PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 1405011-1 1992 Genetic variants of salivary alpha-amylase were studied using isoelectric focusing in a pH gradient of 6-8 and silver staining methods. Silver 111-117 amylase alpha 1A Homo sapiens 20-42 31492693-9 2019 The results from this study demonstrated that lapatinib O-debenzylation and quinone imine-GSH conjugate formation were highly correlated with hepatic CYP3A activity, as measured by midazolam 1"-hydroxylation. Glutathione 90-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 31492693-9 2019 The results from this study demonstrated that lapatinib O-debenzylation and quinone imine-GSH conjugate formation were highly correlated with hepatic CYP3A activity, as measured by midazolam 1"-hydroxylation. Midazolam 181-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 31492693-10 2019 CYP3A4 played a dominant role in lapatinib bioactivation in all liver tissues evaluated. Lapatinib 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 31492693-13 2019 These findings indicate that individual CYP3A activity, not CYP3A5 genotype alone, is a key determinant of lapatinib bioactivation and likely influences exposure to reactive metabolites. Lapatinib 107-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 31492693-14 2019 SIGNIFICANCE STATEMENT: This study is the first to examine the effect of CYP3A5 genotype, total CYP3A activity, and CYP3A5-selective activity on lapatinib bioactivation in individual human liver tissues. Lapatinib 145-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 31492693-15 2019 The results of this investigation indicate that lapatinib bioactivation via oxidative O-debenzylation is highly correlated with total hepatic CYP3A activity, and not CYP3A5 genotype alone. Lapatinib 48-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-147 31492693-16 2019 These findings provide insight into the individual factors, namely, CYP3A activity, that may affect individual exposure to reactive, potentially toxic metabolites of lapatinib. Lapatinib 166-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 31392364-0 2019 Siponimod pharmacokinetics, safety, and tolerability in combination with the potent CYP3A4 inhibitor itraconazole in healthy subjects with different CYP2C9 genotypes. siponimod 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 31625159-5 2019 METHODS: We examined whether CBD inhibits human CYP3A4 and CYP2C19 mediated metabolism of clobazam and N-desmethylclobazam (N-CLB), respectively, and performed studies assessing the effects of CBD on brain and plasma pharmacokinetics of clobazam in mice. Cannabidiol 29-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 31625159-5 2019 METHODS: We examined whether CBD inhibits human CYP3A4 and CYP2C19 mediated metabolism of clobazam and N-desmethylclobazam (N-CLB), respectively, and performed studies assessing the effects of CBD on brain and plasma pharmacokinetics of clobazam in mice. N-desmethylclobazam 103-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 31392364-0 2019 Siponimod pharmacokinetics, safety, and tolerability in combination with the potent CYP3A4 inhibitor itraconazole in healthy subjects with different CYP2C9 genotypes. Itraconazole 101-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 31401678-1 2019 PURPOSE: The purpose of this study was to investigate the potential impact of CYP3A4, CYP3A5, and CYP3A7 polymorphisms on the concentration and efficacy of tacrolimus in a cohort of pediatric patients with nephrotic range proteinuria. Tacrolimus 156-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 31773688-9 2019 CYP3A4*1G polymorphism related to postoperative VAS score, medication dosage and prevalence of adverse reactions in sufentanil group (p<0.05), while it didn"t with those of oxycodone group (p>0.05). Sufentanil 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 31702381-2 2019 Methodology & results: A dual function probe isobutyryl-11-keto-beta-boswellic acid (IKBA) was developed; it possessed a high selectivity toward CYP3A5 and CYP3A enzymes for its two individual metabolites, respectively. 11-keto-boswellic acid 89-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-154 31702381-4 2019 Finally, IKBA was successfully used for the evaluation of the activity of CYP3A5 and CYP3A enzymes in various bio samples. 11-keto-boswellic acid 9-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-79 30953752-8 2019 CYP3A4 and CYP3A5 were identified as the major enzymes responsible for biotransformation of CCT241736 in human, exclusively forming five out of seven metabolites. CCT241736 92-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 31090092-1 2019 5-Hydroxymethyl tolterodine (5-HMT; the active fesoterodine metabolite) is metabolized via the cytochrome P450 (CYP) 2D6 and CYP3A pathways. 5-hydroxymethyl tolterodine 0-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-130 31090092-4 2019 Models predicted and verified mirabegron and desipramine (CYP2D6 substrate) and 5-HMT and ketoconazole (strong CYP3A inhibitor) DDIs. Ketoconazole 90-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-116 31720444-7 2019 Six phytochemicals (Geranin, Apigenin, Fisetin, Luteolin, Phthalic acid and Gallic acid) were predicted to be inhibitors of CYP3A4 and, may slowdown elimination of PIs thereby maintain optimal PIs concentrations. geranin A 20-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 31720444-7 2019 Six phytochemicals (Geranin, Apigenin, Fisetin, Luteolin, Phthalic acid and Gallic acid) were predicted to be inhibitors of CYP3A4 and, may slowdown elimination of PIs thereby maintain optimal PIs concentrations. Apigenin 29-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 31720444-7 2019 Six phytochemicals (Geranin, Apigenin, Fisetin, Luteolin, Phthalic acid and Gallic acid) were predicted to be inhibitors of CYP3A4 and, may slowdown elimination of PIs thereby maintain optimal PIs concentrations. fisetin 39-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 31720444-7 2019 Six phytochemicals (Geranin, Apigenin, Fisetin, Luteolin, Phthalic acid and Gallic acid) were predicted to be inhibitors of CYP3A4 and, may slowdown elimination of PIs thereby maintain optimal PIs concentrations. Luteolin 48-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 31720444-7 2019 Six phytochemicals (Geranin, Apigenin, Fisetin, Luteolin, Phthalic acid and Gallic acid) were predicted to be inhibitors of CYP3A4 and, may slowdown elimination of PIs thereby maintain optimal PIs concentrations. Phthalic Acids 58-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 31720444-7 2019 Six phytochemicals (Geranin, Apigenin, Fisetin, Luteolin, Phthalic acid and Gallic acid) were predicted to be inhibitors of CYP3A4 and, may slowdown elimination of PIs thereby maintain optimal PIs concentrations. Gallic Acid 76-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 31090092-7 2019 5-HMT fractional clearance by CYP3A and CYP2D6 was verified from clinical DDI studies with a potent CYP3A4 inhibitor (ketoconazole) and inducer (rifampicin) in CYP2D6 extensive and poor metabolizers and with a moderate CYP3A inhibitor (fluconazole) in healthy volunteers. Ketoconazole 118-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-35 31090092-1 2019 5-Hydroxymethyl tolterodine (5-HMT; the active fesoterodine metabolite) is metabolized via the cytochrome P450 (CYP) 2D6 and CYP3A pathways. 5-hydroxymethyl tolterodine 29-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-130 31090092-7 2019 5-HMT fractional clearance by CYP3A and CYP2D6 was verified from clinical DDI studies with a potent CYP3A4 inhibitor (ketoconazole) and inducer (rifampicin) in CYP2D6 extensive and poor metabolizers and with a moderate CYP3A inhibitor (fluconazole) in healthy volunteers. Ketoconazole 118-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 31090092-7 2019 5-HMT fractional clearance by CYP3A and CYP2D6 was verified from clinical DDI studies with a potent CYP3A4 inhibitor (ketoconazole) and inducer (rifampicin) in CYP2D6 extensive and poor metabolizers and with a moderate CYP3A inhibitor (fluconazole) in healthy volunteers. Ketoconazole 118-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 31090092-7 2019 5-HMT fractional clearance by CYP3A and CYP2D6 was verified from clinical DDI studies with a potent CYP3A4 inhibitor (ketoconazole) and inducer (rifampicin) in CYP2D6 extensive and poor metabolizers and with a moderate CYP3A inhibitor (fluconazole) in healthy volunteers. Rifampin 145-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-35 31090092-7 2019 5-HMT fractional clearance by CYP3A and CYP2D6 was verified from clinical DDI studies with a potent CYP3A4 inhibitor (ketoconazole) and inducer (rifampicin) in CYP2D6 extensive and poor metabolizers and with a moderate CYP3A inhibitor (fluconazole) in healthy volunteers. Fluconazole 236-247 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-35 31090092-7 2019 5-HMT fractional clearance by CYP3A and CYP2D6 was verified from clinical DDI studies with a potent CYP3A4 inhibitor (ketoconazole) and inducer (rifampicin) in CYP2D6 extensive and poor metabolizers and with a moderate CYP3A inhibitor (fluconazole) in healthy volunteers. Fluconazole 236-247 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 31090092-1 2019 5-Hydroxymethyl tolterodine (5-HMT; the active fesoterodine metabolite) is metabolized via the cytochrome P450 (CYP) 2D6 and CYP3A pathways. fesoterodine 47-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-130 31455676-11 2019 Expression of CYP3A4 and metabolism of triazolam, a typical CYP3A substrate, in the liver of CYP3A/PXR-humanized mice were enhanced in response to rifampicin, a typical human PXR activator. Rifampin 147-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 31441067-0 2019 Functional characterization of 27 CYP3A4 variants on macitentan metabolism in vitro. macitentan 53-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 31441067-4 2019 The aim of this study was to investigate the catalytic characteristics of 27 CYP3A4 protein variants on the metabolism of macitentan in vitro. macitentan 122-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 31441067-10 2019 CONCLUSION: Twenty-seven CYP3A4 protein variants displayed different catalytic characteristics towards macitentan in vitro, especially CYP3A4.5, .17, .20, .23. macitentan 103-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 31441067-10 2019 CONCLUSION: Twenty-seven CYP3A4 protein variants displayed different catalytic characteristics towards macitentan in vitro, especially CYP3A4.5, .17, .20, .23. macitentan 103-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 31455676-4 2019 Oral administration of the human PXR activator rifampicin increased hepatic expression of CYP3A4 mRNA and triazolam (TRZ) 1"- and 4-hydroxylation activities, CYP3A probe activities, in the liver and intestine microsomes of hCYP3A-MAC/hPXR mice. Rifampin 47-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 31455676-4 2019 Oral administration of the human PXR activator rifampicin increased hepatic expression of CYP3A4 mRNA and triazolam (TRZ) 1"- and 4-hydroxylation activities, CYP3A probe activities, in the liver and intestine microsomes of hCYP3A-MAC/hPXR mice. Rifampin 47-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 31455676-4 2019 Oral administration of the human PXR activator rifampicin increased hepatic expression of CYP3A4 mRNA and triazolam (TRZ) 1"- and 4-hydroxylation activities, CYP3A probe activities, in the liver and intestine microsomes of hCYP3A-MAC/hPXR mice. Rifampin 47-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 223-229 31676845-6 2019 In this study, we show that dinaciclib, a potent cyclin dependent kinase inhibitor, significantly increases the basal CYP3A4 and PXR levels in 24 hours. dinaciclib 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 31455676-5 2019 The plasma concentration of TRZ after oral dosing was significantly decreased by rifampicin treatment in hCYP3A-MAC/hPXR mice but not in hCYP3A-MAC mice. Triazolam 28-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 31455676-5 2019 The plasma concentration of TRZ after oral dosing was significantly decreased by rifampicin treatment in hCYP3A-MAC/hPXR mice but not in hCYP3A-MAC mice. Rifampin 81-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 31455676-6 2019 In addition, mass spectrometry imaging analysis showed that rifampicin treatment increased the formation of hydroxy TRZ in the intestine of hCYP3A-MAC/hPXR mice after oral dosing of TRZ. Rifampin 60-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 31455676-6 2019 In addition, mass spectrometry imaging analysis showed that rifampicin treatment increased the formation of hydroxy TRZ in the intestine of hCYP3A-MAC/hPXR mice after oral dosing of TRZ. hydroxide ion 108-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 31455676-6 2019 In addition, mass spectrometry imaging analysis showed that rifampicin treatment increased the formation of hydroxy TRZ in the intestine of hCYP3A-MAC/hPXR mice after oral dosing of TRZ. Triazolam 116-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 31455676-6 2019 In addition, mass spectrometry imaging analysis showed that rifampicin treatment increased the formation of hydroxy TRZ in the intestine of hCYP3A-MAC/hPXR mice after oral dosing of TRZ. Triazolam 182-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 31455676-7 2019 The plasma concentration of 1"- and 4-hydroxy TRZ in portal blood was also increased by rifampicin treatment in hCYP3A-MAC/hPXR mice. 1"- and 4-hydroxy trz 28-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 31455676-7 2019 The plasma concentration of 1"- and 4-hydroxy TRZ in portal blood was also increased by rifampicin treatment in hCYP3A-MAC/hPXR mice. Rifampin 88-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 31455676-11 2019 Expression of CYP3A4 and metabolism of triazolam, a typical CYP3A substrate, in the liver of CYP3A/PXR-humanized mice were enhanced in response to rifampicin, a typical human PXR activator. Triazolam 39-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 30489204-13 2019 In addition, recombinant enzyme incubation experiments demonstrated that CYP3A4 was the predominant P450 responsible for the metabolism of silymarin. Silymarin 139-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 30557096-7 2019 The results indicated that catalpol could inhibit the activity of CYP3A4, CYP2E1 and CYP2C9, with IC50 values of 14.27, 22.4 and 14.69 muM, respectively, but those other CYP isoforms were not affected. catalpol 27-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 31676845-7 2019 We also demonstrated that matured Huh7s can be used for drug induction studies, where CYP3A4, CYP1A2, CYP2C9, and CYP2C19 inductions were achieved following rifampicin treatment. Rifampin 157-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 31731555-0 2019 Interactions of 7,8-Dihydroxyflavone with Serum Albumin as well as with CYP2C9, CYP2C19, CYP3A4, and Xanthine Oxidase Biotransformation Enzymes. 6,7-dihydroxyflavone 16-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 31731555-4 2019 Furthermore, the inhibitory effects of DHF on cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) and xanthine oxidase (XO) enzymes were also tested using in vitro models. 6,7-dihydroxyflavone 39-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 31408697-6 2019 Eplerenone"s primary metabolite, 6 beta-hydroxyeplerenone is formed preferentially via CYP3A4, however, the relative contribution of CYP3A5 to the 21-hydroxyeplerenone metabolite formation is unknown. 6 beta-hydroxyeplerenone 33-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 31647836-10 2019 Based on the reduced exposure of maraviroc observed in this study, increasing the dose of maraviroc may be studied to normalize its moderately reduced exposure following rifabutin co-administration, a moderate inducer of CYP3A4. maraviroc 90-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 221-227 31647836-10 2019 Based on the reduced exposure of maraviroc observed in this study, increasing the dose of maraviroc may be studied to normalize its moderately reduced exposure following rifabutin co-administration, a moderate inducer of CYP3A4. Rifabutin 170-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 221-227 31515991-3 2019 Auriculasin inhibited UGT1A6, UGT1A8, UGT1A10, UGT2B7, CYP2C9, and CYP3A4 strongly at a concentration of 100 muM. auriculasin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 31640597-11 2019 Rhabdomyolysis was most likely induced by toxic plasma concentrations of Simvastatin due to Palbociclibs inhibition of the CYP3A4 enzyme in combination with a decreased hepatic uptake of Simvastatin due to single nucleotide polymorphism rs4149056. Simvastatin 73-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 31408697-0 2019 The relative role of CYP3A4 and CYP3A5 in eplerenone metabolism. Eplerenone 42-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 31408697-5 2019 Eplerenone, an aldosterone antagonist, is also metabolized by CYP3A enzymes, and it has the potential to be an excellent substrate probe for CYP3A4/5. Eplerenone 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 31408697-5 2019 Eplerenone, an aldosterone antagonist, is also metabolized by CYP3A enzymes, and it has the potential to be an excellent substrate probe for CYP3A4/5. Eplerenone 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 31408697-6 2019 Eplerenone"s primary metabolite, 6 beta-hydroxyeplerenone is formed preferentially via CYP3A4, however, the relative contribution of CYP3A5 to the 21-hydroxyeplerenone metabolite formation is unknown. Eplerenone 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 31408697-7 2019 Through in-vitro microsomal incubations with recombinant CYP3A4 and CYP3A5 enzymes, we identified their relative contributions to 21-hydroxyeplerenone metabolism. 21-Hydroxyeplerenone 130-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 31408697-9 2019 Based on these findings, eplerenone has the potential to serve as an in-vivo substrate probe for CYP3A4 by monitoring 6-beta-hydroxy metabolite formation as well as CYP3A4/5 by monitoring 21-hydroxy metabolite formation. Eplerenone 25-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 31603853-4 2019 The aim of this study was to investigate the effects of two biologically active compounds: 2-aminoethane-sulfonic acid (taurine) and 3-hydroxy-4-trimethylaminobutyrate (L-carnitine) on urinary 6beta-hydroxycortisol/cortisol (6beta-OHC/cortisol) metabolic ratio as a biomarker of the CYP3A4 activity of healthy volunteers. 2-aminoethane-sulfonic acid 91-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 283-289 31608899-6 2019 RESULTS The most key anti-CRC targets of FN were identified as tumor protein p53 (TP53), cytochrome P450 3A4 (CYP3A4), ATP binding cassette subfamily G member 2 (ABCG2), tumor necrosis factor (TNF), epidermal growth factor receptor (EGFR), Erb-B2 receptor tyrosine kinase 2 (ERBB2), and cytochrome P450 1A1 (CYP1A1). formononetin 41-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-108 31608899-6 2019 RESULTS The most key anti-CRC targets of FN were identified as tumor protein p53 (TP53), cytochrome P450 3A4 (CYP3A4), ATP binding cassette subfamily G member 2 (ABCG2), tumor necrosis factor (TNF), epidermal growth factor receptor (EGFR), Erb-B2 receptor tyrosine kinase 2 (ERBB2), and cytochrome P450 1A1 (CYP1A1). formononetin 41-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 31603853-4 2019 The aim of this study was to investigate the effects of two biologically active compounds: 2-aminoethane-sulfonic acid (taurine) and 3-hydroxy-4-trimethylaminobutyrate (L-carnitine) on urinary 6beta-hydroxycortisol/cortisol (6beta-OHC/cortisol) metabolic ratio as a biomarker of the CYP3A4 activity of healthy volunteers. Taurine 120-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 283-289 31603853-4 2019 The aim of this study was to investigate the effects of two biologically active compounds: 2-aminoethane-sulfonic acid (taurine) and 3-hydroxy-4-trimethylaminobutyrate (L-carnitine) on urinary 6beta-hydroxycortisol/cortisol (6beta-OHC/cortisol) metabolic ratio as a biomarker of the CYP3A4 activity of healthy volunteers. 3-hydroxy-4-trimethylaminobutyrate 133-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 283-289 31603853-4 2019 The aim of this study was to investigate the effects of two biologically active compounds: 2-aminoethane-sulfonic acid (taurine) and 3-hydroxy-4-trimethylaminobutyrate (L-carnitine) on urinary 6beta-hydroxycortisol/cortisol (6beta-OHC/cortisol) metabolic ratio as a biomarker of the CYP3A4 activity of healthy volunteers. Carnitine 169-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 283-289 31603853-7 2019 The quantification of the 6beta-OHC/cortisol metabolic ratio as a biomarker of CYP3A4 activity in human urine was used for the assessment of CYP3A4 catalytic activity as a non-invasive test. 6beta-ohc 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 31603853-7 2019 The quantification of the 6beta-OHC/cortisol metabolic ratio as a biomarker of CYP3A4 activity in human urine was used for the assessment of CYP3A4 catalytic activity as a non-invasive test. Hydrocortisone 36-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 31603853-13 2019 Results The ratio of 6-6beta-OHC/cortisol was used as a biomarker to study the taurine and L-carnitine influence on CYP3A4 metabolism of cortisol. Taurine 79-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 31603853-13 2019 Results The ratio of 6-6beta-OHC/cortisol was used as a biomarker to study the taurine and L-carnitine influence on CYP3A4 metabolism of cortisol. Carnitine 91-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 31603853-13 2019 Results The ratio of 6-6beta-OHC/cortisol was used as a biomarker to study the taurine and L-carnitine influence on CYP3A4 metabolism of cortisol. Hydrocortisone 137-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 31603853-15 2019 Seven days after the administration of taurine in a dose of 500 mg twice a day, the 6beta-OCH/cortisol ratio was 3.3 +- 0.2, which indicated the increased catalytic activity of CYP3A4 towards cortisol. Taurine 39-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 31603853-15 2019 Seven days after the administration of taurine in a dose of 500 mg twice a day, the 6beta-OCH/cortisol ratio was 3.3 +- 0.2, which indicated the increased catalytic activity of CYP3A4 towards cortisol. 6beta-och 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 31603853-15 2019 Seven days after the administration of taurine in a dose of 500 mg twice a day, the 6beta-OCH/cortisol ratio was 3.3 +- 0.2, which indicated the increased catalytic activity of CYP3A4 towards cortisol. Hydrocortisone 94-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 31603853-15 2019 Seven days after the administration of taurine in a dose of 500 mg twice a day, the 6beta-OCH/cortisol ratio was 3.3 +- 0.2, which indicated the increased catalytic activity of CYP3A4 towards cortisol. Hydrocortisone 192-200 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 31603853-17 2019 Conclusions The results obtained demonstrated the influence of taurine on 6beta-OCH/cortisol metabolic ratio as a biomarker of CYP3A4 catalytic activity to cortisol. Taurine 63-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 31603853-17 2019 Conclusions The results obtained demonstrated the influence of taurine on 6beta-OCH/cortisol metabolic ratio as a biomarker of CYP3A4 catalytic activity to cortisol. -och 79-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 31603853-17 2019 Conclusions The results obtained demonstrated the influence of taurine on 6beta-OCH/cortisol metabolic ratio as a biomarker of CYP3A4 catalytic activity to cortisol. Hydrocortisone 84-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 31601999-2 2019 The high pharmacokinetic variability of fentanyl is assumed to be due to cytochrome P450 3A-mediated (CYP3A) N-dealkylation to norfentanyl in humans. Fentanyl 40-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 31603853-17 2019 Conclusions The results obtained demonstrated the influence of taurine on 6beta-OCH/cortisol metabolic ratio as a biomarker of CYP3A4 catalytic activity to cortisol. Hydrocortisone 156-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 31601999-2 2019 The high pharmacokinetic variability of fentanyl is assumed to be due to cytochrome P450 3A-mediated (CYP3A) N-dealkylation to norfentanyl in humans. norfentanyl 127-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 31358899-4 2019 The CYP3A induction potential was determined by repeatedly dosing XueShuanTong for 15 days in human subjects and by treating cryopreserved human hepatocytes with circulating ginsenosides; midazolam served as a probe substrate. Ginsenosides 174-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-9 31601999-4 2019 In this small study in palliative cancer patients under real-life clinical conditions, the influence of CYP3A on fentanyl variability was investigated. Fentanyl 113-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-109 31601999-9 2019 Both clearances showed a weak correlation and hence a minimal influence of CYP3A on fentanyl elimination. Fentanyl 84-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 31581123-8 2019 The tuberculostatic drug rifampicin is a CYP3A4 inducer, increasing the metabolism of hydrocortisone. Rifampin 25-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 31581123-8 2019 The tuberculostatic drug rifampicin is a CYP3A4 inducer, increasing the metabolism of hydrocortisone. Hydrocortisone 86-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 31358899-4 2019 The CYP3A induction potential was determined by repeatedly dosing XueShuanTong for 15 days in human subjects and by treating cryopreserved human hepatocytes with circulating ginsenosides; midazolam served as a probe substrate. Midazolam 188-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-9 31058459-4 2019 However, the catalytic characteristics of these 27 CYP3A4 variants on oxidizing regorafenib have not being determined. regorafenib 80-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 31012522-2 2019 CBD is metabolized by cytochrome P450 (CYP)3A4 and CYP2C19 with a growing body of evidence suggesting it is also a potent inhibitor of these pathways. Cannabidiol 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-46 31202736-5 2019 In this study, we showed that treatment with the indirect CAR activator phenobarbital activated transcription of the CYP3A4 gene in three-dimensionally (3D)-cultured HepG2 cells. Phenobarbital 72-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 31202736-7 2019 Moreover, okadaic acid and epidermal growth factor, were found to repress phenobarbital-induced CAR nuclear translocation and subsequent activation of the CYP3A4 gene promoter. Okadaic Acid 10-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 31202736-7 2019 Moreover, okadaic acid and epidermal growth factor, were found to repress phenobarbital-induced CAR nuclear translocation and subsequent activation of the CYP3A4 gene promoter. Phenobarbital 74-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 31295464-9 2019 CYP3A95, which shares 79% sequence homology with human CYP3A4 and CYP2D50 catalyzed the conversion of codeine to norcodeine (Km of 104.1 and 526.9 muM, Vmax of 2.8 and 2.6 pmol/min/pmol P450). Codeine 102-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 31295464-9 2019 CYP3A95, which shares 79% sequence homology with human CYP3A4 and CYP2D50 catalyzed the conversion of codeine to norcodeine (Km of 104.1 and 526.9 muM, Vmax of 2.8 and 2.6 pmol/min/pmol P450). norcodeine 113-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 31058419-2 2019 Amlodipine is mainly metabolized by cytochrome P450 (CYP) 3A4, whereas losartan is metabolized by CYP2C9 and CYP3A4. Amlodipine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-61 31058459-5 2019 The purpose of this study was to investigate the catalytic characteristics of 27 CYP3A4 protein variants on the oxidative metabolism of regorafenib in vitro. regorafenib 136-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 31058419-2 2019 Amlodipine is mainly metabolized by cytochrome P450 (CYP) 3A4, whereas losartan is metabolized by CYP2C9 and CYP3A4. Losartan 71-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 31058459-0 2019 Functional characterization of 27 CYP3A4 protein variants to metabolize regorafenib in vitro. regorafenib 72-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 31058459-6 2019 METHOD: Wild-type CYP3A4.1 or other variants was incubated with 0.5-20 mumol/L regorafenib for 30 minutes. regorafenib 79-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 31058459-1 2019 AIM: Regorafenib is a tyrosine kinase inhibitor that is mainly metabolized by CYP3A4. regorafenib 5-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 31058459-9 2019 CONCLUSION: This study is the first to investigate the function of 27 CYP3A4 protein variants on the metabolism of regorafenib in vitro, and it may provide some valuable information for further research in clinic. regorafenib 115-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 31058459-2 2019 The genetic polymorphism of CYP3A4 would contribute to differences in metabolism of regorafenib. regorafenib 84-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 31269280-11 2019 Hence, a [14 C]midazolam microdosing approach may be used as an alternative to a therapeutic dose of midazolam to study developmental changes in hepatic CYP3A activity in young children. Midazolam 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-158 31288127-5 2019 The imidazole derivatives were more toxic to mammalian cells and more potently inhibited the activity of CYP3A4, which is one of the main causes of azole toxicity. imidazole 4-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 31222796-2 2019 Because at the commonly used milligram doses (250-750 mg) chlorzoxazone acts as an inhibitor of the CYP3A4/5 marker substrate midazolam, previous attempts failed to combine both drugs in a common phenotyping cocktail. Chlorzoxazone 58-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 31222796-0 2019 Simultaneous phenotyping of CYP2E1 and CYP3A using oral chlorzoxazone and midazolam microdoses. Chlorzoxazone 56-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 31222796-0 2019 Simultaneous phenotyping of CYP2E1 and CYP3A using oral chlorzoxazone and midazolam microdoses. Midazolam 74-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 31520256-7 2019 Drugs interacting with DOACs (P-glycoprotein/CYP3A4) were used by 6460 (20%) of patients. doacs 23-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 31520256-13 2019 Polypharmacy was associated with adverse outcomes and attenuated the advantage in risk of major bleeding among rivaroxaban users, particularly in the presence of P-glycoprotein/CYP3A4-modulating drugs. Rivaroxaban 111-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 30825074-2 2019 Although there are in vitro studies showing that myricetin inhibits human cytochrome P450 (CYP) 2D6 and CYP3A, the inhibitory mechanisms of myricetin on CYP enzymes are still unclear. myricetin 49-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-109 30825074-4 2019 METHODS: This study was performed to investigate the inhibitory effects of myricetin on human CYP3A4, CYP2B6, CYP2C9, CYP2D6 and rat CYP3A2, CYP2B1, CYP2C11, CYP2D1 through the cocktail approach using ultra-performance liquid chromatography tandem mass spectrometry. myricetin 75-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 30825074-9 2019 CONCLUSIONS: In conclusion, this study indicates that myricetin inhibited CYP3A4/3A2, CYP2C9/2C11, CYP2D6/2D1 and CYP2B1 by various mechanisms with different Ki values. myricetin 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-84 30993551-1 2019 BACKGROUND AND OBJECTIVES: A recent report indicated that the pharmacodynamic interaction between clopidogrel and vonoprazan leading to attenuation of the anti-platelet effect of clopidogrel was unlikely to be caused by the inhibition of cytochrome P450 (CYP) 2B6, CYP2C19, or CYP3A4/5 by vonoprazan, based on in vitro CYP inhibition data. Clopidogrel 98-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 277-285 30993551-1 2019 BACKGROUND AND OBJECTIVES: A recent report indicated that the pharmacodynamic interaction between clopidogrel and vonoprazan leading to attenuation of the anti-platelet effect of clopidogrel was unlikely to be caused by the inhibition of cytochrome P450 (CYP) 2B6, CYP2C19, or CYP3A4/5 by vonoprazan, based on in vitro CYP inhibition data. 1-(5-(2-fluorophenyl)-1-(pyridin-3-ylsulfonyl)-1H-pyrrol-3-yl)-N-methylmethanamine 114-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 277-285 30993551-2 2019 The current report investigates another important antiplatelet inhibitor, prasugrel, that is also activated through metabolism by CYP2B6, CYP2C19 and CYP3A4/5, for its CYP-based DDI potential with vonoprazan. Prasugrel Hydrochloride 74-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-158 30993551-2 2019 The current report investigates another important antiplatelet inhibitor, prasugrel, that is also activated through metabolism by CYP2B6, CYP2C19 and CYP3A4/5, for its CYP-based DDI potential with vonoprazan. Didanosine 178-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-158 31288127-5 2019 The imidazole derivatives were more toxic to mammalian cells and more potently inhibited the activity of CYP3A4, which is one of the main causes of azole toxicity. Azoles 8-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 30993551-2 2019 The current report investigates another important antiplatelet inhibitor, prasugrel, that is also activated through metabolism by CYP2B6, CYP2C19 and CYP3A4/5, for its CYP-based DDI potential with vonoprazan. 1-(5-(2-fluorophenyl)-1-(pyridin-3-ylsulfonyl)-1H-pyrrol-3-yl)-N-methylmethanamine 197-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-158 31617197-0 2019 Effect of CYP3A4, CYP3A5, ABCB1 Gene Polymorphisms on Rivaroxaban Pharmacokinetics in Patients Undergoing Total Hip and Knee Replacement Surgery. Rivaroxaban 54-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 31002385-0 2019 Use of 4beta-Hydroxycholesterol Plasma Concentrations as an Endogenous Biomarker of CYP3A Activity: Clinical Validation in Individuals With Type 2 Diabetes. cholest-5-ene-3,4-diol 7-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-89 31002385-4 2019 Activity of CYP3A was lower in the T2D population compared with nondiabetic subjects; this decrease was reflected in 4beta-OHC concentrations (24.33 vs. 12.58 ng/mL; P < 0.0001) and 4beta-OHC ratio (0.13 vs. 0.09 (x 104 ); P < 0.0002). ohc 123-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 31002385-5 2019 These results suggest that 4beta-OHC should be considered as a valid, convenient, and easy to use endogenous biomarker of CYP3A activity in patients. 4beta-ohc 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-127 31617197-4 2019 AIM: Evaluation of CYP3A4, CYP3A5 and ABCB1 gene polymorphisms influence on rivaroxaban pharmacokinetics and prothrombin time dynamics in patients undergoing total hip and knee replacement surgery. Rivaroxaban 76-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 31394259-6 2019 CaCO-2 cell uptake assay and human liver microsome studies proved that ARV is a substrate of CYP3A4 but not of P-gp efflux pump. omega-N-Allylarginine 71-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 31399494-1 2019 Erythromycin is a substrate of cytochrome P4503A4 (CYP3A4) and multiple drug transporters. Erythromycin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-49 31094010-2 2019 Teneligliptin is metabolized by CYP3A4, and glimepiride might be partly metabolized by CYP3A4. glimepiride 44-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 31094010-2 2019 Teneligliptin is metabolized by CYP3A4, and glimepiride might be partly metabolized by CYP3A4. 3-(4-(4-(3-methyl-1-phenyl-1H-pyrazol-5-yl)piperazin-1-yl)pyrrolidin-2-ylcarbonyl)thiazolidine 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 31399494-1 2019 Erythromycin is a substrate of cytochrome P4503A4 (CYP3A4) and multiple drug transporters. Erythromycin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 31399494-12 2019 Maximum velocity of uptake transport, CYP3A4 clearance, total passive diffusion, and others were found to collectively control 14CO2 production rates. 14co2 127-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 31526233-6 2019 On the other hand, treatment of HepaRG cells with RMP resulted in a significant increase in mRNA expression for CYP2B6 (6.68-fold, p = 0.007) and CYP3A4 (111.96-fold, p = 0.001), whereas NR1I3 expression decreased (0.46-fold, p = 0.033). Rifampin 50-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 31421085-6 2019 KEY FINDINGS: At 100 muM, licoricidin strongly inhibited CYP2C9, CYP2C19, CYP3A4, UGT1A3, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT2B4, UGT2B7, UGT2B15, and UGT2B17. licoricidin 26-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 31465819-13 2019 The treatment of hepatocytes from two male human donors with 0.5-25 muM metazachlor or 500 muM NaPB for 4 days resulted in increases in CYP2B6 and CYP3A4 mRNA levels but had no effect on hepatocyte RDS. metazachlor 72-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 31588879-0 2019 Impact of CYP3A4/5 and ABCB1 polymorphisms on tacrolimus exposure and response in pediatric primary nephrotic syndrome. Tacrolimus 46-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-18 31588879-1 2019 Aim: To evaluate the impact of CYP3A4*1G, CYP3A5*3 and ABCB1-C3435T polymorphisms on tacrolimus concentrations, efficacy and tolerance in pediatric primary nephrotic syndrome. Tacrolimus 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 31588879-6 2019 Conclusion: The genotypes of CYP3A4*1G and CYP3A5*3 rather than ABCB1-C3435T potentially predicted tacrolimus exposure and clinical response in pediatric primary nephrotic syndrome. Tacrolimus 99-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 31108125-9 2019 Testosterone 2beta-hydroxylation was diminished in CYP3A94217Asn and CYP3A95392Thr. Testosterone 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 31108125-9 2019 Testosterone 2beta-hydroxylation was diminished in CYP3A94217Asn and CYP3A95392Thr. Testosterone 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 31108125-10 2019 Ketoconazole inhibited 2beta-hydroxylation differently in the five variants with the most pronounced inhibition obtained for CYP3A95392Thr. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-130 31611799-3 2019 Currently, phenotyping studies for CYP3A involve the administration of midazolam and collection of timed blood samples up to 24-48 hours in order to determine an area under the plasma concentration time curve (AUC). Midazolam 71-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-40 29676195-7 2019 The results indicate that sophocarpine could inhibit the activity of CYP3A4 and 2C9, with the IC50 values of 12.22 and 15.96 muM, respectively, but that other CYP isoforms were not affected. sophocarpine 26-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-83 29676195-8 2019 Enzyme kinetic studies showed that sophocarpine is not only a noncompetitive inhibitor of CYP3A4 but also a competitive inhibitor of CYP2C9, with Ki values of 6.74 and 9.19 muM, respectively. sophocarpine 35-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 29676195-9 2019 Also, sophocarpine is a time-dependent inhibitor of CYP3A4 with Kinact/KI value of 0.082/21.54 muM-1 min-1. sophocarpine 6-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 29676195-11 2019 The in vitro studies of sophocarpine with CYP isoforms suggested that sophocarpine has the potential to cause pharmacokinetic drug interactions with other co-administered drugs metabolized by CYP3A4 and 2C9. sophocarpine 24-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-206 29676195-11 2019 The in vitro studies of sophocarpine with CYP isoforms suggested that sophocarpine has the potential to cause pharmacokinetic drug interactions with other co-administered drugs metabolized by CYP3A4 and 2C9. sophocarpine 70-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-206 31569378-4 2019 Validation of RGs was performed by an expression analysis of CYP3A4 and CYP1A2 on rifampicin and beta-naphthoflavone induction, respectively. Rifampin 82-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 31569378-4 2019 Validation of RGs was performed by an expression analysis of CYP3A4 and CYP1A2 on rifampicin and beta-naphthoflavone induction, respectively. beta-Naphthoflavone 97-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 31611799-4 2019 The key challenge that limits the use of midazolam-based phenotyping for CYP3A in academic research settings and preclude the use of this approach in a clinical setting is the logistical burden of collecting frequent blood samples for up to 48 h post dose following the administration of a probe drug +- an interacting drug. Midazolam 41-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 31611799-9 2019 Conclusion: On this basis, it is proposed that a 3-h assessment of midazolam AUC (AUC0-3) represents a viable strategy to reduce the logistical burden associated with the assessment of CYP3A phenotype. Midazolam 67-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-190 31456404-5 2019 These methods were applied to a soluble N-terminally truncated CYP3A4 form, and the results show that there are few changes in the average structure upon binding ketoconazole, ritonavir, or midazolam. Ketoconazole 162-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 31616470-0 2019 The Impact of CYP3A4*22 on Tacrolimus Pharmacokinetics and Outcome in Clinical Practice at a Single Kidney Transplant Center. Tacrolimus 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 31616470-1 2019 Background: Although there is evidence that the CYP3A4*22 variant should be considered in tacrolimus dosing in renal transplantation, its impact beyond tacrolimus dose requirements remains controversial. Tacrolimus 90-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 31616470-12 2019 Conclusion: At our transplantation center, both CYP3A5*3 and, to a lesser extent, CYP3A4*22 affect tacrolimus pharmacokinetics early after onset of therapy with consequences for steady-state treatment in routine clinical practice. Tacrolimus 99-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 30488748-8 2019 Time dependent CYP3A4/5 inhibition was noted for testosterone and midazolam with IC50 shift of 10.9- and 39.9-fold, respectively. Testosterone 49-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 30488748-8 2019 Time dependent CYP3A4/5 inhibition was noted for testosterone and midazolam with IC50 shift of 10.9- and 39.9-fold, respectively. Midazolam 66-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 30488748-9 2019 With midazolam, the kinact and KI values of ZYTP1 were 0.075 min-1 and 4.47 microM for the CYP3A4/5 time dependent inhibition, respectively. Midazolam 5-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 31456404-5 2019 These methods were applied to a soluble N-terminally truncated CYP3A4 form, and the results show that there are few changes in the average structure upon binding ketoconazole, ritonavir, or midazolam. Ritonavir 176-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 31456404-5 2019 These methods were applied to a soluble N-terminally truncated CYP3A4 form, and the results show that there are few changes in the average structure upon binding ketoconazole, ritonavir, or midazolam. Midazolam 190-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 31527544-4 2019 In a previous study, we reported that CYP3A4 is primarily responsible for the formation of OH-LOX in human liver microsomes. oh-lox 91-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 31414593-0 2019 Tofacitinib Is a Mechanism-Based Inactivator of Cytochrome P450 3A4. tofacitinib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-67 31414593-2 2019 TFT was found to show concentration-, time-, and NADPH-dependent inhibition of CYP3A4, and irreversibility of the inactivation was also observed. NADP 49-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 31414593-6 2019 Furthermore, ketoconazole attenuated TFT-mediated CYP3A4 inactivation. Ketoconazole 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 31414593-9 2019 Multiple P450 enzymes, including CYPs2C19, 3A4, 2D6, and 1A2, participated in the metabolism of TFT to the epoxide, while the formation of the aldehyde was mainly catalyzed by CYP3A4. Aldehydes 143-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 31540101-6 2019 In the reporter gene assays, all sesquiterpenes significantly induced cytochrome P450 3A4 expression via pregnane X receptor interaction. Sesquiterpenes 33-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-89 31527544-5 2019 Although metabolism by CYP3A4 does not produce active metabolites, it can affect the conversion of LOX into trans-/cis-LOX, since CYP3A4 activity modulates the substrate LOX concentration. loxoprofen 99-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 31527544-5 2019 Although metabolism by CYP3A4 does not produce active metabolites, it can affect the conversion of LOX into trans-/cis-LOX, since CYP3A4 activity modulates the substrate LOX concentration. loxoprofen 99-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 31527544-5 2019 Although metabolism by CYP3A4 does not produce active metabolites, it can affect the conversion of LOX into trans-/cis-LOX, since CYP3A4 activity modulates the substrate LOX concentration. trans-/cis-lox 108-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 31527544-5 2019 Although metabolism by CYP3A4 does not produce active metabolites, it can affect the conversion of LOX into trans-/cis-LOX, since CYP3A4 activity modulates the substrate LOX concentration. trans-/cis-lox 108-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 31527544-9 2019 Specifically, DEX significantly decreased the concentration of the LOX active metabolite formed by CR, which corresponded to an increased concentration of OH-LOX formed by CYP3A4. Dexamethasone 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 31527544-9 2019 Specifically, DEX significantly decreased the concentration of the LOX active metabolite formed by CR, which corresponded to an increased concentration of OH-LOX formed by CYP3A4. loxoprofen 67-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 31527544-9 2019 Specifically, DEX significantly decreased the concentration of the LOX active metabolite formed by CR, which corresponded to an increased concentration of OH-LOX formed by CYP3A4. oh-lox 155-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 31099107-3 2019 13-O-Demethyl tacrolimus (13-O-DMT) was reported as the major metabolite formed by cytochrome P450 (CYP)3A such as CYP3A5. 13-O-demethyl tacrolimus 0-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-106 31099107-3 2019 13-O-Demethyl tacrolimus (13-O-DMT) was reported as the major metabolite formed by cytochrome P450 (CYP)3A such as CYP3A5. 13-O-demethyl tacrolimus 26-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-106 31173645-0 2019 Effects of CYP3A inhibitors on the pharmacokinetics of quizartinib, a potent and selective FLT3 inhibitor, and its active metabolite. quizartinib 55-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-16 31173645-11 2019 CONCLUSIONS: These results suggest reducing the dose of quizartinib when coadministered with a strong CYP3A inhibitor, but not with a moderate or weak CYP3A inhibitor. quizartinib 56-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 31236938-6 2019 KEY RESULTS: CYP2E1 activity was markedly up-regulated in cancer (6-hydroxychlorzoxazone/chlorzoxazone ratio of 1.30 vs. 2.75), while CYP3A phenotypic activity was repressed in cancer (omeprazole sulfone/omeprazole ratio of 0.23 vs. 0.49). omeprazole sulfone 185-203 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-139 31236938-6 2019 KEY RESULTS: CYP2E1 activity was markedly up-regulated in cancer (6-hydroxychlorzoxazone/chlorzoxazone ratio of 1.30 vs. 2.75), while CYP3A phenotypic activity was repressed in cancer (omeprazole sulfone/omeprazole ratio of 0.23 vs. 0.49). Omeprazole 185-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-139 31309254-0 2019 Cytochrome P450 3A4, 3A5, and 2C8 expression in breast, prostate, lung, endometrial, and ovarian tumors: relevance for resistance to taxanes. Taxoids 133-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 31299239-6 2019 In vitro, axitinib inhibited loperamide metabolism with the IC50 of 18.34 muM for RLM, 1.705 muM for HLM and 1.604 muM for CYP3A4*1, and it was confirmed as a non-competitive inhibitor in all enzymes. Axitinib 10-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 31299239-6 2019 In vitro, axitinib inhibited loperamide metabolism with the IC50 of 18.34 muM for RLM, 1.705 muM for HLM and 1.604 muM for CYP3A4*1, and it was confirmed as a non-competitive inhibitor in all enzymes. Loperamide 29-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 30786012-4 2019 Plasma concentrations of endoxifen were significantly associated with CYP2D6 diplotype (P < 0.0001), CYP3A4*22 genotype (P = 0.0003), and concomitant intake of potent CYP2D6 inhibitors (P < 0.001). 4-hydroxy-N-desmethyltamoxifen 25-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 30786012-6 2019 Finally, the multivariable regression analysis showed that formation of tamoxifen metabolites was independently impacted by CYP2D6 diplotype and CYP3A4*22, CYP2C19*2, and CYP2B6*6 genetic polymorphisms. Tamoxifen 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 30828771-2 2019 To evaluate drug-drug interactions, the impact of ketoconazole, a known strong inhibitor of cytochrome P450 3A4 and P-glycoprotein, was studied. Ketoconazole 50-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-111 31215774-1 2019 Regulatory agencies currently recommend itraconazole (ITZ) as a strong cytochrome P450 3A (CYP3A) inhibitor for clinical drug-drug interaction (DDI) studies. Itraconazole 40-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-89 31215774-1 2019 Regulatory agencies currently recommend itraconazole (ITZ) as a strong cytochrome P450 3A (CYP3A) inhibitor for clinical drug-drug interaction (DDI) studies. Itraconazole 40-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-96 31215774-1 2019 Regulatory agencies currently recommend itraconazole (ITZ) as a strong cytochrome P450 3A (CYP3A) inhibitor for clinical drug-drug interaction (DDI) studies. Itraconazole 54-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-89 31215774-1 2019 Regulatory agencies currently recommend itraconazole (ITZ) as a strong cytochrome P450 3A (CYP3A) inhibitor for clinical drug-drug interaction (DDI) studies. Itraconazole 54-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-96 31250974-1 2019 The drug-drug interaction profile of atorvastatin confirms that disposition is determined by cytochrome P450 (CYP) 3A4 and organic anion transporting polypeptides (OATPs). Atorvastatin 37-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-118 31123759-3 2019 The purpose of this study was to evaluate the potential for a caffeine metabolic ratio to describe variability in CYP3A activity. Caffeine 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 31123759-4 2019 METHODS: The metabolic ratio 1,3,7-trimethyluric acid (TMU) to caffeine was evaluated as a biomarker to describe variability in CYP3A activity in a cohort (n = 28) of healthy 21 to 35-year-old males. Caffeine 63-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-133 31123759-9 2019 CONCLUSION: BSV in CYP3A activity was well described by caffeine/TMU ratios pre- and post-induction. Caffeine 56-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-24 31123759-9 2019 CONCLUSION: BSV in CYP3A activity was well described by caffeine/TMU ratios pre- and post-induction. 1,3,7-trimethyluric acid 65-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-24 31301485-8 2019 Besides absorption, intestinal wall metabolism of testosterone (CYP3A4) was determined by showing a linear formation (R2 = 0.99; up to 165 min) of the main metabolites androstenedione and 6Beta-hydroxytestosterone, indicating no loss of metabolic capacity of the intestinal tissue within the system. Testosterone 50-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 31301485-8 2019 Besides absorption, intestinal wall metabolism of testosterone (CYP3A4) was determined by showing a linear formation (R2 = 0.99; up to 165 min) of the main metabolites androstenedione and 6Beta-hydroxytestosterone, indicating no loss of metabolic capacity of the intestinal tissue within the system. Androstenedione 168-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 31301485-8 2019 Besides absorption, intestinal wall metabolism of testosterone (CYP3A4) was determined by showing a linear formation (R2 = 0.99; up to 165 min) of the main metabolites androstenedione and 6Beta-hydroxytestosterone, indicating no loss of metabolic capacity of the intestinal tissue within the system. 6 beta-hydroxytestosterone 188-213 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 31306750-4 2019 Acalabrutinib is a substrate of PgP and CYP3A4, with a significant fraction of drug metabolized by first pass gut extraction and 25% absolute bioavailability. acalabrutinib 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 31306750-12 2019 The model can then distinguish the interplay between dissolution and first pass extraction and how in vivo stomach pH, saturation of gut PgP, and saturation or inhibition of gut CYP3A4, will impact the pharmacokinetics of acalabrutinib. acalabrutinib 222-235 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 31119768-0 2019 CYP3A4/5 mediates the metabolic detoxification of humantenmine, a highly toxic alkaloid from Gelsemium elegans Benth. humantenmine 50-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 31119768-9 2019 A CYP3A4/5 activity inhibition model was established by intraperitoneally injecting ketoconazole in mice and used to evaluate the role of CYP3A4/5 in HMT detoxification. Ketoconazole 84-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 2-8 31116446-3 2019 Cytochrome P-450 (CYP)2C8, CYP3A, and P-glycoprotein inhibitors can increase the plasma and central nervous system concentrations and radically alter the risk profile of loperamide. Loperamide 170-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 31343441-9 2019 In concordance with previous results, besides CYP1A2, a possible induction of CYP2C19 and CYP3A4 by tobacco smoke, resulting in lower serum concentrations of escitalopram in smokers than in nonsmokers, is suggested. Citalopram 158-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 31433338-8 2019 CYP3A4/5/7 is potentially inhibited by CBD. Cannabidiol 39-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 31270214-4 2019 Increased luciferase activity of a reporter plasmid containing the CYP3A4 promoter region by phenobarbital was augmented by transfection of siRNA for ADAR1 (siADAR1) but not by siADAR2. Phenobarbital 93-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 31270214-5 2019 In addition, the knockdown of ADAR1 resulted in the enhanced induction of CYP2B6 and CYP3A4 mRNA by 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime and phenobarbital, respectively. 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde 100-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 31270214-5 2019 In addition, the knockdown of ADAR1 resulted in the enhanced induction of CYP2B6 and CYP3A4 mRNA by 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime and phenobarbital, respectively. o-(3,4-dichlorobenzyl)oxime 161-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 31270214-5 2019 In addition, the knockdown of ADAR1 resulted in the enhanced induction of CYP2B6 and CYP3A4 mRNA by 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime and phenobarbital, respectively. Phenobarbital 193-206 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 31656654-0 2019 Effect of rifampicin and clarithromycin on the CYP3A activity in patients with Mycobacterium avium complex. Rifampin 10-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 31656654-0 2019 Effect of rifampicin and clarithromycin on the CYP3A activity in patients with Mycobacterium avium complex. Clarithromycin 25-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 31656654-6 2019 Before and after 7-day administration of rifampicin and clarithromycin, the pharmacokinetics of midazolam, a CYP3A-specific probe, were analyzed. Midazolam 96-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-114 31656654-12 2019 Conclusions: Coadministration of rifampicin and clarithromycin may increase CYP3A enzymatic activity. Rifampin 33-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 31656654-12 2019 Conclusions: Coadministration of rifampicin and clarithromycin may increase CYP3A enzymatic activity. Clarithromycin 48-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 31436536-3 2019 Here, we show that in a human CAR (hCAR)-knockout (KO) HepaRG cell line, PB significantly induces the expression of CYP2B6 and CYP3A4, two shared target genes of hCAR and human PXR (hPXR). Phenobarbital 73-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 31436536-4 2019 In human primary hepatocytes and hCAR-KO HepaRG cells, PB-induced expression of CYP3A4 was markedly repressed by genetic knockdown or pharmacological inhibition of hPXR. Phenobarbital 55-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 31150656-13 2019 Taken together, these results demonstrated that CRA has good absorption in both stomach and small intestine, but it could be metabolized partly due to CYP1A2 and CYP3A4 in vivo. corosolic acid 48-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 31480231-0 2019 Structural Insights into the Interaction of Cytochrome P450 3A4 with Suicide Substrates: Mibefradil, Azamulin and 6",7"-Dihydroxybergamottin. Mibefradil 89-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-63 31480231-0 2019 Structural Insights into the Interaction of Cytochrome P450 3A4 with Suicide Substrates: Mibefradil, Azamulin and 6",7"-Dihydroxybergamottin. azamulin 101-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-63 31480231-0 2019 Structural Insights into the Interaction of Cytochrome P450 3A4 with Suicide Substrates: Mibefradil, Azamulin and 6",7"-Dihydroxybergamottin. 6',7'-dihydroxybergamottin 114-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-63 31480231-4 2019 This study provides the first direct insights into the interaction of CYP3A4 with three suicide substrates: mibefradil, an antihypertensive drug quickly withdrawn from the market; a semi-synthetic antibiotic azamulin; and a natural furanocoumarin, 6",7"-dihydroxybergamottin. Mibefradil 108-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 31480231-4 2019 This study provides the first direct insights into the interaction of CYP3A4 with three suicide substrates: mibefradil, an antihypertensive drug quickly withdrawn from the market; a semi-synthetic antibiotic azamulin; and a natural furanocoumarin, 6",7"-dihydroxybergamottin. azamulin 208-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 31480231-4 2019 This study provides the first direct insights into the interaction of CYP3A4 with three suicide substrates: mibefradil, an antihypertensive drug quickly withdrawn from the market; a semi-synthetic antibiotic azamulin; and a natural furanocoumarin, 6",7"-dihydroxybergamottin. Furocoumarins 232-246 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 31480231-4 2019 This study provides the first direct insights into the interaction of CYP3A4 with three suicide substrates: mibefradil, an antihypertensive drug quickly withdrawn from the market; a semi-synthetic antibiotic azamulin; and a natural furanocoumarin, 6",7"-dihydroxybergamottin. 6',7'-dihydroxybergamottin 248-274 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 31293154-0 2019 Characterization of Genetic Variation in CYP3A4 on the Metabolism of Cabozantinib in Vitro. cabozantinib 69-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 31293154-1 2019 Cabozantinib is a multityrosine kinase inhibitor and has a wide range of applications in the clinic, whose metabolism is predominately dependent on CYP3A4. cabozantinib 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 31293154-2 2019 This study was performed to characterize the enzymatic properties of 29 CYP3A4 alleles toward cabozantinib and the functional changes of five selected alleles (the wild-type, CYP3A4.2.8.14 and .15) toward cabozantinib in the presence of ketoconazole. cabozantinib 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 31293154-2 2019 This study was performed to characterize the enzymatic properties of 29 CYP3A4 alleles toward cabozantinib and the functional changes of five selected alleles (the wild-type, CYP3A4.2.8.14 and .15) toward cabozantinib in the presence of ketoconazole. cabozantinib 205-217 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 31293154-5 2019 With the presence of ketoconazole, five tested CYP3A4 alleles, even CYP3A4.14 and .15, exhibited obvious reductions in intrinsic clearance. Ketoconazole 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 31293154-5 2019 With the presence of ketoconazole, five tested CYP3A4 alleles, even CYP3A4.14 and .15, exhibited obvious reductions in intrinsic clearance. Ketoconazole 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 31293154-6 2019 Besides, we compared cabozantinib with regorafenib in relative clearance to confirm that CYP3A4 has the property of substrate specificity. cabozantinib 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 31293154-6 2019 Besides, we compared cabozantinib with regorafenib in relative clearance to confirm that CYP3A4 has the property of substrate specificity. regorafenib 39-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 31293154-7 2019 As the first study of CYP3A4 genetic polymorphisms toward cabozantinib, our observations can provide prediction of an individual"s capability in response to cabozantinib and guidance for medication and treatment of cabozantinib. cabozantinib 58-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 31293154-7 2019 As the first study of CYP3A4 genetic polymorphisms toward cabozantinib, our observations can provide prediction of an individual"s capability in response to cabozantinib and guidance for medication and treatment of cabozantinib. cabozantinib 157-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 31293154-7 2019 As the first study of CYP3A4 genetic polymorphisms toward cabozantinib, our observations can provide prediction of an individual"s capability in response to cabozantinib and guidance for medication and treatment of cabozantinib. cabozantinib 157-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 31136946-1 2019 Possible interaction between clopidogrel and CYP3A4-metabolised atorvastatin or non-CYP3A4-metabolised rosuvastatin was investigated based on pharmacokinetic parameters of clopidogrel and its metabolites as well as the platelet reactivity test in patients undergoing coronary angiography/angioplasty. Atorvastatin 64-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 30945322-1 2019 AIMS: Erlotinib is a tyrosine kinase inhibitor used in the treatment of non-small cell lung cancer highly metabolized by the cytochrome P450 (CYP) 3A. Erlotinib Hydrochloride 6-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-149 30945322-2 2019 Hence, CYP3A4 activity might be a useful predictor of erlotinib pharmacokinetics in personalized medicine. Erlotinib Hydrochloride 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 30945322-3 2019 The effect of erlotinib on CYP3A activity was therefore studied in non-small cell lung cancer patients. Erlotinib Hydrochloride 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 30945322-5 2019 CYP3A activity was assessed using quinine as a probe before and during erlotinib treatment. Quinine 34-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 30945322-12 2019 CONCLUSIONS: An induction of CYP3A activity was observed after 2 months of erlotinib treatment which was also seen when subdividing based on gender. Erlotinib Hydrochloride 75-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 31190414-3 2019 Tac is metabolized in the liver and intestine by the cytochrome P450 3A (CYP3A) isoforms CYP3A4 and CYP3A5. Tacrolimus 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-71 31190414-3 2019 Tac is metabolized in the liver and intestine by the cytochrome P450 3A (CYP3A) isoforms CYP3A4 and CYP3A5. Tacrolimus 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 31190414-3 2019 Tac is metabolized in the liver and intestine by the cytochrome P450 3A (CYP3A) isoforms CYP3A4 and CYP3A5. Tacrolimus 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 31187169-12 2019 This study confirms the need for caution in patients with solid tumors treated with lapatinib, and who are concomitantly receiving drugs that are strong CYP3A inhibitors and/or prolong the QTc. Lapatinib 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-158 31132328-5 2019 Similarly, in HepG2 cells, PA treatment significantly suppressed the CYP3A4 (major subtype of human CYP3A) mRNA level and promoter transcription activity. Palmitates 27-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 31132328-5 2019 Similarly, in HepG2 cells, PA treatment significantly suppressed the CYP3A4 (major subtype of human CYP3A) mRNA level and promoter transcription activity. Palmitates 27-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 30570831-2 2019 In vitro studies show cytochrome P450 (CYP) 3A4 is involved in vemurafenib metabolism, but the effect of strong inducers or inhibitors of CYP3A4 on vemurafenib exposure in vivo is unknown. Vemurafenib 63-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-47 30570831-3 2019 This phase 1, open-label, multicenter study evaluated the effect of rifampicin, a CYP3A4 inducer, on the pharmacokinetics of single-dose vemurafenib in 27 patients with BRAFV600 mutation-positive metastatic malignancy. Rifampin 68-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 31089768-0 2019 The effect of ketoconazole on praziquantel pharmacokinetics and the role of CYP3A4 in the formation of X-OH-praziquantel and not 4-OH-praziquantel. x-oh-praziquantel 103-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 31089768-15 2019 KTZ preferentially inhibited the formation of X-OH-PZQ rather than 4-OH-PZQ, confirming in vitro data which implicates CYP3A4 in the formation of X-OH-PZQ rather than 4-OH-PZQ. Ketoconazole 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 31089768-15 2019 KTZ preferentially inhibited the formation of X-OH-PZQ rather than 4-OH-PZQ, confirming in vitro data which implicates CYP3A4 in the formation of X-OH-PZQ rather than 4-OH-PZQ. x-oh-pzq 146-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 31163215-3 2019 All tested coumarins except a C4 phenyl derivative (11) showed higher inhibitory activities for CYP2A6 over the other CYP isoforms, including CYP1A2, CYP2D6, CYP2E1, CYP3A4, CYP2C8, and CYP2C9. Coumarins 11-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-172 31103741-0 2019 Human CYP3A4-mediated toxification of the pyrrolizidine alkaloid lasiocarpine. Pyrrolizidine Alkaloids 42-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 31103741-0 2019 Human CYP3A4-mediated toxification of the pyrrolizidine alkaloid lasiocarpine. lasiocarpine 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 31103741-7 2019 Experiments with the potent CYP3A/Cyp3a inhibitor ketoconazole and supersomes containing individual human and rat CYPs revealed that enzymes of the CYP3A/Cyp3a family of both species are of major relevance for lasiocarpine metabolism. Ketoconazole 50-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 31103741-7 2019 Experiments with the potent CYP3A/Cyp3a inhibitor ketoconazole and supersomes containing individual human and rat CYPs revealed that enzymes of the CYP3A/Cyp3a family of both species are of major relevance for lasiocarpine metabolism. Ketoconazole 50-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-39 31103741-7 2019 Experiments with the potent CYP3A/Cyp3a inhibitor ketoconazole and supersomes containing individual human and rat CYPs revealed that enzymes of the CYP3A/Cyp3a family of both species are of major relevance for lasiocarpine metabolism. lasiocarpine 210-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 31103741-7 2019 Experiments with the potent CYP3A/Cyp3a inhibitor ketoconazole and supersomes containing individual human and rat CYPs revealed that enzymes of the CYP3A/Cyp3a family of both species are of major relevance for lasiocarpine metabolism. lasiocarpine 210-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-39 31103741-8 2019 To assess if metabolism by human CYP3A4 results in a toxification of lasiocarpine we performed experiments with V79 cells. lasiocarpine 69-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 31103741-11 2019 By contrast, a V79 clone engineered for expression of human CYP3A4 showed concentration-dependent gammaH2AX and micronucleus formation. gammah2ax 98-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 31103741-12 2019 Concluding, our results showed the CYP3A4-dependent formation of genotoxic metabolites of lasiocarpine. lasiocarpine 90-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 30973652-6 2019 Methadone exposure was either decreased or unchanged when it was coadministered with weak to strong CYP3A inhibitors or a moderate CYP3A4 inducer. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 30973652-6 2019 Methadone exposure was either decreased or unchanged when it was coadministered with weak to strong CYP3A inhibitors or a moderate CYP3A4 inducer. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 31399314-5 2019 As a result, RA increased the gene expression of a drug-metabolizing enzyme CYP3A4, as a functional molecule of intestinal mature development, in iPSC-derived intestinal organoids. Tretinoin 13-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 31102151-1 2019 The objective of this study was to determine the impact of polymorphism of CYP3A subfamily isoenzymes (allelic variants of CYP3A4*22 and CYP3A5*3) on the efficacy clopidogrel in patients with an acute coronary syndrome (ACS), who have undergone percutaneous coronary intervention (PCI). Clopidogrel 163-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 31102151-3 2019 The activity of CYP3A4/5 was expressed as the ratio of the concentrations of cortisol and 6beta-hydroxycortisol was performed by using high performance liquid chromatography. Hydrocortisone 77-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 31102151-3 2019 The activity of CYP3A4/5 was expressed as the ratio of the concentrations of cortisol and 6beta-hydroxycortisol was performed by using high performance liquid chromatography. 6 beta-hydroxycortisol 90-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 30227770-5 2019 CYP3A4 expression level was significantly correlated with PTV disappearance rate and metabolite formation. paritaprevir 58-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 30227770-7 2019 This study represents that the major CYP isoform involved in PTV metabolism is CYP3A4, with CYP3A5 having a minor role in PTV metabolism. paritaprevir 61-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 30301385-6 2019 Co-administration of probenecid (an UGT2B7 inhibitor) or fluconazole (an UGT2B7 and CYP3A4 inhibitor) was predicted to increase area under the curve for mirabegron to 115% or 174%, respectively. Probenecid 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 30301385-6 2019 Co-administration of probenecid (an UGT2B7 inhibitor) or fluconazole (an UGT2B7 and CYP3A4 inhibitor) was predicted to increase area under the curve for mirabegron to 115% or 174%, respectively. Fluconazole 57-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 31164198-0 2019 Degradation of pristine and oxidized single wall carbon nanotubes by CYP3A4. Carbon 49-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 31164198-3 2019 In the present investigation, we studied the biodegradation of single-walled carbon nanotubes (SWCNTs) by Cytochrome P450 enzymes (CYP3A4) through using Raman spectroscopy. Carbon 77-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 31417408-14 2019 The genetic polymorphisms of CYP3A4 rs755828176 and NR1I2 rs3814055 were significantly associated with unbound imatinib and N-desmethyl-imatinib dose-adjusted trough plasma levels. Imatinib Mesylate 111-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 31417408-14 2019 The genetic polymorphisms of CYP3A4 rs755828176 and NR1I2 rs3814055 were significantly associated with unbound imatinib and N-desmethyl-imatinib dose-adjusted trough plasma levels. N-desmethylimatinib 124-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 31129163-5 2019 Both, silica NPs (SiO2 NP) and cargo-free PEGylated stealth liposomes resulted in the induction of CYP3A4-activity up to 150% in a dose-dependent manner, with different time-dependent response-patterns as a function of NP-type after a single treatment. Silicon Dioxide 6-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 31129163-5 2019 Both, silica NPs (SiO2 NP) and cargo-free PEGylated stealth liposomes resulted in the induction of CYP3A4-activity up to 150% in a dose-dependent manner, with different time-dependent response-patterns as a function of NP-type after a single treatment. Silicon Dioxide 18-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 31357617-7 2019 Moreover, ENNB1 significantly decreased the hydroxylation rates of the typical CYP3A4-substrate midazolam (MDZ). Midazolam 96-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 31357617-7 2019 Moreover, ENNB1 significantly decreased the hydroxylation rates of the typical CYP3A4-substrate midazolam (MDZ). Midazolam 107-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 31271289-6 2019 Recombinant human CYP screening and CYP inhibition experiments revealed that multiple CYPs, notably CYP1A1, CYP1A2, and CYP3A4, were responsible for the metabolic activation of elemicin. elemicin 177-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 31413581-5 2019 The mechanism of the interaction is due to macrolides" inhibition of CYP3A4 isoenzyme and OAT1B transporter causing increased exposure to statins. Macrolides 43-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 31332230-8 2019 Treatment of spheroids with rifampicin increased CYP3A4 activity, demonstrating the metabolic capacity of HepaRG spheroids. Rifampin 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 31332230-8 2019 Treatment of spheroids with rifampicin increased CYP3A4 activity, demonstrating the metabolic capacity of HepaRG spheroids. heparg 106-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 31312984-4 2019 In this study, the N- and alpha-carbon oxidation processes of lapatinib catalyzed by CYP3A4 were explored by density functional theory method. Nitrogen 19-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 31312984-4 2019 In this study, the N- and alpha-carbon oxidation processes of lapatinib catalyzed by CYP3A4 were explored by density functional theory method. Carbon 32-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 31312984-4 2019 In this study, the N- and alpha-carbon oxidation processes of lapatinib catalyzed by CYP3A4 were explored by density functional theory method. Lapatinib 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 31295928-3 2019 CYP3A4/FMO-activities significantly correlated with the formation of N-desmethylvandetanib/ vandetanib-N-oxide. N-Desmethyl vandetanib 69-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 31295928-3 2019 CYP3A4/FMO-activities significantly correlated with the formation of N-desmethylvandetanib/ vandetanib-N-oxide. vandetanib-n-oxide 92-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 31295928-4 2019 Based on these studies, most of the vandetanib metabolism was attributed to N-desmethylvandetanib/vandetanib-N-oxide to CYP3A4/FMO3. vandetanib 36-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 31295928-4 2019 Based on these studies, most of the vandetanib metabolism was attributed to N-desmethylvandetanib/vandetanib-N-oxide to CYP3A4/FMO3. N-Desmethyl vandetanib 76-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 31295928-4 2019 Based on these studies, most of the vandetanib metabolism was attributed to N-desmethylvandetanib/vandetanib-N-oxide to CYP3A4/FMO3. vandetanib 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 31295928-5 2019 Recombinant CYP3A4 was most efficient to form N-desmethylvandetanib, while FMO1/FMO3 generated N-oxide. N-Desmethyl vandetanib 46-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 31295928-6 2019 Cytochrome b5 stimulated the CYP3A4-catalyzed formation of N-desmethylvandetanib, which is of great importance because CYP3A4 is not only most efficient in generating N-desmethylvandetanib, but also most significant due to its high expression in human liver. N-Desmethyl vandetanib 59-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 31295928-6 2019 Cytochrome b5 stimulated the CYP3A4-catalyzed formation of N-desmethylvandetanib, which is of great importance because CYP3A4 is not only most efficient in generating N-desmethylvandetanib, but also most significant due to its high expression in human liver. N-Desmethyl vandetanib 59-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 31295928-6 2019 Cytochrome b5 stimulated the CYP3A4-catalyzed formation of N-desmethylvandetanib, which is of great importance because CYP3A4 is not only most efficient in generating N-desmethylvandetanib, but also most significant due to its high expression in human liver. N-Desmethyl vandetanib 167-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 31295928-6 2019 Cytochrome b5 stimulated the CYP3A4-catalyzed formation of N-desmethylvandetanib, which is of great importance because CYP3A4 is not only most efficient in generating N-desmethylvandetanib, but also most significant due to its high expression in human liver. N-Desmethyl vandetanib 167-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 31295928-7 2019 Molecular modeling indicated that binding of more than one molecule of vandetanib into the CYP3A4-active center can be responsible for the high efficiency of CYP3A4 N-demethylating vandetanib. vandetanib 71-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 31295928-7 2019 Molecular modeling indicated that binding of more than one molecule of vandetanib into the CYP3A4-active center can be responsible for the high efficiency of CYP3A4 N-demethylating vandetanib. vandetanib 71-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 31295928-7 2019 Molecular modeling indicated that binding of more than one molecule of vandetanib into the CYP3A4-active center can be responsible for the high efficiency of CYP3A4 N-demethylating vandetanib. vandetanib 181-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 31295928-7 2019 Molecular modeling indicated that binding of more than one molecule of vandetanib into the CYP3A4-active center can be responsible for the high efficiency of CYP3A4 N-demethylating vandetanib. vandetanib 181-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 31295928-8 2019 Indeed, the CYP3A4-mediated reaction exhibits kinetics of positive cooperativity and this corresponded to the in silico model, where two vandetanib molecules were found in CYP3A4-active center. vandetanib 137-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 31295928-8 2019 Indeed, the CYP3A4-mediated reaction exhibits kinetics of positive cooperativity and this corresponded to the in silico model, where two vandetanib molecules were found in CYP3A4-active center. vandetanib 137-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 31291311-9 2019 CONCLUSIONS: CYP3A4 rs4646437 was found to be significantly and independently associated with ALT elevation in Japanese patients receiving ASV plus DCV therapy. asunaprevir 139-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 31291311-9 2019 CONCLUSIONS: CYP3A4 rs4646437 was found to be significantly and independently associated with ALT elevation in Japanese patients receiving ASV plus DCV therapy. daclatasvir 148-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 31032736-0 2019 Peppermint (Mentha piperita L.) extract effectively inhibits cytochrome P450 3A4 (CYP3A4) mRNA induction in rifampicin-treated HepG2 cells. Rifampin 108-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 31032736-2 2019 Therefore, here, we examined the suppressive effects of the extracts from seven edible herbs on the induction of CYP3A4 gene expression in rifampicin-treated HepG2 cells. Rifampin 139-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 31032736-5 2019 It suppressed the induction of CYP3A4 mRNA expression by rifampicin in a dose-dependent manner. Rifampin 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 31032736-7 2019 These findings demonstrate that pheophorbide a suppresses the induction of CYP3A4 mRNA expression in rifampicin-treated HepG2 cells. pheophorbide a 32-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 31032736-7 2019 These findings demonstrate that pheophorbide a suppresses the induction of CYP3A4 mRNA expression in rifampicin-treated HepG2 cells. Rifampin 101-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 30845347-0 2019 Effect of CYP3A inhibitors on the pharmacokinetics of pevonedistat in patients with advanced solid tumours. pevonedistat 54-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 30912163-0 2019 Perpetrator effects of ciclosporin (P-glycoprotein inhibitor) and its combination with fluconazole (CYP3A inhibitor) on the pharmacokinetics of rivaroxaban in healthy volunteers. Fluconazole 87-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 30912163-0 2019 Perpetrator effects of ciclosporin (P-glycoprotein inhibitor) and its combination with fluconazole (CYP3A inhibitor) on the pharmacokinetics of rivaroxaban in healthy volunteers. Rivaroxaban 144-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 30912163-1 2019 AIMS: Rivaroxaban exposure is considerably increased by drugs that are combined P-glycoprotein (P-gp) and strong cytochrome P450 (CYP) 3A inhibitors (e.g. ketoconazole). Rivaroxaban 6-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-137 30912163-1 2019 AIMS: Rivaroxaban exposure is considerably increased by drugs that are combined P-glycoprotein (P-gp) and strong cytochrome P450 (CYP) 3A inhibitors (e.g. ketoconazole). Ketoconazole 155-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-137 30912163-2 2019 The aim of the present study was to investigate the effects of the potent P-gp inhibitor ciclosporin and its combination with the moderate CYP3A inhibitor fluconazole on rivaroxaban pharmacokinetics and on CYP3A activity. Cyclosporine 89-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 206-211 30912163-2 2019 The aim of the present study was to investigate the effects of the potent P-gp inhibitor ciclosporin and its combination with the moderate CYP3A inhibitor fluconazole on rivaroxaban pharmacokinetics and on CYP3A activity. Fluconazole 155-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-144 30912163-2 2019 The aim of the present study was to investigate the effects of the potent P-gp inhibitor ciclosporin and its combination with the moderate CYP3A inhibitor fluconazole on rivaroxaban pharmacokinetics and on CYP3A activity. Rivaroxaban 170-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-144 30912163-4 2019 CYP3A4 activity was estimated using a midazolam microdose. Midazolam 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 30912163-6 2019 RESULTS: Compared to baseline, ciclosporin increased rivaroxaban average exposure by 47% (90% confidence interval 28-68%), maximum concentration by 104% (70-146%), and decreased CYP3A4 activity by 34% (25-42%). Cyclosporine 31-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 30912163-7 2019 Ciclosporin combined with fluconazole increased rivaroxaban average exposure by 86% (58-119%) and maximum concentration by 115% (83-153%), which was considerably stronger than observed in historical controls receiving rivaroxaban with fluconazole alone, and decreased CYP3A4 activity by 79% (76-82%). Cyclosporine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 268-274 30912163-7 2019 Ciclosporin combined with fluconazole increased rivaroxaban average exposure by 86% (58-119%) and maximum concentration by 115% (83-153%), which was considerably stronger than observed in historical controls receiving rivaroxaban with fluconazole alone, and decreased CYP3A4 activity by 79% (76-82%). Fluconazole 26-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 268-274 30912163-8 2019 CONCLUSION: Patients treated with rivaroxaban in combination with single modulators of multiple elimination pathways or multiple modulators of single elimination pathways (CYP3A, P-gp) require particular care. Rivaroxaban 34-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-177 31127319-2 2019 Crizotinib is a selective tyrosine kinase inhibitor of ALK, ROS1, and MET and a substrate of CYP3A. Crizotinib 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 31127319-5 2019 Frequency and reasons for use of concomitant CYP3A inducers, including dexamethasone, with crizotinib were characterized. Crizotinib 91-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-50 31127319-8 2019 RESULTS: Dexamethasone was the most commonly used CYP3A inducer (30.4%). Dexamethasone 9-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 30648733-1 2019 Simultaneous competition for cytochrome P450 (CYP) 2C19 and CYP3A4 might diminish clopidogrel"s antiplatelet effect by impacting its metabolic activation. Clopidogrel 82-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 30648733-2 2019 This pharmacoepidemiologic study investigated whether proton pump inhibitors (PPIs) and CYP3A4-metabolized statins individually and jointly increase thrombotic events by attenuating clopidogrel"s effectiveness. Clopidogrel 182-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 30675694-3 2019 METHODS: A PBPK model of hyperforin accounting for the induction of cytochrome P450 (CYP) 3A, CYP2C9 and CYP2C19 was developed in the Simcyp Simulator (version 17) and verified using published, clinically observed pharmacokinetic data. hyperforin 25-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-92 30675694-8 2019 CONCLUSION: In the current study, a PBPK model for hyperforin was successfully developed, with a predictive capability for the interactions of SJW with different CYP3A, CYP2C9 and CYP2C19 substrates. hyperforin 51-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-167 30758919-2 2019 In vitro, lesinurad was shown to be a weak inhibitor of cytochrome P450 (CYP)2C9 and a weak inducer of CYP3A4. lesinurad 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 31044521-1 2019 Acalabrutinib, a selective, covalent Bruton tyrosine kinase inhibitor, is a CYP3A substrate and weak CYP3A/CYP2C8 inhibitor. acalabrutinib 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 31044521-1 2019 Acalabrutinib, a selective, covalent Bruton tyrosine kinase inhibitor, is a CYP3A substrate and weak CYP3A/CYP2C8 inhibitor. acalabrutinib 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 31044521-4 2019 The model reasonably predicted clinically observed acalabrutinib DDI with the CYP3A perpetrators itraconazole (4.80-fold vs. 5.21-fold observed) and rifampicin (0.21-fold vs. 0.23-fold observed). acalabrutinib 51-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 31044521-4 2019 The model reasonably predicted clinically observed acalabrutinib DDI with the CYP3A perpetrators itraconazole (4.80-fold vs. 5.21-fold observed) and rifampicin (0.21-fold vs. 0.23-fold observed). Itraconazole 97-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 31044521-5 2019 An increase of two to threefold acalabrutinib area under the curve was predicted for coadministration with moderate CYP3A inhibitors. acalabrutinib 32-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 31028057-0 2019 Indinavir Increases Midazolam N-Glucuronidation in Humans: Identification of an Alternate CYP3A Inhibitor Using an In Vitro to In Vivo Approach. Indinavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 31028057-1 2019 Midazolam is a widely used index substrate for assessing effects of xenobiotics on CYP3A activity. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 31028057-2 2019 A previous study involving human hepatocytes showed the primary route of midazolam metabolism, 1"-hydroxylation, shifted to N-glucuronidation in the presence of the CYP3A inhibitor ketoconazole, which may lead to an overprediction of the magnitude of a xenobiotic-midazolam interaction. Midazolam 73-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-170 31028057-2 2019 A previous study involving human hepatocytes showed the primary route of midazolam metabolism, 1"-hydroxylation, shifted to N-glucuronidation in the presence of the CYP3A inhibitor ketoconazole, which may lead to an overprediction of the magnitude of a xenobiotic-midazolam interaction. Nitrogen 124-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-170 31028057-2 2019 A previous study involving human hepatocytes showed the primary route of midazolam metabolism, 1"-hydroxylation, shifted to N-glucuronidation in the presence of the CYP3A inhibitor ketoconazole, which may lead to an overprediction of the magnitude of a xenobiotic-midazolam interaction. Ketoconazole 181-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-170 31028057-2 2019 A previous study involving human hepatocytes showed the primary route of midazolam metabolism, 1"-hydroxylation, shifted to N-glucuronidation in the presence of the CYP3A inhibitor ketoconazole, which may lead to an overprediction of the magnitude of a xenobiotic-midazolam interaction. Midazolam 264-273 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-170 31028057-5 2019 Compared with vehicle, indinavir (10 muM) inhibited midazolam 1"-hydroxylation by recombinant CYP3A4, human liver microsomes, and high-CYP3A activity cryopreserved human hepatocytes by >=70%; the IC50 obtained with hepatocytes (2.7 muM) was within reported human unbound indinavir Cmax (<=5 muM). Indinavir 23-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 31028057-5 2019 Compared with vehicle, indinavir (10 muM) inhibited midazolam 1"-hydroxylation by recombinant CYP3A4, human liver microsomes, and high-CYP3A activity cryopreserved human hepatocytes by >=70%; the IC50 obtained with hepatocytes (2.7 muM) was within reported human unbound indinavir Cmax (<=5 muM). Indinavir 23-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-99 31028057-5 2019 Compared with vehicle, indinavir (10 muM) inhibited midazolam 1"-hydroxylation by recombinant CYP3A4, human liver microsomes, and high-CYP3A activity cryopreserved human hepatocytes by >=70%; the IC50 obtained with hepatocytes (2.7 muM) was within reported human unbound indinavir Cmax (<=5 muM). Midazolam 52-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 31028057-5 2019 Compared with vehicle, indinavir (10 muM) inhibited midazolam 1"-hydroxylation by recombinant CYP3A4, human liver microsomes, and high-CYP3A activity cryopreserved human hepatocytes by >=70%; the IC50 obtained with hepatocytes (2.7 muM) was within reported human unbound indinavir Cmax (<=5 muM). Midazolam 52-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-99 31048453-9 2019 11-OH-THC was depleted by UGTs (fm = 0.67 and Km,u = 39 nM), CYP3A4 (fm = 0.18, Km,u = 824 nM), and CYP2C9 (fm = 0.15, Km,u = 33 nM). 11-Hydroxytetrahydrocannabinol 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 31068367-5 2019 To describe the pharmacokinetic interaction profile of alectinib in a complete fashion, its possible inhibitory properties toward clinically relevant P450 enzymes (i.e., CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP3A4, or CYP3A5) were evaluated using human P450-expressing insect microsomes, revealing alectinib as a poor interactor. alectinib 55-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 31068367-6 2019 Advantageously for its use in pharmacotherapy, alectinib further exhibited negligible potential to cause any changes in expression of ABCB1, ABCG2, ABCC1, CYP1A2, CYP3A4, and CYP2B6 in intestine, liver, and NSCLC models. alectinib 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 31084979-7 2019 The most frequent interactions were amiodarone-statin for CYP3A4 and atorvastatin-verapamil-diltiazem for P-gp. Amiodarone 36-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 31102650-0 2019 Microdosed midazolam for the determination of cytochrome P450 3A activity: Development and clinical evaluation of a buccal film. Midazolam 11-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-64 31102650-3 2019 The activity of CYP3A can be monitored using the CYP3A substrate midazolam. Midazolam 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-21 31102650-3 2019 The activity of CYP3A can be monitored using the CYP3A substrate midazolam. Midazolam 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 31102650-7 2019 It was the aim of the present study to clinically evaluate a novel buccal film containing microdoses of midazolam for assessment of CYP3A activity. Midazolam 104-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-137 30564916-10 2019 Significant contribution to the in vitro metabolism of THJ-018 and THJ-2201 originated from CYP2B6, CYP2C19, CYP3A4, and CYP3A5. thj 55-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 30564916-10 2019 Significant contribution to the in vitro metabolism of THJ-018 and THJ-2201 originated from CYP2B6, CYP2C19, CYP3A4, and CYP3A5. thj 67-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 30253726-3 2019 Midostaurin is primarily metabolized by the liver through the CYP3A4 enzyme with fecal excretion accounting for 95% of the dose (4% recovered as unchanged drug). midostaurin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 31064695-8 2019 Subgroup analysis indicated that the CYP3A4*1G/*1G homozygote was associated with poor prognosis at 1 year among patients with stable high-intensity atorvastatin therapy (40-80 mg/d) after adjustment for conventional factors in the additive model (OR = 8.16; 95% confidence interval, 1.50-44.44; P = .015) and recessive model (OR = 9.06; 95% confidence interval, 1.72-47.64; P = .009). Atorvastatin 149-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 30058048-0 2019 Drug-metabolizing enzymes CYP3A as a link between tacrolimus and vitamin D in renal transplant recipients: is it relevant in clinical practice? Tacrolimus 50-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-31 30058048-0 2019 Drug-metabolizing enzymes CYP3A as a link between tacrolimus and vitamin D in renal transplant recipients: is it relevant in clinical practice? Vitamin D 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-31 30058048-1 2019 CYP3A enzymes are involved in the metabolism of calcineurin inhibitor tacrolimus as well as vitamin D. Tacrolimus 70-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 30058048-1 2019 CYP3A enzymes are involved in the metabolism of calcineurin inhibitor tacrolimus as well as vitamin D. Vitamin D 92-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 30058048-2 2019 In this review, we summarize the clinical aspects of CYP3A-mediated metabolism of tacrolimus and vitamin D with emphasis on the influence of single-nucleotide polymorphisms on tacrolimus disposition. Tacrolimus 82-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 30058048-2 2019 In this review, we summarize the clinical aspects of CYP3A-mediated metabolism of tacrolimus and vitamin D with emphasis on the influence of single-nucleotide polymorphisms on tacrolimus disposition. Tacrolimus 176-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 30058048-3 2019 We describe the utility of 4beta hydroxycholesterol as a marker of CYP3A activity. cholest-5-ene-3,4-diol 27-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-72 31288895-7 2019 These results revealed that flucloxacillin might have weak pharmacokinetic interactions on midazolam metabolized into 1"-hydroxy midazolam, indicating that there was weak induction to CYP3A by flucloxacillin and that there was at least 30.80 % of metabolic behaviour in change with bioavailability decreased by 38.11 % that took effect to flucloxacillin metabolism for liver injury in CPY3A4 poor metabolic polymorphisms. Floxacillin 28-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-189 31288895-7 2019 These results revealed that flucloxacillin might have weak pharmacokinetic interactions on midazolam metabolized into 1"-hydroxy midazolam, indicating that there was weak induction to CYP3A by flucloxacillin and that there was at least 30.80 % of metabolic behaviour in change with bioavailability decreased by 38.11 % that took effect to flucloxacillin metabolism for liver injury in CPY3A4 poor metabolic polymorphisms. Midazolam 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-189 31288895-7 2019 These results revealed that flucloxacillin might have weak pharmacokinetic interactions on midazolam metabolized into 1"-hydroxy midazolam, indicating that there was weak induction to CYP3A by flucloxacillin and that there was at least 30.80 % of metabolic behaviour in change with bioavailability decreased by 38.11 % that took effect to flucloxacillin metabolism for liver injury in CPY3A4 poor metabolic polymorphisms. 1-hydroxymethylmidazolam 118-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-189 31288895-7 2019 These results revealed that flucloxacillin might have weak pharmacokinetic interactions on midazolam metabolized into 1"-hydroxy midazolam, indicating that there was weak induction to CYP3A by flucloxacillin and that there was at least 30.80 % of metabolic behaviour in change with bioavailability decreased by 38.11 % that took effect to flucloxacillin metabolism for liver injury in CPY3A4 poor metabolic polymorphisms. Floxacillin 193-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-189 31288895-7 2019 These results revealed that flucloxacillin might have weak pharmacokinetic interactions on midazolam metabolized into 1"-hydroxy midazolam, indicating that there was weak induction to CYP3A by flucloxacillin and that there was at least 30.80 % of metabolic behaviour in change with bioavailability decreased by 38.11 % that took effect to flucloxacillin metabolism for liver injury in CPY3A4 poor metabolic polymorphisms. Floxacillin 193-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-189 31487643-0 2019 Relationships between endogenous CYP3A markers and plasma amlodipine exposure and metabolism in early postpartum and non-peripartum women with hypertension. Amlodipine 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 31487643-1 2019 OBJECTIVE: This study aimed to evaluate the relationship between endogenous CYP3A markers and plasma amlodipine (AML) exposure and metabolism parameters in early postpartum and non-peripartum women. Amlodipine 101-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 31487643-12 2019 AML metabolism and plasma 4beta-OHC may be useful as CYP3A markers in early postpartum and non-peripartum women. 4beta-ohc 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 31102695-0 2019 Vitamin E analogues differentially inhibit human cytochrome P450 3A (CYP3A)-mediated oxidative metabolism of lithocholic acid: Impact of delta-tocotrienol on lithocholic acid cytotoxicity. Vitamin E 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-67 31102695-0 2019 Vitamin E analogues differentially inhibit human cytochrome P450 3A (CYP3A)-mediated oxidative metabolism of lithocholic acid: Impact of delta-tocotrienol on lithocholic acid cytotoxicity. Vitamin E 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 31102695-0 2019 Vitamin E analogues differentially inhibit human cytochrome P450 3A (CYP3A)-mediated oxidative metabolism of lithocholic acid: Impact of delta-tocotrienol on lithocholic acid cytotoxicity. Lithocholic Acid 109-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-67 31102695-0 2019 Vitamin E analogues differentially inhibit human cytochrome P450 3A (CYP3A)-mediated oxidative metabolism of lithocholic acid: Impact of delta-tocotrienol on lithocholic acid cytotoxicity. Lithocholic Acid 109-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 31102695-0 2019 Vitamin E analogues differentially inhibit human cytochrome P450 3A (CYP3A)-mediated oxidative metabolism of lithocholic acid: Impact of delta-tocotrienol on lithocholic acid cytotoxicity. Lithocholic Acid 158-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 31102695-1 2019 Lithocholic acid is a cytotoxic bile acid oxidized at the C-3 position by human cytochrome P450 3A (CYP3A) to form 3-ketocholanoic acid, but it is not known whether this metabolite is cytotoxic. Lithocholic Acid 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-98 31102695-1 2019 Lithocholic acid is a cytotoxic bile acid oxidized at the C-3 position by human cytochrome P450 3A (CYP3A) to form 3-ketocholanoic acid, but it is not known whether this metabolite is cytotoxic. Lithocholic Acid 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 31102695-1 2019 Lithocholic acid is a cytotoxic bile acid oxidized at the C-3 position by human cytochrome P450 3A (CYP3A) to form 3-ketocholanoic acid, but it is not known whether this metabolite is cytotoxic. Bile Acids and Salts 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-98 31102695-1 2019 Lithocholic acid is a cytotoxic bile acid oxidized at the C-3 position by human cytochrome P450 3A (CYP3A) to form 3-ketocholanoic acid, but it is not known whether this metabolite is cytotoxic. Bile Acids and Salts 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 31102695-1 2019 Lithocholic acid is a cytotoxic bile acid oxidized at the C-3 position by human cytochrome P450 3A (CYP3A) to form 3-ketocholanoic acid, but it is not known whether this metabolite is cytotoxic. 3-ketocholanoic acid 115-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-98 31102695-1 2019 Lithocholic acid is a cytotoxic bile acid oxidized at the C-3 position by human cytochrome P450 3A (CYP3A) to form 3-ketocholanoic acid, but it is not known whether this metabolite is cytotoxic. 3-ketocholanoic acid 115-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 31102695-3 2019 In the present study, the hypothesis to be tested is that tocotrienols inhibit CYP3A-catalyzed lithocholic acid 3-oxidation, thereby influencing lithocholic acid cytotoxicity. Tocotrienols 58-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-84 31102695-3 2019 In the present study, the hypothesis to be tested is that tocotrienols inhibit CYP3A-catalyzed lithocholic acid 3-oxidation, thereby influencing lithocholic acid cytotoxicity. Lithocholic Acid 95-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-84 31102695-3 2019 In the present study, the hypothesis to be tested is that tocotrienols inhibit CYP3A-catalyzed lithocholic acid 3-oxidation, thereby influencing lithocholic acid cytotoxicity. Lithocholic Acid 145-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-84 31102695-4 2019 Our enzyme catalysis experiments indicated that human recombinant CYP3A5 in addition to CYP3A4, liver microsomes, and intestinal microsomes catalyzed lithocholic acid 3-oxidation to form 3-ketocholanoic acid. Lithocholic Acid 150-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 31102695-4 2019 Our enzyme catalysis experiments indicated that human recombinant CYP3A5 in addition to CYP3A4, liver microsomes, and intestinal microsomes catalyzed lithocholic acid 3-oxidation to form 3-ketocholanoic acid. 3-ketocholanoic acid 187-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 31102695-6 2019 alpha-Tocotrienol, gamma-tocotrienol, delta-tocotrienol, and a tocotrienol-rich vitamin E mixture, but not alpha-tocopherol (a vitamin E analogue), differentially inhibited lithocholic acid 3-oxidation catalyzed by liver and intestinal microsomes and recombinant CYP3A4 and CYP3A5. tocotrienol, alpha 0-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 263-269 31102695-6 2019 alpha-Tocotrienol, gamma-tocotrienol, delta-tocotrienol, and a tocotrienol-rich vitamin E mixture, but not alpha-tocopherol (a vitamin E analogue), differentially inhibited lithocholic acid 3-oxidation catalyzed by liver and intestinal microsomes and recombinant CYP3A4 and CYP3A5. Vitamin E 80-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 263-269 31102695-6 2019 alpha-Tocotrienol, gamma-tocotrienol, delta-tocotrienol, and a tocotrienol-rich vitamin E mixture, but not alpha-tocopherol (a vitamin E analogue), differentially inhibited lithocholic acid 3-oxidation catalyzed by liver and intestinal microsomes and recombinant CYP3A4 and CYP3A5. Lithocholic Acid 173-189 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 263-269 31102695-7 2019 Compared to lithocholic acid 3-oxidation, CYP3A-catalyzed testosterone 6beta-hydroxylation was inhibited to a lesser extent by alpha-tocotrienol, gamma-tocotrienol, delta-tocotrienol, and a tocotrienol-rich vitamin E mixture. Lithocholic Acid 12-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 31102695-7 2019 Compared to lithocholic acid 3-oxidation, CYP3A-catalyzed testosterone 6beta-hydroxylation was inhibited to a lesser extent by alpha-tocotrienol, gamma-tocotrienol, delta-tocotrienol, and a tocotrienol-rich vitamin E mixture. testosterone 6beta 58-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 31102695-7 2019 Compared to lithocholic acid 3-oxidation, CYP3A-catalyzed testosterone 6beta-hydroxylation was inhibited to a lesser extent by alpha-tocotrienol, gamma-tocotrienol, delta-tocotrienol, and a tocotrienol-rich vitamin E mixture. tocotrienol, alpha 127-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 31102695-7 2019 Compared to lithocholic acid 3-oxidation, CYP3A-catalyzed testosterone 6beta-hydroxylation was inhibited to a lesser extent by alpha-tocotrienol, gamma-tocotrienol, delta-tocotrienol, and a tocotrienol-rich vitamin E mixture. plastochromanol 8 146-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 31102695-7 2019 Compared to lithocholic acid 3-oxidation, CYP3A-catalyzed testosterone 6beta-hydroxylation was inhibited to a lesser extent by alpha-tocotrienol, gamma-tocotrienol, delta-tocotrienol, and a tocotrienol-rich vitamin E mixture. tocotrienol, delta 165-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 31102695-7 2019 Compared to lithocholic acid 3-oxidation, CYP3A-catalyzed testosterone 6beta-hydroxylation was inhibited to a lesser extent by alpha-tocotrienol, gamma-tocotrienol, delta-tocotrienol, and a tocotrienol-rich vitamin E mixture. Tocotrienols 133-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 31102695-7 2019 Compared to lithocholic acid 3-oxidation, CYP3A-catalyzed testosterone 6beta-hydroxylation was inhibited to a lesser extent by alpha-tocotrienol, gamma-tocotrienol, delta-tocotrienol, and a tocotrienol-rich vitamin E mixture. Vitamin E 207-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 31250333-0 2019 A Pediatric Covariate Function for CYP3A-Mediated Midazolam Clearance Can Scale Clearance of Selected CYP3A Substrates in Children. Midazolam 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-40 31250333-0 2019 A Pediatric Covariate Function for CYP3A-Mediated Midazolam Clearance Can Scale Clearance of Selected CYP3A Substrates in Children. Midazolam 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 31250333-2 2019 Here we evaluate when a pediatric covariate function for midazolam clearance can be used to scale clearance of other CYP3A substrates. Midazolam 57-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-122 31250333-7 2019 According to the framework, a midazolam covariate function will lead to systemically accurate clearance scaling (absolute prediction error (PE) < 30%) for CYP3A substrates binding to albumin with an extraction ratio between 0.35 and 0.65 when binding < 10% in adults, between 0.05 and 0.55 when binding > 90%, and with an extraction ratio ranging between these values when binding between 10 and 90%. Midazolam 30-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-160 31250333-10 2019 We defined for which CYP3A substrates a pediatric covariate function for midazolam clearance can accurately scale plasma clearance in children. Midazolam 73-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-26 31239454-8 2019 Furthermore, the results indicate that coumarin (CYP2A), midazolam (CYP3A), tolbutamide (CYP2C), and dextromethorphan (CYP2D) are as selective for porcine as for human CYP450. Midazolam 57-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 31460189-0 2019 Potent CYP3A4 Inhibitors Derived from Dillapiol and Sesamol. 5-allyl 6,7-dimethoxy 1,3-benzodioxole 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 31460189-0 2019 Potent CYP3A4 Inhibitors Derived from Dillapiol and Sesamol. sesamol 52-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 31460189-5 2019 These compounds are 106 and 46 times more potent than dillapiol whose IC50 for the inhibition of CYP3A4 is 9.2 muM. 5-allyl 6,7-dimethoxy 1,3-benzodioxole 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 31083930-0 2019 A Covalently Attached Progesterone Molecule Outcompetes the Binding of Free Progesterone at an Allosteric Site of Cytochrome P450 3A4. Progesterone 22-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-133 31083930-0 2019 A Covalently Attached Progesterone Molecule Outcompetes the Binding of Free Progesterone at an Allosteric Site of Cytochrome P450 3A4. Progesterone 76-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-133 31083930-4 2019 Progesterone (PRG) is a known allosteric activator of CYP3A4-catalyzed 7-benzyloxy-4-trifluoromethylcoumarin (BFC) debenzylation. Progesterone 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 31083930-4 2019 Progesterone (PRG) is a known allosteric activator of CYP3A4-catalyzed 7-benzyloxy-4-trifluoromethylcoumarin (BFC) debenzylation. Progesterone 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 31083930-4 2019 Progesterone (PRG) is a known allosteric activator of CYP3A4-catalyzed 7-benzyloxy-4-trifluoromethylcoumarin (BFC) debenzylation. 7-benzyloxy-4-trifluoromethylcoumarin 71-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 31083930-4 2019 Progesterone (PRG) is a known allosteric activator of CYP3A4-catalyzed 7-benzyloxy-4-trifluoromethylcoumarin (BFC) debenzylation. 7-benzyloxy-4-trifluoromethylcoumarin 110-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 31218462-0 2019 Guidance for Rifampin and Midazolam Dosing Protocols To Study Intestinal and Hepatic Cytochrome P450 (CYP) 3A4 Induction and De-induction. Rifampin 13-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-110 31218462-0 2019 Guidance for Rifampin and Midazolam Dosing Protocols To Study Intestinal and Hepatic Cytochrome P450 (CYP) 3A4 Induction and De-induction. Midazolam 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-110 31218462-3 2019 To collate published data regarding induction of CYP3A4 expression by rifampin and identify an optimal protocol to study DDIs using physiologically based pharmacokinetic (PBPK) modelling. Rifampin 70-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 31218462-4 2019 The University of Washington Drug Interaction Database was searched for published data regarding induction of CYP3A4 by rifampin. Rifampin 120-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 31218462-5 2019 A verified PBPK model was used to define the optimal dose, duration, timing and route of administration of rifampin and midazolam to assess induction of intestinal and hepatic CYP3A4 by rifampin. Rifampin 186-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 31218462-9 2019 Intestinal CYP3A4 expression returned to baseline in > 90% of participants within 7 days of rifampin cessation, whereas induction of hepatic CYP3A4 persisted for greater than 7 days in > 50% of participants. Rifampin 92-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 30925039-11 2019 Nonetheless, CYP3A4 was more selective at steps leading to TBF-A, making it more effective in terbinafine bioactivation based on metabolic split ratios for competing pathways. tbf-a 59-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 30925039-11 2019 Nonetheless, CYP3A4 was more selective at steps leading to TBF-A, making it more effective in terbinafine bioactivation based on metabolic split ratios for competing pathways. Terbinafine 94-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 30925039-13 2019 Clinical data on drug interactions support the CYP3A4 role in terbinafine metabolism, while CYP2C19 remains understudied. Terbinafine 62-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 30938510-5 2019 CYP3A family was the predominant enzyme catalyzing the bioactivation of icaritin. icaritin 72-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 31009883-2 2019 In which, the TiO2 nanotube arrays in-situ assembled with g-C3N4 (TNA/g-C3N4) was used as a photoanode, and a cytochrome P450 3A4 (CYP3A4) enzyme was immobilized in the porous ITO/CuO films to fabricate an ITO/CuO/CYP3A4 photocathode. titanium dioxide 14-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-129 31009883-2 2019 In which, the TiO2 nanotube arrays in-situ assembled with g-C3N4 (TNA/g-C3N4) was used as a photoanode, and a cytochrome P450 3A4 (CYP3A4) enzyme was immobilized in the porous ITO/CuO films to fabricate an ITO/CuO/CYP3A4 photocathode. titanium dioxide 14-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 31009883-2 2019 In which, the TiO2 nanotube arrays in-situ assembled with g-C3N4 (TNA/g-C3N4) was used as a photoanode, and a cytochrome P450 3A4 (CYP3A4) enzyme was immobilized in the porous ITO/CuO films to fabricate an ITO/CuO/CYP3A4 photocathode. titanium dioxide 14-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 214-220 31047967-3 2019 Rifampicin was chosen as the CYP3A /P-GP inducer. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 31047967-11 2019 DDIs of rifampicin with CYP3A or P-GP substrates following oral versus intravenous administration to human were successfully predicted using the developed semi-PBPK model. Rifampin 8-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 31312405-5 2019 DL5050 preferentially induced the expression of CYP2B6 (target of hCAR) over CYP3A4 (target of hPXR) on both the mRNA and protein levels. CHEMBL4465050 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 31212673-15 2019 From the head and neck cancer (HNC) gene expression dataset, the proposed method identified two additional genes (CYP3A4 and NOVA1) that are significantly enriched in linoleic acid metabolism, drug metabolism, steroid hormone biosynthesis and metabolic pathways. Linoleic Acid 167-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 31212673-15 2019 From the head and neck cancer (HNC) gene expression dataset, the proposed method identified two additional genes (CYP3A4 and NOVA1) that are significantly enriched in linoleic acid metabolism, drug metabolism, steroid hormone biosynthesis and metabolic pathways. Steroids 210-217 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 30737956-5 2019 However, CYP3A4 activity was not well maintained under dimethyl sulfoxide (DMSO)-free conditions (13-18 days), dramatically reducing drug metabolism capability. Dimethyl Sulfoxide 55-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 30737956-5 2019 However, CYP3A4 activity was not well maintained under dimethyl sulfoxide (DMSO)-free conditions (13-18 days), dramatically reducing drug metabolism capability. Dimethyl Sulfoxide 75-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 30652261-5 2019 A lot of important drug interaction data have been published that must also be taken into account when oxycodone is used concomitantly with cytochrome P450 (CYP) 3A inducers and inhibitors and/or CYP2D6 inhibitors. Oxycodone 103-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-164 30918015-0 2019 Stereoselective Oxidation Kinetics of Deoxycholate in Recombinant and Microsomal CYP3A Enzymes: Deoxycholate 19-Hydroxylation Is an In Vitro Marker of CYP3A7 Activity. Deoxycholic Acid 38-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 30918015-0 2019 Stereoselective Oxidation Kinetics of Deoxycholate in Recombinant and Microsomal CYP3A Enzymes: Deoxycholate 19-Hydroxylation Is an In Vitro Marker of CYP3A7 Activity. Deoxycholic Acid 96-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 30918015-2 2019 It was recently disclosed that the major secondary BA, deoxycholate (DCA) species, is stereoselectively oxidized to tertiary BAs exclusively by CYP3A enzymes. Bile Acids and Salts 51-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-149 30918015-2 2019 It was recently disclosed that the major secondary BA, deoxycholate (DCA) species, is stereoselectively oxidized to tertiary BAs exclusively by CYP3A enzymes. Deoxycholic Acid 55-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-149 30918015-2 2019 It was recently disclosed that the major secondary BA, deoxycholate (DCA) species, is stereoselectively oxidized to tertiary BAs exclusively by CYP3A enzymes. Deoxycholic Acid 69-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-149 30918015-2 2019 It was recently disclosed that the major secondary BA, deoxycholate (DCA) species, is stereoselectively oxidized to tertiary BAs exclusively by CYP3A enzymes. Bile Acids and Salts 125-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-149 30918015-4 2019 The stereoselective oxidation of DCA fit well with Hill kinetics at 1-300 muM in both recombinant CYP3A enzymes and pooled HLMs. Deoxycholic Acid 33-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 30918015-6 2019 Correlation between DCA oxidation and testosterone 6beta-hydroxylation in 14 adult single-donor HLMs provided proof-of-concept evidence that DCA 19-hydroxylation is an in vitro marker reaction for CYP3A7 activity, whereas oxidation at other sites represents mixed indicators for CYP3A4 and CYP3A7 activities. Deoxycholic Acid 141-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 279-285 30918015-7 2019 Deactivation caused by DCA-induced cytochrome P450-cytochrome P420 conversion, as shown by the spectral titrations of isolated CYP3A proteins, was observed when DCA levels were near or higher than the critical micelle concentration (about 1500 muM). Deoxycholic Acid 23-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 30918015-7 2019 Deactivation caused by DCA-induced cytochrome P450-cytochrome P420 conversion, as shown by the spectral titrations of isolated CYP3A proteins, was observed when DCA levels were near or higher than the critical micelle concentration (about 1500 muM). Deoxycholic Acid 161-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 30918015-9 2019 The disclosed kinetic and functional roles of CYP3A isoforms in disposing of the gut bacteria-derived DCA may help in understanding the structural and functional mechanisms of CYP3A. Deoxycholic Acid 102-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-51 30918015-9 2019 The disclosed kinetic and functional roles of CYP3A isoforms in disposing of the gut bacteria-derived DCA may help in understanding the structural and functional mechanisms of CYP3A. Deoxycholic Acid 102-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-181 30962288-11 2019 However, the cell viability in clopidogrel- and ketoconazole (CYP3A4 inhibitor)-treated CYP2C19-KO HLCs was significantly enhanced as compared with that in clopidogrel- and DMSO-treated CYP2C19-KO HLCs. Ketoconazole 48-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 30962288-11 2019 However, the cell viability in clopidogrel- and ketoconazole (CYP3A4 inhibitor)-treated CYP2C19-KO HLCs was significantly enhanced as compared with that in clopidogrel- and DMSO-treated CYP2C19-KO HLCs. Dimethyl Sulfoxide 173-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 30992242-2 2019 Activities of CYP2C9, CYP2C19, and CYP3A4 were determined by using the prototypical substrates tolbutamide, omeprazole and midazolam, respectively. Tolbutamide 95-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 30992242-2 2019 Activities of CYP2C9, CYP2C19, and CYP3A4 were determined by using the prototypical substrates tolbutamide, omeprazole and midazolam, respectively. Omeprazole 108-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 30992242-2 2019 Activities of CYP2C9, CYP2C19, and CYP3A4 were determined by using the prototypical substrates tolbutamide, omeprazole and midazolam, respectively. Midazolam 123-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 31101589-4 2019 Rifamycin stimulated PXR transcriptional activity in two PXR reporter cell lines and induced expression of two genes known to be regulated by PXR and are directly involved in cellular detoxification: CYP3A4 and PgP. rifamycin SV 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 31101589-5 2019 Moreover, CYP3A4 metabolic activity was induced by rifamycin in HepG2 cells. rifamycin SV 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 31101589-8 2019 Thus, rifamycin exhibits potent anti-inflammatory activities, characterized by in vitro PXR activation and concomitant CYP3A4 and PgP induction, in parallel with potent NFkappaB inhibition and concomitant IL8 inhibition. rifamycin SV 6-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 30306496-0 2019 Effect of 95% Ethanol Khat Extract and Cathinone on in vitro Human Recombinant Cytochrome P450 (CYP) 2C9, CYP2D6, and CYP3A4 Activity. cathinone 39-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 30306496-4 2019 This study aimed to reveal the inhibitory potencies of khat ethanol extract (KEE) and its major active ingredient (cathinone) on human cytochrome P450 (CYP) 2C9, CYP2D6, and CYP3A4 enzymes activities, which are collectively responsible for metabolizing 70-80% clinically used drugs. Ethanol 60-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 30306496-4 2019 This study aimed to reveal the inhibitory potencies of khat ethanol extract (KEE) and its major active ingredient (cathinone) on human cytochrome P450 (CYP) 2C9, CYP2D6, and CYP3A4 enzymes activities, which are collectively responsible for metabolizing 70-80% clinically used drugs. cathinone 115-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 30991128-9 2019 The CYP450 isoforms CYP2C19 and CYP3A4 were involved in rac-myclobutanil and S-(+)-myclobutanil metabolism. systhane 60-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 30991128-9 2019 The CYP450 isoforms CYP2C19 and CYP3A4 were involved in rac-myclobutanil and S-(+)-myclobutanil metabolism. systhane 77-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 30511200-9 2019 Patients administered TAS-114 exhibited linear PK and CYP3A4 induction, with no effect on the PK of S-1. TAS-114 22-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 30815689-9 2019 CYP3A4*22 rs35599367 was associated with higher plasma tenofovir alafenamide AUC0-24 at day 56. tenofovir alafenamide 55-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 30633368-8 2019 A multivariable linear regression model incorporating hepatic cytochrome P450 (CYP) 3A4 abundance, albumin concentration, hepatic CYP1A2 abundance, hepatic CYP2C19 abundance, and intestinal CYP2C19 abundance provided robust prediction of axitinib AUCSS (R2 = 0.890; P < .001). Axitinib 238-246 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-87 30633368-10 2019 Variability in axitinib AUCSS is primarily driven by differences in hepatic CYP3A4 abundance and albumin concentration. Axitinib 15-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 30861159-4 2019 In wild-type CYP3A4 rs2242480 (TT) carriers, patients who took calcium channel blockers had lower tacrolimus stable doses than those without the concomitant medications (P < 1 x 10-4 ). Tacrolimus 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 30861159-8 2019 Our finding suggested that wild-type CYP3A4 rs2242480 (TT) carriers should be more cautious to take tacrolimus when they are coadministrated with calcium channel blockers, and CYP3A5 rs776746 (AA) carriers may need higher tacrolimus dosage when they are in combination with hypertension. Tacrolimus 100-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 30861159-8 2019 Our finding suggested that wild-type CYP3A4 rs2242480 (TT) carriers should be more cautious to take tacrolimus when they are coadministrated with calcium channel blockers, and CYP3A5 rs776746 (AA) carriers may need higher tacrolimus dosage when they are in combination with hypertension. Tacrolimus 222-232 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 30920135-5 2019 We also observed that stromal CYP3A4 expression is up-regulated by drugs commonly used in AML induction therapy, cytarabine, etoposide and daunorubicin, resulting in cross-resistance. Cytarabine 113-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 30920135-5 2019 We also observed that stromal CYP3A4 expression is up-regulated by drugs commonly used in AML induction therapy, cytarabine, etoposide and daunorubicin, resulting in cross-resistance. Etoposide 125-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 30920135-5 2019 We also observed that stromal CYP3A4 expression is up-regulated by drugs commonly used in AML induction therapy, cytarabine, etoposide and daunorubicin, resulting in cross-resistance. Daunorubicin 139-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 30920135-7 2019 The up-regulation of CYP3A4 associated with disease control was reversed by clarithromycin, a potent inhibitor of CYP3A4. Clarithromycin 76-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 30920135-7 2019 The up-regulation of CYP3A4 associated with disease control was reversed by clarithromycin, a potent inhibitor of CYP3A4. Clarithromycin 76-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 29558838-2 2019 Midostaurin is a major cytochrome P450 3A4 (CYP3A4) substrate. midostaurin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-42 29558838-2 2019 Midostaurin is a major cytochrome P450 3A4 (CYP3A4) substrate. midostaurin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 29558838-3 2019 Coadministration with a strong CYP3A4 inhibitor or inducer can lead to a potential increase or decrease in midostaurin exposure. midostaurin 107-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 29558838-6 2019 Isavuconazole, a moderate CYP3A4 inhibitor, was successfully initiated and maintained, while midostaurin therapy was also administered. isavuconazole 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 29558838-7 2019 Clinicians should be aware and exercise caution when using midostaurin with CYP3A4 inhibitors and inducers. midostaurin 59-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 31261526-5 2019 The most commonly reported genotype was CYP3A53/3, which was strongly associated with cyclosporine A (CsA) and tacrolimus (FK506). Cyclosporine 86-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-49 31261526-5 2019 The most commonly reported genotype was CYP3A53/3, which was strongly associated with cyclosporine A (CsA) and tacrolimus (FK506). Cyclosporine 102-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-49 31261526-5 2019 The most commonly reported genotype was CYP3A53/3, which was strongly associated with cyclosporine A (CsA) and tacrolimus (FK506). Tacrolimus 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-49 31261526-5 2019 The most commonly reported genotype was CYP3A53/3, which was strongly associated with cyclosporine A (CsA) and tacrolimus (FK506). Tacrolimus 123-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-49 31025537-7 2019 The presence of CYP3A4*1B allele was evaluated on the basis of agarose gel electrophoresis. Sepharose 63-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 30981185-11 2019 RESULTS: Passively diffused constituents of the methanol acai extract (IC50 of 28.03 microg/microl) demonstrated the highest inhibition potential, and, at 1.5 microg/microl, induced significant changes in CYP3A4 gene expression. Methanol 48-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 205-211 30981185-15 2019 CONCLUSION: The passively absorbable portion of a methanol acai extract exhibited inhibition and induction effects on CYP3A4 suggesting the potential to produce botanical-drug interactions. Methanol 50-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 31045868-16 2019 Population PK models including CYP3A5 and CYP3A4 genotypes will be considered to guide initial tacrolimus dosing. Tacrolimus 95-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 29889646-0 2019 Time-dependent inhibition (TDI) of CYP1A2 by a CYP3A4-mediated reactive metabolite: proposal for a novel mechanism of irreversible TDI by a non-suicide substrate. Toluene 2,4-Diisocyanate 27-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 29889646-10 2019 In addition, DSP-1053 TDI of CYP1A2 in human liver microsomes was drastically reduced not only by addition of a CYP3A4 inhibitor, but also by addition of potassium cyanide (KCN), which is a trapping agent for iminium ions. iminium 209-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 30044681-3 2019 Mavacamten does not inhibit CYP enzymes, but at high concentrations relative to anticipated therapeutic concentrations induces CYP2B6 and CYP3A4 enzymes in vitro. MYK-461 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 31145690-0 2019 Drug-drug interaction (DDI) assessments of ruxolitinib, a dual substrate of CYP3A4 and CYP2C9, using a verified physiologically based pharmacokinetic (PBPK) model to support regulatory submissions. ruxolitinib 43-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 31145690-1 2019 Ruxolitinib is mainly metabolized by cytochrome P450 (CYP) enzymes CYP3A4 and CYP2C9 followed by minor contributions of other hepatic CYP enzymes in vitro. ruxolitinib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 31145690-2 2019 A physiologically based pharmacokinetic (PBPK) model was established to evaluate the changes in the ruxolitinib systemic exposures with co-administration of CYP3A4 and CYP2C9 perpetrators. ruxolitinib 100-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 31145690-3 2019 The fractions metabolized in the liver via oxidation by CYP enzymes (fm,CYP3A4 = 0.75, fm,CYP2C9 = 0.19, and fm,CYPothers = 0.06) for an initial ruxolitinib model based on in vitro data were optimized (0.43, 0.56, and 0.01, respectively) using the observed exposure changes of ruxolitinib (10 mg) with co-administered ketoconazole (200 mg). ruxolitinib 145-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 31145690-7 2019 The estimated AUC ratios of ruxolitinib by co-administration of the moderate CYP3A4 inhibitor erythromycin (500 mg) and the strong CYP3A4 inducer rifampicin (600 mg) were within a 20% error compared with the clinically observed values. ruxolitinib 28-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 31145690-7 2019 The estimated AUC ratios of ruxolitinib by co-administration of the moderate CYP3A4 inhibitor erythromycin (500 mg) and the strong CYP3A4 inducer rifampicin (600 mg) were within a 20% error compared with the clinically observed values. ruxolitinib 28-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 31145690-7 2019 The estimated AUC ratios of ruxolitinib by co-administration of the moderate CYP3A4 inhibitor erythromycin (500 mg) and the strong CYP3A4 inducer rifampicin (600 mg) were within a 20% error compared with the clinically observed values. Rifampin 146-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 31145690-9 2019 Furthermore, an AUC increase of ruxolitinib in the absence or presence of the dual CYP3A4 and CYP2C9 inhibitor fluconazole (100-400 mg) was prospectively estimated to be 1.94- to 4.31-fold. ruxolitinib 32-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 31145690-11 2019 A ruxolitinib PBPK model with optimized fm,CYP3A4 and fm,CYP2C9 was established to evaluate victim DDI risks. ruxolitinib 2-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 31145690-12 2019 The previous minimal PBPK model was supported by the FDA for the dose reduction strategy, halving the dose with the concomitant use of strong CYP3A4 inhibitors and dual inhibitors on CYP2C9 and CYP3A4, such as fluconazole at <=200 mg. Fluconazole simulation results were used as supportive evidence in discussions with the FDA and EMA about ruxolitinib dose adjustment when co-administering perpetrator drugs. Fluconazole 210-221 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 31191607-4 2019 Here, we found decreased CYP3A4 and increased miR-200a-3p and miR-150-5p in LO2 cells with free fatty acid (FFA)-induced steatosis. Fatty Acids, Nonesterified 91-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 31191607-4 2019 Here, we found decreased CYP3A4 and increased miR-200a-3p and miR-150-5p in LO2 cells with free fatty acid (FFA)-induced steatosis. Fatty Acids, Nonesterified 108-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 31191607-8 2019 These results suggest that miR-200a-3p and miR-150-5p, through directly targeting 3"-UTR of CYP3A4, contribute to the development of FFA-induced steatosis. Fatty Acids, Nonesterified 133-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 30848264-1 2019 Organotin anticancer agent di-n-butyl-di-(4-chlorobenzohydroxamato)tin(iv) (DBDCT) exerted an inhibitory effect on its major metabolic enzyme cytochrome CYP3A. di-n-butyl-di-(4-chlorobenzohydroxamato)tin(iv) 27-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-158 30848264-1 2019 Organotin anticancer agent di-n-butyl-di-(4-chlorobenzohydroxamato)tin(iv) (DBDCT) exerted an inhibitory effect on its major metabolic enzyme cytochrome CYP3A. dbdct 76-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-158 30848264-2 2019 But whether hepatic drug-metabolizing enzymes and their regulatory nuclear receptors including pregnane PXR and constitutive androstane CAR binding with retinoid receptor RXR as a heterodimer are involved in the DBDCT-mediated regulation of CYP3A remains unclear. androstane 125-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 241-246 30926609-0 2019 Active-site differences between substrate-free and ritonavir-bound cytochrome P450 (CYP) 3A5 reveal plasticity differences between CYP3A5 and CYP3A4. Ritonavir 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 30926609-6 2019 We have previously shown that the structure of the CYP3A5-ritonavir complex differs substantially from that of the CYP3A4-ritonavir complex. Ritonavir 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 30926609-6 2019 We have previously shown that the structure of the CYP3A5-ritonavir complex differs substantially from that of the CYP3A4-ritonavir complex. Ritonavir 122-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 30926609-10 2019 Comparison with the CYP3A5-ritonavir complex confirmed conserved CYP3A5 structural features and indicated differences in plasticity between CYP3A4 and CYP3A5 that favor alternative ritonavir conformations. Ritonavir 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 30926609-10 2019 Comparison with the CYP3A5-ritonavir complex confirmed conserved CYP3A5 structural features and indicated differences in plasticity between CYP3A4 and CYP3A5 that favor alternative ritonavir conformations. Ritonavir 181-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 30951590-6 2019 Being primarily metabolized through the CYP3A4 pathway, fostamatinib is subject to drug-drug interactions and concomitant administration with strong CYP3A4 inhibitors or inducers can affect fostamatinib exposure. fostamatinib 56-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 30951590-6 2019 Being primarily metabolized through the CYP3A4 pathway, fostamatinib is subject to drug-drug interactions and concomitant administration with strong CYP3A4 inhibitors or inducers can affect fostamatinib exposure. fostamatinib 190-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 30951590-6 2019 Being primarily metabolized through the CYP3A4 pathway, fostamatinib is subject to drug-drug interactions and concomitant administration with strong CYP3A4 inhibitors or inducers can affect fostamatinib exposure. fostamatinib 190-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 31156436-2 2019 Metabolized mainly by CYP3A and being a substrate of P-glycoprotein (P-gp), CsA is susceptible to drug-drug interactions. Cyclosporine 76-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-27 30737835-2 2019 Since prednisone is known to induce the cytochrome P450 iso-enzyme CYP3A4, which is the main metabolizing enzyme of docetaxel in the liver, a potential drug-drug interaction may occur. Prednisone 6-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 30737835-2 2019 Since prednisone is known to induce the cytochrome P450 iso-enzyme CYP3A4, which is the main metabolizing enzyme of docetaxel in the liver, a potential drug-drug interaction may occur. Docetaxel 116-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 30985942-7 2019 The PBPK model predicted that the AUC for mirabegron with itraconazole (a CYP3A4 inhibitor) was 4.12-times that in healthy elderly subjects administered mirabegron alone, and predicted that the proportional change in AUC for desipramine (a CYP2D6 substrate) with mirabegron was greater than that in healthy subjects. Itraconazole 58-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 30985942-7 2019 The PBPK model predicted that the AUC for mirabegron with itraconazole (a CYP3A4 inhibitor) was 4.12-times that in healthy elderly subjects administered mirabegron alone, and predicted that the proportional change in AUC for desipramine (a CYP2D6 substrate) with mirabegron was greater than that in healthy subjects. Desipramine 225-236 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 30637977-4 2019 The results demonstrate that Ser119 in CYP3A4 and Glu374 in CYP3A5 formed direct hydrogen bonding with SE, respectively. Hydrogen 81-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 30637977-5 2019 Additionally, one water molecule located between the B-C loop and the I helix mediated different hydrogen-bonding networks between CYP3A4/3A5 and SE. Water 18-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 30637977-5 2019 Additionally, one water molecule located between the B-C loop and the I helix mediated different hydrogen-bonding networks between CYP3A4/3A5 and SE. Hydrogen 97-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 30762084-7 2019 RESULTS: In the population pharmacokinetic analysis for gefitinib, alpha1-acid glycoprotein (AGP), age, body weight, and concomitant use of cytochrome P450 3A4 inducers were significant covariates on oral clearance (CL/F). Gefitinib 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-159 30762084-7 2019 RESULTS: In the population pharmacokinetic analysis for gefitinib, alpha1-acid glycoprotein (AGP), age, body weight, and concomitant use of cytochrome P450 3A4 inducers were significant covariates on oral clearance (CL/F). Fluorine 219-220 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-159 30810914-2 2019 As suvorexant is metabolized primarily by Cytochrome P450 3A (CYP3A), and its pharmacokinetics may be affected by CYP3A modulators, the effects of CYP3A inhibitors (ketoconazole or diltiazem) or an inducer (rifampin [rifampicin]) on the pharmacokinetics, safety, and tolerability of suvorexant were investigated. suvorexant 3-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-60 30810914-2 2019 As suvorexant is metabolized primarily by Cytochrome P450 3A (CYP3A), and its pharmacokinetics may be affected by CYP3A modulators, the effects of CYP3A inhibitors (ketoconazole or diltiazem) or an inducer (rifampin [rifampicin]) on the pharmacokinetics, safety, and tolerability of suvorexant were investigated. suvorexant 3-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 30810914-2 2019 As suvorexant is metabolized primarily by Cytochrome P450 3A (CYP3A), and its pharmacokinetics may be affected by CYP3A modulators, the effects of CYP3A inhibitors (ketoconazole or diltiazem) or an inducer (rifampin [rifampicin]) on the pharmacokinetics, safety, and tolerability of suvorexant were investigated. suvorexant 3-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 30810914-2 2019 As suvorexant is metabolized primarily by Cytochrome P450 3A (CYP3A), and its pharmacokinetics may be affected by CYP3A modulators, the effects of CYP3A inhibitors (ketoconazole or diltiazem) or an inducer (rifampin [rifampicin]) on the pharmacokinetics, safety, and tolerability of suvorexant were investigated. suvorexant 3-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 30888624-7 2019 After a 14-day washout, 600 mg of rifampin (rifampicin), a strong CYP3A4 inducer, as well as an inducer of UGT enzymes and a weak inducer of CYP1A2, was administered once daily on days 15-21. Rifampin 34-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 30895461-0 2019 Correction to: Effect of CYP3A Inhibition and Induction on the Pharmacokinetics of Suvorexant: Two Phase I, Open-Label, Fixed-Sequence Trials in Healthy Subjects. suvorexant 83-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-30 30367352-0 2019 Impact of CYP3A4*22 on Pazopanib Pharmacokinetics in Cancer Patients. pazopanib 23-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 30367352-6 2019 CONCLUSION: This analysis shows that CYP3A4*22 heterozygotes have a substantial lower pazopanib clearance and that dose adjustments based on CYP3A4*22 status could be considered. pazopanib 86-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 30367352-6 2019 CONCLUSION: This analysis shows that CYP3A4*22 heterozygotes have a substantial lower pazopanib clearance and that dose adjustments based on CYP3A4*22 status could be considered. pazopanib 86-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 30694595-2 2019 Three phase I DDI studies were conducted in healthy subjects to characterize the DDI profile of tezacaftor/ivacaftor with cytochrome P450 (CYP)3A substrates, CYP3A inhibitors, and a permeability glycoprotein (P-gp) substrate. tezacaftor 96-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-145 30694595-2 2019 Three phase I DDI studies were conducted in healthy subjects to characterize the DDI profile of tezacaftor/ivacaftor with cytochrome P450 (CYP)3A substrates, CYP3A inhibitors, and a permeability glycoprotein (P-gp) substrate. tezacaftor 96-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-163 30694595-2 2019 Three phase I DDI studies were conducted in healthy subjects to characterize the DDI profile of tezacaftor/ivacaftor with cytochrome P450 (CYP)3A substrates, CYP3A inhibitors, and a permeability glycoprotein (P-gp) substrate. ivacaftor 107-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-145 30694595-10 2019 Strong CYP3A inhibitors significantly increase the exposures of tezacaftor and ivacaftor. tezacaftor 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-12 30694595-10 2019 Strong CYP3A inhibitors significantly increase the exposures of tezacaftor and ivacaftor. ivacaftor 79-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-12 30730615-6 2019 Overall, ASP8477 was a weak inhibitor for CYP3A4 and CYP2C9, a moderate to strong inhibitor for CYP2C19, and a weak to strong inhibitor for CYP2D6, with doses from 20 to 100 mg. pyridin-3-yl 4-(phenylcarbamoyl)piperidine-1-carboxylate 9-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 30762305-1 2019 This study provides whole-body physiologically-based pharmacokinetic models of the strong index cytochrome P450 (CYP)1A2 inhibitor and moderate CYP3A4 inhibitor fluvoxamine and of the sensitive CYP1A2 substrate theophylline. Fluvoxamine 161-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 30762305-1 2019 This study provides whole-body physiologically-based pharmacokinetic models of the strong index cytochrome P450 (CYP)1A2 inhibitor and moderate CYP3A4 inhibitor fluvoxamine and of the sensitive CYP1A2 substrate theophylline. Theophylline 211-223 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 30787101-11 2019 In vitro studies confirmed CYP2C8 and CYP3A4 roles in apalutamide metabolism. apalutamide 54-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 30982160-2 2019 Teneligliptin is a potent, selective, and long-lasting DPP-4 inhibitor with a t1/2 of approximately 24 h and unique pharmacokinetic properties: it is metabolized by cytochrome P450 (CYP) 3A4 and flavin-containing monooxygenase 3 (FMO3), or excreted from the kidney in an unchanged form. 3-(4-(4-(3-methyl-1-phenyl-1H-pyrazol-5-yl)piperazin-1-yl)pyrrolidin-2-ylcarbonyl)thiazolidine 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-190 30955332-4 2019 The MeOH extract exhibited significant inhibition of the major human CYP450 isozymes (CYP3A4, CYP1A2, CYP2D6, CYP2C9, and CYP2C19). Methanol 4-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 31639687-3 2019 Alternatively, CYP3A4 and CYP3A5 can form norhydrocodone and dihydrocodeine. norhydrocodone 42-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 31639687-3 2019 Alternatively, CYP3A4 and CYP3A5 can form norhydrocodone and dihydrocodeine. dihydrocodeine 61-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 30748026-0 2019 4beta-Hydroxycholesterol as an Endogenous Biomarker for CYP3A Activity: Literature Review and Critical Evaluation. cholest-5-ene-3,4-diol 0-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 30748026-1 2019 A number of cytochrome P450 (CYP)3A phenotyping probes have been used to characterize the drug interaction potential of new molecular entities; of these, midazolam has emerged as the gold standard. Midazolam 154-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-35 30748026-2 2019 Recently, plasma 4beta-hydroxycholesterol (4beta-OHC), the metabolite of CYP3A-mediated cholesterol metabolism, has been championed as an endogenous biomarker for CYP3A, particularly during chronic conditions where CYP3A activity is altered by disease and in long-term treatment studies where midazolam administration is not optimal. cholest-5-ene-3,4-diol 17-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 30748026-2 2019 Recently, plasma 4beta-hydroxycholesterol (4beta-OHC), the metabolite of CYP3A-mediated cholesterol metabolism, has been championed as an endogenous biomarker for CYP3A, particularly during chronic conditions where CYP3A activity is altered by disease and in long-term treatment studies where midazolam administration is not optimal. cholest-5-ene-3,4-diol 17-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-168 30748026-2 2019 Recently, plasma 4beta-hydroxycholesterol (4beta-OHC), the metabolite of CYP3A-mediated cholesterol metabolism, has been championed as an endogenous biomarker for CYP3A, particularly during chronic conditions where CYP3A activity is altered by disease and in long-term treatment studies where midazolam administration is not optimal. cholest-5-ene-3,4-diol 17-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-168 30748026-2 2019 Recently, plasma 4beta-hydroxycholesterol (4beta-OHC), the metabolite of CYP3A-mediated cholesterol metabolism, has been championed as an endogenous biomarker for CYP3A, particularly during chronic conditions where CYP3A activity is altered by disease and in long-term treatment studies where midazolam administration is not optimal. 4beta-ohc 43-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 30748026-2 2019 Recently, plasma 4beta-hydroxycholesterol (4beta-OHC), the metabolite of CYP3A-mediated cholesterol metabolism, has been championed as an endogenous biomarker for CYP3A, particularly during chronic conditions where CYP3A activity is altered by disease and in long-term treatment studies where midazolam administration is not optimal. 4beta-ohc 43-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-168 30748026-2 2019 Recently, plasma 4beta-hydroxycholesterol (4beta-OHC), the metabolite of CYP3A-mediated cholesterol metabolism, has been championed as an endogenous biomarker for CYP3A, particularly during chronic conditions where CYP3A activity is altered by disease and in long-term treatment studies where midazolam administration is not optimal. 4beta-ohc 43-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-168 30748026-2 2019 Recently, plasma 4beta-hydroxycholesterol (4beta-OHC), the metabolite of CYP3A-mediated cholesterol metabolism, has been championed as an endogenous biomarker for CYP3A, particularly during chronic conditions where CYP3A activity is altered by disease and in long-term treatment studies where midazolam administration is not optimal. Cholesterol 30-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 30748026-2 2019 Recently, plasma 4beta-hydroxycholesterol (4beta-OHC), the metabolite of CYP3A-mediated cholesterol metabolism, has been championed as an endogenous biomarker for CYP3A, particularly during chronic conditions where CYP3A activity is altered by disease and in long-term treatment studies where midazolam administration is not optimal. Cholesterol 30-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-168 30748026-2 2019 Recently, plasma 4beta-hydroxycholesterol (4beta-OHC), the metabolite of CYP3A-mediated cholesterol metabolism, has been championed as an endogenous biomarker for CYP3A, particularly during chronic conditions where CYP3A activity is altered by disease and in long-term treatment studies where midazolam administration is not optimal. Cholesterol 30-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-168 30748026-2 2019 Recently, plasma 4beta-hydroxycholesterol (4beta-OHC), the metabolite of CYP3A-mediated cholesterol metabolism, has been championed as an endogenous biomarker for CYP3A, particularly during chronic conditions where CYP3A activity is altered by disease and in long-term treatment studies where midazolam administration is not optimal. Midazolam 293-302 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 30748026-3 2019 Multiple studies in humans have shown that 4beta-OHC can qualitatively differentiate among weak, moderate, and potent CYP3A induction when an inducer, typically rifampin, is administered for up to 2 weeks. 4beta-ohc 43-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-123 30748026-3 2019 Multiple studies in humans have shown that 4beta-OHC can qualitatively differentiate among weak, moderate, and potent CYP3A induction when an inducer, typically rifampin, is administered for up to 2 weeks. Rifampin 161-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-123 30748026-6 2019 However, sufficiently powered studies assessing the ability of 4beta-OHC or 4beta-OHC:cholesterol ratios to measure CYP3A activity (ie, predictive performance) have not been conducted to date. Cholesterol 86-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 30683357-0 2019 Assessment of electrocatalytic hydroxylase activity of cytochrome P450 3A4 (CYP3A4) by means of derivatization of 6beta-hydroxycortisol by sulfuric acid for fluorimetric assay. 6 beta-hydroxycortisol 114-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-74 30683357-0 2019 Assessment of electrocatalytic hydroxylase activity of cytochrome P450 3A4 (CYP3A4) by means of derivatization of 6beta-hydroxycortisol by sulfuric acid for fluorimetric assay. 6 beta-hydroxycortisol 114-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 30683357-0 2019 Assessment of electrocatalytic hydroxylase activity of cytochrome P450 3A4 (CYP3A4) by means of derivatization of 6beta-hydroxycortisol by sulfuric acid for fluorimetric assay. sulfuric acid 139-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-74 30683357-0 2019 Assessment of electrocatalytic hydroxylase activity of cytochrome P450 3A4 (CYP3A4) by means of derivatization of 6beta-hydroxycortisol by sulfuric acid for fluorimetric assay. sulfuric acid 139-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 30683357-1 2019 We used rapid one-step derivatization of 6beta-hydroxylated hydrocortisone by sulfuric acid for fluorimetric determination of CYP3A4-dependent hydroxylase reaction in the electrochemical system. 6beta-hydroxylated hydrocortisone 41-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 30683357-1 2019 We used rapid one-step derivatization of 6beta-hydroxylated hydrocortisone by sulfuric acid for fluorimetric determination of CYP3A4-dependent hydroxylase reaction in the electrochemical system. sulfuric acid 78-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 30683357-2 2019 We have shown that CYP3A4 substrate - hydrocortisone - and its 6beta-hydroxylated product have different emission wavelengths at an excitation lambdaex = 365 nm after treatment with sulfuric acid:ethanol (3:1) mixture (lambdaem = 525 +- 2 nm and lambdaem = 427 +- 2 nm, respectively). Hydrocortisone 38-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 30683357-2 2019 We have shown that CYP3A4 substrate - hydrocortisone - and its 6beta-hydroxylated product have different emission wavelengths at an excitation lambdaex = 365 nm after treatment with sulfuric acid:ethanol (3:1) mixture (lambdaem = 525 +- 2 nm and lambdaem = 427 +- 2 nm, respectively). sulfuric acid 182-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 30683357-2 2019 We have shown that CYP3A4 substrate - hydrocortisone - and its 6beta-hydroxylated product have different emission wavelengths at an excitation lambdaex = 365 nm after treatment with sulfuric acid:ethanol (3:1) mixture (lambdaem = 525 +- 2 nm and lambdaem = 427 +- 2 nm, respectively). Ethanol 196-203 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 29779438-3 2019 Other CYP enzymes contributing to the metabolism of one or more of the three pyrethroids were CYP1A2, CYP2C8, CYP2C9*1, CYP2D6*1, CYP3A4 and CYP3A5. Pyrethrins 77-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 29790809-5 2019 Cytochrome p450 (CYP) 2D6 was found to be the dominant CYP enzyme involved in the biotransformation of leelamine to its hydroxylated metabolite, whereas CYP2C19, CYP1A1, and CYP3A4 contributed to some extent. dehydroabietylamine 103-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 30783000-2 2019 This article discusses DDIs between doravirine, a nonnucleoside reverse transcriptase inhibitor (NNRTI), and cytochrome P450 3A (CYP3A) substrates and drugs that modulate CYP3A activity. doravirine 36-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-176 30783000-4 2019 Coadministration of doravirine with CYP3A inhibitors (ritonavir or ketoconazole) increased doravirine exposure approximately 3-fold. doravirine 20-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 30783000-4 2019 Coadministration of doravirine with CYP3A inhibitors (ritonavir or ketoconazole) increased doravirine exposure approximately 3-fold. Ritonavir 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 30783000-4 2019 Coadministration of doravirine with CYP3A inhibitors (ritonavir or ketoconazole) increased doravirine exposure approximately 3-fold. Ketoconazole 67-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 30783000-4 2019 Coadministration of doravirine with CYP3A inhibitors (ritonavir or ketoconazole) increased doravirine exposure approximately 3-fold. doravirine 91-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 30783000-7 2019 Overall, the coadministration of doravirine with CYP3A inhibitors and substrates is, therefore, supported by these data together with efficacy and safety data from clinical trials, while coadministration with strong CYP3A inducers, such as rifampin, cannot be recommended. doravirine 33-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 30783000-8 2019 Concomitant dosing with rifabutin (a CYP3A inducer less potent than rifampin) is acceptable if doravirine dosing is adjusted from once to twice daily; however, the effect of other moderate inducers on doravirine pharmacokinetics is unknown. Rifabutin 24-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-42 30912932-0 2019 Structure-Activity Relationships of Rationally Designed Ritonavir Analogues: Impact of Side-Group Stereochemistry, Headgroup Spacing, and Backbone Composition on the Interaction with CYP3A4. Ritonavir 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 183-189 30912932-1 2019 In a continuing effort to identify structural attributes required for strong binding and potent inhibition of human drug-metabolizing CYP3A4, we designed ten ritonavir-like analogues differing in the side-group stereochemistry, backbone atomic composition, and headgroup spacing. Ritonavir 158-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 30912932-5 2019 Comparison of the subseries and individual compounds showed that CYP3A4 only weakly discriminates between side-group configurations, associates more tightly with the pyridyl-ethyl-linker analogues, and strongly disfavors the N-containing backbone. Nitrogen 225-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 30971754-3 2019 First, we assessed the inhibitory effects of ten time-dependent CYP3A inhibitors on midazolam 1"-hydroxylation in human liver microsomes. Midazolam 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 30520061-6 2019 The relative induction ratios of DHI on CYP1A2, CYP2B6 and CYP3A4 activity were calculated by LC-MS/MS. dehydrosoyasaponin I 33-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 30520061-8 2019 The LC-MS/MS data showed DHI intensively inhibit CYP2A6 activity and the intensity of inhibition was followed by CYP2C8, CYP3A4, CYP2C19, CYP2B6, CYP2D6, CYP1A2, CYP2E1 and CYP2C9 in vitro. dehydrosoyasaponin I 25-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 30520061-9 2019 The results of RT-PCR showed that there is a certain induction of DHI on CYP3A4 mRNA in human primary hepatocytes in vitro. dehydrosoyasaponin I 66-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 30589098-1 2019 AIMS: In vitro study showed that benidipine is exclusively metabolized by cytochrome P450 (CYP) 3A. benidipine 33-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-98 30589098-12 2019 CYP3A activity using midazolam did not appear to correlate with oral clearance of benidipine. Midazolam 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 30094711-7 2019 The main elimination route of dabrafenib is the oxidative metabolism via CYP3A4/2C8 and biliary excretion. dabrafenib 30-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-83 30094711-11 2019 Considering that dabrafenib is a substrate of CYP3A4/2C8 and is a CYP3A4/2B6/2C inducer, drug-drug interactions are expected with dabrafenib. dabrafenib 17-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-56 30094711-11 2019 Considering that dabrafenib is a substrate of CYP3A4/2C8 and is a CYP3A4/2B6/2C inducer, drug-drug interactions are expected with dabrafenib. dabrafenib 130-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-56 30639283-4 2019 The template shape was determined mainly through reciprocal comparisons of simulation results with available experiment data mainly on recombinant CYP3A4-mediated reactions of polyaromatic hydrocarbon (PAH) ligands. polyaromatic hydrocarbon 176-200 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 30639283-4 2019 The template shape was determined mainly through reciprocal comparisons of simulation results with available experiment data mainly on recombinant CYP3A4-mediated reactions of polyaromatic hydrocarbon (PAH) ligands. p-Aminohippuric Acid 202-205 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 30361928-2 2019 Clopidogrel is metabolized to the pharmacologically active metabolite H4 and its isomers by multiple CYPs, including CYP2C19 and CYP3A4. Clopidogrel 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 30361928-6 2019 RESULTS: It was found that vonoprazan is not a significant direct inhibitor of any CYP isoforms (IC50 >= 16 muM), but shows the potential for TDI of CYP2B6, CYP2C19, and CYP3A4/5. 1-(5-(2-fluorophenyl)-1-(pyridin-3-ylsulfonyl)-1H-pyrrol-3-yl)-N-methylmethanamine 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 30412271-8 2019 netupitant is metabolized by cytochrome P450 3A4 to 3 major pharmacologically active metabolites (M1, M2, and M3). netupitant 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-48 31510073-1 2019 The Cytochrome P450 family of heme-containing proteins plays a major role in catalyzing phase I metabolic reactions, and the CYP3A4 subtype is responsible for the metabolism of many currently marketed drugs. Heme 30-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 31571937-0 2019 Functional characteristics of CYP3A4 allelic variants on the metabolism of loperamide in vitro. Loperamide 75-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 31571937-2 2019 Loperamide, identified as a CYP3A4 substrate, is prone to misuse and abuse and has high risks of life-threatening cardiotoxicity. Loperamide 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 31571937-3 2019 Methods: Thus, this study is designed to evaluate the enzymatic characteristics of 29 CYP3A4 alleles toward loperamide in vitro, including the 7 novel CYP3A4 variants (*28-*34). Loperamide 108-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 31571937-6 2019 Conclusion: As the first study to identify the properties of these CYP3A4 variants toward loperamide metabolism, our investigation may establish the genotype-phenotype relationship for loperamide, predict an individual"s capability in response to loperamide, and provide some guidance of clinical medication and treatment for loperamide. Loperamide 90-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 31571937-6 2019 Conclusion: As the first study to identify the properties of these CYP3A4 variants toward loperamide metabolism, our investigation may establish the genotype-phenotype relationship for loperamide, predict an individual"s capability in response to loperamide, and provide some guidance of clinical medication and treatment for loperamide. Loperamide 185-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 31571937-6 2019 Conclusion: As the first study to identify the properties of these CYP3A4 variants toward loperamide metabolism, our investigation may establish the genotype-phenotype relationship for loperamide, predict an individual"s capability in response to loperamide, and provide some guidance of clinical medication and treatment for loperamide. Loperamide 185-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 31571937-6 2019 Conclusion: As the first study to identify the properties of these CYP3A4 variants toward loperamide metabolism, our investigation may establish the genotype-phenotype relationship for loperamide, predict an individual"s capability in response to loperamide, and provide some guidance of clinical medication and treatment for loperamide. Loperamide 185-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 30422319-4 2019 The objective of this analysis was to examine the pharmacokinetics of rolapitant in healthy subjects and assess drug-drug interactions between rolapitant and midazolam (a CYP3A substrate), ketoconazole (a CYP3A inhibitor), or rifampin (a CYP3A4 inducer). Midazolam 158-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-176 30422319-7 2019 Coadministration of ketoconazole with rolapitant had no effects on rolapitant maximum concentration and resulted in an approximately 20% increase in the area under the concentration-time curve of rolapitant, suggesting that strong CYP3A inhibitors have minimal inhibitory effects on rolapitant exposure. Ketoconazole 20-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 231-236 30826567-0 2019 Factors involved in phenoconversion of CYP3A using 4beta-hydroxycholesterol in stable kidney transplant recipients. cholest-5-ene-3,4-diol 51-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 29199506-7 2019 Potent inducers of cytochrome P450 isoenzyme CYP3A4, as phenytoin, could induce inadequate responses due to increased imatinib clearance and low imatinib trough plasma levels. Phenytoin 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 29199506-7 2019 Potent inducers of cytochrome P450 isoenzyme CYP3A4, as phenytoin, could induce inadequate responses due to increased imatinib clearance and low imatinib trough plasma levels. Imatinib Mesylate 118-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 29199506-7 2019 Potent inducers of cytochrome P450 isoenzyme CYP3A4, as phenytoin, could induce inadequate responses due to increased imatinib clearance and low imatinib trough plasma levels. Imatinib Mesylate 145-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 29523051-4 2019 Verapamil"s inhibition of both permeability-glycoprotein (P-gp) and CYP3A4 is suspected to have led to the adverse side effects seen in our patient. Verapamil 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30799725-11 2019 Conclusion: This study revealed the possible association of IL-17 G-197A with cyclosporine metabolism and transplant rejection after LT, which might be partly related to the upregulations of CYP3A4/5 dependent on PXR. Cyclosporine 78-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-199 30653754-0 2019 Effect of panaxytriol on cytochrome P450 3A4 via the pregnane X receptor regulatory pathway. panaxytriol 10-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-44 30790160-1 2019 Warfarin is dependent on multiple hepatic enzymes for metabolism while apixaban is a substrate for P-glycoprotein (P-gp) transport and hepatic CYP3A4 metabolism. apixaban 71-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 30826567-4 2019 We measured plasma concentrations of the above compounds in stable kidney transplant recipients, and evaluated their relations with phenoconversion of CYP3A evaluated by plasma concentration of 4beta-hydroxycholesterol, a biomarker of CYP3A activity. cholest-5-ene-3,4-diol 194-218 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-156 30826567-10 2019 Only plasma indoxyl sulfate concentration was significantly higher in recipients with CYP3A phenoconversion compared to those without phenoconversion. Indican 12-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 30826567-11 2019 CONCLUSIONS: These findings suggest that higher plasma indoxyl sulfate concentration may be involved in CYP3A phenoconversion. Indican 55-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-109 30826567-12 2019 Dose adjustment of drugs metabolized by CYP3A may be needed in patients with CYP3A5*1 allele and high blood indoxyl sulfate. Indican 108-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 30826567-3 2019 Indoxyl sulfate, parathyroid hormone (PTH), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) have been reported to cause CYP3A downregulation in renal failure. Indican 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-143 30745395-6 2019 No induction of CYP1A2 or -2B6 was observed in cultured human hepatocytes; small increases in CYP3A4 mRNA (<=20%) were reported at doravirine concentrations of >=10 muM but with no corresponding increase in enzyme activity. doravirine 131-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 30931962-0 2019 Influence of CYP3A4/5 and ABC transporter polymorphisms on lenvatinib plasma trough concentrations in Japanese patients with thyroid cancer. lenvatinib 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 30931962-1 2019 Lenvatinib is a substrate of cytochrome P450 (CYP) 3A and ATP-binding cassette (ABC) transporters. lenvatinib 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-53 30931962-2 2019 In this study, we aimed to evaluate how CYP3A4/5 and ABC transporter polymorphisms affected the mean steady-state dose-adjusted plasma trough concentrations (C0) of lenvatinib in a cohort of 40 Japanese patients with thyroid cancer. lenvatinib 165-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 30931962-5 2019 However, the mean dose-adjusted C0 values of lenvatinib in patients with the CYP3A4*1/*1 genotype and ABCC2 -24T allele were significantly higher than those in patients with the CYP3A4*1G allele and -24C/C genotype, respectively (P = 0.018 and 0.036, respectively). lenvatinib 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 30931962-5 2019 However, the mean dose-adjusted C0 values of lenvatinib in patients with the CYP3A4*1/*1 genotype and ABCC2 -24T allele were significantly higher than those in patients with the CYP3A4*1G allele and -24C/C genotype, respectively (P = 0.018 and 0.036, respectively). lenvatinib 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 30931962-6 2019 In multivariate analysis, CYP3A4 genotype and total bilirubin were independent factors influencing the dose-adjusted C0 of lenvatinib (P = 0.010 and 0.046, respectively). lenvatinib 123-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 30931962-8 2019 Lenvatinib pharmacokinetics were significantly influenced by the CYP3A4*1G polymorphism. lenvatinib 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 30931962-9 2019 If the target plasma concentration of lenvatinib for efficacy or toxicity is determined, elucidation of the details of the CYP3A4*1G genotype may facilitate decision-making related to the appropriate initial lenvatinib dosage to achieve optimal plasma concentrations. lenvatinib 38-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 30745395-3 2019 Kinetic studies confirmed that cytochrome P450 3A (CYP3A) plays a major role in the metabolism of doravirine, with ~20-fold-higher catalytic efficiency for CYP3A4 versus CYP3A5. doravirine 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-49 30745395-3 2019 Kinetic studies confirmed that cytochrome P450 3A (CYP3A) plays a major role in the metabolism of doravirine, with ~20-fold-higher catalytic efficiency for CYP3A4 versus CYP3A5. doravirine 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 30919109-3 2019 Cortisol, at plasma concentrations observed during the third trimester (~ 800 nM), either alone or in combination with other pregnancy-related hormones, induces CYP3A activity in SCHH and HepaRG cells when cultured in dexamethasone-free media. Dexamethasone 218-231 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-166 30745395-8 2019 In summary, these in vitro findings indicate that CYP3A4 and CYP3A5 mediate the metabolism of doravirine, although with different catalytic efficiencies. doravirine 94-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 30919109-4 2019 To determine the mechanism(s) by which cortisol induces CYP3A activity, HepaRG cells were pre-incubated in dexamethasone-free medium and then incubated for 72 h with cortisol (798 nM). Hydrocortisone 39-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 30919109-4 2019 To determine the mechanism(s) by which cortisol induces CYP3A activity, HepaRG cells were pre-incubated in dexamethasone-free medium and then incubated for 72 h with cortisol (798 nM). Hydrocortisone 166-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 30745395-3 2019 Kinetic studies confirmed that cytochrome P450 3A (CYP3A) plays a major role in the metabolism of doravirine, with ~20-fold-higher catalytic efficiency for CYP3A4 versus CYP3A5. doravirine 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 30919109-6 2019 CYP3A4, and not CYP3A5, was found to be the dominant contributor to total CYP3A activity in control- and cortisol-treated HepaRG cells. Hydrocortisone 105-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 30745395-9 2019 Clinical trials reported elsewhere confirm that doravirine is subject to drug-drug interactions (DDIs) via CYP3A inhibitors and inducers, but they support the notion that DDIs (either direction) are unlikely via other major drug-metabolizing enzymes and transporters. doravirine 48-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-112 30919109-6 2019 CYP3A4, and not CYP3A5, was found to be the dominant contributor to total CYP3A activity in control- and cortisol-treated HepaRG cells. Hydrocortisone 105-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 30919109-10 2019 These data indicate that PXR plays a central role in cortisol-mediated induction of CYP3A activity during pregnancy and suggests that other enzymes and transporters, such as CYP2B6 and P-glycoprotein, may also be induced during pregnancy via the same mechanism(s). Hydrocortisone 53-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-89 30898762-6 2019 We found that CYP3A4 plays a major role in BMSC-mediated inhibition in the activity of 3 different FLT3 TKIs (sorafenib, quizartinib, and gilteritinib) against FLT3/ITD acute myeloid leukemia (AML). Sorafenib 110-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 30919109-8 2019 Cortisol-mediated CYP3A4 induction in HepaRG cells was primarily mediated by GR-dependent PXR induction pathway and to a smaller extent via a PXR-independent pathway. Hydrocortisone 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 30898762-6 2019 We found that CYP3A4 plays a major role in BMSC-mediated inhibition in the activity of 3 different FLT3 TKIs (sorafenib, quizartinib, and gilteritinib) against FLT3/ITD acute myeloid leukemia (AML). quizartinib 121-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 30898762-6 2019 We found that CYP3A4 plays a major role in BMSC-mediated inhibition in the activity of 3 different FLT3 TKIs (sorafenib, quizartinib, and gilteritinib) against FLT3/ITD acute myeloid leukemia (AML). gilteritinib 138-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 30898762-7 2019 Furthermore, clarithromycin, a clinically active CYP3A4 inhibitor, significantly reversed the protective effects of BMSCs. Clarithromycin 13-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 30901927-8 2019 Clotrimazole, a potent CYP3A4 inhibitor, significantly increased Papp,pig of the CYP3A4 substrates midazolam, verapamil and tamoxifen and significantly decreased the formation of their main metabolites. Clotrimazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 31057647-0 2019 Panax ginseng Inhibits Metabolism of Diester Alkaloids by Downregulating CYP3A4 Enzyme Activity via the Pregnane X Receptor. diester alkaloids 37-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 31057647-13 2019 The kinetic plots indicated that the KM and V max values of CYP3A4 were 10.08 +- 3.26 muM and 0.12 +- 0.01nmol mg protein-1 min-1 for aconitine, 131.3 +- 99.75 muM and 0.73 +- 0.44 nmol mg protein-1 min-1 for mesaconitine, and 17.05 +- 9.70 muM and 0.16 +- 0.04 nmol mg protein-1 min-1 for hypaconitine, respectively. Aconitine 134-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 31057647-13 2019 The kinetic plots indicated that the KM and V max values of CYP3A4 were 10.08 +- 3.26 muM and 0.12 +- 0.01nmol mg protein-1 min-1 for aconitine, 131.3 +- 99.75 muM and 0.73 +- 0.44 nmol mg protein-1 min-1 for mesaconitine, and 17.05 +- 9.70 muM and 0.16 +- 0.04 nmol mg protein-1 min-1 for hypaconitine, respectively. mesaconitine 209-221 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 31057647-13 2019 The kinetic plots indicated that the KM and V max values of CYP3A4 were 10.08 +- 3.26 muM and 0.12 +- 0.01nmol mg protein-1 min-1 for aconitine, 131.3 +- 99.75 muM and 0.73 +- 0.44 nmol mg protein-1 min-1 for mesaconitine, and 17.05 +- 9.70 muM and 0.16 +- 0.04 nmol mg protein-1 min-1 for hypaconitine, respectively. hypaconitine 290-302 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 31057647-14 2019 The in vitro mean intrinsic clearance rates by CYP3A4 were 0.0119, 0.0056, and 0.0091 mL nmol CYP-1 min-1 for aconitine, mesaconitine, and hypaconitine, respectively. Aconitine 110-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 31057647-14 2019 The in vitro mean intrinsic clearance rates by CYP3A4 were 0.0119, 0.0056, and 0.0091 mL nmol CYP-1 min-1 for aconitine, mesaconitine, and hypaconitine, respectively. mesaconitine 121-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 31057647-14 2019 The in vitro mean intrinsic clearance rates by CYP3A4 were 0.0119, 0.0056, and 0.0091 mL nmol CYP-1 min-1 for aconitine, mesaconitine, and hypaconitine, respectively. hypaconitine 139-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 31057647-16 2019 CYP3A4 had a larger effect on diester alkaloid metabolism than the other human CYP isoforms, CYP1A2, CYP2C9, and CYP2E1. diester alkaloid 30-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 30901927-8 2019 Clotrimazole, a potent CYP3A4 inhibitor, significantly increased Papp,pig of the CYP3A4 substrates midazolam, verapamil and tamoxifen and significantly decreased the formation of their main metabolites. Clotrimazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 30901927-8 2019 Clotrimazole, a potent CYP3A4 inhibitor, significantly increased Papp,pig of the CYP3A4 substrates midazolam, verapamil and tamoxifen and significantly decreased the formation of their main metabolites. LY 165163 65-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 30901927-8 2019 Clotrimazole, a potent CYP3A4 inhibitor, significantly increased Papp,pig of the CYP3A4 substrates midazolam, verapamil and tamoxifen and significantly decreased the formation of their main metabolites. Midazolam 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 30901927-8 2019 Clotrimazole, a potent CYP3A4 inhibitor, significantly increased Papp,pig of the CYP3A4 substrates midazolam, verapamil and tamoxifen and significantly decreased the formation of their main metabolites. Midazolam 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 30901927-8 2019 Clotrimazole, a potent CYP3A4 inhibitor, significantly increased Papp,pig of the CYP3A4 substrates midazolam, verapamil and tamoxifen and significantly decreased the formation of their main metabolites. Tamoxifen 124-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 30901927-8 2019 Clotrimazole, a potent CYP3A4 inhibitor, significantly increased Papp,pig of the CYP3A4 substrates midazolam, verapamil and tamoxifen and significantly decreased the formation of their main metabolites. Tamoxifen 124-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 30840584-3 2019 We also examined the effects of pretreatment with menthol on the cytotoxic activity of paclitaxel (PAC) and vincristine (VIN), which are substrates of CYP3A4, in the cells. Vincristine 108-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 30931282-2 2019 Drugs interacting with colchicine metabolism through CYP3A4 can accelerate accumulation and toxicity. Colchicine 23-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 30785734-0 2019 Allosteric Interactions in Human Cytochrome P450 CYP3A4: The Role of Phenylalanine 213. Phenylalanine 69-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 30785734-1 2019 The role of Phe213 in the allosteric mechanism of human cytochrome P450 CYP3A4 was studied using a combination of progesterone (PGS) and carbamazepine (CBZ) as probe substrates. Progesterone 114-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 30785734-1 2019 The role of Phe213 in the allosteric mechanism of human cytochrome P450 CYP3A4 was studied using a combination of progesterone (PGS) and carbamazepine (CBZ) as probe substrates. Progesterone 128-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 30785734-1 2019 The role of Phe213 in the allosteric mechanism of human cytochrome P450 CYP3A4 was studied using a combination of progesterone (PGS) and carbamazepine (CBZ) as probe substrates. Carbamazepine 137-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 30785734-1 2019 The role of Phe213 in the allosteric mechanism of human cytochrome P450 CYP3A4 was studied using a combination of progesterone (PGS) and carbamazepine (CBZ) as probe substrates. Carbamazepine 152-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 30887238-4 2019 Moderate interactions [mean AUC fold change, <= 2.08 (midazolam) or 2.36 (simvastatin)] was predicted for CYP3A4 probe substrates and weak interactions (mean AUC fold change, <= 1.29-1.97) were predicted for CYP2C19, CYP2C9, and CYP2D6 substrates. Midazolam 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 30887238-4 2019 Moderate interactions [mean AUC fold change, <= 2.08 (midazolam) or 2.36 (simvastatin)] was predicted for CYP3A4 probe substrates and weak interactions (mean AUC fold change, <= 1.29-1.97) were predicted for CYP2C19, CYP2C9, and CYP2D6 substrates. Simvastatin 74-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 30840584-2 2019 In the present study, we investigated changes in the expression of cytochrome P450 isoform CYP3A4mRNA after treating human hepatocellular carcinoma HepG2 cells with menthol. Menthol 165-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 30840584-3 2019 We also examined the effects of pretreatment with menthol on the cytotoxic activity of paclitaxel (PAC) and vincristine (VIN), which are substrates of CYP3A4, in the cells. Paclitaxel 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 30840584-3 2019 We also examined the effects of pretreatment with menthol on the cytotoxic activity of paclitaxel (PAC) and vincristine (VIN), which are substrates of CYP3A4, in the cells. Vincristine 121-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 30840584-7 2019 Results The gene expression level of CYP3A4 in HepG2 cells was significantly reduced by treatment with menthol for 1 day. Menthol 103-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 30840584-10 2019 Conclusions These results demonstrate that menthol enhanced the anti-tumor effects of PAC and VIN through the downregulation of CYP3A4 in HepG2 cells without exerting cytotoxic activity. Menthol 43-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 30841426-9 2019 Our results indicated that SJZ enhanced the anti-lung cancer effects of gefitinib via the key targets ABCG2, ABCC1, ABAT, GSR, CYP1A2, ALOX5, CYP3A4, PLA2G1B and PLA2G2A and the key metabolites 2-oxoglutarate, taurocholic acid, oxidized glutathione and linoleic acid. Gefitinib 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 30541878-8 2019 In vitro studies showed that esaxerenone was a substrate of CYP3A and multiple UDP-glucuronosyltransferase isoforms. esaxerenone 29-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 30704835-3 2019 We previously reported that the 2,4-diamino-5-cyanopyrimidine derivative 2 was a potent PKCtheta inhibitor; however, it exhibited CYP3A4 time-dependent inhibition (TDI). 2,4-Diaminopyrimidine-5-carbonitrile 32-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 30428505-0 2019 Physiologically-based pharmacokinetic modelling to predict oprozomib CYP3A drug-drug interaction potential in patients with advanced malignancies. ONX 0912 59-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 30428505-10 2019 CONCLUSIONS: These results indicate oprozomib has a low potential to inhibit the metabolism of CYP3A4 substrates in humans. ONX 0912 36-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 30573465-0 2019 Suppression of Hepatic CYP3A4 Expression and Activity by 3-Methylcholanthrene in Humanized PXR-CAR-CYP3A4/3A7 Mice. Methylcholanthrene 57-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 30573465-0 2019 Suppression of Hepatic CYP3A4 Expression and Activity by 3-Methylcholanthrene in Humanized PXR-CAR-CYP3A4/3A7 Mice. Methylcholanthrene 57-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 30573465-1 2019 Polycyclic aromatic hydrocarbons (PAHs) are environmental pollutants that activate the aryl hydrocarbon receptor, thereby triggering a range of biologic responses, exemplified by the induction of CYP1A1 PAHs can also regulate the expression of members of the CYP3A subfamily, with reports of mainly suppressive effects on mouse hepatic Cyp3a11 expression, but paradoxically both inductive and suppressive effects on human hepatic CYP3A4 expression. Polycyclic Aromatic Hydrocarbons 0-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 430-436 30088221-1 2019 OBJECTIVES: The aim of this study was to assess the pharmacokinetics (PK) and safety/tolerability of siponimod in healthy subjects when coadministered with (1) the moderate cytochrome P450 (CYP) 2C9 and CYP3A inhibitor fluconazole (Study A), and (2) with three different CYP2C9 genotype variants (Study B). siponimod 101-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-208 30606729-0 2019 Continuum of Host-Gut Microbial Co-metabolism: Host CYP3A4/3A7 are Responsible for Tertiary Oxidations of Deoxycholate Species. Deoxycholic Acid 106-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 30606729-5 2019 Metabolic inhibition assays in human liver microsomes and recombinant P450 assays revealed that CYP3A4 and CYP3A7 were responsible for the regioselective oxidations of both DCA and its conjugated forms, glycodeoxycholate (GDCA) and taurodeoxycholate (TDCA). Deoxycholic Acid 173-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 30606729-5 2019 Metabolic inhibition assays in human liver microsomes and recombinant P450 assays revealed that CYP3A4 and CYP3A7 were responsible for the regioselective oxidations of both DCA and its conjugated forms, glycodeoxycholate (GDCA) and taurodeoxycholate (TDCA). Glycodeoxycholic Acid 203-220 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 30606729-5 2019 Metabolic inhibition assays in human liver microsomes and recombinant P450 assays revealed that CYP3A4 and CYP3A7 were responsible for the regioselective oxidations of both DCA and its conjugated forms, glycodeoxycholate (GDCA) and taurodeoxycholate (TDCA). Glycodeoxycholic Acid 222-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 30606729-5 2019 Metabolic inhibition assays in human liver microsomes and recombinant P450 assays revealed that CYP3A4 and CYP3A7 were responsible for the regioselective oxidations of both DCA and its conjugated forms, glycodeoxycholate (GDCA) and taurodeoxycholate (TDCA). Taurodeoxycholic Acid 232-249 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 30573465-1 2019 Polycyclic aromatic hydrocarbons (PAHs) are environmental pollutants that activate the aryl hydrocarbon receptor, thereby triggering a range of biologic responses, exemplified by the induction of CYP1A1 PAHs can also regulate the expression of members of the CYP3A subfamily, with reports of mainly suppressive effects on mouse hepatic Cyp3a11 expression, but paradoxically both inductive and suppressive effects on human hepatic CYP3A4 expression. Polycyclic Aromatic Hydrocarbons 34-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 430-436 30573465-3 2019 The present study used 3-methylcholanthrene (MC) as a model PAH to characterize the in vivo regulation of CYP3A4 expression and activity in humanized pregnane X receptor-constitutive androstane receptor-CYP3A4/3A7 mice. Methylcholanthrene 23-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 31159144-0 2019 Non-coplanar and coplanar polychlorinated biphenyls potentiate genotoxicity of aflatoxin B1 in a human hepatocyte line by enhancing CYP1A2 and CYP3A4 expression. Polychlorinated Biphenyls 26-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 30573465-3 2019 The present study used 3-methylcholanthrene (MC) as a model PAH to characterize the in vivo regulation of CYP3A4 expression and activity in humanized pregnane X receptor-constitutive androstane receptor-CYP3A4/3A7 mice. Methylcholanthrene 23-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 30573465-3 2019 The present study used 3-methylcholanthrene (MC) as a model PAH to characterize the in vivo regulation of CYP3A4 expression and activity in humanized pregnane X receptor-constitutive androstane receptor-CYP3A4/3A7 mice. Methylcholanthrene 45-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 30573465-7 2019 MC treatment suppressed hepatic CYP3A4 in female mice at 72 hours postdosing at the mRNA, protein, and catalytic activity levels. Methylcholanthrene 0-2 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 30606729-7 2019 The regioselective oxidations of DCA, GDCA, and TDCA by CYP3A4 and CYP3A7 may help eliminate host-toxic DCA species. Deoxycholic Acid 33-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 30606729-7 2019 The regioselective oxidations of DCA, GDCA, and TDCA by CYP3A4 and CYP3A7 may help eliminate host-toxic DCA species. Glycodeoxycholic Acid 38-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 30606729-7 2019 The regioselective oxidations of DCA, GDCA, and TDCA by CYP3A4 and CYP3A7 may help eliminate host-toxic DCA species. Deoxycholic Acid 39-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 31159144-0 2019 Non-coplanar and coplanar polychlorinated biphenyls potentiate genotoxicity of aflatoxin B1 in a human hepatocyte line by enhancing CYP1A2 and CYP3A4 expression. Aflatoxin B1 79-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 29120670-0 2019 Correlation Between Steroid-Induced Osteonecrosis of The Femoral Head and Hepatic CYP3A Activity: A Systematic Review and Meta-Analysis. Steroids 20-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-87 30540686-5 2019 These findings suggest that possible autoinduction of drug metabolism by higher total daily doses and induction of cytochrome P450 isoform 3A4 (CYP3A4) by cigarette smoke in liver could be the potential causes of increased total clearance of bisoprolol in patients with ACS. Bisoprolol 242-252 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-142 30540686-5 2019 These findings suggest that possible autoinduction of drug metabolism by higher total daily doses and induction of cytochrome P450 isoform 3A4 (CYP3A4) by cigarette smoke in liver could be the potential causes of increased total clearance of bisoprolol in patients with ACS. Bisoprolol 242-252 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 30660696-4 2019 Upon oral administration of lorlatinib, the plasma AUC0-8h in CYP3A4-humanized mice was ~1.8-fold lower than in wild-type and Cyp3a-/- mice. lorlatinib 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 30660696-6 2019 Moreover, simultaneous pharmacological inhibition of P-glycoprotein and CYP3A4 with oral elacridar and ritonavir in CYP3A4-humanized mice profoundly increased lorlatinib brain concentrations, but not its oral availability or other relative tissue distribution. Ritonavir 103-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 30660696-6 2019 Moreover, simultaneous pharmacological inhibition of P-glycoprotein and CYP3A4 with oral elacridar and ritonavir in CYP3A4-humanized mice profoundly increased lorlatinib brain concentrations, but not its oral availability or other relative tissue distribution. lorlatinib 159-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 30660696-8 2019 The absolute oral bioavailability of lorlatinib over 8 h in wild-type, Cyp3a-/-, and CYP3A4-humanized mice was 81.6%, 72.9%, and 58.5%, respectively. lorlatinib 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 30660696-9 2019 Lorlatinib thus has good oral bioavailability, which is markedly restricted by human CYP3A4 but not by mouse Cyp3a. lorlatinib 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 29120670-4 2019 This study aims to review the investigations on the hepatic CYP3A (cytochrome P4503A enzyme) genetic polymorphisms in steroid-induced ONFH patients. Steroids 118-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 29120670-4 2019 This study aims to review the investigations on the hepatic CYP3A (cytochrome P4503A enzyme) genetic polymorphisms in steroid-induced ONFH patients. Steroids 118-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-91 29120670-8 2019 The odds ratios, standard mean difference, and 95% confidence intervals were calculated to assess the effect of hepatic CYP3A activity on the rabbit model with steroid-induced ONFH. Steroids 160-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-125 29120670-11 2019 RESULTS: High hepatic CYP3A activity significantly decreased the risk for steroid-induced ONFH in the rabbit model (p <. Steroids 74-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-27 29120670-13 2019 The CYP3A gene may be potentially associated with increased risk of steroid-induced ONFH in the human allele model. Steroids 68-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-9 29120670-14 2019 CONCLUSION: The study suggests that high hepatic CYP3A activity decreases the risk of steroid-induced ONFH. Steroids 86-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 30573512-2 2019 Hyperforin is one constituent of SJW that alters CYP3A4 expression by activation of the nuclear receptor pregnane X receptor (PXR). hyperforin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 30467864-5 2019 KEY FINDINGS: The active substances betulinic acid (BA) and ursolic acid (UA) strongly inhibited CYP3A4 activity while UA and lupeol moderately inhibited CYP2C19. betulinic acid 36-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 30467864-5 2019 KEY FINDINGS: The active substances betulinic acid (BA) and ursolic acid (UA) strongly inhibited CYP3A4 activity while UA and lupeol moderately inhibited CYP2C19. betulinic acid 52-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 30467864-5 2019 KEY FINDINGS: The active substances betulinic acid (BA) and ursolic acid (UA) strongly inhibited CYP3A4 activity while UA and lupeol moderately inhibited CYP2C19. ursolic acid 60-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 30467864-5 2019 KEY FINDINGS: The active substances betulinic acid (BA) and ursolic acid (UA) strongly inhibited CYP3A4 activity while UA and lupeol moderately inhibited CYP2C19. ursolic acid 74-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 30799432-0 2019 Effect of Multidrug-Resistant 1 (MDR1) and CYP3A4*1B Polymorphisms on Cyclosporine-Based Immunosuppressive Therapy in Renal Transplant Patients. Cyclosporine 70-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 30668439-2 2019 HYPOTHESIS/PURPOSE: This study dwells into the interaction details involving ABC-transporters, CYP3A4, GST and cytotoxic effects of resveratrol on different cell lines. Resveratrol 132-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 30668439-7 2019 The resveratrol inhibited both CYP3A4 and GST enzymatic activity in a concentration-dependent way and induced apoptosis in the resistance cell lines because of increased levels of caspase-3, -8,-6/9 and incremental phosphatidyl serine (PS) exposure as detected by flow cytometry. Resveratrol 4-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 30668439-8 2019 The treatment of Caco-2 cells with resveratrol showed significantly lower p-gp, MRP1, BCRP, CYP3A4, GST, and hPXR mRNA levels in a 48 h observation. Resveratrol 35-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 30668439-9 2019 CONCLUSION: The result confirmed resveratrol mediated inhibition of ABC-transporters" overall efflux functions, and its expression, and apoptosis as well as metabolic enzymes GST and CYP3A4 activity. Resveratrol 33-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 183-189 30622215-0 2019 Belinostat, at Its Clinically Relevant Concentrations, Inhibits Rifampicin-Induced CYP3A4 and MDR1 Gene Expression. belinostat 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 30622215-0 2019 Belinostat, at Its Clinically Relevant Concentrations, Inhibits Rifampicin-Induced CYP3A4 and MDR1 Gene Expression. Rifampin 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 30622215-8 2019 BEL repressed rifampicin-induced gene expression of CYP3A4 and multidrug resistance protein 1, as well as their respective protein activities. belinostat 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 30622215-8 2019 BEL repressed rifampicin-induced gene expression of CYP3A4 and multidrug resistance protein 1, as well as their respective protein activities. Rifampin 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 30799432-4 2019 The aim of this study was to determine the relationship between CYP3A4*1B and MDR1 polymorphisms and dose requirements to achieve the target therapeutic range for CsA. Cyclosporine 163-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 30799432-7 2019 RESULTS Patients with the CYP3A4*1/*1 genotype received the lowest mean dose of CsA compared to CYP3A4*1/*1B, and had a higher average drug concentration in the blood. Cyclosporine 80-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 30823561-5 2019 The metabolism of 25B-NBF was catalyzed by CYP1A1, CYP1A2, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2J2, CYP3A4, and UGT2B7 enzymes. SSW3KY7SWW 18-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 30873161-5 2019 CAAP48-treatment resulted in an accumulation of the hepatocyte-specific intracellular enzymes aspartate- and alanine-transaminase and impaired the activity of the hepatic multidrug resistant-associated protein 2 and cytochrome P450 3A4. caap48- 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-235 30576102-4 2019 In silico predictions with ADMET Predictor and MetaDrug software suggested a role of CYP1A2, CYP2A6, CYP2B6, CYP2E1, and CYP3A4 in the metabolism of chiral PCBs. Polychlorinated Biphenyls 156-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 30808332-6 2019 CONCLUSION: Simvastatin, as well as lovastatin, because of their CYP3A4 metabolism, and to a lesser extent atorvastatin, which is only partially metabolized by CYP3A4, are the HMG-CoA reductase inhibitors with the greatest risk of drug interactions and should not be used in patients under HIV-therapy. Simvastatin 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 30808332-6 2019 CONCLUSION: Simvastatin, as well as lovastatin, because of their CYP3A4 metabolism, and to a lesser extent atorvastatin, which is only partially metabolized by CYP3A4, are the HMG-CoA reductase inhibitors with the greatest risk of drug interactions and should not be used in patients under HIV-therapy. Lovastatin 36-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 30808332-6 2019 CONCLUSION: Simvastatin, as well as lovastatin, because of their CYP3A4 metabolism, and to a lesser extent atorvastatin, which is only partially metabolized by CYP3A4, are the HMG-CoA reductase inhibitors with the greatest risk of drug interactions and should not be used in patients under HIV-therapy. Atorvastatin 107-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 30858735-0 2019 Modeling and simulation of the endogenous CYP3A induction marker 4beta-hydroxycholesterol during enasidenib treatment. cholest-5-ene-3,4-diol 65-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 30676743-2 2019 This study investigated the interaction of recombinant CYP3A4 with a nonspecific inhibitor metyrapone, antifungal drug fluconazole, and protease inhibitor phenylmethanesulfonyl fluoride (PMSF). Metyrapone 91-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 30676743-2 2019 This study investigated the interaction of recombinant CYP3A4 with a nonspecific inhibitor metyrapone, antifungal drug fluconazole, and protease inhibitor phenylmethanesulfonyl fluoride (PMSF). Phenylmethylsulfonyl Fluoride 187-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 30676743-3 2019 Metyrapone and fluconazole are classic type II ligands that inhibit CYP3A4 with medium strength by ligating to the heme iron, whereas PMSF, lacking the heme-ligating moiety, acts as a weak type I ligand and inhibitor of CYP3A4. Metyrapone 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30676743-3 2019 Metyrapone and fluconazole are classic type II ligands that inhibit CYP3A4 with medium strength by ligating to the heme iron, whereas PMSF, lacking the heme-ligating moiety, acts as a weak type I ligand and inhibitor of CYP3A4. Metyrapone 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 30676743-3 2019 Metyrapone and fluconazole are classic type II ligands that inhibit CYP3A4 with medium strength by ligating to the heme iron, whereas PMSF, lacking the heme-ligating moiety, acts as a weak type I ligand and inhibitor of CYP3A4. Fluconazole 15-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30676743-3 2019 Metyrapone and fluconazole are classic type II ligands that inhibit CYP3A4 with medium strength by ligating to the heme iron, whereas PMSF, lacking the heme-ligating moiety, acts as a weak type I ligand and inhibitor of CYP3A4. Fluconazole 15-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 30676743-3 2019 Metyrapone and fluconazole are classic type II ligands that inhibit CYP3A4 with medium strength by ligating to the heme iron, whereas PMSF, lacking the heme-ligating moiety, acts as a weak type I ligand and inhibitor of CYP3A4. Heme 115-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30676743-3 2019 Metyrapone and fluconazole are classic type II ligands that inhibit CYP3A4 with medium strength by ligating to the heme iron, whereas PMSF, lacking the heme-ligating moiety, acts as a weak type I ligand and inhibitor of CYP3A4. Iron 120-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30676743-3 2019 Metyrapone and fluconazole are classic type II ligands that inhibit CYP3A4 with medium strength by ligating to the heme iron, whereas PMSF, lacking the heme-ligating moiety, acts as a weak type I ligand and inhibitor of CYP3A4. Phenylmethylsulfonyl Fluoride 134-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 30676743-9 2019 Moreover, its hydrolysis product, phenylmethanesulfonic acid, can also access and be retained in the CYP3A4 active site. phenylmethanesulfonic acid 34-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 30858735-5 2019 Results: The PK model showed that enasidenib plasma concentrations were adequately described by a one-compartment model with first-order absorption and elimination; the PD model showed a high capacity to induce CYP3A (Emax=7.36) and a high enasidenib plasma concentration to produce half of maximum CYP3A induction (EC50 =31,400 ng/mL). enasidenib 34-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-216 30858735-0 2019 Modeling and simulation of the endogenous CYP3A induction marker 4beta-hydroxycholesterol during enasidenib treatment. enasidenib 97-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 30858735-4 2019 A semi-mechanistic nonlinear mixed effect PK/PD model was successfully developed to characterize enasidenib plasma PK and to assess enasidenib-induced CYP3A activity. enasidenib 132-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-156 30858735-5 2019 Results: The PK model showed that enasidenib plasma concentrations were adequately described by a one-compartment model with first-order absorption and elimination; the PD model showed a high capacity to induce CYP3A (Emax=7.36) and a high enasidenib plasma concentration to produce half of maximum CYP3A induction (EC50 =31,400 ng/mL). enasidenib 34-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 299-304 30858735-7 2019 Although the EC50 value for CYP3A induction by enasidenib is high, CYP3A induction was observed due to significant drug accumulation. enasidenib 47-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 30858735-8 2019 Conclusion: CYP3A induction following enasidenib dosing should be considered when prescribing concomitant medication metabolized via this pathway. enasidenib 38-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 30778299-4 2019 Reaction phenotyping and chemical inhibition assays showed that CYP3A4 and CYP3A5 were key enzymes responsible for BFT 5beta-hydroxylation. bufotalin 115-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 30390556-0 2019 Study on the inhibitory effect of furafylline and troleandomycin in the 7-methoxyresorufin-O-demethylase and nifedipine oxidase activities in hepatic microsomes from four poultry species using high-performance liquid chromatography coupled with fluorescence and ultraviolet detection. furafylline 34-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-127 30390556-0 2019 Study on the inhibitory effect of furafylline and troleandomycin in the 7-methoxyresorufin-O-demethylase and nifedipine oxidase activities in hepatic microsomes from four poultry species using high-performance liquid chromatography coupled with fluorescence and ultraviolet detection. Troleandomycin 50-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-127 30390556-1 2019 The present study reports the in vitro studies with furafylline and troleandomycin (TAO) as specific inhibitors of activities 7-methoxyresorufin-O-demethylase (MROD) and nifedipine oxidase, catalyzed by cytochrome P450 1 A2 (CYP1 A2) and 3A4 human enzymes, respectively, in hepatic microsomes of quail, duck, turkey and chicken. furafylline 52-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-188 30390556-1 2019 The present study reports the in vitro studies with furafylline and troleandomycin (TAO) as specific inhibitors of activities 7-methoxyresorufin-O-demethylase (MROD) and nifedipine oxidase, catalyzed by cytochrome P450 1 A2 (CYP1 A2) and 3A4 human enzymes, respectively, in hepatic microsomes of quail, duck, turkey and chicken. Troleandomycin 68-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-188 30778299-6 2019 Furthermore, molecular docking simulations showed that BFT could bind on two different ligand-binding sites on both CYP3A4 and CYP3A5, which partially explained the different kinetic behaviors of BFT in CYP3A4 and CYP3A5. bufotalin 196-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 30778299-5 2019 Kinetic analyses demonstrated that BFT 5beta-hydroxylation in both HLMs and human CYP3A4 followed the biphasic kinetics, while BFT 5beta-hydroxylation in CYP3A5 followed substrate inhibition kinetics. bufotalin 35-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 30778299-7 2019 These findings are very helpful for elucidating the phase I metabolism of BFT in human and for deeper understanding the key interactions between CYP3A enzymes and bufadienolides, as well as for the development of bufadienolide-type drugs with improved pharmacokinetic and safety profiles. bufotalin 74-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-150 30778299-6 2019 Furthermore, molecular docking simulations showed that BFT could bind on two different ligand-binding sites on both CYP3A4 and CYP3A5, which partially explained the different kinetic behaviors of BFT in CYP3A4 and CYP3A5. bufotalin 55-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 30778299-7 2019 These findings are very helpful for elucidating the phase I metabolism of BFT in human and for deeper understanding the key interactions between CYP3A enzymes and bufadienolides, as well as for the development of bufadienolide-type drugs with improved pharmacokinetic and safety profiles. Bufanolides 163-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-150 30778299-6 2019 Furthermore, molecular docking simulations showed that BFT could bind on two different ligand-binding sites on both CYP3A4 and CYP3A5, which partially explained the different kinetic behaviors of BFT in CYP3A4 and CYP3A5. bufotalin 55-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 30778299-7 2019 These findings are very helpful for elucidating the phase I metabolism of BFT in human and for deeper understanding the key interactions between CYP3A enzymes and bufadienolides, as well as for the development of bufadienolide-type drugs with improved pharmacokinetic and safety profiles. bufadienolide 163-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-150 30778299-6 2019 Furthermore, molecular docking simulations showed that BFT could bind on two different ligand-binding sites on both CYP3A4 and CYP3A5, which partially explained the different kinetic behaviors of BFT in CYP3A4 and CYP3A5. bufotalin 196-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 30447161-5 2019 Surprisingly, sulfaphenazole appeared to be a potent inhibitor of 5"-hydroxylation of flucloxacillin by both recombinant CYP3A4 and CYP3A7. Sulfaphenazole 14-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 30607545-1 2019 INTRODUCTION: Aprepitant, a selective neurokinin-1 receptor antagonist approved for prevention of chemotherapy-induced nausea and vomiting (CINV), is an inhibitor of the cytochrome P450 3A4 (CYP3A4) enzyme, which is involved in the clearance of several chemotherapeutic agents. cinv 140-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-189 30466000-2 2019 The involvement of selected enzymes (CYP1A2, CYP2C19, CYP2E1, CYP3 A4, UGT1A1, UGT1A6, and UGT2B7) in the metabolism of RA and the inhibitory effect of RA on the enzyme activity were comprehensively evaluated using human recombinant isozyme system. rosmarinic acid 120-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-69 30447161-5 2019 Surprisingly, sulfaphenazole appeared to be a potent inhibitor of 5"-hydroxylation of flucloxacillin by both recombinant CYP3A4 and CYP3A7. Floxacillin 86-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 30447161-6 2019 CONCLUSIONS AND IMPLICATIONS: The combined results show that the 5"-hydroxylation of flucloxacillin is primarily catalysed by CYP3A4, CYP3A7 and CYP2C9. Floxacillin 85-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 29802543-11 2019 Because bortezomib undergoes extensive metabolism by hepatic cytochrome P450 3A4 and 2C19 enzymes, certain strong cytochrome P450 3A4 inducers and inhibitors can also alter the systemic exposure of bortezomib. Bortezomib 8-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-89 29998574-1 2019 CYP3A enzymes participate in the elimination of ticagrelor and the bioactivation of clopidogrel and prasugrel. Clopidogrel 84-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 29998574-1 2019 CYP3A enzymes participate in the elimination of ticagrelor and the bioactivation of clopidogrel and prasugrel. Prasugrel Hydrochloride 100-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 29998574-5 2019 CYP3A4*22 carriers also showed more pronounced platelet inhibition at 24 hours after ticagrelor ingestion than the controls (43% vs. 21%; P = 0.029). Ticagrelor 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29802543-11 2019 Because bortezomib undergoes extensive metabolism by hepatic cytochrome P450 3A4 and 2C19 enzymes, certain strong cytochrome P450 3A4 inducers and inhibitors can also alter the systemic exposure of bortezomib. Bortezomib 8-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-80 29802543-11 2019 Because bortezomib undergoes extensive metabolism by hepatic cytochrome P450 3A4 and 2C19 enzymes, certain strong cytochrome P450 3A4 inducers and inhibitors can also alter the systemic exposure of bortezomib. Bortezomib 198-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-89 29802543-11 2019 Because bortezomib undergoes extensive metabolism by hepatic cytochrome P450 3A4 and 2C19 enzymes, certain strong cytochrome P450 3A4 inducers and inhibitors can also alter the systemic exposure of bortezomib. Bortezomib 198-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-80 29901213-3 2019 A stepwise approach was taken to qualify the interaction model of an existing letermovir physiologically based pharmacokinetic model to predict letermovir interactions with CYP3A and OATP1B. letermovir 78-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-178 29901213-3 2019 A stepwise approach was taken to qualify the interaction model of an existing letermovir physiologically based pharmacokinetic model to predict letermovir interactions with CYP3A and OATP1B. letermovir 144-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-178 29901213-4 2019 The model was then used to prospectively predict the interaction between letermovir and CYP2C8 substrates such as repaglinide, a substrate of CYP2C8, CYP3A, and OATP1B. letermovir 73-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 29901213-4 2019 The model was then used to prospectively predict the interaction between letermovir and CYP2C8 substrates such as repaglinide, a substrate of CYP2C8, CYP3A, and OATP1B. repaglinide 114-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 29901213-7 2019 In addition, midazolam interactions with letermovir at therapeutic doses were also simulated to confirm that letermovir is a moderate CYP3A inhibitor. letermovir 109-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-139 30284597-5 2019 RESULTS: Moderate CYP3A4 inhibition by diltiazem (240 mg/day) increased the Cmax and AUC0- of ACT-541468 by 1.4-fold (90% confidence interval (CI): 1.2-1.6) and 2.4-fold (90% CI: 2.0-2.8), respectively, and prolonged t1/2 by 80% (90% CI: 60-90) without affecting tmax. Diltiazem 39-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 30442649-5 2019 As victims, five new drugs were identified as sensitive substrates: abemeciclib, midostaurin, and neratinib for CYP3A and glecaprevir and voxilaprevir for OATP1B1/1B3. neratinib 98-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-117 30442651-5 2019 [14C]Acalabrutinib was metabolized to more than three dozen metabolites detectable by liquid chromatography-tandem mass spectrometry, with primary metabolism by CYP3A-mediated oxidation of the pyrrolidine ring, thiol conjugation of the butynamide warhead, and amide hydrolysis. Carbon-14 1-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-166 30442651-5 2019 [14C]Acalabrutinib was metabolized to more than three dozen metabolites detectable by liquid chromatography-tandem mass spectrometry, with primary metabolism by CYP3A-mediated oxidation of the pyrrolidine ring, thiol conjugation of the butynamide warhead, and amide hydrolysis. acalabrutinib 5-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-166 30442651-5 2019 [14C]Acalabrutinib was metabolized to more than three dozen metabolites detectable by liquid chromatography-tandem mass spectrometry, with primary metabolism by CYP3A-mediated oxidation of the pyrrolidine ring, thiol conjugation of the butynamide warhead, and amide hydrolysis. pyrrolidine 193-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-166 30442651-5 2019 [14C]Acalabrutinib was metabolized to more than three dozen metabolites detectable by liquid chromatography-tandem mass spectrometry, with primary metabolism by CYP3A-mediated oxidation of the pyrrolidine ring, thiol conjugation of the butynamide warhead, and amide hydrolysis. Sulfhydryl Compounds 211-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-166 30442651-5 2019 [14C]Acalabrutinib was metabolized to more than three dozen metabolites detectable by liquid chromatography-tandem mass spectrometry, with primary metabolism by CYP3A-mediated oxidation of the pyrrolidine ring, thiol conjugation of the butynamide warhead, and amide hydrolysis. butynamide warhead 236-254 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-166 30442651-5 2019 [14C]Acalabrutinib was metabolized to more than three dozen metabolites detectable by liquid chromatography-tandem mass spectrometry, with primary metabolism by CYP3A-mediated oxidation of the pyrrolidine ring, thiol conjugation of the butynamide warhead, and amide hydrolysis. Amides 241-246 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-166 30442651-6 2019 A major active, circulating, pyrrolidine ring-opened metabolite, ACP-5862 (4-[8-amino-3-[4-(but-2-ynoylamino)butanoyl]imidazo[1,5-a]pyrazin-1-yl]-N-(2-pyridyl)benzamide), was produced by CYP3A oxidation.Novel enol thioethers from the 2-butynamide warhead arose from glutathione and/or cysteine Michael additions and were subject to hydrolysis to a beta-ketoamide. acp 65-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-192 30442651-6 2019 A major active, circulating, pyrrolidine ring-opened metabolite, ACP-5862 (4-[8-amino-3-[4-(but-2-ynoylamino)butanoyl]imidazo[1,5-a]pyrazin-1-yl]-N-(2-pyridyl)benzamide), was produced by CYP3A oxidation.Novel enol thioethers from the 2-butynamide warhead arose from glutathione and/or cysteine Michael additions and were subject to hydrolysis to a beta-ketoamide. 4-[8-amino-3-[4-(but-2-ynoylamino)butanoyl]imidazo[1,5-a]pyrazin-1-yl]-n-(2-pyridyl)benzamide 75-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-192 30678826-9 2019 Interestingly, several metabolites including the 4-hydroxyl form of CPA (4-OH-CPA) and phosphamide mustard were detected in the CYP2B6, CYP2C19, and CYP3A4 expression systems, but not in the CYP2C9 and CYP2D6 system. 4-hydroxyl 49-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 30218411-1 2019 BACKGROUND: CYP3A4 is a major enzyme catalyzing the metabolism of endogenous steroids that play an important role in the etiology of carcinogenesis. Steroids 77-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 30205156-11 2019 With the current extensive knowledge on the reactions and pathways of metabolism of vitamin D, especially those catalyzed by CYP24A1, CYP27A1, CYP27B1, CYP3A4 and CYP11A1, it is likely that many other of the resulting hydroxyvitamin D metabolites will be measured in human serum in the future, some contributing to a more detailed understanding of vitamin D status in health and disease. Vitamin D 225-234 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 30205156-11 2019 With the current extensive knowledge on the reactions and pathways of metabolism of vitamin D, especially those catalyzed by CYP24A1, CYP27A1, CYP27B1, CYP3A4 and CYP11A1, it is likely that many other of the resulting hydroxyvitamin D metabolites will be measured in human serum in the future, some contributing to a more detailed understanding of vitamin D status in health and disease. Vitamin D 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 30205156-11 2019 With the current extensive knowledge on the reactions and pathways of metabolism of vitamin D, especially those catalyzed by CYP24A1, CYP27A1, CYP27B1, CYP3A4 and CYP11A1, it is likely that many other of the resulting hydroxyvitamin D metabolites will be measured in human serum in the future, some contributing to a more detailed understanding of vitamin D status in health and disease. Hydroxycholecalciferols 218-234 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 30678826-9 2019 Interestingly, several metabolites including the 4-hydroxyl form of CPA (4-OH-CPA) and phosphamide mustard were detected in the CYP2B6, CYP2C19, and CYP3A4 expression systems, but not in the CYP2C9 and CYP2D6 system. Dimethoate 87-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 30678826-13 2019 Additionally, CPA metabolites like 4-OH-CPA and phosphamide mustard produced by human CYP2B6, CYP2C9, CYP2C19, and CYP3A4 are suggested to be major determinants of micronucleus induction by CPA. Dimethoate 48-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 30345530-7 2019 Genistein considerably inhibited P-glycoprotein-mediated drug efflux in 22Rv1 cells and CYP3A4 activity in microsomes. Genistein 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 30287909-8 2019 These data together with those reporting that the CYP3A4 and ESR2 SNPs correlate with the expression of TRIM4 and ESR2 mRNAs in PBMCs (ranging from P = 1.98 x 10-6 to P = 2.0 x 10-35), and that the CYP2C9rs1799853 SNP modulates the efficiency of multiple drugs, suggest that steroid hormone-related genes may have a role in determining the response to anti-TNF drugs.KEY POINTS Polymorphisms within the CYP3A4 and CYP2C9 loci correlate with changes in DAS28 after treatment with anti-TNF drugs. Steroids 275-290 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 30295407-1 2019 INTRODUCTION: Isavuconazole, a triazole antifungal, is an inhibitor of cytochrome P450 3A4, which also metabolizes tacrolimus and sirolimus. isavuconazole 14-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-90 30295407-1 2019 INTRODUCTION: Isavuconazole, a triazole antifungal, is an inhibitor of cytochrome P450 3A4, which also metabolizes tacrolimus and sirolimus. Triazoles 31-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-90 30295407-1 2019 INTRODUCTION: Isavuconazole, a triazole antifungal, is an inhibitor of cytochrome P450 3A4, which also metabolizes tacrolimus and sirolimus. Tacrolimus 115-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-90 30295407-1 2019 INTRODUCTION: Isavuconazole, a triazole antifungal, is an inhibitor of cytochrome P450 3A4, which also metabolizes tacrolimus and sirolimus. Sirolimus 130-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-90 29375004-5 2019 Contributions of CYP3A4 and CYP2C9 to metabolism of deoxypodophyllotoxin and nateglinide were also predicted. deoxypodophyllotoxin 52-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 29375004-5 2019 Contributions of CYP3A4 and CYP2C9 to metabolism of deoxypodophyllotoxin and nateglinide were also predicted. Nateglinide 77-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 29375004-7 2019 Predicted contributions of CYP3A4 to formations of 6beta-hydroxytestosterone, 1"-hydroxymidazolam, norverapamil, ortho-hydroxyatorvastatin and para-hydroxyatorvastatin using other probes were 47.46-219.46%, 21.62-98.87%, 186.49-462.44%, 21.87-101.15% and 53.62-247.97%, respectively. 6 beta-hydroxytestosterone 51-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 29375004-8 2019 Predicted contributions of CYP3A4 and CYP2C9 to nateglinide metabolism were 8.18-37.84% and 36.08-94.04%, separately. Nateglinide 48-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 30345530-10 2019 Yet, the inhibitory effects of genistein on drug efflux in 22Rv1 cells and on microsomal CYP3A4 activity raise the possibility that genistein can affect taxane effects on CRPC cells in other circumstances than those we studied, which merits further research. Genistein 132-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 30580183-2 2019 Concomitant treatment with ticagrelor, a moderate CYP3A4 inhibitor, and CYP3A4-metabolized statins such as atorvastatin, might lead to an increased risk of muscle-related adverse events. Ticagrelor 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 30342195-17 2019 To further investigate the regulatory mechanisms, we found that ginsenosides enhanced the rifampicin-induced pregnane X receptor (PXR) transactivation of the CYP3A4 promoter. Ginsenosides 64-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 30342195-17 2019 To further investigate the regulatory mechanisms, we found that ginsenosides enhanced the rifampicin-induced pregnane X receptor (PXR) transactivation of the CYP3A4 promoter. Rifampin 90-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 30342195-18 2019 Treatment of hPXR-over-expressed cells with ginsenosides increased the rifampicin-inducible expression of CYP3A4 in a concentration-dependent manner. Ginsenosides 44-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 30342195-18 2019 Treatment of hPXR-over-expressed cells with ginsenosides increased the rifampicin-inducible expression of CYP3A4 in a concentration-dependent manner. Rifampin 71-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 30587336-3 2019 We previously reported that acetaminophen (APAP) caused accumulation of functional CYP3A protein via inhibition of CYP3A protein degradation through reduction of glycoprotein 78 (gp78), an E3 ligase of the ubiquitin proteasome system. Acetaminophen 28-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 30587336-3 2019 We previously reported that acetaminophen (APAP) caused accumulation of functional CYP3A protein via inhibition of CYP3A protein degradation through reduction of glycoprotein 78 (gp78), an E3 ligase of the ubiquitin proteasome system. Acetaminophen 28-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 30587336-3 2019 We previously reported that acetaminophen (APAP) caused accumulation of functional CYP3A protein via inhibition of CYP3A protein degradation through reduction of glycoprotein 78 (gp78), an E3 ligase of the ubiquitin proteasome system. Acetaminophen 43-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 30587336-3 2019 We previously reported that acetaminophen (APAP) caused accumulation of functional CYP3A protein via inhibition of CYP3A protein degradation through reduction of glycoprotein 78 (gp78), an E3 ligase of the ubiquitin proteasome system. Acetaminophen 43-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 30587336-4 2019 Furthermore, N-acetyl-m-aminophenol, a regioisomer of APAP causes CYP3A protein accumulation, whereas p-acetamidobezoic acid, in which a hydroxy group of APAP was substituted for a carboxy group, did not lead to the same effects. 3-hydroxyacetanilide 13-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 30587336-4 2019 Furthermore, N-acetyl-m-aminophenol, a regioisomer of APAP causes CYP3A protein accumulation, whereas p-acetamidobezoic acid, in which a hydroxy group of APAP was substituted for a carboxy group, did not lead to the same effects. Acetaminophen 54-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 30587336-7 2019 Four compounds, including salicylate, increased CYP3A enzyme activity and led to the accumulation of functional CYP3A protein similarly to APAP. Salicylates 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 30587336-7 2019 Four compounds, including salicylate, increased CYP3A enzyme activity and led to the accumulation of functional CYP3A protein similarly to APAP. Salicylates 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-117 30587336-11 2019 When SB203580, a p38 MAPK inhibitor, was co-administered with APAP, the inhibitory effects of APAP on CYP3A protein degradation were suppressed. SB 203580 5-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 30587336-11 2019 When SB203580, a p38 MAPK inhibitor, was co-administered with APAP, the inhibitory effects of APAP on CYP3A protein degradation were suppressed. Acetaminophen 62-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 30587336-13 2019 Salicylate derivatives may also suppress the CYP3A protein degradation. Salicylates 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-50 30658513-11 2019 Strong inhibitors and inducers of CYP3A4 and p-glycoprotein should be avoided in patients treated with rivaroxaban, apixaban, and edoxaban. Rivaroxaban 103-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 30572203-3 2019 Selective inhibition of intestinal CYP3A4 by grapefruit juice may increase the oral bioavailability of voriconazole in children. Voriconazole 103-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 30500380-5 2019 In addition, we were interested to analyze acute cytotoxicity of the model drug cyclophosphamide (CPA) metabolized by HepG2-2C19 C1 and by a previously generated CYP3A4-overexpressing HepG2 cell clone. Cyclophosphamide 80-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 30609441-1 2019 Amlodipine has a potential to reduce clopidogrel bioactivation through the cytochrome P450 3A4 enzyme in vivo, but the clinical impact of this interaction remains controversial. Amlodipine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-94 30609441-1 2019 Amlodipine has a potential to reduce clopidogrel bioactivation through the cytochrome P450 3A4 enzyme in vivo, but the clinical impact of this interaction remains controversial. Clopidogrel 37-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-94 30658513-11 2019 Strong inhibitors and inducers of CYP3A4 and p-glycoprotein should be avoided in patients treated with rivaroxaban, apixaban, and edoxaban. apixaban 116-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 30658513-11 2019 Strong inhibitors and inducers of CYP3A4 and p-glycoprotein should be avoided in patients treated with rivaroxaban, apixaban, and edoxaban. edoxaban 130-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 30500380-5 2019 In addition, we were interested to analyze acute cytotoxicity of the model drug cyclophosphamide (CPA) metabolized by HepG2-2C19 C1 and by a previously generated CYP3A4-overexpressing HepG2 cell clone. Cyclophosphamide 98-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 30500380-6 2019 Upon 10 mM CPA exposure, we were able to detect its metabolites 4-hydroxy-cyclophosphamide and acrolein in CYP3A4- and CYP2C19-expressing cell clones, but not in parental HepG2 cell line. Cyclophosphamide 11-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 30500380-6 2019 Upon 10 mM CPA exposure, we were able to detect its metabolites 4-hydroxy-cyclophosphamide and acrolein in CYP3A4- and CYP2C19-expressing cell clones, but not in parental HepG2 cell line. 4-hydroxycyclophosphamide 64-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 30500380-6 2019 Upon 10 mM CPA exposure, we were able to detect its metabolites 4-hydroxy-cyclophosphamide and acrolein in CYP3A4- and CYP2C19-expressing cell clones, but not in parental HepG2 cell line. Acrolein 95-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 30580183-2 2019 Concomitant treatment with ticagrelor, a moderate CYP3A4 inhibitor, and CYP3A4-metabolized statins such as atorvastatin, might lead to an increased risk of muscle-related adverse events. Atorvastatin 107-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 30517006-0 2019 CYP3A4/5 Activity Probed with Testosterone and Midazolam: Correlation between Two Substrates at the Microsomal and Enzyme Levels. Testosterone 30-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-8 30627802-0 2019 Sorafenib N-Oxide Is an Inhibitor of Human Hepatic CYP3A4. Sorafenib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 30627802-0 2019 Sorafenib N-Oxide Is an Inhibitor of Human Hepatic CYP3A4. n-oxide 10-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 30627802-1 2019 The multi-kinase inhibitor sorafenib (SOR) is clinically important in the treatment of hepatocellular and renal cancers and undergoes CYP3A4-dependent oxidation in liver to the pharmacologically active N-oxide metabolite (SNO). Sorafenib 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 30627802-5 2019 Enzyme kinetics of CYP3A4-mediated midazolam 1"-hydroxylation in individual human hepatic microsomes were analyzed by non-linear regression and appropriate replots. Midazolam 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 30627802-7 2019 To assess these findings, further molecular docking studies of SOR and SNO with the 1TQN crystal structure of CYP3A4 were undertaken. Sorafenib 63-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 30627802-9 2019 In the optimal docking pose, the N-oxide moiety of SNO was also found to interact directly with the heme moiety of CYP3A4. n-oxide 33-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 30627802-9 2019 In the optimal docking pose, the N-oxide moiety of SNO was also found to interact directly with the heme moiety of CYP3A4. Heme 100-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 30729119-1 2019 Purpose: We evaluated potential drug-drug interactions between cilostazol and simvastatin, both CYP3A substrates, in healthy subjects. Cilostazol 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-101 30517006-0 2019 CYP3A4/5 Activity Probed with Testosterone and Midazolam: Correlation between Two Substrates at the Microsomal and Enzyme Levels. Midazolam 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-8 30517006-1 2019 Testosterone (TST) and midazolam (MDZ) are widely used as probes to detect CYP3A4/5 activity, but the data acquired with these two substrates do not correlate well at the microsomal level (per milligram of microsomal protein), and the reason is unclear. Testosterone 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-83 30517006-1 2019 Testosterone (TST) and midazolam (MDZ) are widely used as probes to detect CYP3A4/5 activity, but the data acquired with these two substrates do not correlate well at the microsomal level (per milligram of microsomal protein), and the reason is unclear. Midazolam 23-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-83 30517006-1 2019 Testosterone (TST) and midazolam (MDZ) are widely used as probes to detect CYP3A4/5 activity, but the data acquired with these two substrates do not correlate well at the microsomal level (per milligram of microsomal protein), and the reason is unclear. Midazolam 34-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-83 30517006-2 2019 In this study, CYP3A4/5 activity was probed with TST and MDZ at the microsomal and enzyme levels (per picomole of CYP3A4/5) in 72 human liver samples. Midazolam 57-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-23 30517006-4 2019 Compared with TST, MDZ was found to correlate better with the content of CYP3A4/5 (no correlation vs 0.431) and CYP3A5 (no correlation vs 0.447), and huge variations in enzyme content existed among different genotypes, which explained the lower degree of correlation at the microsomal level. Midazolam 19-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-81 30517006-6 2019 In conclusion, our study demonstrates a high degree of correlation between CYP3A4/5 activity probed with TST and MDZ at the enzyme level but not at the microsomal level and allows us to correctly understand the influence of gene polymorphisms on the correlations. Midazolam 113-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-83 30099888-1 2019 BACKGROUND: It is unknown whether diltiazem, a moderate cytochrome P450 enzyme (CYP3A4) and P-glycoprotein (P-gp) inhibitor, increases the incidence of bleeding events in combination with rivaroxaban, a CYP3A4 and P-gp substrate. Diltiazem 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 28594339-13 2019 Three patients were concomitantly taking cimetidine, which is known to cause inhibition of CYP3A4 and CYP2C8 leading to increased levels of loperamide. Cimetidine 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 28594339-13 2019 Three patients were concomitantly taking cimetidine, which is known to cause inhibition of CYP3A4 and CYP2C8 leading to increased levels of loperamide. Loperamide 140-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 29989304-1 2019 The magnitude of interaction between the CYP3A4 substrate tacrolimus and various CYP3A4 inhibitors is highly unpredictable. Tacrolimus 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 31933482-1 2019 BACKGROUND: Cobicistat (COBI), a CYP3A inhibitor, is a pharmacokinetic enhancer that increases exposures of the HIV protease inhibitors (PIs) atazanavir (ATV) and darunavir (DRV). Cobicistat 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 31933482-1 2019 BACKGROUND: Cobicistat (COBI), a CYP3A inhibitor, is a pharmacokinetic enhancer that increases exposures of the HIV protease inhibitors (PIs) atazanavir (ATV) and darunavir (DRV). Cobicistat 24-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 31933482-1 2019 BACKGROUND: Cobicistat (COBI), a CYP3A inhibitor, is a pharmacokinetic enhancer that increases exposures of the HIV protease inhibitors (PIs) atazanavir (ATV) and darunavir (DRV). Atazanavir Sulfate 142-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 31933482-1 2019 BACKGROUND: Cobicistat (COBI), a CYP3A inhibitor, is a pharmacokinetic enhancer that increases exposures of the HIV protease inhibitors (PIs) atazanavir (ATV) and darunavir (DRV). Atazanavir Sulfate 154-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 31933482-11 2019 CONCLUSIONS: Consistent with COBI-mediated CYP3A inhibition, drospirenone exposure increased following coadministration with COBI-containing regimens, with a greater increase with ATV+COBI. Cobicistat 29-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-48 29989304-1 2019 The magnitude of interaction between the CYP3A4 substrate tacrolimus and various CYP3A4 inhibitors is highly unpredictable. Tacrolimus 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 29989304-2 2019 We investigated whether an individual"s baseline in vivo CYP3A4 activity, assessed using the oral midazolam (MDZ) probe, could be used to predict the magnitude of drug-drug interaction between tacrolimus and the potent CYP3A4 inhibitor itraconazole. Midazolam 98-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 30414935-0 2019 Constitutive androstane receptor weakens the induction of panaxytriol on CYP3A4 by repressing the activation of pregnane X receptor. panaxytriol 58-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 30414935-2 2019 Our previous studies have demonstrated that panaxytriol (PXT) upregulates the expression of CYP3A4 via the PXR regulatory pathway. panaxytriol 44-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 29989304-2 2019 We investigated whether an individual"s baseline in vivo CYP3A4 activity, assessed using the oral midazolam (MDZ) probe, could be used to predict the magnitude of drug-drug interaction between tacrolimus and the potent CYP3A4 inhibitor itraconazole. Midazolam 98-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 29989304-2 2019 We investigated whether an individual"s baseline in vivo CYP3A4 activity, assessed using the oral midazolam (MDZ) probe, could be used to predict the magnitude of drug-drug interaction between tacrolimus and the potent CYP3A4 inhibitor itraconazole. Midazolam 109-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 29989304-2 2019 We investigated whether an individual"s baseline in vivo CYP3A4 activity, assessed using the oral midazolam (MDZ) probe, could be used to predict the magnitude of drug-drug interaction between tacrolimus and the potent CYP3A4 inhibitor itraconazole. Midazolam 109-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 29989304-2 2019 We investigated whether an individual"s baseline in vivo CYP3A4 activity, assessed using the oral midazolam (MDZ) probe, could be used to predict the magnitude of drug-drug interaction between tacrolimus and the potent CYP3A4 inhibitor itraconazole. Tacrolimus 193-203 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 29989304-2 2019 We investigated whether an individual"s baseline in vivo CYP3A4 activity, assessed using the oral midazolam (MDZ) probe, could be used to predict the magnitude of drug-drug interaction between tacrolimus and the potent CYP3A4 inhibitor itraconazole. Tacrolimus 193-203 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 29989304-2 2019 We investigated whether an individual"s baseline in vivo CYP3A4 activity, assessed using the oral midazolam (MDZ) probe, could be used to predict the magnitude of drug-drug interaction between tacrolimus and the potent CYP3A4 inhibitor itraconazole. Itraconazole 236-248 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 29989304-2 2019 We investigated whether an individual"s baseline in vivo CYP3A4 activity, assessed using the oral midazolam (MDZ) probe, could be used to predict the magnitude of drug-drug interaction between tacrolimus and the potent CYP3A4 inhibitor itraconazole. Itraconazole 236-248 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 30713247-4 2019 Major findings were: 1) Cachectic cancer patients had high plasma concentrations of oxycodone via the reduction of CYP3A activity. Oxycodone 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 30930421-6 2019 CYP reaction phenotyping for butyrylfentanyl using human liver microsomes and various anti-CYP antibodies revealed that CYP3A4 was involved in the formation of nor-butyrylfentanyl, (omega-1)-hydroxy-butyrylfentanyl, and beta-hydroxy-butyrylfentanyl. butyrfentanyl 29-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 30302786-2 2019 The objectives of this entry-into-human study were to assess the safety, tolerability, pharmacokinetics (PK) and pharmacodynamics of risdiplam, and the effect of the strong CYP3A inhibitor itraconazole on the PK of risdiplam in healthy male volunteers. Itraconazole 189-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-178 30930421-6 2019 CYP reaction phenotyping for butyrylfentanyl using human liver microsomes and various anti-CYP antibodies revealed that CYP3A4 was involved in the formation of nor-butyrylfentanyl, (omega-1)-hydroxy-butyrylfentanyl, and beta-hydroxy-butyrylfentanyl. nor-butyrylfentanyl 160-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 30930421-6 2019 CYP reaction phenotyping for butyrylfentanyl using human liver microsomes and various anti-CYP antibodies revealed that CYP3A4 was involved in the formation of nor-butyrylfentanyl, (omega-1)-hydroxy-butyrylfentanyl, and beta-hydroxy-butyrylfentanyl. (omega-1)-hydroxy-butyrylfentanyl 181-214 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 30930421-6 2019 CYP reaction phenotyping for butyrylfentanyl using human liver microsomes and various anti-CYP antibodies revealed that CYP3A4 was involved in the formation of nor-butyrylfentanyl, (omega-1)-hydroxy-butyrylfentanyl, and beta-hydroxy-butyrylfentanyl. beta-hydroxy-butyrylfentanyl 220-248 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 31061321-3 2019 This retrospective observational study assessed the relationship between serum iPTH levels and the blood concentration or dosage of tacrolimus, a CYP3A substrate, after oral administration in kidney transplant patients. Tacrolimus 132-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-151 31474719-2 2019 Midazolam, which is predominantly metabolized to 1"-hydroxymidazolam and 4-hydroxymidazolam by CYP3A4, is considered an effective probe for CYP3A4. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 31474719-2 2019 Midazolam, which is predominantly metabolized to 1"-hydroxymidazolam and 4-hydroxymidazolam by CYP3A4, is considered an effective probe for CYP3A4. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 31474719-2 2019 Midazolam, which is predominantly metabolized to 1"-hydroxymidazolam and 4-hydroxymidazolam by CYP3A4, is considered an effective probe for CYP3A4. 1-hydroxymethylmidazolam 49-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 31474719-2 2019 Midazolam, which is predominantly metabolized to 1"-hydroxymidazolam and 4-hydroxymidazolam by CYP3A4, is considered an effective probe for CYP3A4. 4-hydroxymidazolam 73-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 31474719-2 2019 Midazolam, which is predominantly metabolized to 1"-hydroxymidazolam and 4-hydroxymidazolam by CYP3A4, is considered an effective probe for CYP3A4. 4-hydroxymidazolam 73-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 31474719-3 2019 To determine the area under the curve (AUC) of midazolam or midazolam clearance for CYP3A4 activity, multiple plasma samples of midazolam are required. Midazolam 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 31474719-3 2019 To determine the area under the curve (AUC) of midazolam or midazolam clearance for CYP3A4 activity, multiple plasma samples of midazolam are required. Midazolam 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 31474719-3 2019 To determine the area under the curve (AUC) of midazolam or midazolam clearance for CYP3A4 activity, multiple plasma samples of midazolam are required. Midazolam 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 31228606-8 2019 Moreover, the drug-drug interaction and drug-food interaction could be observed by using our human iPS-IECM in the presence of an inducer and inhibitor of CYP3A4, i.e., rifampicin and grape fruit juice, respectively. ips-iecm 99-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 30340248-5 2019 Mean (95% confidence interval) exosome-derived CYP3A4 protein expression pre- and post-rifampicin dosing was 0.24 (0.2-0.28) and 0.42 (0.21-0.65) ng ml-1 exosome concentrate. Rifampin 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 30340248-6 2019 Mean (95% confidence interval) exosome CYP3A4 mRNA expression pre- and post-rifampicin dosing was 6.0 (1.1-32.7) and 48.3 (11.3-104) x 10-11 2-DeltaDeltaCt , respectively. Rifampin 76-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 30340248-8 2019 CONCLUSIONS: Consistent strong concordance was observed between exosome-derived CYP3A4 biomarkers and midazolam CL/F. Midazolam 102-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 30340248-8 2019 CONCLUSIONS: Consistent strong concordance was observed between exosome-derived CYP3A4 biomarkers and midazolam CL/F. Fluorine 115-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 31228606-8 2019 Moreover, the drug-drug interaction and drug-food interaction could be observed by using our human iPS-IECM in the presence of an inducer and inhibitor of CYP3A4, i.e., rifampicin and grape fruit juice, respectively. Rifampin 169-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 31228606-8 2019 Moreover, the drug-drug interaction and drug-food interaction could be observed by using our human iPS-IECM in the presence of an inducer and inhibitor of CYP3A4, i.e., rifampicin and grape fruit juice, respectively. grape fruit juice 184-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 29696643-2 2019 Ritonavir and clopidogrel are inhibitors of CYP3A4 and CYP2C8, respectively. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 29696643-2 2019 Ritonavir and clopidogrel are inhibitors of CYP3A4 and CYP2C8, respectively. Clopidogrel 14-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 30427584-0 2019 Evaluation of Drug-Drug Interactions of Rucaparib and CYP1A2, CYP2C9, CYP2C19, CYP3A, and P-gp Substrates in Patients With an Advanced Solid Tumor. rucaparib 40-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-84 29717476-2 2019 Verified DDI simulations provided dose recommendations for olaparib coadministration with clinically relevant CYP3A4 modulators to eliminate potential risk to patient safety or olaparib efficacy. olaparib 59-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 30238620-3 2019 Although drug interactions arising from reversible inhibition of CYP isozymes by evocalcet were considered unlikely based on the results of in vitro studies and static model analyses, the potential for evocalcet to cause time-dependent inhibition of CYP3A or induction of several CYP isozymes could not be ruled out. Evocalcet 202-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 250-255 29717476-3 2019 When olaparib is given with strong/moderate CYP3A inhibitors, the dose should be reduced to 100/150 mg b.i.d. olaparib 5-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-49 29717476-8 2019 Olaparib was shown to be a weak inhibitor of CYP3A (1.6-fold increase in exposure of a sensitive CYP3A probe) and to have no effect on P-glycoprotein or UGT1A1 substrates. olaparib 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-50 29717476-8 2019 Olaparib was shown to be a weak inhibitor of CYP3A (1.6-fold increase in exposure of a sensitive CYP3A probe) and to have no effect on P-glycoprotein or UGT1A1 substrates. olaparib 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-102 31385766-0 2019 Association Between CYP3A4 and CYP3A5 Genotypes and Cyclosporine"s Blood Levels and Doses among Jordanian Kidney Transplanted Patients BACKGROUND: Cyclosporine is used as an immunosuppressive agent in kidney transplantation. Cyclosporine 52-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 30378493-12 2019 CYP3A families, especially CYP3A4 and CYP3A5, play an important role in the biotransformation of CsA. Cyclosporine 97-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 30336288-11 2019 Identification of orthologous human CYP2C9 and CYP3A4 enzyme families in vultures will be an important further step in explaining the differences in the metabolic pathway(s) of meloxicam and diclofenac for the species. Meloxicam 177-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 30336288-11 2019 Identification of orthologous human CYP2C9 and CYP3A4 enzyme families in vultures will be an important further step in explaining the differences in the metabolic pathway(s) of meloxicam and diclofenac for the species. Diclofenac 191-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 31385766-0 2019 Association Between CYP3A4 and CYP3A5 Genotypes and Cyclosporine"s Blood Levels and Doses among Jordanian Kidney Transplanted Patients BACKGROUND: Cyclosporine is used as an immunosuppressive agent in kidney transplantation. Cyclosporine 147-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 31244435-0 2019 Association of Genetic Variants in CYP3A4, CYP3A5, CYP2C8, and CYP2C19 with Tacrolimus Pharmacokinetics in Renal Transplant Recipients. Tacrolimus 76-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 31702486-1 2019 BACKGROUND: Metoclopramide is mainly metabolized by CYP2D6, CYP3A4, CYP2C19, and CYP1A2 enzymes, while cilostazol is also metabolized by CYP3A4, CYP2C19, and CYP1A2 enzymes. Metoclopramide 12-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 31385766-2 2019 Cyclosporine is predominantly metabolized by CYP3A4 and CYP3A5. Cyclosporine 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 31385766-3 2019 The most commonSingle Nucleotide Polymorphisms (SNPs) affecting cyclosporine metabolism (CYP3A4*1B, CYP3A4*1G,CYP3A4*22 and CYP3A5*3) were investigated among Jordanian kidney transplanted patients to find out the genotypesand allele frequencies of these SNPs. Cyclosporine 64-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 31702486-1 2019 BACKGROUND: Metoclopramide is mainly metabolized by CYP2D6, CYP3A4, CYP2C19, and CYP1A2 enzymes, while cilostazol is also metabolized by CYP3A4, CYP2C19, and CYP1A2 enzymes. cilostazol 103-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 31385766-3 2019 The most commonSingle Nucleotide Polymorphisms (SNPs) affecting cyclosporine metabolism (CYP3A4*1B, CYP3A4*1G,CYP3A4*22 and CYP3A5*3) were investigated among Jordanian kidney transplanted patients to find out the genotypesand allele frequencies of these SNPs. Cyclosporine 64-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 31385766-3 2019 The most commonSingle Nucleotide Polymorphisms (SNPs) affecting cyclosporine metabolism (CYP3A4*1B, CYP3A4*1G,CYP3A4*22 and CYP3A5*3) were investigated among Jordanian kidney transplanted patients to find out the genotypesand allele frequencies of these SNPs. Cyclosporine 64-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 30470150-1 2019 Lopinavir (LPV), an efficient drug for HIV infection treatment, was incorporated into biodegradable PLGA nanocapsules (NCs) embedded in microparticles (MCPs) using the spray-drying technique in an attempt to bypass the P-gp efflux and protect the drug from CYP3A pre-systemic metabolism without ritonavir (RTV). Lopinavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 257-262 30348903-0 2019 Mechanistic In Vitro Studies Indicate that the Clinical Drug-Drug Interaction between Telithromycin and Simvastatin Acid Is Driven by Time-Dependent Inhibition of CYP3A4 with Minimal Effect on OATP1B1. telithromycin 86-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 30348903-0 2019 Mechanistic In Vitro Studies Indicate that the Clinical Drug-Drug Interaction between Telithromycin and Simvastatin Acid Is Driven by Time-Dependent Inhibition of CYP3A4 with Minimal Effect on OATP1B1. simvastatin acid 104-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 30348903-1 2019 A previous attempt to accurately quantify the increased simvastatin acid exposure due to drug-drug interaction (DDI) with coadministered telithromycin, using a mechanistic static model, substantially underpredicted the magnitude of the area under the plasma concentration-time curve ratio (AUCR) based on reversible inhibition of CYP3A4 and organic anion transporting polypeptide 1B1 (OATP1B1). simvastatin acid 56-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 330-336 30348903-1 2019 A previous attempt to accurately quantify the increased simvastatin acid exposure due to drug-drug interaction (DDI) with coadministered telithromycin, using a mechanistic static model, substantially underpredicted the magnitude of the area under the plasma concentration-time curve ratio (AUCR) based on reversible inhibition of CYP3A4 and organic anion transporting polypeptide 1B1 (OATP1B1). telithromycin 137-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 330-336 30348903-2 2019 To reconcile this disconnect between predicted and clinically observed AUCR, telithromycin was evaluated as a time-dependent inhibitor of CYP3A4 in vitro, as well as an inhibitor of OATP1B1. telithromycin 77-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 30348903-6 2019 These results indicate the time-dependent inhibition of CYP3A4 by telithromycin as the primary driver underlying its clinical DDI with simvastatin acid. telithromycin 66-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 30348903-6 2019 These results indicate the time-dependent inhibition of CYP3A4 by telithromycin as the primary driver underlying its clinical DDI with simvastatin acid. simvastatin acid 135-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 29412111-9 2019 Ticagrelor is metabolized mainly by CYP3A4, which does not show functionally relevant genetic variability. Ticagrelor 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 30580179-5 2019 Perampanel is extensively but slowly metabolized via CYP3A4. perampanel 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 31089348-4 2019 Adding verapamil (100 muM), valspodar (5 muM) and ketoconazole (10 muM) significantly enhanced the permeability of REG across mucosal to serosal in the rat jejunum (P < 0.05) suggesting role of CYP 3A4 and/or efflux transporters in oral bioavailability of REG. Verapamil 7-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-204 31089348-4 2019 Adding verapamil (100 muM), valspodar (5 muM) and ketoconazole (10 muM) significantly enhanced the permeability of REG across mucosal to serosal in the rat jejunum (P < 0.05) suggesting role of CYP 3A4 and/or efflux transporters in oral bioavailability of REG. valspodar 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-204 31089348-4 2019 Adding verapamil (100 muM), valspodar (5 muM) and ketoconazole (10 muM) significantly enhanced the permeability of REG across mucosal to serosal in the rat jejunum (P < 0.05) suggesting role of CYP 3A4 and/or efflux transporters in oral bioavailability of REG. Ketoconazole 50-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-204 30371861-4 2019 Fentanyl is a common opiate primarily metabolized by CYP3A4 subtypes. Fentanyl 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 31339834-0 2019 Comparison of Steroid Hormone Hydroxylations by and Docking to Human Cytochromes P450 3A4 and 3A5. Steroids 14-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-97 31339834-1 2019 PURPOSE: Hydroxylation activity at the 6beta-position of steroid hormones (testosterone, progesterone, and cortisol) by human cytochromes P450 (P450 or CYP) 3A4 and CYP3A5 and their molecular docking energy values were compared to understand the catalytic properties of the major forms of human CYP3A, namely, CYP3A4 and CYP3A5. Steroids 57-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-170 28857712-3 2019 Busulfan is metabolized by hepatic oxidation via the cytochrome P450 3A4 system as well as through conjugation with glutathione. Busulfan 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-72 31339834-1 2019 PURPOSE: Hydroxylation activity at the 6beta-position of steroid hormones (testosterone, progesterone, and cortisol) by human cytochromes P450 (P450 or CYP) 3A4 and CYP3A5 and their molecular docking energy values were compared to understand the catalytic properties of the major forms of human CYP3A, namely, CYP3A4 and CYP3A5. Steroids 57-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 310-316 28857712-9 2019 We hypothesize that the increased busulfan levels observed could be related to a cytokine-mediated CYP3A4 suppression. Busulfan 34-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 31339834-1 2019 PURPOSE: Hydroxylation activity at the 6beta-position of steroid hormones (testosterone, progesterone, and cortisol) by human cytochromes P450 (P450 or CYP) 3A4 and CYP3A5 and their molecular docking energy values were compared to understand the catalytic properties of the major forms of human CYP3A, namely, CYP3A4 and CYP3A5. Testosterone 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-170 31339834-1 2019 PURPOSE: Hydroxylation activity at the 6beta-position of steroid hormones (testosterone, progesterone, and cortisol) by human cytochromes P450 (P450 or CYP) 3A4 and CYP3A5 and their molecular docking energy values were compared to understand the catalytic properties of the major forms of human CYP3A, namely, CYP3A4 and CYP3A5. Testosterone 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 310-316 31339834-1 2019 PURPOSE: Hydroxylation activity at the 6beta-position of steroid hormones (testosterone, progesterone, and cortisol) by human cytochromes P450 (P450 or CYP) 3A4 and CYP3A5 and their molecular docking energy values were compared to understand the catalytic properties of the major forms of human CYP3A, namely, CYP3A4 and CYP3A5. Progesterone 89-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-170 31339834-2 2019 METHODS: Testosterone, progesterone, and cortisol 6beta-hydroxylation activities of recombinant CYP3A4 and CYP3A5 were determined by liquid chromatography. Testosterone 9-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 31339834-2 2019 METHODS: Testosterone, progesterone, and cortisol 6beta-hydroxylation activities of recombinant CYP3A4 and CYP3A5 were determined by liquid chromatography. Progesterone 23-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 31339834-1 2019 PURPOSE: Hydroxylation activity at the 6beta-position of steroid hormones (testosterone, progesterone, and cortisol) by human cytochromes P450 (P450 or CYP) 3A4 and CYP3A5 and their molecular docking energy values were compared to understand the catalytic properties of the major forms of human CYP3A, namely, CYP3A4 and CYP3A5. Progesterone 89-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 310-316 31339834-2 2019 METHODS: Testosterone, progesterone, and cortisol 6beta-hydroxylation activities of recombinant CYP3A4 and CYP3A5 were determined by liquid chromatography. Hydrocortisone 41-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 31339834-1 2019 PURPOSE: Hydroxylation activity at the 6beta-position of steroid hormones (testosterone, progesterone, and cortisol) by human cytochromes P450 (P450 or CYP) 3A4 and CYP3A5 and their molecular docking energy values were compared to understand the catalytic properties of the major forms of human CYP3A, namely, CYP3A4 and CYP3A5. Hydrocortisone 107-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-170 31339834-3 2019 Docking simulations of these substrates to the heme moiety of reported crystal structures of CYP3A4 (Protein Data Bank code ITQN) and CYP3A5 (6MJM) were conducted. Heme 47-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 31339834-1 2019 PURPOSE: Hydroxylation activity at the 6beta-position of steroid hormones (testosterone, progesterone, and cortisol) by human cytochromes P450 (P450 or CYP) 3A4 and CYP3A5 and their molecular docking energy values were compared to understand the catalytic properties of the major forms of human CYP3A, namely, CYP3A4 and CYP3A5. Hydrocortisone 107-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 310-316 31339834-4 2019 RESULTS: Michaelis constants (Km) for CYP3A5- mediated 6beta-hydroxylation of testosterone and progesterone were approximately twice those for CYP3A4, whereas the value for cortisol 6beta-hydroxylation mediated by CYP3A5 was similar to the value for that by CYP3A4. Testosterone 78-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 31339834-4 2019 RESULTS: Michaelis constants (Km) for CYP3A5- mediated 6beta-hydroxylation of testosterone and progesterone were approximately twice those for CYP3A4, whereas the value for cortisol 6beta-hydroxylation mediated by CYP3A5 was similar to the value for that by CYP3A4. Testosterone 78-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 258-264 30643090-3 2019 Amenamevir is mainly metabolized by CYP3A, and excreted into feces. ASP2151 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 31339834-4 2019 RESULTS: Michaelis constants (Km) for CYP3A5- mediated 6beta-hydroxylation of testosterone and progesterone were approximately twice those for CYP3A4, whereas the value for cortisol 6beta-hydroxylation mediated by CYP3A5 was similar to the value for that by CYP3A4. Progesterone 95-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 258-264 31339834-5 2019 Maximal velocities (Vmax) of the three steroid hormones 6beta-hydroxylation catalyzed by CYP3A5 were 30%-63% of those by CYP3A4. Steroids 39-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 31339834-7 2019 The differences in the docking energies between CYP3A4 and CYP3A5 for steroid hormones were slightly correlated to the logarithm of CYP3A5/CYP3A4 ratios for Km values (substrate affinity). Steroids 70-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 31339834-7 2019 The differences in the docking energies between CYP3A4 and CYP3A5 for steroid hormones were slightly correlated to the logarithm of CYP3A5/CYP3A4 ratios for Km values (substrate affinity). Steroids 70-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 31339834-9 2019 Molecular docking simulations could partially explain the differences in the accessibility of substrates to the heme moiety of human CYP3A molecules, resulting in the enzymatic affinity of CYP3A4 and CYP3A5. Heme 112-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-138 31339834-9 2019 Molecular docking simulations could partially explain the differences in the accessibility of substrates to the heme moiety of human CYP3A molecules, resulting in the enzymatic affinity of CYP3A4 and CYP3A5. Heme 112-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 28847268-4 2019 Moreover, in vivo oral hypoglycemic activity assay revealed that most of the tested candidates were more potent than the reference drug, sitagliptin, producing rapid onset with long duration of activity that extends to 24 h. Interestingly, the derivatives 11, 16, 18a and 23 showed evidence of mild cytochrome P450 3A4 (CYP3A4) inhibition (IC50; > 210 microM) and their acute toxicity (LD50) was more than 1.9 gm/kg. Sitagliptin Phosphate 137-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 299-318 28847268-4 2019 Moreover, in vivo oral hypoglycemic activity assay revealed that most of the tested candidates were more potent than the reference drug, sitagliptin, producing rapid onset with long duration of activity that extends to 24 h. Interestingly, the derivatives 11, 16, 18a and 23 showed evidence of mild cytochrome P450 3A4 (CYP3A4) inhibition (IC50; > 210 microM) and their acute toxicity (LD50) was more than 1.9 gm/kg. Sitagliptin Phosphate 137-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 320-326 31256150-2 2019 Phenobarbital is an inducer of cytochrome P450 (CYP) 3A, while midazolam is a CYP3A substrate. Phenobarbital 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-55 31256150-2 2019 Phenobarbital is an inducer of cytochrome P450 (CYP) 3A, while midazolam is a CYP3A substrate. Midazolam 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 30320358-9 2019 Our results indicate that by stimulating HIF-1alpha activity, hypoxia downregulates the expression of CYP2B6, CYP3A4 and CYP3A5, that in turn leads to decreased conversion of CPA and IFA into their active forms and thus to diminished cytotoxicity. Cyclophosphamide 175-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 30320358-9 2019 Our results indicate that by stimulating HIF-1alpha activity, hypoxia downregulates the expression of CYP2B6, CYP3A4 and CYP3A5, that in turn leads to decreased conversion of CPA and IFA into their active forms and thus to diminished cytotoxicity. Ifosfamide 183-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 30489455-1 2019 BACKGROUND: CYP3A4/5 and P-glycoprotein (P-gp, ABCB1) affect tacrolimus (TAC) exposure in T cells and kidney cells. Tacrolimus 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-20 30489455-1 2019 BACKGROUND: CYP3A4/5 and P-glycoprotein (P-gp, ABCB1) affect tacrolimus (TAC) exposure in T cells and kidney cells. Tacrolimus 73-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-20 30520338-1 2019 Clonazepam undergoes nitroreduction to 7-amino-clonazepam via CYP3A4/5, followed by acetylation to 7-acetamido-clonazepam via NAT2 enzyme. Clonazepam 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-70 30520338-1 2019 Clonazepam undergoes nitroreduction to 7-amino-clonazepam via CYP3A4/5, followed by acetylation to 7-acetamido-clonazepam via NAT2 enzyme. 7-aminoclonazepam 39-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-70 30544127-5 2019 Enzyme kinetic studies showed that isofraxidin was not only a noncompetitive inhibitor of CYP3A4 but also a competitive inhibitor of CYP1A2 and 2E1, with Ki values of 7.91, 10.14, and 9.30 micromol/L, respectively. isofraxidin 35-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 30544127-6 2019 In addition, isofraxidin is a time-dependent inhibitor for CYP3A4 with Kinact/KI value of 0.047/12.33 micromol/L-1min-1. isofraxidin 13-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 31587003-6 2019 Enzyme kinetic studies showed that cynaroside was not only a noncompetitive inhibitor of CYP3A4 but also a competitive inhibitor of CYP1A2 and 2C9, with Ki values of 7.33, 11.60, and 8.09 mumol/L, respectively. luteolin-7-glucoside 35-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 29479631-2 2019 Tacrolimus is metabolised in the liver and intestine by the cytochrome P450 3A (CYP3A) isoforms CYP3A4 and CYP3A5. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-78 29479631-2 2019 Tacrolimus is metabolised in the liver and intestine by the cytochrome P450 3A (CYP3A) isoforms CYP3A4 and CYP3A5. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-85 29479631-2 2019 Tacrolimus is metabolised in the liver and intestine by the cytochrome P450 3A (CYP3A) isoforms CYP3A4 and CYP3A5. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 31587003-7 2019 In addition, cynaroside is a time-dependent inhibitor for CYP3A4 with Kinact/KI value of 0.049/11.62 mumol/L-1min-1. luteolin-7-glucoside 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 30394306-2 2019 RSV inhibits cytochrome P450 CYP3A4 activity and interacts with the pregnane X receptor (PXR), the central regulator of drug/xenobiotic metabolizing enzyme expression. Resveratrol 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 30394306-6 2019 We found that only polymethoxylated stilbenes are prone to significantly induce CYP2B6 or CYP3A4 in primary human hepatocytes via pregnane X receptor (PXR) interaction. Stilbenes 36-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 30394306-7 2019 Natural resveratrol derivatives such as trans- and cis-RSV, oxyresveratrol, pinostilbene and pterostilbene significantly inhibit CYP3A4/5 enzymatic activities; however, only trans-RSV significantly inhibits CYP3A4/5 activity (both testosterone 6beta-hydroxylation and midazolam 1 -hydroxylation) in micromolar concentrations by a non-competitive mechanism, suggesting a potential risk of food-drug interactions with CYP3A4/5 substrates. Resveratrol 8-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 30394306-7 2019 Natural resveratrol derivatives such as trans- and cis-RSV, oxyresveratrol, pinostilbene and pterostilbene significantly inhibit CYP3A4/5 enzymatic activities; however, only trans-RSV significantly inhibits CYP3A4/5 activity (both testosterone 6beta-hydroxylation and midazolam 1 -hydroxylation) in micromolar concentrations by a non-competitive mechanism, suggesting a potential risk of food-drug interactions with CYP3A4/5 substrates. Resveratrol 8-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 31907914-5 2019 Cariprazine is metabolized by cyp3a4 and to a lesser extent by cyp2d6 enzymes. cariprazine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 30394306-7 2019 Natural resveratrol derivatives such as trans- and cis-RSV, oxyresveratrol, pinostilbene and pterostilbene significantly inhibit CYP3A4/5 enzymatic activities; however, only trans-RSV significantly inhibits CYP3A4/5 activity (both testosterone 6beta-hydroxylation and midazolam 1 -hydroxylation) in micromolar concentrations by a non-competitive mechanism, suggesting a potential risk of food-drug interactions with CYP3A4/5 substrates. Resveratrol 8-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 30394306-7 2019 Natural resveratrol derivatives such as trans- and cis-RSV, oxyresveratrol, pinostilbene and pterostilbene significantly inhibit CYP3A4/5 enzymatic activities; however, only trans-RSV significantly inhibits CYP3A4/5 activity (both testosterone 6beta-hydroxylation and midazolam 1 -hydroxylation) in micromolar concentrations by a non-competitive mechanism, suggesting a potential risk of food-drug interactions with CYP3A4/5 substrates. trans- and cis-rsv 40-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 30394306-7 2019 Natural resveratrol derivatives such as trans- and cis-RSV, oxyresveratrol, pinostilbene and pterostilbene significantly inhibit CYP3A4/5 enzymatic activities; however, only trans-RSV significantly inhibits CYP3A4/5 activity (both testosterone 6beta-hydroxylation and midazolam 1 -hydroxylation) in micromolar concentrations by a non-competitive mechanism, suggesting a potential risk of food-drug interactions with CYP3A4/5 substrates. puag-haad 60-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 30394306-7 2019 Natural resveratrol derivatives such as trans- and cis-RSV, oxyresveratrol, pinostilbene and pterostilbene significantly inhibit CYP3A4/5 enzymatic activities; however, only trans-RSV significantly inhibits CYP3A4/5 activity (both testosterone 6beta-hydroxylation and midazolam 1 -hydroxylation) in micromolar concentrations by a non-competitive mechanism, suggesting a potential risk of food-drug interactions with CYP3A4/5 substrates. puag-haad 60-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 30394306-7 2019 Natural resveratrol derivatives such as trans- and cis-RSV, oxyresveratrol, pinostilbene and pterostilbene significantly inhibit CYP3A4/5 enzymatic activities; however, only trans-RSV significantly inhibits CYP3A4/5 activity (both testosterone 6beta-hydroxylation and midazolam 1 -hydroxylation) in micromolar concentrations by a non-competitive mechanism, suggesting a potential risk of food-drug interactions with CYP3A4/5 substrates. puag-haad 60-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 30394306-7 2019 Natural resveratrol derivatives such as trans- and cis-RSV, oxyresveratrol, pinostilbene and pterostilbene significantly inhibit CYP3A4/5 enzymatic activities; however, only trans-RSV significantly inhibits CYP3A4/5 activity (both testosterone 6beta-hydroxylation and midazolam 1 -hydroxylation) in micromolar concentrations by a non-competitive mechanism, suggesting a potential risk of food-drug interactions with CYP3A4/5 substrates. pinostilbene 76-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 30394306-7 2019 Natural resveratrol derivatives such as trans- and cis-RSV, oxyresveratrol, pinostilbene and pterostilbene significantly inhibit CYP3A4/5 enzymatic activities; however, only trans-RSV significantly inhibits CYP3A4/5 activity (both testosterone 6beta-hydroxylation and midazolam 1 -hydroxylation) in micromolar concentrations by a non-competitive mechanism, suggesting a potential risk of food-drug interactions with CYP3A4/5 substrates. pinostilbene 76-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 30394306-7 2019 Natural resveratrol derivatives such as trans- and cis-RSV, oxyresveratrol, pinostilbene and pterostilbene significantly inhibit CYP3A4/5 enzymatic activities; however, only trans-RSV significantly inhibits CYP3A4/5 activity (both testosterone 6beta-hydroxylation and midazolam 1 -hydroxylation) in micromolar concentrations by a non-competitive mechanism, suggesting a potential risk of food-drug interactions with CYP3A4/5 substrates. pinostilbene 76-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 30394306-7 2019 Natural resveratrol derivatives such as trans- and cis-RSV, oxyresveratrol, pinostilbene and pterostilbene significantly inhibit CYP3A4/5 enzymatic activities; however, only trans-RSV significantly inhibits CYP3A4/5 activity (both testosterone 6beta-hydroxylation and midazolam 1 -hydroxylation) in micromolar concentrations by a non-competitive mechanism, suggesting a potential risk of food-drug interactions with CYP3A4/5 substrates. pterostilbene 93-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 30394306-7 2019 Natural resveratrol derivatives such as trans- and cis-RSV, oxyresveratrol, pinostilbene and pterostilbene significantly inhibit CYP3A4/5 enzymatic activities; however, only trans-RSV significantly inhibits CYP3A4/5 activity (both testosterone 6beta-hydroxylation and midazolam 1 -hydroxylation) in micromolar concentrations by a non-competitive mechanism, suggesting a potential risk of food-drug interactions with CYP3A4/5 substrates. pterostilbene 93-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 30394306-7 2019 Natural resveratrol derivatives such as trans- and cis-RSV, oxyresveratrol, pinostilbene and pterostilbene significantly inhibit CYP3A4/5 enzymatic activities; however, only trans-RSV significantly inhibits CYP3A4/5 activity (both testosterone 6beta-hydroxylation and midazolam 1 -hydroxylation) in micromolar concentrations by a non-competitive mechanism, suggesting a potential risk of food-drug interactions with CYP3A4/5 substrates. pterostilbene 93-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 29297772-6 2019 CC-223 was metabolized by CYP2C9 and CYP3A, while metabolism of M1 was mediated by CYP2C8 and CYP3A. CC-223 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-42 29297772-17 2019 Model based predictions of DDI with ketoconazole were in agreement with observed results enabling prospective predictions of DDIs between CC-223 and CYP3A4 inhibitors. Ketoconazole 36-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 29320899-0 2019 In vitro analysis of itraconazole cis-diastereoisomers inhibition of nine cytochrome P450 enzymes: stereoselective inhibition of CYP3A. Itraconazole 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-134 29320899-6 2019 All ITZ diastereoisomers dose-dependently inhibited CYP3A activity in both used assays, midazolam and testosterone hydroxylation. Midazolam 88-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-57 29320899-6 2019 All ITZ diastereoisomers dose-dependently inhibited CYP3A activity in both used assays, midazolam and testosterone hydroxylation. Testosterone 102-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-57 29394111-0 2019 Functional characterization of 21 CYP3A4 variants on amiodarone metabolism in vitro. Amiodarone 53-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 29394111-3 2019 Genetic polymorphisms of CYP3A4 can produce a significant effect on the efficacy and safety of some drugs, so the purpose of this study was to clarify the catalytic characteristics of 22 CYP3A4 allelic isoforms, including 6 novel variants in Han Chinese population, on the oxidative metabolism of amiodarone in vitro. Amiodarone 297-307 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 29394111-3 2019 Genetic polymorphisms of CYP3A4 can produce a significant effect on the efficacy and safety of some drugs, so the purpose of this study was to clarify the catalytic characteristics of 22 CYP3A4 allelic isoforms, including 6 novel variants in Han Chinese population, on the oxidative metabolism of amiodarone in vitro. Amiodarone 297-307 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 29394111-10 2019 This is the first time report describing all these infrequent alleles for amiodarone metabolism, which can provide fundamental data for further clinical studies on CYP3A4 alleles. Amiodarone 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 30481027-0 2018 Novel Tetrazole-Containing Analogues of Itraconazole as Potent Antiangiogenic Agents with Reduced Cytochrome P450 3A4 Inhibition. 1H-tetrazole 6-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-117 30481027-0 2018 Novel Tetrazole-Containing Analogues of Itraconazole as Potent Antiangiogenic Agents with Reduced Cytochrome P450 3A4 Inhibition. Itraconazole 40-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-117 30481027-2 2018 The wider use of itraconazole in the treatment of cancer, however, has been limited by its potent inhibition of the drug metabolizing enzyme cytochrome P450 3A4 (CYP3A4). Itraconazole 17-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-160 30481027-2 2018 The wider use of itraconazole in the treatment of cancer, however, has been limited by its potent inhibition of the drug metabolizing enzyme cytochrome P450 3A4 (CYP3A4). Itraconazole 17-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 30481027-4 2018 Among these analogues, 15n with tetrazole in place of 1,2,4-triazole exhibited optimal inhibition of human umbilical vein endothelial cell proliferation with an IC50 of 73 nM without a significant effect on CYP3A4 (EC50 > 20 muM). 15n 23-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 30587978-0 2018 Nanostructures of diamond, graphene oxide and graphite inhibit CYP1A2, CYP2D6 and CYP3A4 enzymes and downregulate their genes in liver cells. graphene oxide 27-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 30388368-0 2018 Overcoming Time-Dependent Inhibition (TDI) of Cytochrome P450 3A4 (CYP3A4) Resulting from Bioactivation of a Fluoropyrimidine Moiety. 2-fluoropyrimidine 109-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-65 30388368-0 2018 Overcoming Time-Dependent Inhibition (TDI) of Cytochrome P450 3A4 (CYP3A4) Resulting from Bioactivation of a Fluoropyrimidine Moiety. 2-fluoropyrimidine 109-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 30587978-0 2018 Nanostructures of diamond, graphene oxide and graphite inhibit CYP1A2, CYP2D6 and CYP3A4 enzymes and downregulate their genes in liver cells. Graphite 46-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 29956478-10 2018 According to static predictions, inactivation of CYP3A4 by nintedanib was unlikely to cause drug-drug interactions with clinically used doses of nintedanib, whereas midostaurin was predicted to increase the plasma exposure to CYP3A4-dependent substrates several fold. nintedanib 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 30422622-3 2018 By confining the cytochrome P450 3A4 (CYP3A4) enzyme and TCPP inside the pores of Au@CNC, a high metabolic activity is achieved by using 7-ethoxytrifluoromethyl coumarin as the substrate because of the three-dimensional hierarchical porous structure, large surface area, and fast electron transfer capacity of Au@CNC. tetracarboxyphenylporphine 57-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-36 30422622-3 2018 By confining the cytochrome P450 3A4 (CYP3A4) enzyme and TCPP inside the pores of Au@CNC, a high metabolic activity is achieved by using 7-ethoxytrifluoromethyl coumarin as the substrate because of the three-dimensional hierarchical porous structure, large surface area, and fast electron transfer capacity of Au@CNC. tetracarboxyphenylporphine 57-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 30422622-3 2018 By confining the cytochrome P450 3A4 (CYP3A4) enzyme and TCPP inside the pores of Au@CNC, a high metabolic activity is achieved by using 7-ethoxytrifluoromethyl coumarin as the substrate because of the three-dimensional hierarchical porous structure, large surface area, and fast electron transfer capacity of Au@CNC. Gold 82-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-36 30422622-3 2018 By confining the cytochrome P450 3A4 (CYP3A4) enzyme and TCPP inside the pores of Au@CNC, a high metabolic activity is achieved by using 7-ethoxytrifluoromethyl coumarin as the substrate because of the three-dimensional hierarchical porous structure, large surface area, and fast electron transfer capacity of Au@CNC. Gold 82-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 30422622-3 2018 By confining the cytochrome P450 3A4 (CYP3A4) enzyme and TCPP inside the pores of Au@CNC, a high metabolic activity is achieved by using 7-ethoxytrifluoromethyl coumarin as the substrate because of the three-dimensional hierarchical porous structure, large surface area, and fast electron transfer capacity of Au@CNC. 7-ethoxytrifluoromethyl coumarin 137-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-36 30422622-3 2018 By confining the cytochrome P450 3A4 (CYP3A4) enzyme and TCPP inside the pores of Au@CNC, a high metabolic activity is achieved by using 7-ethoxytrifluoromethyl coumarin as the substrate because of the three-dimensional hierarchical porous structure, large surface area, and fast electron transfer capacity of Au@CNC. 7-ethoxytrifluoromethyl coumarin 137-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 30422622-3 2018 By confining the cytochrome P450 3A4 (CYP3A4) enzyme and TCPP inside the pores of Au@CNC, a high metabolic activity is achieved by using 7-ethoxytrifluoromethyl coumarin as the substrate because of the three-dimensional hierarchical porous structure, large surface area, and fast electron transfer capacity of Au@CNC. Gold 310-312 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-36 30422622-3 2018 By confining the cytochrome P450 3A4 (CYP3A4) enzyme and TCPP inside the pores of Au@CNC, a high metabolic activity is achieved by using 7-ethoxytrifluoromethyl coumarin as the substrate because of the three-dimensional hierarchical porous structure, large surface area, and fast electron transfer capacity of Au@CNC. Gold 310-312 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 30581412-7 2018 Older AEDs, acting on cytochrome P450 isoenzymes, and especially on CYP3A4, such as phenobarbital, phenytoin, and carbamazepine are more likely to significantly reduce the anticoagulant effect of DOACs (especially rivaroxaban, apixaban, and edoxaban). Phenobarbital 84-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30581412-7 2018 Older AEDs, acting on cytochrome P450 isoenzymes, and especially on CYP3A4, such as phenobarbital, phenytoin, and carbamazepine are more likely to significantly reduce the anticoagulant effect of DOACs (especially rivaroxaban, apixaban, and edoxaban). Phenytoin 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30581412-7 2018 Older AEDs, acting on cytochrome P450 isoenzymes, and especially on CYP3A4, such as phenobarbital, phenytoin, and carbamazepine are more likely to significantly reduce the anticoagulant effect of DOACs (especially rivaroxaban, apixaban, and edoxaban). Carbamazepine 114-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30581412-7 2018 Older AEDs, acting on cytochrome P450 isoenzymes, and especially on CYP3A4, such as phenobarbital, phenytoin, and carbamazepine are more likely to significantly reduce the anticoagulant effect of DOACs (especially rivaroxaban, apixaban, and edoxaban). doacs 196-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30581412-7 2018 Older AEDs, acting on cytochrome P450 isoenzymes, and especially on CYP3A4, such as phenobarbital, phenytoin, and carbamazepine are more likely to significantly reduce the anticoagulant effect of DOACs (especially rivaroxaban, apixaban, and edoxaban). Rivaroxaban 214-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30581412-7 2018 Older AEDs, acting on cytochrome P450 isoenzymes, and especially on CYP3A4, such as phenobarbital, phenytoin, and carbamazepine are more likely to significantly reduce the anticoagulant effect of DOACs (especially rivaroxaban, apixaban, and edoxaban). apixaban 227-235 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30581412-7 2018 Older AEDs, acting on cytochrome P450 isoenzymes, and especially on CYP3A4, such as phenobarbital, phenytoin, and carbamazepine are more likely to significantly reduce the anticoagulant effect of DOACs (especially rivaroxaban, apixaban, and edoxaban). edoxaban 241-249 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30248338-4 2018 The mRNA levels of hepatic VDR- and vitamin D-related genes [cytochrome P450 (CYP) 2R1, CYP27A1, and CYP3A4] were higher in NAFL patients compared with normal liver subjects. Vitamin D 36-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 29956478-3 2018 Dovitinib, midostaurin and nintedanib exhibited an increased inhibition of CYP3A4 after a 30-min. 4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 29956478-3 2018 Dovitinib, midostaurin and nintedanib exhibited an increased inhibition of CYP3A4 after a 30-min. midostaurin 11-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 29956478-3 2018 Dovitinib, midostaurin and nintedanib exhibited an increased inhibition of CYP3A4 after a 30-min. nintedanib 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 29956478-6 2018 The inhibitory mechanism of CYP3A4 by midostaurin and nintedanib, but not by dovitinib, was consistent with irreversible mechanism-based inhibition. midostaurin 38-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 29956478-6 2018 The inhibitory mechanism of CYP3A4 by midostaurin and nintedanib, but not by dovitinib, was consistent with irreversible mechanism-based inhibition. nintedanib 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 29956478-10 2018 According to static predictions, inactivation of CYP3A4 by nintedanib was unlikely to cause drug-drug interactions with clinically used doses of nintedanib, whereas midostaurin was predicted to increase the plasma exposure to CYP3A4-dependent substrates several fold. midostaurin 165-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 226-232 29956478-11 2018 Furthermore, based on reversible inhibition, masitinib and vatalanib were predicted to increase the plasma exposure to sensitive CYP2C8 and CYP3A4 substrates by >=2-fold. masitinib 45-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 29956478-11 2018 Furthermore, based on reversible inhibition, masitinib and vatalanib were predicted to increase the plasma exposure to sensitive CYP2C8 and CYP3A4 substrates by >=2-fold. vatalanib 59-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 29956478-12 2018 In summary, our data identify midostaurin and nintedanib as time-dependent inhibitors of CYP3A4 and detect a risk of drug-drug interactions between vatalanib and CYP2C8 substrates, and between masitinib, midostaurin and vatalanib and CYP3A4 substrates. midostaurin 30-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 29956478-12 2018 In summary, our data identify midostaurin and nintedanib as time-dependent inhibitors of CYP3A4 and detect a risk of drug-drug interactions between vatalanib and CYP2C8 substrates, and between masitinib, midostaurin and vatalanib and CYP3A4 substrates. midostaurin 30-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 234-240 29956478-12 2018 In summary, our data identify midostaurin and nintedanib as time-dependent inhibitors of CYP3A4 and detect a risk of drug-drug interactions between vatalanib and CYP2C8 substrates, and between masitinib, midostaurin and vatalanib and CYP3A4 substrates. nintedanib 46-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 29956478-12 2018 In summary, our data identify midostaurin and nintedanib as time-dependent inhibitors of CYP3A4 and detect a risk of drug-drug interactions between vatalanib and CYP2C8 substrates, and between masitinib, midostaurin and vatalanib and CYP3A4 substrates. nintedanib 46-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 234-240 29956478-12 2018 In summary, our data identify midostaurin and nintedanib as time-dependent inhibitors of CYP3A4 and detect a risk of drug-drug interactions between vatalanib and CYP2C8 substrates, and between masitinib, midostaurin and vatalanib and CYP3A4 substrates. vatalanib 148-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 234-240 30171692-0 2018 CYP3A4-mediated effects of rifampicin on the pharmacokinetics of vilaprisan and its UGT1A1-mediated effects on bilirubin glucuronidation in humans. Rifampin 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 30171692-0 2018 CYP3A4-mediated effects of rifampicin on the pharmacokinetics of vilaprisan and its UGT1A1-mediated effects on bilirubin glucuronidation in humans. vilaprisan 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 30192025-1 2018 AIMS: We assessed the potential mutual interaction of oral macitentan (cytochrome P450 (CYP) 3A4 substrate) at steady-state with single-dose oral rivaroxaban (CYP3A4 and P-glycoprotein substrate) and evaluated the effect of the CYP3A and P-glycoprotein inducer St John"s wort (SJW) on the pharmacokinetics of these drugs in healthy volunteers. macitentan 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-96 30192025-1 2018 AIMS: We assessed the potential mutual interaction of oral macitentan (cytochrome P450 (CYP) 3A4 substrate) at steady-state with single-dose oral rivaroxaban (CYP3A4 and P-glycoprotein substrate) and evaluated the effect of the CYP3A and P-glycoprotein inducer St John"s wort (SJW) on the pharmacokinetics of these drugs in healthy volunteers. macitentan 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 30171692-0 2018 CYP3A4-mediated effects of rifampicin on the pharmacokinetics of vilaprisan and its UGT1A1-mediated effects on bilirubin glucuronidation in humans. Bilirubin 111-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 30192025-1 2018 AIMS: We assessed the potential mutual interaction of oral macitentan (cytochrome P450 (CYP) 3A4 substrate) at steady-state with single-dose oral rivaroxaban (CYP3A4 and P-glycoprotein substrate) and evaluated the effect of the CYP3A and P-glycoprotein inducer St John"s wort (SJW) on the pharmacokinetics of these drugs in healthy volunteers. macitentan 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-164 30171692-1 2018 AIMS: The primary aim of the present study was to quantify the effects of rifampicin, a strong cytochrome P450 (CYP) 3A4 inducer, on the pharmacokinetics of the new selective progesterone receptor modulator, vilaprisan. Rifampin 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-120 30192025-1 2018 AIMS: We assessed the potential mutual interaction of oral macitentan (cytochrome P450 (CYP) 3A4 substrate) at steady-state with single-dose oral rivaroxaban (CYP3A4 and P-glycoprotein substrate) and evaluated the effect of the CYP3A and P-glycoprotein inducer St John"s wort (SJW) on the pharmacokinetics of these drugs in healthy volunteers. Rivaroxaban 146-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-164 30171692-1 2018 AIMS: The primary aim of the present study was to quantify the effects of rifampicin, a strong cytochrome P450 (CYP) 3A4 inducer, on the pharmacokinetics of the new selective progesterone receptor modulator, vilaprisan. vilaprisan 208-218 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-120 30171692-13 2018 Therefore, it is recommended that the use of strong CYP3A4 inducers is avoided when taking vilaprisan. vilaprisan 91-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 30218442-0 2018 Increased tacrolimus blood concentration by Beni-Madonna - a new hybrid citrus cultivar categorized as "Tangor", in a liver transplant patient: likely furanocoumarin-mediated inhibition of CYP3A4 or P-glycoprotein. Furocoumarins 151-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 30171779-1 2018 AIM: We report on two Phase 1, open-label, single-arm studies assessing the effect of osimertinib on simvastatin (CYP3A substrate) and rosuvastatin (breast cancer resistance protein substrate [BCRP] substrate) exposure in patients with advanced epidermal growth factor receptor (EGFR)-mutated non-small cell lung cancer who have progressed after treatment with an EGFR tyrosine kinase inhibitor, to determine, upon coadministration, whether osimertinib could affect the exposure of these agents. osimertinib 86-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 29153269-12 2018 Interactions between seasons and CYP27A1 rs933994, CYP3A4 rs2246709 on plasma 25(OH)D concentrations were also observed. 25(oh)d 78-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 29153269-14 2018 CONCLUSIONS: Genetic mutants in vitamin D pathway (GC, CYP3A4, CYP24A1, and NADSYN1/DHCR7) had significant associations with 25(OH)D levels among pregnant women in southeast China. Vitamin D 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 29569712-1 2018 Rifampin demonstrated dose-dependent relative induction between cytochrome P (CYP)3A and P-glycoprotein (P-gp), organic anion transporting polypeptides (OATPs), or CYP2C9; P-gp, OATP, and CYP2C9 induction was one drug-drug interaction (DDI) category lower than that observed for CYP3A across a wide range of pregnane X receptor (PXR) agonism. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-84 29153269-14 2018 CONCLUSIONS: Genetic mutants in vitamin D pathway (GC, CYP3A4, CYP24A1, and NADSYN1/DHCR7) had significant associations with 25(OH)D levels among pregnant women in southeast China. 25(oh)d 125-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 29569712-1 2018 Rifampin demonstrated dose-dependent relative induction between cytochrome P (CYP)3A and P-glycoprotein (P-gp), organic anion transporting polypeptides (OATPs), or CYP2C9; P-gp, OATP, and CYP2C9 induction was one drug-drug interaction (DDI) category lower than that observed for CYP3A across a wide range of pregnane X receptor (PXR) agonism. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 279-284 30311747-4 2018 The area under the concentration-time curve (AUC) ratios of midazolam were above 0.80, indicating that induction of CYP3A by evofosfamide administered weekly is unlikely to occur in humans. TH 302 125-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 29569712-2 2018 The objective of this study was to determine if these relationships could be utilized to predict transporter induction by other CYP3A inducers (rifabutin and carbamazepine) and of another P-gp substrate, sofosbuvir. Rifabutin 144-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-133 29569712-2 2018 The objective of this study was to determine if these relationships could be utilized to predict transporter induction by other CYP3A inducers (rifabutin and carbamazepine) and of another P-gp substrate, sofosbuvir. Carbamazepine 158-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-133 29569712-6 2018 Induction of P-gp, CYP2C9, and decreased sofosbuvir exposure were successfully predicted by observed CYP3A induction. Sofosbuvir 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 29569723-2 2018 The objective of this study was to establish relative induction relationships between CYP3A and drug transporters (P-glycoprotein (P-gp), organic anion transporting polypeptide (OATP), and breast cancer resistance protein (BCRP)) or other P450s (CYP2C9 and CYP1A2) using ascending doses of the prototypical pregnane xenobiotic receptor (PXR) agonist, rifampin, to elicit weak, moderate, and strong PXR agonism. Rifampin 351-359 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 29574693-6 2018 Multivariable analysis indicated that consideration of baseline weight, body mass index, and CYP2C8, CYP3A4, and P-gp abundance strongly predicts steady-state dabrafenib trough concentration above 48 ng/mL (ROC AUC = 0.94; accuracy = 86%). dabrafenib 159-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 29633238-0 2018 Drinking Ethanol Has Few Acute Effects on CYP2C9, CYP2C19, NAT2, and P-Glycoprotein Activities but Somewhat Inhibits CYP1A2, CYP2D6, and Intestinal CYP3A: So What? Ethanol 9-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-153 30105453-1 2018 PURPOSE: To assess the potential pharmacokinetic (PK) interactions between siponimod and rifampin, a strong CYP3A4/moderate CYP2C9 inducer, in healthy subjects. siponimod 75-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 30533000-2 2018 Pharmacokinetic drug-drug interaction between mitotane, a strong CYP3A4 inducer, and etoposide, which is a substrate of CYP3A4, may contribute to chemoresistance. Mitotane 46-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 30533000-2 2018 Pharmacokinetic drug-drug interaction between mitotane, a strong CYP3A4 inducer, and etoposide, which is a substrate of CYP3A4, may contribute to chemoresistance. Mitotane 46-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 30533000-2 2018 Pharmacokinetic drug-drug interaction between mitotane, a strong CYP3A4 inducer, and etoposide, which is a substrate of CYP3A4, may contribute to chemoresistance. Etoposide 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 30105453-1 2018 PURPOSE: To assess the potential pharmacokinetic (PK) interactions between siponimod and rifampin, a strong CYP3A4/moderate CYP2C9 inducer, in healthy subjects. Rifampin 89-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 30105453-14 2018 CONCLUSIONS: The study findings suggest that in the presence of rifampin, a strong CYP3A4/moderate CYP2C9 inducer, siponimod showed significant decrease in Cmax,ss (45%) and AUCtau,ss (57%) in healthy subjects. Rifampin 64-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 30167757-3 2018 As drug interaction studies with buprenorphine are limited, we wanted to investigate the effect of voriconazole, a strong CYP3A4 inhibitor, on the pharmacokinetics and pharmacodynamics of oral buprenorphine. Voriconazole 99-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 30167757-11 2018 CONCLUSIONS: Voriconazole greatly increases exposure to oral buprenorphine, mainly by inhibiting intestinal and liver CYP3A4. Voriconazole 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 30167757-11 2018 CONCLUSIONS: Voriconazole greatly increases exposure to oral buprenorphine, mainly by inhibiting intestinal and liver CYP3A4. Buprenorphine 61-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 30167757-13 2018 Although oral buprenorphine is not commonly used, this interaction may become relevant in patients receiving sublingual buprenorphine together with voriconazole or other CYP3A4 or transporter inhibitors. Buprenorphine 14-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 29785610-10 2018 Troleandomycin and verapamil displayed quasi-irreversible MDI of CYP3A4; MIC formation was observed, while no formation of CYP-dependent GSH adducts occurred. Troleandomycin 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 29785610-10 2018 Troleandomycin and verapamil displayed quasi-irreversible MDI of CYP3A4; MIC formation was observed, while no formation of CYP-dependent GSH adducts occurred. Verapamil 19-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 29876844-0 2018 Nutritional Status Differentially Alters Cytochrome P450 3A4 (CYP3A4) and Uridine 5"-Diphospho-Glucuronosyltransferase (UGT) Mediated Drug Metabolism: Effect of Short-Term Fasting and High Fat Diet on Midazolam Metabolism. Midazolam 201-210 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 29876844-5 2018 RESULTS: Short-term fasting increased CYP3A4-mediated midazolam clearance by 12% (p < 0.01) and decreased UGT-mediated metabolism apparent 1-OH-midazolam clearance by 13% (p < 0.01) by decreasing the ratio of clearance and the fraction metabolite formed (DeltaCL1-OH-MDZ/f1-OH-MDZ). Midazolam 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 29876844-8 2018 CONCLUSIONS: Short-term fasting differentially alters midazolam metabolism by increasing CYP3A4-mediated metabolism but by decreasing UGT-mediated metabolism. Midazolam 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 30047107-5 2018 Review findings show doravirine is well-absorbed, exhibits moderate protein binding activity, and is extensively metabolized by cytochrome P450 enzymes (specifically CYP3A). doravirine 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-171 30047107-7 2018 Drug interaction studies have shown doravirine does not affect the pharmacokinetics of dolutegravir or atorvastatin but may have its pharmacokinetics altered by rifampicin (rifampin) and other rifamycins (CYP3A inducers) and ritonavir (CYP3A inhibitor). doravirine 36-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 205-210 30047107-7 2018 Drug interaction studies have shown doravirine does not affect the pharmacokinetics of dolutegravir or atorvastatin but may have its pharmacokinetics altered by rifampicin (rifampin) and other rifamycins (CYP3A inducers) and ritonavir (CYP3A inhibitor). doravirine 36-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 236-241 30179260-5 2018 The metabolism of nilotinib is primarily via hepatic cytochrome P450 (CYP) 3A4 according to in vitro studies. nilotinib 18-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-78 29744741-6 2018 Furthermore, 1 microM naltrexone hydrochloride inhibited CYP3A4 enzyme activity, the most by 37.9% followed by CYP2C9 (36.5%) and CYP2D6 (31.8%). Naltrexone 22-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 29779093-8 2018 The contribution ratio of CYP3A4 to the metabolic clearance of finerenone derived from these values was 0.88-0.89 and was consistent with estimations based on in vitro data, with the remaining metabolic clearance due to CYP2C8 involvement. finerenone 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 29779093-9 2018 CONCLUSION: Finerenone is predominantly metabolized by CYP3A4 in the gut wall and liver. finerenone 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 29785610-9 2018 Mifepristone displayed irreversible MDI of CYP3A4, formation of CYP-dependent GSH adducts was observed, while CYP-mediated covalent binding occurred which was decreased in the presence of GSH. Mifepristone 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 30422888-0 2018 Investigating the Effect of Demographics, Clinical Characteristics, and Polymorphism of MDR-1, CYP1A2, CYP3A4, and CYP3A5 on Clopidogrel Resistance. Clopidogrel 125-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 29905956-0 2018 Population Pharmacokinetic/Pharmacodynamic Analyses of Avatrombopag in Patients With Chronic Liver Disease and Optimal Dose Adjustment Guide With Concomitantly Administered CYP3A and CYP2C9 Inhibitors. avatrombopag 55-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-178 30179260-6 2018 In the clinical setting, exposure to nilotinib was significantly reduced by the induction of CYP3A4 with rifampicin and significantly increased by the inhibition of CYP3A with ketoconazole. nilotinib 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 30179260-6 2018 In the clinical setting, exposure to nilotinib was significantly reduced by the induction of CYP3A4 with rifampicin and significantly increased by the inhibition of CYP3A with ketoconazole. nilotinib 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 30179260-6 2018 In the clinical setting, exposure to nilotinib was significantly reduced by the induction of CYP3A4 with rifampicin and significantly increased by the inhibition of CYP3A with ketoconazole. Rifampin 105-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 30179260-6 2018 In the clinical setting, exposure to nilotinib was significantly reduced by the induction of CYP3A4 with rifampicin and significantly increased by the inhibition of CYP3A with ketoconazole. Rifampin 105-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 30179260-7 2018 Additionally, nilotinib is a competitive inhibitor of CYP3A4/5, CYP2C8, CYP2C9, CYP2D6, and uridine diphosphate glucuronosyltransferase 1A1. nilotinib 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-62 28782406-0 2018 Severe sunitinib-induced myelosuppression in a patient with a CYP 3A4 polymorphism. Sunitinib 7-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-69 29846137-0 2018 A drug-drug interaction study of ibrutinib with moderate/strong CYP3A inhibitors in patients with B-cell malignancies. ibrutinib 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 30205091-2 2018 Methadone undergoes N-demethylation by multiple cytochrome P450 (CYP) enzymes including CYP3A4, CYP2B6, CYP2C19, CYP2D6, CYP2C9, and CYP2C8. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 30205091-2 2018 Methadone undergoes N-demethylation by multiple cytochrome P450 (CYP) enzymes including CYP3A4, CYP2B6, CYP2C19, CYP2D6, CYP2C9, and CYP2C8. Nitrogen 20-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 30205091-3 2018 In vivo, polymorphism effects on methadone systemic exposure have been noted for CYP2B6, CYP3A4, and CYP2D6. Methadone 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 29846137-1 2018 This was an open-label, multicenter, phase-1 study to evaluate the drug interaction between steady-state ibrutinib and moderate (erythromycin) and strong (voriconazole) CYP3A inhibitors in patients with B-cell malignancies and to confirm dosing recommendations. ibrutinib 105-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-174 30122094-3 2018 OBJECTIVE: This study investigates the inhibitory effects of Friedelin on the major human liver CYP isoforms (CYP3A4, 1A2, 2A6, 2E1, 2D6, 2C9, 2C19 and 2C8). friedelin 61-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 31070542-9 2018 DISCUSSION AND CONCLUSIONS: The in vitro studies of bergenin with CYP isoforms indicate that bergenin has the potential to cause pharmacokinetic drug interactions with other co-administered drugs metabolized by CYP3A4, 2E1 and 2C9. bergenin 93-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-230 30122094-5 2018 RESULTS: The results indicate that Friedelin inhibited the activity of CYP3A4 and 2E1, with the IC50 values of 10.79 and 22.54 muM, respectively, but other CYP isoforms were not affected. friedelin 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-85 30122094-6 2018 Enzyme kinetic studies showed that Friedelin is not only a noncompetitive inhibitor of CYP3A4, but also a competitive inhibitor of CYP2E1, with Ki values of 6.16 and 18.02 muM, respectively. friedelin 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 30122094-7 2018 In addition, Friedelin is a time-dependent inhibitor of CYP3A4 with Kinact/Ki value of 4.84 nM/min. friedelin 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 30122094-8 2018 DISCUSSION AND CONCLUSION: The in vitro studies of Friedelin with CYP isoforms suggested that Friedelin has the potential to cause pharmacokinetic drug interactions with other co-administered drugs metabolized by CYP3A4 and 2E1. friedelin 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 213-227 30122094-8 2018 DISCUSSION AND CONCLUSION: The in vitro studies of Friedelin with CYP isoforms suggested that Friedelin has the potential to cause pharmacokinetic drug interactions with other co-administered drugs metabolized by CYP3A4 and 2E1. friedelin 94-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 213-227 30532626-3 2018 In the present study, ethanol extracts of 58 medicinal plants, belonging to 27 families, were evaluated for potential activities in CYP3A4 induction in HepG2 cells by reporter gene assay. Ethanol 22-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 30346772-4 2018 Compound 2 was developed improving aqueous solubility and eliminating CYP3A4 time-dependent inhibition starting from the earlier described inhibitor 1 (AZ20). AZ20 152-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 28385095-6 2018 Enzyme kinetic studies showed that PTM was not only a non-competitive inhibitor of CYP3A4, but also a competitive inhibitor of CYP1A2 and 2C9, with Ki values of 7.33, 11.60 and 8.09 muM, respectively. ptm 35-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 29191071-0 2018 Allosteric activation of cytochrome P450 3A4 by efavirenz facilitates midazolam binding. Midazolam 70-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-44 29191071-2 2018 The purpose of this study is to investigate the heteroactivation mechanism of CYP3A4 by efavirenz, which enhances metabolism of midazolam in vivo, in terms of its binding to CYP3A4 with in vitro spectroscopic methods. Midazolam 128-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 29191071-2 2018 The purpose of this study is to investigate the heteroactivation mechanism of CYP3A4 by efavirenz, which enhances metabolism of midazolam in vivo, in terms of its binding to CYP3A4 with in vitro spectroscopic methods. Midazolam 128-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 29191071-4 2018 Efavirenz exhibited a type II spectral change with binding to CYP3A4 indicating a possible inhibitor. efavirenz 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 29191071-8 2018 These results propose that efavirenz affects midazolam-binding via binding to the peripheral site which is apart from the active site of CYP3A4. Midazolam 45-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 30381583-0 2018 Impact of CYP3A4*1G Polymorphism on Fentanyl Analgesia Assessed by Analgesia Nociception Index in Chinese Patients Undergoing Hysteroscopy. Fentanyl 36-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 30381583-13 2018 Conclusion: CYP3A4*1G polymorphism associated with the analgesic efficacy of intraoperative fentanyl in the patients undergoing hysteroscopy under general anesthesia. Fentanyl 92-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 30125880-2 2018 Herein, a facile electrochemical enzymatic nanoreactor (CYP3A4/PNGFs) is constructed by immobilizing CYP3A4 inside polydopamine (PDA) modified nanoporous graphene foams (PNGFs) whose pore diameter is controllable by the template of silica spheres. polydopamine 115-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 30125880-2 2018 Herein, a facile electrochemical enzymatic nanoreactor (CYP3A4/PNGFs) is constructed by immobilizing CYP3A4 inside polydopamine (PDA) modified nanoporous graphene foams (PNGFs) whose pore diameter is controllable by the template of silica spheres. polydopamine 115-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 30125880-2 2018 Herein, a facile electrochemical enzymatic nanoreactor (CYP3A4/PNGFs) is constructed by immobilizing CYP3A4 inside polydopamine (PDA) modified nanoporous graphene foams (PNGFs) whose pore diameter is controllable by the template of silica spheres. Silicon Dioxide 232-238 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 30125880-2 2018 Herein, a facile electrochemical enzymatic nanoreactor (CYP3A4/PNGFs) is constructed by immobilizing CYP3A4 inside polydopamine (PDA) modified nanoporous graphene foams (PNGFs) whose pore diameter is controllable by the template of silica spheres. polydopamine 129-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 30125880-5 2018 At the pore diameter of about 65 nm, CYP3A4 shows the highest affinity to testosterone with the Michaelis-Menten constant (Kmapp) of 110.70 +- 18 muM and the relatively higher reaction rate with the Imax value of 11.85 +- 1.20 nA, which is due to the maintained native configuration and larger amount of immobilized enzyme. Testosterone 74-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 30125880-2 2018 Herein, a facile electrochemical enzymatic nanoreactor (CYP3A4/PNGFs) is constructed by immobilizing CYP3A4 inside polydopamine (PDA) modified nanoporous graphene foams (PNGFs) whose pore diameter is controllable by the template of silica spheres. polydopamine 129-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 30125880-6 2018 Furthermore, the constructed CYP3A4/PNGF-1 nanoreactor is successfully applied to the metabolism of three steroid hormones (testosterone, estrone and progesterone), and the order of the calculated Kmapp values is consistent with literature. Steroids 106-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 30125880-2 2018 Herein, a facile electrochemical enzymatic nanoreactor (CYP3A4/PNGFs) is constructed by immobilizing CYP3A4 inside polydopamine (PDA) modified nanoporous graphene foams (PNGFs) whose pore diameter is controllable by the template of silica spheres. Graphite 154-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 30125880-6 2018 Furthermore, the constructed CYP3A4/PNGF-1 nanoreactor is successfully applied to the metabolism of three steroid hormones (testosterone, estrone and progesterone), and the order of the calculated Kmapp values is consistent with literature. Testosterone 124-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 30340067-0 2018 Quantitative analysis of 4beta- and 4alpha-hydroxycholesterol in human plasma and serum by UHPLC/ESI-HR-MS. Cholesterol oxidation product 4beta-hydroxycholesterol (4beta-OHC) may possibly be used as an endogenous biomarker of CYP3A enzyme activity and as CYP3A4 is involved in the metabolism of approximately 50% of the drugs in clinical use, the monitoring of CYP3A activity by 4beta-OHC plasma or serum levels, may be of clinical significance. 4beta- and 4alpha-hydroxycholesterol 25-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 226-231 30125880-6 2018 Furthermore, the constructed CYP3A4/PNGF-1 nanoreactor is successfully applied to the metabolism of three steroid hormones (testosterone, estrone and progesterone), and the order of the calculated Kmapp values is consistent with literature. Estrone 138-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 30125880-6 2018 Furthermore, the constructed CYP3A4/PNGF-1 nanoreactor is successfully applied to the metabolism of three steroid hormones (testosterone, estrone and progesterone), and the order of the calculated Kmapp values is consistent with literature. Progesterone 150-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 30340067-10 2018 The method was successfully used for the determination of 4beta-OHC and 4alpha-OHC concentrations in clinical plasma and serum samples collected before and after treatment with a known CYP3A4 inducer rifampicin. Rifampin 200-210 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 30340067-0 2018 Quantitative analysis of 4beta- and 4alpha-hydroxycholesterol in human plasma and serum by UHPLC/ESI-HR-MS. Cholesterol oxidation product 4beta-hydroxycholesterol (4beta-OHC) may possibly be used as an endogenous biomarker of CYP3A enzyme activity and as CYP3A4 is involved in the metabolism of approximately 50% of the drugs in clinical use, the monitoring of CYP3A activity by 4beta-OHC plasma or serum levels, may be of clinical significance. 4beta- and 4alpha-hydroxycholesterol 25-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 255-261 30340067-0 2018 Quantitative analysis of 4beta- and 4alpha-hydroxycholesterol in human plasma and serum by UHPLC/ESI-HR-MS. Cholesterol oxidation product 4beta-hydroxycholesterol (4beta-OHC) may possibly be used as an endogenous biomarker of CYP3A enzyme activity and as CYP3A4 is involved in the metabolism of approximately 50% of the drugs in clinical use, the monitoring of CYP3A activity by 4beta-OHC plasma or serum levels, may be of clinical significance. 4beta- and 4alpha-hydroxycholesterol 25-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 255-260 30340067-0 2018 Quantitative analysis of 4beta- and 4alpha-hydroxycholesterol in human plasma and serum by UHPLC/ESI-HR-MS. Cholesterol oxidation product 4beta-hydroxycholesterol (4beta-OHC) may possibly be used as an endogenous biomarker of CYP3A enzyme activity and as CYP3A4 is involved in the metabolism of approximately 50% of the drugs in clinical use, the monitoring of CYP3A activity by 4beta-OHC plasma or serum levels, may be of clinical significance. Cholesterol 108-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 226-231 30340067-0 2018 Quantitative analysis of 4beta- and 4alpha-hydroxycholesterol in human plasma and serum by UHPLC/ESI-HR-MS. Cholesterol oxidation product 4beta-hydroxycholesterol (4beta-OHC) may possibly be used as an endogenous biomarker of CYP3A enzyme activity and as CYP3A4 is involved in the metabolism of approximately 50% of the drugs in clinical use, the monitoring of CYP3A activity by 4beta-OHC plasma or serum levels, may be of clinical significance. Cholesterol 108-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 255-261 30340067-0 2018 Quantitative analysis of 4beta- and 4alpha-hydroxycholesterol in human plasma and serum by UHPLC/ESI-HR-MS. Cholesterol oxidation product 4beta-hydroxycholesterol (4beta-OHC) may possibly be used as an endogenous biomarker of CYP3A enzyme activity and as CYP3A4 is involved in the metabolism of approximately 50% of the drugs in clinical use, the monitoring of CYP3A activity by 4beta-OHC plasma or serum levels, may be of clinical significance. Cholesterol 108-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 255-260 30340067-0 2018 Quantitative analysis of 4beta- and 4alpha-hydroxycholesterol in human plasma and serum by UHPLC/ESI-HR-MS. Cholesterol oxidation product 4beta-hydroxycholesterol (4beta-OHC) may possibly be used as an endogenous biomarker of CYP3A enzyme activity and as CYP3A4 is involved in the metabolism of approximately 50% of the drugs in clinical use, the monitoring of CYP3A activity by 4beta-OHC plasma or serum levels, may be of clinical significance. cholest-5-ene-3,4-diol 138-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 226-231 30340067-0 2018 Quantitative analysis of 4beta- and 4alpha-hydroxycholesterol in human plasma and serum by UHPLC/ESI-HR-MS. Cholesterol oxidation product 4beta-hydroxycholesterol (4beta-OHC) may possibly be used as an endogenous biomarker of CYP3A enzyme activity and as CYP3A4 is involved in the metabolism of approximately 50% of the drugs in clinical use, the monitoring of CYP3A activity by 4beta-OHC plasma or serum levels, may be of clinical significance. cholest-5-ene-3,4-diol 138-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 255-261 30340067-0 2018 Quantitative analysis of 4beta- and 4alpha-hydroxycholesterol in human plasma and serum by UHPLC/ESI-HR-MS. Cholesterol oxidation product 4beta-hydroxycholesterol (4beta-OHC) may possibly be used as an endogenous biomarker of CYP3A enzyme activity and as CYP3A4 is involved in the metabolism of approximately 50% of the drugs in clinical use, the monitoring of CYP3A activity by 4beta-OHC plasma or serum levels, may be of clinical significance. cholest-5-ene-3,4-diol 138-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 255-260 30340067-0 2018 Quantitative analysis of 4beta- and 4alpha-hydroxycholesterol in human plasma and serum by UHPLC/ESI-HR-MS. Cholesterol oxidation product 4beta-hydroxycholesterol (4beta-OHC) may possibly be used as an endogenous biomarker of CYP3A enzyme activity and as CYP3A4 is involved in the metabolism of approximately 50% of the drugs in clinical use, the monitoring of CYP3A activity by 4beta-OHC plasma or serum levels, may be of clinical significance. 4beta-ohc 164-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 226-231 30340067-0 2018 Quantitative analysis of 4beta- and 4alpha-hydroxycholesterol in human plasma and serum by UHPLC/ESI-HR-MS. Cholesterol oxidation product 4beta-hydroxycholesterol (4beta-OHC) may possibly be used as an endogenous biomarker of CYP3A enzyme activity and as CYP3A4 is involved in the metabolism of approximately 50% of the drugs in clinical use, the monitoring of CYP3A activity by 4beta-OHC plasma or serum levels, may be of clinical significance. 4beta-ohc 164-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 255-261 30340067-0 2018 Quantitative analysis of 4beta- and 4alpha-hydroxycholesterol in human plasma and serum by UHPLC/ESI-HR-MS. Cholesterol oxidation product 4beta-hydroxycholesterol (4beta-OHC) may possibly be used as an endogenous biomarker of CYP3A enzyme activity and as CYP3A4 is involved in the metabolism of approximately 50% of the drugs in clinical use, the monitoring of CYP3A activity by 4beta-OHC plasma or serum levels, may be of clinical significance. 4beta-ohc 164-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 255-260 30142539-0 2018 Interactions of casticin, ipriflavone, and resveratrol with serum albumin and their inhibitory effects on CYP2C9 and CYP3A4 enzymes. casticin 16-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 29926893-0 2018 CYP3A4 gene polymorphism is correlated with individual consumption of sufentanil. Sufentanil 70-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29926893-3 2018 The cytochrome P-450 3A4 (CYP3A4) gene has been reported to contribute significantly to human liver microsomal oxidation of sufentanil and alfentanil. Sufentanil 124-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-24 29926893-3 2018 The cytochrome P-450 3A4 (CYP3A4) gene has been reported to contribute significantly to human liver microsomal oxidation of sufentanil and alfentanil. Sufentanil 124-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 29926893-3 2018 The cytochrome P-450 3A4 (CYP3A4) gene has been reported to contribute significantly to human liver microsomal oxidation of sufentanil and alfentanil. Alfentanil 139-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-24 29926893-3 2018 The cytochrome P-450 3A4 (CYP3A4) gene has been reported to contribute significantly to human liver microsomal oxidation of sufentanil and alfentanil. Alfentanil 139-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 29926893-5 2018 We then investigated the correlation between sufentanil (an opioid analgesic) consumption and CYP3A4 genetic polymorphism. Sufentanil 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 29926893-7 2018 Interestingly, the parturients with homozygous CYP3A4*1G showed less sufentanil consumption compared with those having the wild-type genotype. Sufentanil 69-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 29926893-8 2018 CONCLUSION: In summary, we found a correlation between CYP3A4 genetic polymorphism and sufentanil consumption. Sufentanil 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 30142539-8 2018 Our results suggest that high intake of CAS and RES may interfere with the albumin-binding of Site II ligands as well as the metabolism of drugs by CYP2C9 and/or CYP3A4 enzymes, while large doses of IPR may affect the CYP3A4-catalyzed biotransformation of some drugs. casticin 40-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 30142539-8 2018 Our results suggest that high intake of CAS and RES may interfere with the albumin-binding of Site II ligands as well as the metabolism of drugs by CYP2C9 and/or CYP3A4 enzymes, while large doses of IPR may affect the CYP3A4-catalyzed biotransformation of some drugs. casticin 40-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 218-224 30142539-0 2018 Interactions of casticin, ipriflavone, and resveratrol with serum albumin and their inhibitory effects on CYP2C9 and CYP3A4 enzymes. Resveratrol 43-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 30142539-8 2018 Our results suggest that high intake of CAS and RES may interfere with the albumin-binding of Site II ligands as well as the metabolism of drugs by CYP2C9 and/or CYP3A4 enzymes, while large doses of IPR may affect the CYP3A4-catalyzed biotransformation of some drugs. Resveratrol 48-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 30142539-8 2018 Our results suggest that high intake of CAS and RES may interfere with the albumin-binding of Site II ligands as well as the metabolism of drugs by CYP2C9 and/or CYP3A4 enzymes, while large doses of IPR may affect the CYP3A4-catalyzed biotransformation of some drugs. Resveratrol 48-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 218-224 30142539-7 2018 Our main observations are the following: (1) Polyphenols formed stable complexes with albumin (K = 104-105 L/mol); (2) CAS and RES slightly displaced naproxen from human albumin, while albumin-binding of warfarin was not affected; (3) CAS and RES significantly inhibited CYP2C9, with CAS being as potent as the positive control warfarin; (4) each polyphenol significantly inhibited CYP3A4, with RES being stronger and CAS slightly weaker than the known inhibitor naringenin. Polyphenols 45-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 382-388 30142539-7 2018 Our main observations are the following: (1) Polyphenols formed stable complexes with albumin (K = 104-105 L/mol); (2) CAS and RES slightly displaced naproxen from human albumin, while albumin-binding of warfarin was not affected; (3) CAS and RES significantly inhibited CYP2C9, with CAS being as potent as the positive control warfarin; (4) each polyphenol significantly inhibited CYP3A4, with RES being stronger and CAS slightly weaker than the known inhibitor naringenin. casticin 119-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 382-388 30362120-5 2018 Inhibition studies with chemical inhibitors and antibodies suggested that arachidonic acid, the substrate of CYP2J2, and CYP2J2-specific antibody effectively inhibited the formation of SYL-927-M in HLMs whereas no significant inhibition was observed with the inhibitors for CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1 and CYP3A4, demonstrating that CYP2J2 was primarily responsible for the formation of SYL-927-M. Arachidonic Acid 74-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 326-332 30502764-7 2018 Further investigation showed that GA (17 : 1) had less cytotoxicity in primary rat hepatocytes than in HepG2 cells and that the toxicity was enhanced through CYP1A- and CYP3A-mediated metabolism. ginkgolic acid 34-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-174 30044899-0 2018 Amenamevir: Studies of Potential CYP3A-Mediated Pharmacokinetic Interactions With Midazolam, Cyclosporine, and Ritonavir in Healthy Volunteers. ASP2151 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 29870591-1 2018 Amenamevir (formerly ASP2151) induces cytochrome P450 (CYP)2B6 and CYP3A4 and inhibits CYP2C8. ASP2151 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 29870591-1 2018 Amenamevir (formerly ASP2151) induces cytochrome P450 (CYP)2B6 and CYP3A4 and inhibits CYP2C8. ASP2151 21-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 30044899-0 2018 Amenamevir: Studies of Potential CYP3A-Mediated Pharmacokinetic Interactions With Midazolam, Cyclosporine, and Ritonavir in Healthy Volunteers. Midazolam 82-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 30044899-3 2018 Three studies were done in healthy volunteers to investigate potential CYP3A pharmacokinetic interactions with the following drugs: (1) Midazolam (probe substrate for CYP3A): After 10 days" pretreatment with amenamevir 400 mg daily, geometric mean maximum concentration of drug in blood plasma (Cmax ) and area under the plasma drug concentration-time curve from time zero to infinity (AUC0- ) of midazolam 7.5 mg were about 68% and 51%, respectively, of those after midazolam alone. ASP2151 208-218 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-76 30044899-5 2018 (3) Ritonavir (inhibitor of CYP3A): When given with single doses of ritonavir 600 mg, geometric mean Cmax of amenamevir after 400-mg and 1200-mg single doses was, respectively, about 1.4 and 1.6 times higher, and geometric mean AUC0- about 2.6 and 3.3 times higher, than after amenamevir alone. Ritonavir 4-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 30044899-0 2018 Amenamevir: Studies of Potential CYP3A-Mediated Pharmacokinetic Interactions With Midazolam, Cyclosporine, and Ritonavir in Healthy Volunteers. Cyclosporine 93-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 30044899-5 2018 (3) Ritonavir (inhibitor of CYP3A): When given with single doses of ritonavir 600 mg, geometric mean Cmax of amenamevir after 400-mg and 1200-mg single doses was, respectively, about 1.4 and 1.6 times higher, and geometric mean AUC0- about 2.6 and 3.3 times higher, than after amenamevir alone. Ritonavir 68-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 30044899-0 2018 Amenamevir: Studies of Potential CYP3A-Mediated Pharmacokinetic Interactions With Midazolam, Cyclosporine, and Ritonavir in Healthy Volunteers. Ritonavir 111-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 30044899-5 2018 (3) Ritonavir (inhibitor of CYP3A): When given with single doses of ritonavir 600 mg, geometric mean Cmax of amenamevir after 400-mg and 1200-mg single doses was, respectively, about 1.4 and 1.6 times higher, and geometric mean AUC0- about 2.6 and 3.3 times higher, than after amenamevir alone. ASP2151 109-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 30044899-5 2018 (3) Ritonavir (inhibitor of CYP3A): When given with single doses of ritonavir 600 mg, geometric mean Cmax of amenamevir after 400-mg and 1200-mg single doses was, respectively, about 1.4 and 1.6 times higher, and geometric mean AUC0- about 2.6 and 3.3 times higher, than after amenamevir alone. ASP2151 278-288 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 30044899-2 2018 Amenamevir is both a substrate and inducer of cytochrome P450 (CYP) 3A4. ASP2151 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-71 30044899-6 2018 Amenamevir has the potential to be involved in CYP3A-mediated pharmacokinetic interactions in clinical practice. ASP2151 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 30607725-1 2018 A method for determination of hydroxylase activity of cytochrome P450 3A4 (CYP3A4) towards its substrate hydrocortisone using fluorescent analysis of the product was developed. Hydrocortisone 105-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-73 30607725-1 2018 A method for determination of hydroxylase activity of cytochrome P450 3A4 (CYP3A4) towards its substrate hydrocortisone using fluorescent analysis of the product was developed. Hydrocortisone 105-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 30607725-2 2018 6beta-hydroxycortisol, formed during CYP3A4-dependent electrocatalysis, has a characteristic fluorescent peak at lambda = 427 +- 2 nm after treating with the sulfuric acid : ethanol (3 : 1) mixture and excitation at lambda = 365 nm, which is different from the substrate (hydrocortisone) fluorescence (lambda = 525 +- 2 nm). 6 beta-hydroxycortisol 0-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 30607725-2 2018 6beta-hydroxycortisol, formed during CYP3A4-dependent electrocatalysis, has a characteristic fluorescent peak at lambda = 427 +- 2 nm after treating with the sulfuric acid : ethanol (3 : 1) mixture and excitation at lambda = 365 nm, which is different from the substrate (hydrocortisone) fluorescence (lambda = 525 +- 2 nm). sulfuric acid 158-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 30607725-2 2018 6beta-hydroxycortisol, formed during CYP3A4-dependent electrocatalysis, has a characteristic fluorescent peak at lambda = 427 +- 2 nm after treating with the sulfuric acid : ethanol (3 : 1) mixture and excitation at lambda = 365 nm, which is different from the substrate (hydrocortisone) fluorescence (lambda = 525 +- 2 nm). Ethanol 174-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 30607725-2 2018 6beta-hydroxycortisol, formed during CYP3A4-dependent electrocatalysis, has a characteristic fluorescent peak at lambda = 427 +- 2 nm after treating with the sulfuric acid : ethanol (3 : 1) mixture and excitation at lambda = 365 nm, which is different from the substrate (hydrocortisone) fluorescence (lambda = 525 +- 2 nm). Hydrocortisone 272-286 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 30607725-4 2018 The developed analytical approach was used to determine the kinetic parameters of CYP3A4-dependent hydrocortisone hydroxylation. Hydrocortisone 99-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 30395700-6 2018 In the presence of human liver microsomes, SR9009 was biotransformed to 13 metabolites by CYP3A4, CYP3A5, CYP2C19, and CYP2D6 isoenzymes. SR9009 43-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 30039199-1 2018 PURPOSE: CYP3A4, CYP2C19, and CYP3A5 are primarily involved in the metabolism of cilostazol. Cilostazol 81-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 30158250-11 2018 To investigate the mechanism of CYP3A4 mRNA upregulation, we analyzed the phosphorylation of STAT5 after celecoxib treatment and found it to be significantly increased. Celecoxib 105-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 30166405-2 2018 In a cohort of 50 renal transplant recipients who underwent quantification of CYP3A4 activity using the oral midazolam drug probe, we confirmed that CYP3A5 genotype is the single most important determinant of tacrolimus metabolite/parent ratio [CYP3A5 expressors displayed 2.7- and 2-fold higher relative exposure to 13-desmethyltacrolimus (DMT) and 31-DMT, respectively; P < 0.001]. Midazolam 109-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 30166405-2 2018 In a cohort of 50 renal transplant recipients who underwent quantification of CYP3A4 activity using the oral midazolam drug probe, we confirmed that CYP3A5 genotype is the single most important determinant of tacrolimus metabolite/parent ratio [CYP3A5 expressors displayed 2.7- and 2-fold higher relative exposure to 13-desmethyltacrolimus (DMT) and 31-DMT, respectively; P < 0.001]. Tacrolimus 209-219 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 30166405-4 2018 Additional analyses in 16 healthy volunteers showed that dual pharmacological inhibition of CYP3A4 and P-glycoprotein using itraconazole resulted in increased tacrolimus metabolite/parent ratios (+65%, +112%, and 25% for 13-, 15-, and 31-DMT, respectively; P < 0.01). Itraconazole 124-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 30166405-4 2018 Additional analyses in 16 healthy volunteers showed that dual pharmacological inhibition of CYP3A4 and P-glycoprotein using itraconazole resulted in increased tacrolimus metabolite/parent ratios (+65%, +112%, and 25% for 13-, 15-, and 31-DMT, respectively; P < 0.01). Tacrolimus 159-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 29749631-1 2018 The antianginal agent ranolazine (Ranexa ) is metabolized primarily by cytochrome P450-3A (CYP3A) enzymes. Ranolazine 22-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-89 30166405-4 2018 Additional analyses in 16 healthy volunteers showed that dual pharmacological inhibition of CYP3A4 and P-glycoprotein using itraconazole resulted in increased tacrolimus metabolite/parent ratios (+65%, +112%, and 25% for 13-, 15-, and 31-DMT, respectively; P < 0.01). dmt 238-241 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 29749631-1 2018 The antianginal agent ranolazine (Ranexa ) is metabolized primarily by cytochrome P450-3A (CYP3A) enzymes. Ranolazine 22-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-96 29749631-1 2018 The antianginal agent ranolazine (Ranexa ) is metabolized primarily by cytochrome P450-3A (CYP3A) enzymes. Ranolazine 34-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-89 29749631-1 2018 The antianginal agent ranolazine (Ranexa ) is metabolized primarily by cytochrome P450-3A (CYP3A) enzymes. Ranolazine 34-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-96 29749631-2 2018 Coadministration with strong CYP3A inhibitors, such as ketoconazole and posaconazole, is contraindicated due to risk of QT prolongation from high levels of ranolazine. Ketoconazole 55-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 29749631-2 2018 Coadministration with strong CYP3A inhibitors, such as ketoconazole and posaconazole, is contraindicated due to risk of QT prolongation from high levels of ranolazine. posaconazole 72-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 29749631-2 2018 Coadministration with strong CYP3A inhibitors, such as ketoconazole and posaconazole, is contraindicated due to risk of QT prolongation from high levels of ranolazine. Ranolazine 156-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 30196760-1 2018 AIM: This study aimed to investigate the effect of CYP3A4 and CYP3A5 genotypes on clinical outcomes of docetaxel treatment. Docetaxel 103-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 30196760-8 2018 CONCLUSION: The allelic variants CYP3A4*22 and CYP3A5*3 contribute to the interpatient variations of docetaxel. Docetaxel 101-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 30253203-9 2018 In Cyp3a-/- mice, brigatinib plasma exposure increased 1.3-fold, and was subsequently 1.8-fold reduced by transgenic overexpression of human CYP3 A4 in liver and intestine. brigatinib 18-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-148 30336495-0 2018 The Influence of CYP3A4 Polymorphism in Sex Steroids as a Risk Factor for Breast Cancer. Steroids 44-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 29095659-1 2018 Rifampicin (RIF), a typical ligand of human pregnane X receptor (PXR), powerfully induces the expression of cytochrome P450 3A4 (CYP3A4) in humans. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-127 30138636-5 2018 Apatinib was a weak inhibitor of human CYP2E1 (IC50>10 muM) but inhibited CYP2B6/2B1 and CYP2D6/2D1 in a competitive way (Ki = 3.84/0.59 and 5.41/0.87 muM), and inhibited CYP3A4/3A2 and rat CYP2E1 in a mixed way (Ki = 11.50/1.83 and 13.06 muM). apatinib 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 29095659-1 2018 Rifampicin (RIF), a typical ligand of human pregnane X receptor (PXR), powerfully induces the expression of cytochrome P450 3A4 (CYP3A4) in humans. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 29095659-1 2018 Rifampicin (RIF), a typical ligand of human pregnane X receptor (PXR), powerfully induces the expression of cytochrome P450 3A4 (CYP3A4) in humans. Rifampin 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-127 29095659-1 2018 Rifampicin (RIF), a typical ligand of human pregnane X receptor (PXR), powerfully induces the expression of cytochrome P450 3A4 (CYP3A4) in humans. Rifampin 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 30595680-4 2018 In this study, we aimed to evaluate the impact of renal impairment severity-dependent accumulation of indoxyl sulfate on hepatic CYP3A activity using metabolic markers. Indican 102-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-134 30382126-5 2018 In addition, FSK-treated HepaRG cells displayed enhanced activities of CYP3A4, NTCP and OATPs when compared to untreated cells. Colforsin 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 30380747-6 2018 OFIE, hydrolyzed (hdl) OFIE, and several flavonols induced the transcriptional activities of both CYP2B6 and CYP3A4 genes in HepG2 cells. Flavonols 41-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 30234976-0 2018 Metabolic Susceptibility of 2-Chlorothioxanthone and Its Toxic Effects on mRNA and Protein Expression and Activities of Human CYP1A2 and CYP3A4 Enzymes. 2-chlorothioxanthen-9-one 28-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 30234976-4 2018 2-Chlorothioxanthone (2-Cl-TX) significantly inhibited the enzymatic activities of CYP1A2 and CYP3A4 with IC50 of 8.36 and 0.86 muM, respectively. 2-chlorothioxanthen-9-one 0-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 30234976-6 2018 2-Cl-TX at 2.5 muM caused 2.19-fold and 1.98-fold overexpression of CYP1A2 and CYP3A4, respectively. 2-cl 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 30234976-4 2018 2-Chlorothioxanthone (2-Cl-TX) significantly inhibited the enzymatic activities of CYP1A2 and CYP3A4 with IC50 of 8.36 and 0.86 muM, respectively. 2-cl-tx 22-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 30234976-8 2018 Results from this study, including the metabolic susceptibility of residual 2-Cl-TX, the proposed metabolites and the significant toxic effect on the activities, mRNA, and protein expression of CYP1A2 and CYP3A4, are vital to the human health and safety risk assessment from this ubiquitous xenobiotic. 2-cl 76-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 205-211 30234976-5 2018 The exposure to 2-Cl-TX at 2.5 muM up-regulated the mRNA expression of CYP1A2 and CYP3A4 in human hepatocellular carcinoma cells to 3.03-fold and 2.02-fold, respectively. 2-cl 16-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 29744867-9 2018 In Cyp3a-/- mice, the plasma exposure of lorlatinib was increased 1.3-fold, but was then twofold reduced upon transgenic overexpression of human CYP3A4 in liver and intestine, whereas relative tissue distribution of lorlatinib remained unaltered. lorlatinib 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 30326853-14 2018 CONCLUSIONS: Our study showed that concomitant use of CYP3A4 inducers and H2-antagonist/PPI, liver metastasis, and age >= 65 were associated with erlotinib-induced hepatotoxicity. Erlotinib Hydrochloride 149-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 29744867-11 2018 Moreover, oral availability of lorlatinib is markedly restricted by CYP3A4 activity. lorlatinib 31-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30072148-1 2018 BACKGROUND: Concomitant use of statins metabolized by the cytochrome P450 isoenzyme 3A4 (CYP3A4) and CYP3A4-inhibiting macrolide antibiotics may confer an increased risk of renal failure. macrolide antibiotics 119-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 30010032-5 2018 The results showed that the prototype of 3,4-DCPB was metabolized by multiple CYP450 enzymes into three metabolites, and the predominant isoforms were CYP2D6 (metabolite M1), CYP1A2 (M2), CYP2C19 and CYP3A4 (M3), respectively., in the presence of beta-NADPH (1 mM) in RLMs or rhCYP450s. 3,4-dichlorophenyl-propenoyl-sec-butylamine 41-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 30072148-4 2018 In propensity score-matched analyses, we compared the risk of serious renal events during episodes of concomitant use of statins and CYP3A4-inhibiting macrolides (n = 71,521) with episodes of use of statins alone (n = 285,488) and, as the primary analysis, with episodes of concomitant use of statins and an active comparator (penicillin V, n = 139,446). Macrolides 151-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 30071242-0 2018 Essential oils of culinary herbs and spices activate PXR and induce CYP3A4 in human intestinal and hepatic in vitro models. Oils, Volatile 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 30349375-10 2018 LINE-1 ORF-1p increased the transcription factor activity of PXR by interacting with PXR and enhancing its cytoplasmic/nuclear translocation, and recruiting PXR to its downstream gene promoter, in turn enhancing the expression of the sorafenib resistance-related genes, CYP3A4 and mdr-1. Sorafenib 234-243 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 270-276 30145177-11 2018 Moreover, overexpression of miR-186-3p inhibitor reversed the G2/M cell cycle arrest induced by DB in L-02/CYP3A4 cells. diosbulbin B 96-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 30301254-0 2018 The Inhibitory Effect of Flavonoid Aglycones on the Metabolic Activity of CYP3A4 Enzyme. Flavonoids 25-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 30301254-4 2018 The aim of this study was to focus on possible interactions between the 30 most commonly encountered flavonoid aglycones on the metabolic activity of CYP3A4 enzyme. Flavonoids 101-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 30301254-5 2018 6beta-hydroxylation of testosterone was used as marker reaction of CYP3A4 activity. Testosterone 23-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 30301254-8 2018 Out of the 30 flavonoids tested, 7 significantly inhibited CYP3A4, most prominent being acacetin that inhibited 95% of enzyme activity at 1 microM concentration. Flavonoids 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 30301254-8 2018 Out of the 30 flavonoids tested, 7 significantly inhibited CYP3A4, most prominent being acacetin that inhibited 95% of enzyme activity at 1 microM concentration. acacetin 88-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 30301254-10 2018 These results alert on possible flavonoid-drug interactions on the level of CYP3A4. Flavonoids 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 30323605-3 2018 Cariprazine is metabolized in two steps by CYP3A4 to didesmethyl-cariprazine (DDCAR). cariprazine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 30323605-3 2018 Cariprazine is metabolized in two steps by CYP3A4 to didesmethyl-cariprazine (DDCAR). didesmethylcariprazine 53-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 30323605-3 2018 Cariprazine is metabolized in two steps by CYP3A4 to didesmethyl-cariprazine (DDCAR). didesmethylcariprazine 78-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 30226084-1 2018 AIM: To develop an LC-MS/MS assay to quantitate well-tolerated substrates; midazolam (CYP3A), omeprazole (CYP2C19), dextromethorphan (CYP2D6), losartan (CYP2C9) and their respective metabolites" concentrations in plasma samples. Midazolam 75-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 30142320-1 2018 Aflatoxin B1 (AFB1) is bioactivated by cytochrome P450 (CYP) 3A isoforms in humans to generate the highly reactive epoxide intermediate AFB1-8,9-epoxide (AFBO), causing hepatotoxicity and hepatocarcinoma. Aflatoxin B1 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-63 30142320-1 2018 Aflatoxin B1 (AFB1) is bioactivated by cytochrome P450 (CYP) 3A isoforms in humans to generate the highly reactive epoxide intermediate AFB1-8,9-epoxide (AFBO), causing hepatotoxicity and hepatocarcinoma. Epoxy Compounds 115-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-63 30142320-1 2018 Aflatoxin B1 (AFB1) is bioactivated by cytochrome P450 (CYP) 3A isoforms in humans to generate the highly reactive epoxide intermediate AFB1-8,9-epoxide (AFBO), causing hepatotoxicity and hepatocarcinoma. aflatoxin B1-2,3-oxide 136-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-63 30142320-1 2018 Aflatoxin B1 (AFB1) is bioactivated by cytochrome P450 (CYP) 3A isoforms in humans to generate the highly reactive epoxide intermediate AFB1-8,9-epoxide (AFBO), causing hepatotoxicity and hepatocarcinoma. aflatoxin B1-2,3-oxide 154-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-63 30114388-5 2018 Our results demonstrate that in both systems the formation of the ferrous carbene-derived MIC is relatively slow, reversible and is not associated with the accumulation of the ferric carbene intermediate, as takes place in the case of CYP3A4 and podophylotoxin. ferrous carbene 66-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 235-241 30142320-6 2018 Interestingly, we uncovered the dual and reverse roles of Phe-304 in CYP3A46, CYP3A5 and CYP3A4 in AFB1 oxidation. Phenylalanine 58-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 30142320-7 2018 Unlike the pi-pi interaction between the Phe-304 phenyl of CYP3A4 and the AFB1 aromatic ring, Phe-304 of CYP3A46 may function to provide steric hindrance to bind AFB1. Phenylalanine 41-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 30002078-0 2018 Biotransformation of Ilaprazole in Human Liver Microsomes and Human: Role of CYP3A4 in Ilaprazole Clearance and Drug-Drug Interaction. ilaprazole 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 30115511-3 2018 Then we used structure based design, first modifying the CYP3A4 crystal structure (pdb code: 4NY4) by adding an oxyferryl moiety to the heme, followed by validating the modified structure to obtain the 1" and 4 position oxidation products of midazolam and then recapitulating the metabolism patterns deciphered previously for 1 and analogs. oxyferryl 112-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 30115511-3 2018 Then we used structure based design, first modifying the CYP3A4 crystal structure (pdb code: 4NY4) by adding an oxyferryl moiety to the heme, followed by validating the modified structure to obtain the 1" and 4 position oxidation products of midazolam and then recapitulating the metabolism patterns deciphered previously for 1 and analogs. Heme 136-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 30115511-3 2018 Then we used structure based design, first modifying the CYP3A4 crystal structure (pdb code: 4NY4) by adding an oxyferryl moiety to the heme, followed by validating the modified structure to obtain the 1" and 4 position oxidation products of midazolam and then recapitulating the metabolism patterns deciphered previously for 1 and analogs. Midazolam 242-251 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 29991576-4 2018 CYP3A4 phenotype was measured as serum concentration of 4beta-hydroxycholesterol (4betaOHC) by ultra-performance liquid chromatography-tandem mass spectrometry in samples collected prior to and 3 months after initiation of treatment with TNF-alpha inhibitors. cholest-5-ene-3,4-diol 56-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29991576-4 2018 CYP3A4 phenotype was measured as serum concentration of 4beta-hydroxycholesterol (4betaOHC) by ultra-performance liquid chromatography-tandem mass spectrometry in samples collected prior to and 3 months after initiation of treatment with TNF-alpha inhibitors. 4betaohc 82-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 30002078-0 2018 Biotransformation of Ilaprazole in Human Liver Microsomes and Human: Role of CYP3A4 in Ilaprazole Clearance and Drug-Drug Interaction. ilaprazole 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 30002078-3 2018 Sulfoxide oxidation of ilaprazole is catalyzed mainly by CYP3A4. sulfoxide 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 30002078-3 2018 Sulfoxide oxidation of ilaprazole is catalyzed mainly by CYP3A4. ilaprazole 23-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 30219715-3 2018 In human liver microsomes (HLMs), a concentration-dependent inhibition of celecoxib hydroxylation by quinidine was observed after CYP2C9 and CYP3A4 were inhibited. Celecoxib 74-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 30219715-3 2018 In human liver microsomes (HLMs), a concentration-dependent inhibition of celecoxib hydroxylation by quinidine was observed after CYP2C9 and CYP3A4 were inhibited. Quinidine 101-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 30002078-4 2018 Thus, it has been widely accepted that CYP3A4 plays a major role in the clearance of ilaprazole in humans. ilaprazole 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 30219715-4 2018 In individual HLMs with variable CYP2D6 activities, a significant correlation was observed between celecoxib hydroxylation and CYP2D6-selective dextromethorphan O-demethylation when CYP2C9 and CYP3A4 activities were suppressed (r = 0.97, P < 0.0001). Celecoxib 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 193-199 30018103-6 2018 ADT S-oxidation is catalyzed by FMO 1 and 3, and to a minor extent by CYP enzymes such as CYP3A4. adt 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 30068519-0 2018 Physiologically Based Pharmacokinetic Model of Itraconazole and Two of Its Metabolites to Improve the Predictions and the Mechanistic Understanding of CYP3A4 Drug-Drug Interactions. Itraconazole 47-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 30068519-1 2018 Physiologically based pharmacokinetic (PBPK) modeling for itraconazole using a bottom-up approach is challenging, not only due to complex saturable pharmacokinetics (PK) and the presence of three metabolites exhibiting CYP3A4 inhibition, but also because of discrepancies in reported in vitro data. Itraconazole 58-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 30068519-7 2018 In addition, itraconazole DDIs with midazolam and other CYP3A4 substrates were successfully predicted within a 2-fold error. Itraconazole 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 29947950-2 2018 Cytochrome P450 (CYP) 2D6 and CYP3A are the two major enzymes responsible for tamsulosin metabolism. Tamsulosin 78-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-35 29762875-2 2018 In vitro data showed that pomalidomide is a substrate of multiple cytochrome P450 (CYP) isozymes and that its oxidative metabolism is mediated primarily by CYP1A2 and CYP3A4, with minor contributions from CYP2C19 and CYP2D6. pomalidomide 26-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 167-173 29557529-6 2018 Both elbasvir and grazoprevir are substrates of cytochrome P450 (CYP) 3A4 enzyme, but mechanistic experiments were lacking to demonstrate the role of other enzymes and the precise relative % contribution of CYP3A4. 2-(pyrrolidin-2-yl)-5-(2-(4-(5-(pyrrolidin-2-yl)-1H-imidazol-2-yl)phenyl)benzofuran-5-yl)-1H-imidazole 5-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 29992479-4 2018 CYP3A and P-gp inducers and body-surface area were shown to impact everolimus exposure, justifying dose adjustments. Everolimus 67-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 29733119-0 2018 Correspondence between the CYP2C19 and CYP3A4 genotypes with the inferred metabolizer phenotype by omeprazole administration in Mexican healthy children. Omeprazole 99-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 29733119-3 2018 Therefore, we aimed to complete a formal evaluation of the diagnostic value of CYP2C19 and CYP3A4 genes for predicting metabolizer phenotypes established by omeprazole (OME) administration in 118 healthy children from Jalisco (western Mexico). Omeprazole 169-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 29027845-0 2018 The potent mechanism-based inactivation of CYP2D6 and CYP3A4 with fusidic acid in in vivo bioaccumulation. Fusidic Acid 66-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 29027845-6 2018 Metoprolol alpha-hydroxylation and midazolam 1"-hydroxylation were used as marker reactions for CYP2D6 and CYP3A4 activities, and HPLC-MS/MS measurement was also utilised. Metoprolol 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 29092680-8 2018 Our in vitro Z-215 metabolism study showed that the major isozyme contributing to the oxidation of Z-215, including the formation of Z-215 sulphone, was CYP3A4. z-215 13-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 29027845-11 2018 Inhibition of CYP2D6 and CYP3A4 activity was found to require the presence of NADPH. NADP 78-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 29092680-8 2018 Our in vitro Z-215 metabolism study showed that the major isozyme contributing to the oxidation of Z-215, including the formation of Z-215 sulphone, was CYP3A4. z-215 99-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 29092680-8 2018 Our in vitro Z-215 metabolism study showed that the major isozyme contributing to the oxidation of Z-215, including the formation of Z-215 sulphone, was CYP3A4. z-215 sulphone 133-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 30178440-1 2018 Zolpidem is predominantly metabolized by CYP3A4, and to a lesser extent by CYP2C9, CYP1A2, CYP2D6 and CYP2C19. Zolpidem 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 30086269-0 2018 The enhancement of cardiotoxicity that results from inhibiton of CYP 3A4 activity and hERG channel by berberine in combination with statins. Berberine 102-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-72 30086269-7 2018 Based on these findings, berberine in combination with statins has a greater inhibitory effect on CYP3A4 activity and CYP3A4 protein and mRNA expression than berberine alone. Berberine 25-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 30086269-7 2018 Based on these findings, berberine in combination with statins has a greater inhibitory effect on CYP3A4 activity and CYP3A4 protein and mRNA expression than berberine alone. Berberine 25-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 30086269-10 2018 These results indicate that berberine in combination with statins can increase cardiotoxicity by inhibiting CYP3A4 and hERG channel. Berberine 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 30283337-0 2018 The Modulatory Role of CYP3A4 in Dictamnine-Induced Hepatotoxicity. dictamnine 33-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 30283337-3 2018 Dictamnine (DTN), the main alkaloid from DC, possesses a furan ring which was suspected of being responsible for hepatotoxicity via metabolic activation primarily by CYP3A4. dictamnine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-172 30283337-3 2018 Dictamnine (DTN), the main alkaloid from DC, possesses a furan ring which was suspected of being responsible for hepatotoxicity via metabolic activation primarily by CYP3A4. dictamnine 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-172 30283337-3 2018 Dictamnine (DTN), the main alkaloid from DC, possesses a furan ring which was suspected of being responsible for hepatotoxicity via metabolic activation primarily by CYP3A4. furan 57-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-172 30283337-4 2018 Herein, the present study aimed to evaluate the role of CYP3A4 in DTN-induced liver injury. dictamnine 66-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 30283337-6 2018 Furthermore, the toxicity was increased in CYP3A4-induced PHH by rifampicin, and CYP3A4 over-expressed (OE) HepG2 and L02 cells. Rifampin 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 30283337-7 2018 Contrarily, the cytotoxicity was decreased in CYP3A4-inhibited PHH and CYP3A4 OE HepG2 and L02 cells inhibited by ketoconazole (KTZ). Ketoconazole 114-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 30283337-7 2018 Contrarily, the cytotoxicity was decreased in CYP3A4-inhibited PHH and CYP3A4 OE HepG2 and L02 cells inhibited by ketoconazole (KTZ). Ketoconazole 114-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 30283337-7 2018 Contrarily, the cytotoxicity was decreased in CYP3A4-inhibited PHH and CYP3A4 OE HepG2 and L02 cells inhibited by ketoconazole (KTZ). Ketoconazole 128-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 30283337-7 2018 Contrarily, the cytotoxicity was decreased in CYP3A4-inhibited PHH and CYP3A4 OE HepG2 and L02 cells inhibited by ketoconazole (KTZ). Ketoconazole 128-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 30283337-10 2018 Collectively, our findings illustrated that DTN-induced hepatotoxicity correlated well with the expression of CYP3A4, namely inhibition of CYP3A4 alleviated the toxicity both in vitro and in vivo, and induction aggravated the toxicity effects. dictamnine 44-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 30283337-10 2018 Collectively, our findings illustrated that DTN-induced hepatotoxicity correlated well with the expression of CYP3A4, namely inhibition of CYP3A4 alleviated the toxicity both in vitro and in vivo, and induction aggravated the toxicity effects. dictamnine 44-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 29753067-0 2018 Drug interaction study of flavonoids toward CYP3A4 and their quantitative structure activity relationship (QSAR) analysis for predicting potential effects. Flavonoids 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 29753067-4 2018 Some flavonoids such as licoflavone (12) and irilone (30) exhibited the selective inhibition toward CYP3 A4 rather than other major human CYPs. Flavonoids 5-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-107 29753067-4 2018 Some flavonoids such as licoflavone (12) and irilone (30) exhibited the selective inhibition toward CYP3 A4 rather than other major human CYPs. licoflavone 24-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-107 29753067-4 2018 Some flavonoids such as licoflavone (12) and irilone (30) exhibited the selective inhibition toward CYP3 A4 rather than other major human CYPs. irilone 45-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-107 29753067-8 2018 Finally, a quantitative structure-activity relationship (QSAR) of flavonoids with their inhibitory effects toward CYP3 A4 was established using computational methods. Flavonoids 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-121 29753067-9 2018 Our findings illustrated the high risk of herb-drug interactions (HDIs) caused by flavonoids and revealed the vital structures requirement of natural flavonoids for the HDIs with clinical drugs eliminated by CYP3 A4. Flavonoids 150-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 208-215 29958895-0 2018 Steroid bioconjugation to a CYP3A4 allosteric site and its effect on substrate binding and coupling efficiency. Steroids 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 29958895-6 2018 Recently, we demonstrated that steroid bioconjugation at the allosteric site results in an increase in activity of CYP3A4 toward testosterone and 7-benzyloxy-4-trifluoromethylcoumarin oxidation. Steroids 31-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 29958895-6 2018 Recently, we demonstrated that steroid bioconjugation at the allosteric site results in an increase in activity of CYP3A4 toward testosterone and 7-benzyloxy-4-trifluoromethylcoumarin oxidation. Testosterone 129-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 29958895-6 2018 Recently, we demonstrated that steroid bioconjugation at the allosteric site results in an increase in activity of CYP3A4 toward testosterone and 7-benzyloxy-4-trifluoromethylcoumarin oxidation. 7-benzyloxy-4-trifluoromethylcoumarin 146-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 29958895-7 2018 Here, using the established bioconjugation methodology, we show how steroid bioconjugation at the allosteric site affects the heme spin state, the binding affinity (KS) of CYP3A4 for testosterone, as well as the enzyme coupling efficiency. Steroids 68-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 29958895-7 2018 Here, using the established bioconjugation methodology, we show how steroid bioconjugation at the allosteric site affects the heme spin state, the binding affinity (KS) of CYP3A4 for testosterone, as well as the enzyme coupling efficiency. Potassium 165-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 29958895-7 2018 Here, using the established bioconjugation methodology, we show how steroid bioconjugation at the allosteric site affects the heme spin state, the binding affinity (KS) of CYP3A4 for testosterone, as well as the enzyme coupling efficiency. Testosterone 183-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 30385190-5 2019 The obtained results demonstrated that fipronil may undergo a clearance by the liver and it is exclusively metabolized by the CYP3A4 isoform. fipronil 39-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 30319126-6 2018 Enzalutamide is rapidly metabolized by the liver, mainly through the CYP2C8 and to a lesser extent by CYP3A4/5 so that its metabolism may be altered when cytochrome isoenzyme inductor or inhibitor drugs are given concomitantly. enzalutamide 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 30319126-7 2018 Moreover, enzalutamide may require dose adjustment for other drugs since it is a potent inductor of CYP3A4 and a moderate inductor of CYP2C9 y el CYP2C19. enzalutamide 10-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 30178440-5 2018 In addition, since zolpidem is metabolized at a high rate by CYP3A4, the effect of CYP2C9*3 allele on the pharmacokinetics of zolpidem was also observed in the condition where CYP3A4 was sufficiently inhibited by the steady-state concentration of clarithromycin, a potent CYP3A4 inhibitor. Zolpidem 19-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 29504673-5 2018 Six pathway inhibitor combinations were identified with a moderate inhibitory potential (>=2.0 < 5.0): five with chlorzoxazone, R-EDDP, S-EDDP and noroxycodone production by CYP3A4, and R- and S-EDDP production by CYP2B6; and one for the meprobamate effect on noroxycodone production by CYP3A4. noroxycodone 153-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 30178440-5 2018 In addition, since zolpidem is metabolized at a high rate by CYP3A4, the effect of CYP2C9*3 allele on the pharmacokinetics of zolpidem was also observed in the condition where CYP3A4 was sufficiently inhibited by the steady-state concentration of clarithromycin, a potent CYP3A4 inhibitor. Zolpidem 19-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 30178440-5 2018 In addition, since zolpidem is metabolized at a high rate by CYP3A4, the effect of CYP2C9*3 allele on the pharmacokinetics of zolpidem was also observed in the condition where CYP3A4 was sufficiently inhibited by the steady-state concentration of clarithromycin, a potent CYP3A4 inhibitor. Zolpidem 19-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 30178440-5 2018 In addition, since zolpidem is metabolized at a high rate by CYP3A4, the effect of CYP2C9*3 allele on the pharmacokinetics of zolpidem was also observed in the condition where CYP3A4 was sufficiently inhibited by the steady-state concentration of clarithromycin, a potent CYP3A4 inhibitor. Zolpidem 126-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 30178440-5 2018 In addition, since zolpidem is metabolized at a high rate by CYP3A4, the effect of CYP2C9*3 allele on the pharmacokinetics of zolpidem was also observed in the condition where CYP3A4 was sufficiently inhibited by the steady-state concentration of clarithromycin, a potent CYP3A4 inhibitor. Zolpidem 126-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 30178440-5 2018 In addition, since zolpidem is metabolized at a high rate by CYP3A4, the effect of CYP2C9*3 allele on the pharmacokinetics of zolpidem was also observed in the condition where CYP3A4 was sufficiently inhibited by the steady-state concentration of clarithromycin, a potent CYP3A4 inhibitor. Zolpidem 126-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 30178440-5 2018 In addition, since zolpidem is metabolized at a high rate by CYP3A4, the effect of CYP2C9*3 allele on the pharmacokinetics of zolpidem was also observed in the condition where CYP3A4 was sufficiently inhibited by the steady-state concentration of clarithromycin, a potent CYP3A4 inhibitor. Clarithromycin 247-261 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 30178440-5 2018 In addition, since zolpidem is metabolized at a high rate by CYP3A4, the effect of CYP2C9*3 allele on the pharmacokinetics of zolpidem was also observed in the condition where CYP3A4 was sufficiently inhibited by the steady-state concentration of clarithromycin, a potent CYP3A4 inhibitor. Clarithromycin 247-261 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 30178440-5 2018 In addition, since zolpidem is metabolized at a high rate by CYP3A4, the effect of CYP2C9*3 allele on the pharmacokinetics of zolpidem was also observed in the condition where CYP3A4 was sufficiently inhibited by the steady-state concentration of clarithromycin, a potent CYP3A4 inhibitor. Clarithromycin 247-261 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 30178440-9 2018 Even with the potent CYP3A4 inhibitor clarithromycin present at steady-state concentrations, there were no significant differences in the exposure of zolpidem, except for elimination half-life (t1/2). Clarithromycin 38-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 29945292-4 2018 EXPERIMENTAL APPROACH: The effects of IMP on PXR-modulated cytochrome P450 3A4 (CYP3A4) expression were assessed using a PXR transactivation assay, a mammalian two-hybrid assay, a competitive ligand-binding assay, analysis of CYP3A4 mRNA and protein expression levels and measurement of CYP3A4 activity using a cell-based reporter gene assay and in vitro model. imperatorin 38-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-78 30171694-0 2018 CYP3A but not P-gp plays a relevant role in the in vivo intestinal and hepatic clearance of the delta-specific phosphoinositide-3 kinase inhibitor leniolisib. leniolisib 147-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 30171694-1 2018 This study investigated the effect of itraconazole, a strong dual inhibitor of cytochrome P450 (CYP) 3A4 and P-glycoprotein (P-gp), on the single dose pharmacokinetics of leniolisib. Itraconazole 38-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-104 30171694-7 2018 These findings suggest that the interaction with itraconazole occurred mainly systemically through inhibition of CYP3A, and corroborate our in vitro findings that leniolisib is neither a sensitive CYP3A substrate nor a relevant in vivo substrate for intestinal or hepatic P-gp. Itraconazole 49-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-118 30171694-8 2018 Assuming itraconazole levels achieved complete inhibition of CYP3A, the fractional contribution of CYP3A to the overall disposition of leniolisib is estimated to be about 50%. Itraconazole 9-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-66 30171694-8 2018 Assuming itraconazole levels achieved complete inhibition of CYP3A, the fractional contribution of CYP3A to the overall disposition of leniolisib is estimated to be about 50%. leniolisib 135-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-66 30171694-8 2018 Assuming itraconazole levels achieved complete inhibition of CYP3A, the fractional contribution of CYP3A to the overall disposition of leniolisib is estimated to be about 50%. leniolisib 135-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-104 30171694-9 2018 The concomitant use of leniolisib with strong inhibitors of CYP3A as well as strong and moderate inducers of CYP3A is best avoided. leniolisib 23-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 30171694-9 2018 The concomitant use of leniolisib with strong inhibitors of CYP3A as well as strong and moderate inducers of CYP3A is best avoided. leniolisib 23-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-114 29945292-4 2018 EXPERIMENTAL APPROACH: The effects of IMP on PXR-modulated cytochrome P450 3A4 (CYP3A4) expression were assessed using a PXR transactivation assay, a mammalian two-hybrid assay, a competitive ligand-binding assay, analysis of CYP3A4 mRNA and protein expression levels and measurement of CYP3A4 activity using a cell-based reporter gene assay and in vitro model. imperatorin 38-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 29923436-0 2018 Quantitative Evaluation of Cytochrome P450 3A4 Inhibition and Hepatotoxicity in HepaRG 3-D Spheroids. heparg 3-d spheroids 80-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-46 29226313-2 2018 Alectinib and its major active metabolite M4 exhibited drug-drug interaction (DDI) potential through cytochrome P450 (CYP) enzymes CYP3A4 and CYP2C8 in vitro. alectinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 29226313-5 2018 The PBPK modeling has provided mechanistic insight into the low victim DDI risk of alectinib through CYP3A4 by a novel two-dimensional analysis for fmCYP3A4 and FG , and demonstrated negligible CYPs 2C8 and 3A4 enzyme-modulating effects at clinically relevant exposure. alectinib 83-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 29991575-0 2018 Comparison of Antifungal Azole Interactions with Adult Cytochrome P450 3A4 versus Neonatal Cytochrome P450 3A7. Azoles 25-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-74 29991575-1 2018 Adult drug metabolism is dominated by cytochrome P450 3A4 (CYP3A4), which is often inhibited by antifungal azole drugs, resulting in potential alterations in drug metabolism and adverse drug/drug interactions. Azoles 107-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-57 29991575-1 2018 Adult drug metabolism is dominated by cytochrome P450 3A4 (CYP3A4), which is often inhibited by antifungal azole drugs, resulting in potential alterations in drug metabolism and adverse drug/drug interactions. Azoles 107-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 29991575-5 2018 Thirteen different azoles were then evaluated for binding and inhibition of purified human CYP3A4 versus CYP3A7. Azoles 19-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 29991575-7 2018 Across this wide range of potencies, CYP3A4 was consistently inhibited more strongly than CYP3A7, with clotrimazole being the least selective (1.5-fold) inhibitor and econazole the most selective (12-fold). Clotrimazole 103-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 29991575-7 2018 Across this wide range of potencies, CYP3A4 was consistently inhibited more strongly than CYP3A7, with clotrimazole being the least selective (1.5-fold) inhibitor and econazole the most selective (12-fold). Econazole 167-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 29991575-9 2018 Most bound to CYP3A4 via coordination to the heme iron, but several also demonstrated evidence of a distinct binding mode at low concentrations. Heme 45-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 29991575-9 2018 Most bound to CYP3A4 via coordination to the heme iron, but several also demonstrated evidence of a distinct binding mode at low concentrations. Iron 50-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 29991575-10 2018 However, only posaconazole inhibited CYP3A4. posaconazole 14-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 29991575-13 2018 Overall, although the details of binding interactions do vary, the same azole compounds inhibit both enzymes, albeit with weaker interactions with CYP3A7 compared with CYP3A4. Azoles 72-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 30170758-3 2018 Rifampin induces UGT1A9, UGT2B7, CYP3A4, and CYP3A5. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 29923436-6 2018 Levels of midazolam, a specific substrate of CYP3A4, were used to determine the long-term metabolic capacity of CYP3A4. Midazolam 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 29923436-6 2018 Levels of midazolam, a specific substrate of CYP3A4, were used to determine the long-term metabolic capacity of CYP3A4. Midazolam 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 29663428-15 2018 A 4-hour, but not the 1-, 2-, and 6-hour, single concentration accurately estimated midazolam area under the curve during constitutive CYP3A conditions in healthy adults. Midazolam 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-140 29982690-3 2018 This study also evaluated effects of CYP3A4 inhibition on PK of GSK2881078. GSK2881078 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 29663428-1 2018 Midazolam is the preferred probe to phenotype cytochrome P450 (CYP) 3A activity. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-70 29663428-3 2018 Midazolam concentrations from adults during CYP3A constitutive conditions were obtained from previous studies after single, oral or intravenous administration. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-49 29982690-8 2018 The effect of CYP3A4 inhibition on GSK2881078 PK was evaluated in a separate cohort. GSK2881078 35-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 29982690-13 2018 The effect of CYP3A4 inhibition on GKS2881078 PK was unlikely to be of clinical significance. gks2881078 35-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 29733390-1 2018 Background: Tacrolimus, a drug for prevention of rejection after kidney transplantation, has a narrow therapeutic window and is metabolized by the cytochrome P540 3A (CYP3A) system. Tacrolimus 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-165 30429697-4 2018 Vincristine is a known CYP3A4 and CYP3A5 substrate, and concomitant administration with fluconazole or voriconazole has been reported to increase vincristine toxicity and peripheral neuropathy, but there is limited literature on posaconazole in this regard. Vincristine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 29399736-6 2018 In hyperoxic HepaRG cultures, urea cycle activity, bile acid synthesis, CytochromeP450 3A4 (CYP3A4) activity and ammonia elimination were 165-266% increased. heparg 13-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-90 29399736-6 2018 In hyperoxic HepaRG cultures, urea cycle activity, bile acid synthesis, CytochromeP450 3A4 (CYP3A4) activity and ammonia elimination were 165-266% increased. heparg 13-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 29733390-1 2018 Background: Tacrolimus, a drug for prevention of rejection after kidney transplantation, has a narrow therapeutic window and is metabolized by the cytochrome P540 3A (CYP3A) system. Tacrolimus 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 167-172 30072626-6 2018 Based on the results for the formation of metabolites when incubated in dexamethasone-induced microsomes, incubation with ketoconazole, and human recombinant cDNA-expressed cytochrome P450s, we identified CYP3A4 and CYP3A5 as the major CYP isoforms involved in the hydroxylation of loxoprofen (M3 and M4). Dexamethasone 72-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 205-211 30463833-2 2018 As a complex containing several kinds of flavonoids, FLCWK has the potential to impact the drug metabolism enzyme P450 3A4 (CYP3A4) and nuclear receptors. Flavonoids 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 30463833-7 2018 FLCWK highly induced CYP3A4 luciferase activity mediated by PXR in PXRCYP3A4 co-transfected cells. flcwk 0-5 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 30479741-2 2018 It is believed that nafcillin causes CYP3A4 enzyme induction which decreases warfarin"s half-life. Nafcillin 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 30479741-2 2018 It is believed that nafcillin causes CYP3A4 enzyme induction which decreases warfarin"s half-life. Warfarin 77-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 30479741-3 2018 The onset of CYP3A4 induction by nafcillin occurs within the first 7 days, but maximal effects may take up to 2 weeks. Nafcillin 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 29925743-10 2018 TSH ratio showed more than 1.0 in all patients with depression and CYP3A4 inducer users. Thyrotropin 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 30159173-4 2018 Both rivaroxaban and amiodarone are substrates for the CYP3A4 hepatic pathway, and concomitant use can result in increased plasma rivaroxaban levels causing an increased propensity to bleeding. Rivaroxaban 5-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 30159173-4 2018 Both rivaroxaban and amiodarone are substrates for the CYP3A4 hepatic pathway, and concomitant use can result in increased plasma rivaroxaban levels causing an increased propensity to bleeding. Amiodarone 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 30159173-4 2018 Both rivaroxaban and amiodarone are substrates for the CYP3A4 hepatic pathway, and concomitant use can result in increased plasma rivaroxaban levels causing an increased propensity to bleeding. Rivaroxaban 130-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 30072626-6 2018 Based on the results for the formation of metabolites when incubated in dexamethasone-induced microsomes, incubation with ketoconazole, and human recombinant cDNA-expressed cytochrome P450s, we identified CYP3A4 and CYP3A5 as the major CYP isoforms involved in the hydroxylation of loxoprofen (M3 and M4). Ketoconazole 122-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 205-211 30072626-6 2018 Based on the results for the formation of metabolites when incubated in dexamethasone-induced microsomes, incubation with ketoconazole, and human recombinant cDNA-expressed cytochrome P450s, we identified CYP3A4 and CYP3A5 as the major CYP isoforms involved in the hydroxylation of loxoprofen (M3 and M4). loxoprofen 282-292 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 205-211 29283173-0 2018 CYP3A4 inducer and inhibitor strongly affect the pharmacokinetics of triptolide and its derivative in rats. triptolide 69-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29353349-8 2018 Daclatasvir has low-to-moderate clearance with the predominant route of elimination via cytochrome P450 3A4-mediated metabolism and P-glycoprotein excretion and intestinal secretion. daclatasvir 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-107 29283173-4 2018 In vitro studies using recombinant human cytochrome P450 enzyme demonstrated that cytochrome P450 3A4 (CYP3A4) was predominant in the metabolism of triptolide and (5R)-5-hydroxytriptolide, accounting for 94.2% and 64.2% of the metabolism, respectively. triptolide 148-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-101 29283173-4 2018 In vitro studies using recombinant human cytochrome P450 enzyme demonstrated that cytochrome P450 3A4 (CYP3A4) was predominant in the metabolism of triptolide and (5R)-5-hydroxytriptolide, accounting for 94.2% and 64.2% of the metabolism, respectively. triptolide 148-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 29283173-4 2018 In vitro studies using recombinant human cytochrome P450 enzyme demonstrated that cytochrome P450 3A4 (CYP3A4) was predominant in the metabolism of triptolide and (5R)-5-hydroxytriptolide, accounting for 94.2% and 64.2% of the metabolism, respectively. 5alpha-Hydroxytriptolide 163-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-101 29283173-4 2018 In vitro studies using recombinant human cytochrome P450 enzyme demonstrated that cytochrome P450 3A4 (CYP3A4) was predominant in the metabolism of triptolide and (5R)-5-hydroxytriptolide, accounting for 94.2% and 64.2% of the metabolism, respectively. 5alpha-Hydroxytriptolide 163-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 30231963-5 2018 Aflatoxin-induced HCC rat models expressing CYP3A4*1, CYP3A5*3, CYP2C19*2, and CYP2D6*10 were established and treated with sorafenib at certain time points. Aflatoxins 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 29704845-11 2018 To our knowledge, this is the first report to demonstrate an inhibitory effect of nefazodone on hepatic CYP1A and CYP3A-like proteins in rainbow trout. nefazodone 82-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 29694732-6 2018 Coadministration of fingolimod at steady-state carbamazepine concentrations resulted in increased fingolimod CL/F by 67% through the induction of CYP3A4, a cytochrome with negligible involvement in fingolimod clearance in an uninduced state. Fingolimod Hydrochloride 20-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 30117082-1 2018 Zolpidem is indicated for the short-term treatment of insomnia and it is predominantly metabolized by CYP3A4, and to a lesser extent by CYP2C19, CYP1A2, and CYP2C9. Zolpidem 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 29353349-10 2018 As a result, the dose of daclatasvir should be reduced from 60 to 30 mg once daily when co-administered with strong inhibitors of cytochrome P450 3A4. daclatasvir 25-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-149 29353349-12 2018 The dose of daclatasvir should be increased from 60 to 90 mg once daily when co-administered with moderate inducers of cytochrome P450 3A4. daclatasvir 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-138 29353349-13 2018 Co-administration of daclatasvir with strong inducers of cytochrome P450 3A4 is contraindicated. daclatasvir 21-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-76 29920787-2 2018 Single nucleotide polymorphisms (SNPs) in genes important to tacrolimus bioavailability and clearance (ABCB1, CYP3A4, and CYP3A5) are associated with differences in tacrolimus pharmacokinetics. Tacrolimus 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 29773500-6 2018 The pharmacokinetics of rivaroxaban were affected by creatinine clearance, alanine aminotransferase, and use of CYP3A4 or P-gp inhibitors. Rivaroxaban 24-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 29920787-2 2018 Single nucleotide polymorphisms (SNPs) in genes important to tacrolimus bioavailability and clearance (ABCB1, CYP3A4, and CYP3A5) are associated with differences in tacrolimus pharmacokinetics. Tacrolimus 165-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 29920787-6 2018 Compared with CYP3A poor metabolizers (PM), time to therapeutic tacrolimus trough was increased by 5.1 +- 1.6 days for CYP3A extensive metabolizers (EM, P < 0.001). Tacrolimus 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-124 29739809-3 2018 Bosutinib is a substrate of CYP3A4 and P-glycoprotein and exhibits pH-dependent solubility with moderate intestinal permeability. bosutinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 29739809-8 2018 These results suggested that bosutinib DDI mechanism could involve not only CYP3A4-mediated metabolism but also P-glycoprotein-mediated efflux on absorption. bosutinib 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 30040022-0 2018 Tacrolimus population pharmacokinetic models according to CYP3A5/CYP3A4/POR genotypes in Chinese Han renal transplant patients. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 29851709-1 2018 PURPOSE/BACKGROUND: The antipsychotic agent lurasidone (Latuda ) is metabolized by Cytochrome P450-3A (CYP3A) enzymes. Lurasidone Hydrochloride 44-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-101 29851709-1 2018 PURPOSE/BACKGROUND: The antipsychotic agent lurasidone (Latuda ) is metabolized by Cytochrome P450-3A (CYP3A) enzymes. Lurasidone Hydrochloride 44-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 29851709-1 2018 PURPOSE/BACKGROUND: The antipsychotic agent lurasidone (Latuda ) is metabolized by Cytochrome P450-3A (CYP3A) enzymes. Lurasidone Hydrochloride 56-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-101 29851709-1 2018 PURPOSE/BACKGROUND: The antipsychotic agent lurasidone (Latuda ) is metabolized by Cytochrome P450-3A (CYP3A) enzymes. Lurasidone Hydrochloride 56-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 29851709-2 2018 Coadministration with strong CYP3A inhibitors (such as ketoconazole, posaconazole, and ritonavir) is contraindicated due to the risk of sedation and movement disorders from high levels of lurasidone. Ketoconazole 55-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 29851709-2 2018 Coadministration with strong CYP3A inhibitors (such as ketoconazole, posaconazole, and ritonavir) is contraindicated due to the risk of sedation and movement disorders from high levels of lurasidone. posaconazole 69-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 29851709-2 2018 Coadministration with strong CYP3A inhibitors (such as ketoconazole, posaconazole, and ritonavir) is contraindicated due to the risk of sedation and movement disorders from high levels of lurasidone. Ritonavir 87-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 29851709-2 2018 Coadministration with strong CYP3A inhibitors (such as ketoconazole, posaconazole, and ritonavir) is contraindicated due to the risk of sedation and movement disorders from high levels of lurasidone. Lurasidone Hydrochloride 188-198 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 29723418-3 2018 Rifabutin, an alternative antibiotic used to treat tuberculosis, may have a lower-magnitude effect on CYP3A. Rifabutin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 29766610-3 2018 In the present study, we developed a sensitive and reliable method for the simultaneous determination of 6beta-OHF and cortisol in human plasma using high-performance liquid chromatography/tandem mass spectrometry together with picolinylester derivatization or nonderivatization methods and 6beta-[9,11,12,12-2 H4 ]hydroxycortisol and [1,2,4,19-13 C4 ]cortisol as internal standards for in vivo CYP3A phenotyping in humans. 6beta-ohf 105-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 395-400 29746397-2 2018 It is converted to an active metabolite N-desmethylclobazam (NCLB) by CYP3A4, which is then broken down to an inactive metabolite by CYP2C19. N-desmethylclobazam 40-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 29649093-0 2018 Comparison of CYP3A4-Inducing Capacity of Enzyme-Inducing Antiepileptic Drugs Using 4beta-Hydroxycholesterol as Biomarker. cholest-5-ene-3,4-diol 84-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 29649093-2 2018 The aim of this study was to estimate CYP3A4-inductive potency of EIAEDs by comparing CYP3A4 activity in patients treated with carbamazepine, phenobarbital, or phenytoin. Carbamazepine 127-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 29649093-2 2018 The aim of this study was to estimate CYP3A4-inductive potency of EIAEDs by comparing CYP3A4 activity in patients treated with carbamazepine, phenobarbital, or phenytoin. Phenobarbital 142-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 29649093-2 2018 The aim of this study was to estimate CYP3A4-inductive potency of EIAEDs by comparing CYP3A4 activity in patients treated with carbamazepine, phenobarbital, or phenytoin. Phenobarbital 142-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 29746397-2 2018 It is converted to an active metabolite N-desmethylclobazam (NCLB) by CYP3A4, which is then broken down to an inactive metabolite by CYP2C19. N-desmethylclobazam 61-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 29649093-2 2018 The aim of this study was to estimate CYP3A4-inductive potency of EIAEDs by comparing CYP3A4 activity in patients treated with carbamazepine, phenobarbital, or phenytoin. Phenytoin 160-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 29746397-3 2018 This study characterizes the impact of CYP3A4 and CYP2C19 drug interactions on CLB and NCLB serum concentrations (Cp) and concentration/dose (Cp/D) ratios in pediatric patients with epilepsy. Clobazam 79-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 29649093-2 2018 The aim of this study was to estimate CYP3A4-inductive potency of EIAEDs by comparing CYP3A4 activity in patients treated with carbamazepine, phenobarbital, or phenytoin. Phenytoin 160-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 29649093-3 2018 METHODS: Residual serum samples from patients treated with EIAEDs or levetiracetam were collected from a therapeutic drug monitoring service for analysis of 4beta-hydroxycholesterol (4betaOHC), which is an indicator of CYP3A4 activity. cholest-5-ene-3,4-diol 157-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 29746397-3 2018 This study characterizes the impact of CYP3A4 and CYP2C19 drug interactions on CLB and NCLB serum concentrations (Cp) and concentration/dose (Cp/D) ratios in pediatric patients with epilepsy. N-desmethylclobazam 87-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 29649093-3 2018 METHODS: Residual serum samples from patients treated with EIAEDs or levetiracetam were collected from a therapeutic drug monitoring service for analysis of 4beta-hydroxycholesterol (4betaOHC), which is an indicator of CYP3A4 activity. 4betaohc 183-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 30087611-5 2018 1"-OH-midazolam formation (reflecting CYP3A4 activity) increased by a factor of 5-8 in both cell models, while the formation of alpha-OH-metoprolol increased by a factor of 6 in HepaRG cells and of 1.4 in primary human hepatocytes. 1"-oh-midazolam 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 29649093-10 2018 CONCLUSIONS: This study shows that phenytoin and carbamazepine have approximately twice the CYP3A4-inducing potency of phenobarbital. Phenytoin 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 29649093-10 2018 CONCLUSIONS: This study shows that phenytoin and carbamazepine have approximately twice the CYP3A4-inducing potency of phenobarbital. Carbamazepine 49-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 29649093-10 2018 CONCLUSIONS: This study shows that phenytoin and carbamazepine have approximately twice the CYP3A4-inducing potency of phenobarbital. Phenobarbital 119-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 29649093-11 2018 The results indicate that 2-fold higher doses of CYP3A4-metabolized drugs may generally be required during concurrent treatment with phenytoin or carbamazepine compared with phenobarbital. Phenytoin 133-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 29649093-11 2018 The results indicate that 2-fold higher doses of CYP3A4-metabolized drugs may generally be required during concurrent treatment with phenytoin or carbamazepine compared with phenobarbital. Carbamazepine 146-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 29649093-11 2018 The results indicate that 2-fold higher doses of CYP3A4-metabolized drugs may generally be required during concurrent treatment with phenytoin or carbamazepine compared with phenobarbital. Phenobarbital 174-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 28891378-3 2018 The manufacturer"s data suggests that cobicistat is a more selective CYP3A4 inhibitor than ritonavir. Cobicistat 38-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 30062590-0 2018 Characterization of Intestinal and Hepatic CYP3A-Mediated Metabolism of Midazolam in Children Using a Physiological Population Pharmacokinetic Modelling Approach. Midazolam 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-48 30062590-2 2018 Our aim is to characterize both intestinal and hepatic CYP3A-mediated metabolism of midazolam in children in order to predict first-pass and systemic metabolism of CYP3A substrates. Midazolam 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 30062590-2 2018 Our aim is to characterize both intestinal and hepatic CYP3A-mediated metabolism of midazolam in children in order to predict first-pass and systemic metabolism of CYP3A substrates. Midazolam 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-169 30087611-6 2018 Inhibition studies using human liver microsomes showed that CYP3A4, 2B6, and 2C9 together contributed 19.0 +- 2.6% (mean +- 95%CI) to O-demethylation, 4.0 +- 0.7% to alpha-hydroxylation, and 7.6 +- 1.7% to N-dealkylation of metoprolol. Nitrogen 206-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-71 30087611-6 2018 Inhibition studies using human liver microsomes showed that CYP3A4, 2B6, and 2C9 together contributed 19.0 +- 2.6% (mean +- 95%CI) to O-demethylation, 4.0 +- 0.7% to alpha-hydroxylation, and 7.6 +- 1.7% to N-dealkylation of metoprolol. Metoprolol 224-234 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-71 30087611-7 2018 In supersomes overexpressing CYP3A4, metoprolol was alpha-hydroxylated in a reaction inhibited by the CYP3A4-specific inhibitor ketoconazole, but not by the CYP2D6-specific inhibitor quinidine. Metoprolol 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 30087611-7 2018 In supersomes overexpressing CYP3A4, metoprolol was alpha-hydroxylated in a reaction inhibited by the CYP3A4-specific inhibitor ketoconazole, but not by the CYP2D6-specific inhibitor quinidine. Metoprolol 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 30087611-7 2018 In supersomes overexpressing CYP3A4, metoprolol was alpha-hydroxylated in a reaction inhibited by the CYP3A4-specific inhibitor ketoconazole, but not by the CYP2D6-specific inhibitor quinidine. Ketoconazole 128-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 30087611-7 2018 In supersomes overexpressing CYP3A4, metoprolol was alpha-hydroxylated in a reaction inhibited by the CYP3A4-specific inhibitor ketoconazole, but not by the CYP2D6-specific inhibitor quinidine. Ketoconazole 128-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 29678659-0 2018 Association of CYP3A4*1B genotype with Cyclosporin A pharmacokinetics in renal transplant recipients: A meta-analysis. Cyclosporine 39-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 30087611-9 2018 CYP3A4, 2B6, and 2C9, which are inducible by rifampicin, contribute to alpha-hydroxylation, O-demethylation, and N-dealkylation of metoprolol. Rifampin 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-11 29678659-2 2018 CYP3A4*1B is reported to be associated with CsA pharmacokinetics parameters, but the relevance is still in dispute. Cyclosporine 44-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 30087611-9 2018 CYP3A4, 2B6, and 2C9, which are inducible by rifampicin, contribute to alpha-hydroxylation, O-demethylation, and N-dealkylation of metoprolol. Metoprolol 131-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-11 29678659-3 2018 Therefore, a meta-analysis was employed to evaluate the influence of CYP3A4*1B on CsA pharmacokinetics at different post-transplantation times in adult renal transplant recipients. Cyclosporine 82-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 29636360-8 2018 LY3023414 pharmacokinetics demonstrated dose-dependent increase in exposure with >= 90% target inhibition at doses >=150 mg. DDI analysis demonstrated LY3023414 to be a weak inhibitor of CYP3A4. LY3023414 151-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 29678659-11 2018 CONCLUSIONS: CYP3A4*1B is associated with CsA C0/Dose ratio in renal transplant recipients which indicates patients with CYP3A4*1B allele require lower dose of CsA to reach target blood concentration compared with the CYP3A4*1 carriers. Cyclosporine 42-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 29678659-11 2018 CONCLUSIONS: CYP3A4*1B is associated with CsA C0/Dose ratio in renal transplant recipients which indicates patients with CYP3A4*1B allele require lower dose of CsA to reach target blood concentration compared with the CYP3A4*1 carriers. Cyclosporine 42-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 29678659-11 2018 CONCLUSIONS: CYP3A4*1B is associated with CsA C0/Dose ratio in renal transplant recipients which indicates patients with CYP3A4*1B allele require lower dose of CsA to reach target blood concentration compared with the CYP3A4*1 carriers. Cyclosporine 42-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 29678659-11 2018 CONCLUSIONS: CYP3A4*1B is associated with CsA C0/Dose ratio in renal transplant recipients which indicates patients with CYP3A4*1B allele require lower dose of CsA to reach target blood concentration compared with the CYP3A4*1 carriers. Cyclosporine 160-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 29678659-11 2018 CONCLUSIONS: CYP3A4*1B is associated with CsA C0/Dose ratio in renal transplant recipients which indicates patients with CYP3A4*1B allele require lower dose of CsA to reach target blood concentration compared with the CYP3A4*1 carriers. Cyclosporine 160-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 29678659-11 2018 CONCLUSIONS: CYP3A4*1B is associated with CsA C0/Dose ratio in renal transplant recipients which indicates patients with CYP3A4*1B allele require lower dose of CsA to reach target blood concentration compared with the CYP3A4*1 carriers. Cyclosporine 160-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 29792708-4 2018 The rate of conversion of midazolam to its 1-hydroxy metabolite was used to assess in vitro CYP3A4 activity in human liver microsomes (HLM). Midazolam 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 29702137-11 2018 This may be a consequence of a reduced metabolism of venlafaxine to the inactive metabolite N-desmethylvenlafaxine via CYP3A4, the main metabolizing enzyme for quetiapine, and a shift towards a higher proportion of the active metabolite ODVEN. Venlafaxine Hydrochloride 53-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 29702137-11 2018 This may be a consequence of a reduced metabolism of venlafaxine to the inactive metabolite N-desmethylvenlafaxine via CYP3A4, the main metabolizing enzyme for quetiapine, and a shift towards a higher proportion of the active metabolite ODVEN. N-desmethylvenlafaxine 92-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 29702137-11 2018 This may be a consequence of a reduced metabolism of venlafaxine to the inactive metabolite N-desmethylvenlafaxine via CYP3A4, the main metabolizing enzyme for quetiapine, and a shift towards a higher proportion of the active metabolite ODVEN. Quetiapine Fumarate 160-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 29792708-9 2018 CYP3A4 protein expression was significantly lower in NAFL and NASH donors ( p < 0.05) and accounted for significant midazolam hydroxylation variability in a multiple linear regression analysis (beta = 0.869, r2 = 0.762, P < 0.01). Midazolam 119-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29869311-1 2018 Ritonavir is an anti-viral compound that has also been employed extensively as a CYP3A4 and P-glycoprotein (Pgp) inhibitor to boost the pharmacokinetic performance of compounds that undergo first pass metabolism. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 29668485-3 2018 Pharmacokinetic assays of sirolimus are available as this drug has a precise therapeutic window and blood levels might be influenced by CYP3A4 polymorphisms and drug interactions. Sirolimus 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 29691891-0 2018 Kuypers and Vanhove reply to "Was 4beta-hydroxycholesterol ever going to be a useful marker of CYP3A4 activity?" cholest-5-ene-3,4-diol 34-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 29464732-0 2018 Was 4beta-hydroxycholesterol ever going to be a useful marker of CYP3A4 activity? cholest-5-ene-3,4-diol 4-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 29749106-1 2018 reply to "Was 4beta-hydroxycholesterol ever going to be a useful marker of CYP3A4 activity?" cholest-5-ene-3,4-diol 14-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 29695615-11 2018 The P450-mediated oxidative metabolism of SAM-760 was still primarily attributed to CYP3A (33%), with minor contributions from P450 isoforms CYP2C19 and CYP2D6. UNII-4JEH3BL51N 42-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-89 29712725-3 2018 CsA is an inhibitor of organic anion transporting polypeptide (OATP)1B1 and CYP3A4, and GEM and its glucuronide (GEM-glu) inhibit OATP1B1 and CYP2C8. Cyclosporine 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 29695615-12 2018 Thus, the disposition of [14C]SAM-760 in human hepatocytes via novel sulfonamide metabolism and CYP3A verified the lower than expected clinical DDI when SAM-760 was coadministered with ketoconazole. Carbon-14 26-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-101 29695615-12 2018 Thus, the disposition of [14C]SAM-760 in human hepatocytes via novel sulfonamide metabolism and CYP3A verified the lower than expected clinical DDI when SAM-760 was coadministered with ketoconazole. Ketoconazole 185-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-101 29635009-1 2018 Lumefantrine is a widely used antimalarial in children in sub-Saharan Africa and is predominantly metabolised by CYP3A4. Lumefantrine 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 29635009-2 2018 The concomitant use of lumefantrine with the antiretroviral efavirenz, which is metabolised by CYP2B6 and is an inducer of CYP3A4, increases the risk of lumefantrine failure and can result in an increased recrudescence rate in HIV-infected children. Lumefantrine 23-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 29989011-1 2018 The aim of the present study was to investigate the potential effect of thymoquinone (TQ) on the metabolic activity of four major drug metabolizing enzymes in human liver microsomes, namely cytochrome P450 (CYP) 1A2, CYP2C9, CYP2D6 and CYP3A4. thymoquinone 72-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 236-242 29572563-2 2018 Inherent between subject variability in clearance of CYP3A4 substrates is substantial; by way of example, midazolam clearance varies by > 10-fold between individuals before considering the impact of extrinsic factors. Midazolam 106-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 29027195-0 2018 TSPYL Family Regulates CYP17A1 and CYP3A4 Expression: Potential Mechanism Contributing to Abiraterone Response in Metastatic Castration-Resistant Prostate Cancer. abiraterone 90-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 29027195-3 2018 Here we show that TSPYLs, especially TSPYL 1, 2, and 4, can regulate the expression of many CYP genes, including CYP17A1, a key enzyme in androgen biosynthesis, and CYP3A4, an enzyme that catalyzes the metabolism of abiraterone, a CYP17 inhibitor. abiraterone 216-227 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 29027195-4 2018 Furthermore, a common TSPYL1 single nucleotide polymorphism (SNP), rs3828743 (G/A) (Pro62Ser), abolishes TSPYL1"s ability to suppress CYP3A4 expression, resulting in reduced abiraterone concentrations and increased cell proliferation. abiraterone 174-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 29989011-7 2018 However, at 10 microM TQ, CYP2C9 enzyme activity was maximally inhibited by 69.69%, followed by CYP3A4 (23.59%) > CYP1A2 (23.51%) > CYP2D6 (11.42%). thymoquinone 22-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 29989011-1 2018 The aim of the present study was to investigate the potential effect of thymoquinone (TQ) on the metabolic activity of four major drug metabolizing enzymes in human liver microsomes, namely cytochrome P450 (CYP) 1A2, CYP2C9, CYP2D6 and CYP3A4. thymoquinone 86-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 236-242 29989011-2 2018 The inhibition of CYP enzymatic activities by TQ was evaluated by incubating typical substrates (phenacetin for CYP1A2, tolbutamide for CYP2C9, dextromethorphan for CYP2D6, and testosterone for CYP3A4) with human liver microsomes and NADPH in the absence or presence of TQ (1, 10 and 100 microM). thymoquinone 46-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 28685622-3 2018 PF-06282999 is an inducer of CYP3A4 mRNA and midazolam-1"-hydroxylase activity in human hepatocytes, which is consistent with PF-06282999-dose dependent decreases in mean maximal plasma concentrations (Cmax) and area under the plasma concentration time curve (AUC) of midazolam in humans following 14-day treatment with PF-06282999. pyrazofurin 0-2 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 28685622-8 2018 TaqMan gene expression analysis of human hepatocytes treated with PF-06282999 and the prototypical PXR agonist rifampin demonstrated increases in mRNA for CYP3A4 and related CYPs that are regulated by PXR. Rifampin 112-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 28737453-16 2018 Selexipag is an inhibitor of CYP2C8 and CYP2C9 and induces CYP3A4 and CYP2C9 in vitro. selexipag 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 30155396-6 2018 Discussion: Phenytoin is an inducer of cytochrome P450 3A4, and quetiapine is a substrate of this enzyme. Phenytoin 12-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-58 29601950-0 2018 Association between MDR1/CYP3A4/OPRM1 gene polymorphisms and the post-caesarean fentanyl analgesic effect on Chinese women. Fentanyl 80-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 29601950-1 2018 OBJECTIVE: Our study aimed to evaluate the association between the multidrug resistance 1 (MDR1)/cytochrome P450 3A4 (CYP3A4)/mu-opioid receptor (OPRM1) gene polymorphisms and the post-caesarean analgesic effect of fentanyl on Chinese women. Fentanyl 215-223 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-116 29601950-1 2018 OBJECTIVE: Our study aimed to evaluate the association between the multidrug resistance 1 (MDR1)/cytochrome P450 3A4 (CYP3A4)/mu-opioid receptor (OPRM1) gene polymorphisms and the post-caesarean analgesic effect of fentanyl on Chinese women. Fentanyl 215-223 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 29601950-7 2018 Subjects with the CYP3A4*1G/*1G genotype needed less fentanyl to achieve pain control than that needed by subjects carrying the CYP3A4*1/*1 and CYP3A4*1/*1G genotypes in the first post-operative 24 h and 48 h (P < 0.05), and the MAP/HR/Cor/Ang-1 levels gradually decreased immediately after surgery and in the first post-operative 24 h. 3. Fentanyl 53-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 29601950-10 2018 CONCLUSION: These results indicated that the MDR1/CYP3A4/OPRM1 gene polymorphisms influenced the fentanyl consumption and the physiological effects of intravenous analgesia in the Chinese women who received lower segment caesarean section surgeries. Fentanyl 97-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 29804290-0 2018 Tacrolimus Elimination in Four Patients With a CYP3A5*3/*3 CYP3A4*22/*22 Genotype Combination. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 29804290-1 2018 Cytochrome P450 3A5 (CYP3A5) and cytochrome P450 3A4 (CYP3A4) are the predominate enzymes responsible for tacrolimus metabolism. Tacrolimus 106-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-52 29804290-1 2018 Cytochrome P450 3A5 (CYP3A5) and cytochrome P450 3A4 (CYP3A4) are the predominate enzymes responsible for tacrolimus metabolism. Tacrolimus 106-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 29804290-2 2018 The presence of CYP3A4 and CYP3A5 genetic variants significantly affects tacrolimus clearance and dose requirements. Tacrolimus 73-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 29727298-9 2018 RESULTS: According to in silico and in vitro analysis results, the most probable metabolizer of phenazepam is CYP3A4. phenazepam 96-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 29727298-10 2018 By the in vivo study results, CYP3A activity decreased sufficiently (from 3.8 [95% CI: 2.94-4.65] to 2.79 [95% CI: 2.02-3.55], p=0.017) between the start and finish of treatment in patients who were prescribed just phenazepam. phenazepam 215-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-35 29727298-11 2018 CONCLUSIONS: Experimental in silico and in vivo studies confirmed that the original Russian benzodiazepine phenazepam was the substrate of CYP3A4 isoenzyme. Benzodiazepines 92-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 29727298-11 2018 CONCLUSIONS: Experimental in silico and in vivo studies confirmed that the original Russian benzodiazepine phenazepam was the substrate of CYP3A4 isoenzyme. phenazepam 107-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 29941014-2 2018 Associations of CYP3A4-mediated metabolism of quinine, with inflammatory biomarkers were investigated in patients undergoing maintenance hemodialysis (HD). Quinine 46-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 29949932-9 2018 SKN was found to be a UDP-glucuronosyltransferases (UGT) 1A9 inhibitor, whereas it induced transactivation of the human pregnane X receptor-mediated cytochrome P450 (CYP) 3A4 gene. sakuranetin 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-174 29904810-5 2018 Moreover, recent evidence has demonstrated that numerous cardiovascular medications, ranging from antihypertensive medication to antiarrhythmics, are known to interact with the CYP3A4 and/or P-gp system increasing the toxicity potential of colchicine. Colchicine 240-250 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 30131925-2 2018 Ranolazine has previously been linked to the development of statin-induced myopathy, because it also inhibits CYP3A4, which increases serum statin levels. Ranolazine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 29950882-0 2018 CYP3A and CYP2C19 activity in urine in relation to CYP3A4, CYP3A5, and CYP2C19 polymorphisms in Russian peptic ulcer patients taking omeprazole. Omeprazole 133-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 29950882-3 2018 Purpose: The aim of the study was to find if CYP3A4*22, CYP3A5*3, CYP2C19*2, CYP2C19*3, and CYP2C19*17 genotypes are connected with CYP3A and CYP2C19 activities in Russian peptic ulcer patients taking omeprazole. Omeprazole 201-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 29950882-3 2018 Purpose: The aim of the study was to find if CYP3A4*22, CYP3A5*3, CYP2C19*2, CYP2C19*3, and CYP2C19*17 genotypes are connected with CYP3A and CYP2C19 activities in Russian peptic ulcer patients taking omeprazole. Omeprazole 201-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-50 29950882-10 2018 A statistically significant difference in CYP3A activity (Mann-Whitney test) was found between CYP2C19 EMs vs CYP2C19 IMs+PMs (p=0.006), between CYP2C19 UMs vs CYP2C19 IMs+PMs (p=0.018), and in multiple comparison Kruskal-Wallis test (p=0.014). pms 122-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 29950882-10 2018 A statistically significant difference in CYP3A activity (Mann-Whitney test) was found between CYP2C19 EMs vs CYP2C19 IMs+PMs (p=0.006), between CYP2C19 UMs vs CYP2C19 IMs+PMs (p=0.018), and in multiple comparison Kruskal-Wallis test (p=0.014). pms 172-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 29950882-11 2018 Conclusion: In CYP2C19 IMs+PMs, CYP3A activity was significantly lower than in CYP2C19 EMs and UMs. pms 27-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-37 29869546-0 2018 The Use of Carbamazepine to Expedite Metabolism of Risperidone Long-Acting Injection Through Induction of CYP3A4 in a Patient With Extrapyramidal Symptoms. Carbamazepine 11-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 29620050-13 2018 Based on early reported human pharmacokinetics, drug interaction indices were 0.16 for CYP3A4 and 0.02 for CYP2C9, suggesting that anlotinib had a low propensity to precipitate drug interactions on these enzymes. anlotinib 131-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 29869546-0 2018 The Use of Carbamazepine to Expedite Metabolism of Risperidone Long-Acting Injection Through Induction of CYP3A4 in a Patient With Extrapyramidal Symptoms. Risperidone 51-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 29557814-9 2018 Our study showed that the concomitant use of CYP3A4 inhibitors, smoking, and exon 21 affected the time to reach gefitinib-induced hepatotoxicity. Gefitinib 112-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 29325225-0 2018 Influence of CYP2D6, CYP3A4, CYP3A5 and ABCB1 Polymorphisms on Pharmacokinetics and Safety of Aripiprazole in Healthy Volunteers. Aripiprazole 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 29325225-1 2018 The aim of this study was to investigate the effect of polymorphisms in cytochrome P450 (CYP) 2D6, CYP3A4 and CYP3A5 enzymes and in P-glycoprotein (P-gp) on the pharmacokinetics and safety of aripiprazole and, its active metabolite, dehydro-aripiprazole, in 148 healthy volunteers from six bioequivalence trials receiving a single oral dose of aripiprazole. Aripiprazole 192-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 29345044-6 2018 TAK-063 was metabolized mainly by CYP2C8 and CYP3A4/5, while incubation with human liver microsomes produced the major human metabolite, M-I as well as several unknown minor metabolites. 1-(2-fluoro-4-(1H-pyrazol-1-yl)phenyl)-5-methoxy-3-(1-phenyl-1H-pyrazol-5-yl)pyridazin-4(1H)-one 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 29325225-1 2018 The aim of this study was to investigate the effect of polymorphisms in cytochrome P450 (CYP) 2D6, CYP3A4 and CYP3A5 enzymes and in P-glycoprotein (P-gp) on the pharmacokinetics and safety of aripiprazole and, its active metabolite, dehydro-aripiprazole, in 148 healthy volunteers from six bioequivalence trials receiving a single oral dose of aripiprazole. dehydroaripiprazole 233-253 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 29325225-1 2018 The aim of this study was to investigate the effect of polymorphisms in cytochrome P450 (CYP) 2D6, CYP3A4 and CYP3A5 enzymes and in P-glycoprotein (P-gp) on the pharmacokinetics and safety of aripiprazole and, its active metabolite, dehydro-aripiprazole, in 148 healthy volunteers from six bioequivalence trials receiving a single oral dose of aripiprazole. Aripiprazole 241-253 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 29504153-0 2018 Relevance of CYP3A4*20, UGT1A1*37 and UGT1A1*28 variants in irinotecan-induced severe toxicity. Irinotecan 60-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 29616291-5 2018 We demonstrated that CYP3A4, 3A5, and 2D6 were the major enzymes that metabolize dronedarone, and that CYP3A7, 2E1, 2C19, 2C18, 1A1, and 2B6 also metabolize dronedarone, but to a lesser extent. Dronedarone 81-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 29616291-5 2018 We demonstrated that CYP3A4, 3A5, and 2D6 were the major enzymes that metabolize dronedarone, and that CYP3A7, 2E1, 2C19, 2C18, 1A1, and 2B6 also metabolize dronedarone, but to a lesser extent. Dronedarone 157-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 29616291-6 2018 Our data showed that the cytotoxicity of dronedarone was decreased in CYP3A4-, 3A5-, or 2D6-overexpressing cells compared to the control HepG2 cells, indicating that the parent dronedarone has higher potency than the metabolites to induce cytotoxicity in these cells. Dronedarone 41-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 29616291-6 2018 Our data showed that the cytotoxicity of dronedarone was decreased in CYP3A4-, 3A5-, or 2D6-overexpressing cells compared to the control HepG2 cells, indicating that the parent dronedarone has higher potency than the metabolites to induce cytotoxicity in these cells. Dronedarone 177-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 29741901-6 2018 We have examined the sulfoxidation of S-omeprazole to omeprazole sulfone metabolite by CYP3A4, and the observed activation free energy barrier is 9.9 kcal/mol. Omeprazole 38-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 29741901-6 2018 We have examined the sulfoxidation of S-omeprazole to omeprazole sulfone metabolite by CYP3A4, and the observed activation free energy barrier is 9.9 kcal/mol. omeprazole sulfone 54-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 29741901-7 2018 The computational results reveal that CYP2C19 exclusively metabolizes R-omeprazole to hydroxyomeprazole, which is hydrophilic and can easily excrete, whereas CYP3A4 metabolizes S-omeprazole to lipophilic sulfone; hence, the excretion of this metabolite would be relatively slower from the body. r-omeprazole 70-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 29741901-7 2018 The computational results reveal that CYP2C19 exclusively metabolizes R-omeprazole to hydroxyomeprazole, which is hydrophilic and can easily excrete, whereas CYP3A4 metabolizes S-omeprazole to lipophilic sulfone; hence, the excretion of this metabolite would be relatively slower from the body. 5-hydroxymethylomeprazole 86-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 29741901-7 2018 The computational results reveal that CYP2C19 exclusively metabolizes R-omeprazole to hydroxyomeprazole, which is hydrophilic and can easily excrete, whereas CYP3A4 metabolizes S-omeprazole to lipophilic sulfone; hence, the excretion of this metabolite would be relatively slower from the body. Omeprazole 177-189 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 29741901-7 2018 The computational results reveal that CYP2C19 exclusively metabolizes R-omeprazole to hydroxyomeprazole, which is hydrophilic and can easily excrete, whereas CYP3A4 metabolizes S-omeprazole to lipophilic sulfone; hence, the excretion of this metabolite would be relatively slower from the body. Sulfones 204-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 29504153-3 2018 As CYP3A4 is also an irinotecan-metabolizing enzyme, our study aimed to elucidate the influence of the CYP3A4*20 loss-of-function allele in the toxicity profile of these patients. Irinotecan 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-9 29504153-3 2018 As CYP3A4 is also an irinotecan-metabolizing enzyme, our study aimed to elucidate the influence of the CYP3A4*20 loss-of-function allele in the toxicity profile of these patients. Irinotecan 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 29767851-7 2018 Lower 25-OHD levels were also associated with increased expression of CYP3A4, and with decreased expression of GC (also termed DBP) and VDR, three genes involved in vitamin D metabolism. 25-ohd 6-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 29759884-0 2018 Assessment of induced CYP3A activity in pregnant women using 4beta-hydroxycholesterol: Cholesterol ratio as an appropriate metabolic marker. cholest-5-ene-3,4-diol 61-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-27 29572333-8 2018 Only idelalisib showed strong inhibition of CYP3A, and lumacaftor behaved as a strong CYP3A inducer. idelalisib 5-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-49 29572333-8 2018 Only idelalisib showed strong inhibition of CYP3A, and lumacaftor behaved as a strong CYP3A inducer. lumacaftor 55-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 29759884-0 2018 Assessment of induced CYP3A activity in pregnant women using 4beta-hydroxycholesterol: Cholesterol ratio as an appropriate metabolic marker. Cholesterol 87-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-27 29759884-5 2018 RESULTS: An increased 4beta-hydroxycholesterol/cholesterol ratio, consistent with high CYP3A activity, was observed in pregnant women compared with that in non-pregnant women; however, no differences were observed among trimesters. cholest-5-ene-3,4-diol 22-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 29759884-7 2018 CONCLUSIONS: We observed an increase in the activity of CYP3A following but not during pregnancy when measured using the 4beta-hydroxycholesterol/cholesterol ratio. cholest-5-ene-3,4-diol 121-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 29759884-7 2018 CONCLUSIONS: We observed an increase in the activity of CYP3A following but not during pregnancy when measured using the 4beta-hydroxycholesterol/cholesterol ratio. Cholesterol 134-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 29759884-8 2018 In addition, based on our results, we suggest that the plasma 4beta-hydroxycholesterol/cholesterol ratio be used to measure CYP3A activity in pregnant women. Hydroxycholesterols 68-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-129 29759884-8 2018 In addition, based on our results, we suggest that the plasma 4beta-hydroxycholesterol/cholesterol ratio be used to measure CYP3A activity in pregnant women. Cholesterol 75-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-129 29727013-9 2018 RESULTS: There was a strong, consistent, and highly significant relationship between everolimus exposure and efficacy, measured by TN-Cmin and SF, regardless of patient"s age and concomitant use of cytochrome P450 3A4 (CYP3A4) inhibitors/inducers. Everolimus 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 29546446-0 2018 CYP3A4 and GCK genetic polymorphisms are the risk factors of tacrolimus-induced new-onset diabetes after transplantation in renal transplant recipients. Tacrolimus 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29546446-1 2018 PURPOSE: We intend to investigate the association between tacrolimus-induced new-onset diabetes after transplantation (NODAT) and polymorphisms of CYP3A4, CYP3A5, ATP-binding cassette transporter sub-family C member 8 (ABCC8), and glucokinase (GCK) in renal transplant recipients. Tacrolimus 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 29546446-7 2018 The lower concentration/dose or fasting serum glucose was in CYP3A4 *1/*1 carriers than that in *18B/*18B carriers in all the renal transplant recipients (p < 0.05), respectively. Glucose 46-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 29546446-10 2018 CONCLUSIONS: The polymorphisms of CYP3A4 *18B and GCK G-30A were related to NODAT induced by tacrolimus. Tacrolimus 93-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 29848078-4 2018 In silico molecular docking was applied to analyze the change in the CYP3A4-alprazolam-binding conformation when ethanol was coadministered with alprazolam. Alprazolam 76-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 29848078-4 2018 In silico molecular docking was applied to analyze the change in the CYP3A4-alprazolam-binding conformation when ethanol was coadministered with alprazolam. Ethanol 113-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 29848078-4 2018 In silico molecular docking was applied to analyze the change in the CYP3A4-alprazolam-binding conformation when ethanol was coadministered with alprazolam. Alprazolam 145-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 29848078-7 2018 Molecular docking results suggested that the conformation of CYP3A4 with alprazolam changed when ethanol was bound to the SER119 residue, which seems critical in the process of CYP3A4-alprazolam binding. Alprazolam 73-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 29848078-7 2018 Molecular docking results suggested that the conformation of CYP3A4 with alprazolam changed when ethanol was bound to the SER119 residue, which seems critical in the process of CYP3A4-alprazolam binding. Alprazolam 73-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 29848078-7 2018 Molecular docking results suggested that the conformation of CYP3A4 with alprazolam changed when ethanol was bound to the SER119 residue, which seems critical in the process of CYP3A4-alprazolam binding. Ethanol 97-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 29848078-7 2018 Molecular docking results suggested that the conformation of CYP3A4 with alprazolam changed when ethanol was bound to the SER119 residue, which seems critical in the process of CYP3A4-alprazolam binding. Ethanol 97-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 29848078-7 2018 Molecular docking results suggested that the conformation of CYP3A4 with alprazolam changed when ethanol was bound to the SER119 residue, which seems critical in the process of CYP3A4-alprazolam binding. Alprazolam 184-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 29848078-7 2018 Molecular docking results suggested that the conformation of CYP3A4 with alprazolam changed when ethanol was bound to the SER119 residue, which seems critical in the process of CYP3A4-alprazolam binding. Alprazolam 184-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 29848078-8 2018 CONCLUSIONS: Ethanol might increase the toxicity of alprazolam by inhibiting the activity of CYP3A4, although other pharmacokinetic processes may be affected. Ethanol 13-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 29848078-8 2018 CONCLUSIONS: Ethanol might increase the toxicity of alprazolam by inhibiting the activity of CYP3A4, although other pharmacokinetic processes may be affected. Alprazolam 52-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 29848078-9 2018 Ethanol could change the conformation of CYP3A4 and affect alprazolam binding. Ethanol 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 29848078-9 2018 Ethanol could change the conformation of CYP3A4 and affect alprazolam binding. Alprazolam 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 29589331-4 2018 A typical value for ASV clearance (CL/F) was 50.8 L/h, increasing by 43% after 2 days to a CL/F of 72.5 L/h at steady-state, likely due to auto-induction of cytochrome P450 3A4 (CYP3A4). asunaprevir 20-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-176 29442148-4 2018 Common single-nucleotide polymorphisms (SNPs) in biotransformation enzymes CYP3A4 and CYP3A5 (CYP3A4*1G and CYP3A5*3) were genotyped by PCR-direct sequencing. single-nucleotide 7-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 29442148-4 2018 Common single-nucleotide polymorphisms (SNPs) in biotransformation enzymes CYP3A4 and CYP3A5 (CYP3A4*1G and CYP3A5*3) were genotyped by PCR-direct sequencing. single-nucleotide 7-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 29745466-0 2018 First-Pass CYP3A-Mediated Metabolism of Midazolam in the Gut Wall and Liver in Preterm Neonates. Midazolam 40-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-16 29589331-4 2018 A typical value for ASV clearance (CL/F) was 50.8 L/h, increasing by 43% after 2 days to a CL/F of 72.5 L/h at steady-state, likely due to auto-induction of cytochrome P450 3A4 (CYP3A4). asunaprevir 20-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 29464464-7 2018 Also, pazopanib is metabolised by the CYP3A4 isoform of the cytochrome P450 group. pazopanib 6-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 29867477-14 2018 Midazolam and tolbutamide are considered good substrates to evaluate porcine CYP3A/2C enzymes, respectively. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 29393971-4 2018 Oliceridine is primarily hepatically metabolized by CYP3A4 and CYP2D6. ((3-methoxythiophen-2-yl)methyl)((2-(9-(pyridin-2-yl)-6-oxaspiro(4.5)decan-9-yl)ethyl))amine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 29412463-3 2018 In vitro, presatovir is a substrate of the efflux transporters P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) and hepatic uptake transporters organic anion transporting polypeptide (OATP) 1B1 and OATP1B3 and is slowly metabolized by cytochrome P450 (CYP) 3A4 and CYP3A5. presatovir 10-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 252-277 29412463-4 2018 This study enrolled 64 healthy subjects to evaluate the effect of cyclosporine, a P-gp, BCRP, and OATP1B1/1B3 inhibitor; rifampin, a strong CYP3A4 and P-gp inducer; efavirenz, a moderate CYP3A4 inducer; and cobicistat, a potent CYP3A inhibitor, on presatovir pharmacokinetics. Rifampin 121-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 29412463-4 2018 This study enrolled 64 healthy subjects to evaluate the effect of cyclosporine, a P-gp, BCRP, and OATP1B1/1B3 inhibitor; rifampin, a strong CYP3A4 and P-gp inducer; efavirenz, a moderate CYP3A4 inducer; and cobicistat, a potent CYP3A inhibitor, on presatovir pharmacokinetics. Rifampin 121-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 28539103-5 2018 A limited number of reports are available which discuss reduced atypical antipsychotic concentrations secondary to oxcarbazepine CYP3A4 induction. Oxcarbazepine 115-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 28539103-9 2018 This report should encourage the completion of in vitro and clinical studies and the publication of case reports describing the possible inductive effects of oxcarbazepine on atypical antipsychotics (including cariprazine, lurasidone, quetiapine, aripiprazole, brexpiprazole, iloperidone, and risperidone) mediated by induction of the CYP3A4 metabolic pathway. Oxcarbazepine 158-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 335-341 28657402-8 2018 In a further study, olaparib (2-200 muM) functioned as a time-dependent inhibitor of CYP3A4/5 (KI, 72.2 muM and Kinact, 0.0675 min-1). olaparib 20-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 28657402-9 2018 Assessment of the CYP induction potential of olaparib (0.061-44 muM) showed minor concentration-related increases in CYP1A2 and more marked increases in CYP2B6 and CYP3A4 mRNA, compared with positive control activity; however, no significant change in CYP3A4/5 enzyme activity was observed. olaparib 45-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 28657402-9 2018 Assessment of the CYP induction potential of olaparib (0.061-44 muM) showed minor concentration-related increases in CYP1A2 and more marked increases in CYP2B6 and CYP3A4 mRNA, compared with positive control activity; however, no significant change in CYP3A4/5 enzyme activity was observed. olaparib 45-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 252-258 29247536-6 2018 Hepatocarcinoma cells in the self-organized liver organoids in 3D LEMgel (LEMgel organoids) showed an epithelial phenotype and expressed ALB, CYP3A4, E-cadherin, and ASGPR. lemgel organoids 74-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 29427135-1 2018 Amlodipine, a commonly prescribed anti-hypertensive drug, shows increased systemic exposure with cytochrome P450 (CYP) 3A inhibitors. Amlodipine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-121 29427135-2 2018 Ritonavir (RTV) is a potent mechanism-based and reversible CYP3A inhibitor and moderate inducer that is used as a pharmacokinetic enhancer in several antiviral treatment regimens. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 29427135-2 2018 Ritonavir (RTV) is a potent mechanism-based and reversible CYP3A inhibitor and moderate inducer that is used as a pharmacokinetic enhancer in several antiviral treatment regimens. Ritonavir 11-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 29427135-3 2018 Drug-drug interaction (DDI) between RTV and amlodipine is due to mixed inhibition and induction of CYP3A4, which is challenging to predict without a mechanistic model that accounts for the complexity of both mechanisms occurring simultaneously. Ritonavir 36-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 29427135-3 2018 Drug-drug interaction (DDI) between RTV and amlodipine is due to mixed inhibition and induction of CYP3A4, which is challenging to predict without a mechanistic model that accounts for the complexity of both mechanisms occurring simultaneously. Amlodipine 44-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 29665350-10 2018 Induction of the model PXR target gene CYP3A4 by PAs was verified at the mRNA, protein and enzyme activity level. Pyrrolizidine Alkaloids 49-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 29665350-11 2018 In conclusion, PXR activation and PXR-mediated induction of CYP3A4 expression by PAs seem to be structure-dependent. Pyrrolizidine Alkaloids 81-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 29675530-0 2018 Hepatoprotective activity of iridoids, seco-iridoids and analog glycosides from Gentianaceae on HepG2 cells via CYP3A4 induction and mitochondrial pathway. Glycosides 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 29675530-7 2018 Amarogentin displayed the most clear inductive effect on CYP3A4 mRNA levels in the HepG2 cells. amarogentin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 29675530-9 2018 Amarogentin displayed obvious inductive effect on CYP3A4 mRNA levels in the HepG2 cells. amarogentin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 29867477-7 2018 Activity measurements were performed with substrates of major human CYP450 enzymes: midazolam (CYP3A), tolbutamide (CYP2C), and chlorzoxazone (CYP2E). Midazolam 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-100 29867477-14 2018 Midazolam and tolbutamide are considered good substrates to evaluate porcine CYP3A/2C enzymes, respectively. Tolbutamide 14-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 29780235-5 2018 In clinical practice, the process of phenotyping of CYP isoenzymes and some endogenous substrates in the ratio of cortisol to 6beta-hydroxycortisol in urine for the evaluation of CYP3A4 activity has been deemed to be a quite promising, safe and minimally invasive method for patients nowadays. Hydrocortisone 114-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 29160300-0 2018 Genome-wide association study identifies the common variants in CYP3A4 and CYP3A5 responsible for variation in tacrolimus trough concentration in Caucasian kidney transplant recipients. Tacrolimus 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 29160300-1 2018 The immunosuppressant tacrolimus (TAC) is metabolized by both cytochrome P450 3A4 (CYP3A4) and CYP3A5 enzymes. Tacrolimus 22-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-81 29160300-1 2018 The immunosuppressant tacrolimus (TAC) is metabolized by both cytochrome P450 3A4 (CYP3A4) and CYP3A5 enzymes. Tacrolimus 22-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 29780235-5 2018 In clinical practice, the process of phenotyping of CYP isoenzymes and some endogenous substrates in the ratio of cortisol to 6beta-hydroxycortisol in urine for the evaluation of CYP3A4 activity has been deemed to be a quite promising, safe and minimally invasive method for patients nowadays. 6 beta-hydroxycortisol 126-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 29736778-0 2018 Effects of polymorphisms in NR1I2, CYP3A4, and ABC transporters on the steady-state plasma trough concentrations of bosutinib in Japanese patient with chronic myeloid leukemia. bosutinib 116-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 29736778-9 2018 Because patients with the NR1I2 7635G/G or 8055T/T genotype may have increased activity of pregnane X receptor-regulated genes and thereafter higher intestinal expression of CYP3A4 and ABC efflux drug transporters, these patients may have a lower bosutinib C0. bosutinib 247-256 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 29498947-8 2018 Ketoconazole (CYP3A4 inhibitor) increased maximum plasma concentration 19% and increased the area under the curve 77%. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 29274758-2 2018 The DOACs are P-glycoprotein (P-gp) and cytochrome p-450 (CYP3A4) substrates. doacs 4-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 29274758-3 2018 Direct oral anticoagulant levels may be increased by the concomitant use of potent dual P-gp/CYP3A4 inhibitors, such as amiodarone, which can potentially translate into adverse clinical outcomes. Amiodarone 120-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 29765150-9 2018 AZD1208 increased CYP3A4 activity after multiple dosing, resulting in increased drug clearance. AZD1208 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 29728928-0 2018 Effects of diltiazem, a moderate inhibitor of CYP3A4, on the pharmacokinetics of tamsulosin in different CYP2D6 genotypes. Diltiazem 11-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 29728928-1 2018 Tamsulosin, a selective antagonist of the alpha1-adrenoceptor, is primarily metabolized by CYP3A4 and CYP2D6, and tamsulosin exposure is significantly increased according to the genetic polymorphism of CYP2D6. Tamsulosin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 29728928-2 2018 In this study, we investigated the effects of diltiazem, a moderate inhibitor of CYP3A4, on the pharmacokinetics of tamsulosin in subjects with different CYP2D6 genotypes. Diltiazem 46-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 29719052-6 2018 Testosterone 6beta-hydroxylation and midazolam 1"-hydroxylation, which are catalysed by both CYP3A4 and CYP3A5 in liver microsomes, were decreased by 25% and 45%, respectively, in the presence of 0.1 mg/ml SO-SWCNT. Testosterone 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 29719052-6 2018 Testosterone 6beta-hydroxylation and midazolam 1"-hydroxylation, which are catalysed by both CYP3A4 and CYP3A5 in liver microsomes, were decreased by 25% and 45%, respectively, in the presence of 0.1 mg/ml SO-SWCNT. Midazolam 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 29719052-6 2018 Testosterone 6beta-hydroxylation and midazolam 1"-hydroxylation, which are catalysed by both CYP3A4 and CYP3A5 in liver microsomes, were decreased by 25% and 45%, respectively, in the presence of 0.1 mg/ml SO-SWCNT. Carbon 209-214 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 28875498-3 2018 CYP2C19 and CYP3A4 are involved in the metabolism of clopidogrel, prasugrel, esomeprazole, and vonoprazan. 1-(5-(2-fluorophenyl)-1-(pyridin-3-ylsulfonyl)-1H-pyrrol-3-yl)-N-methylmethanamine 95-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 29377228-7 2018 CYP2C19 and CYP3A4 are predominantly involved in the metabolism of omeprazole despite their relatively low activities compared to adults. Omeprazole 67-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 29384591-7 2018 MECHANISM: Induction of CYP3A and potentially phase I metabolism (SULT2A1) by carbamazepine. Carbamazepine 78-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 28877336-0 2018 Identification of omega- or (omega-1)-Hydroxylated Medium-Chain Acylcarnitines as Novel Urinary Biomarkers for CYP3A Activity. omega- or (omega-1) 18-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-116 29468841-2 2018 In vitro metabolism data suggested osimertinib is a substrate of cytochrome P450 (CYP)3A4/5, a weak inducer of CYP3A, and an inhibitor of breast cancer resistance protein (BCRP). osimertinib 35-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-116 29468841-5 2018 Based on observed clinical data and PBPK simulations, the recommended dose of osimertinib when dosed with strong CYP3A inducers is 160 mg once daily. osimertinib 78-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-118 28875498-3 2018 CYP2C19 and CYP3A4 are involved in the metabolism of clopidogrel, prasugrel, esomeprazole, and vonoprazan. Clopidogrel 53-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 28875498-3 2018 CYP2C19 and CYP3A4 are involved in the metabolism of clopidogrel, prasugrel, esomeprazole, and vonoprazan. Prasugrel Hydrochloride 66-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 28875498-3 2018 CYP2C19 and CYP3A4 are involved in the metabolism of clopidogrel, prasugrel, esomeprazole, and vonoprazan. Esomeprazole 77-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 28877336-0 2018 Identification of omega- or (omega-1)-Hydroxylated Medium-Chain Acylcarnitines as Novel Urinary Biomarkers for CYP3A Activity. acylcarnitine 64-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-116 29490903-9 2018 In vitro studies demonstrated that CYP3A4 mediated the formation of the N-oxide metabolite (M4), which was further metabolized by glucuronyl transferases (UGTs) to form M8, as M4 was absent in plasma and only trace levels were present in the urine. n-oxide 72-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 29490903-11 2018 Overall, the major clearance route of verinurad is metabolism via UGTs and CYP3A4 and CYP2C8. verinurad 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 29352982-0 2018 Inhibition of CYP3A by Antimalarial Piperaquine and Its Metabolites in Human Liver Microsomes With IVIV Extrapolation. piperaquine 36-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 29227563-3 2018 In this study, we observed gene and protein expression of CYP3A4/5 in both human skin and tissue-engineered skin equivalents (TESEs), and enzyme activity was detected using the model substrate benzyl-O-methyl-cyanocoumarin. benzyl-o-methyl-cyanocoumarin 193-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 29596975-4 2018 CYP2C9, CYP3A4, and CYP3A5 were involved in the formation of FMS S-oxide, which was further metabolized to BR-A-557 by CYP3A4/5. Oxides 65-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 29596975-4 2018 CYP2C9, CYP3A4, and CYP3A5 were involved in the formation of FMS S-oxide, which was further metabolized to BR-A-557 by CYP3A4/5. Oxides 65-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 29596975-9 2018 In addition, simultaneous determination of the FMS metabolites may be used to evaluate CYP2C9 and CYP3A4/5 activity. fimasartan 47-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 29279486-2 2018 Methods The level of serum 4beta-hydroxycholesterol (4betaHC), a surrogate marker of CYP3A4 activity, was determined by LC-MS/MS in samples obtained from patients with HCV infection (CHCs) as well as healthy control subjects (CTLs). cholest-5-ene-3,4-diol 27-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 29279486-2 2018 Methods The level of serum 4beta-hydroxycholesterol (4betaHC), a surrogate marker of CYP3A4 activity, was determined by LC-MS/MS in samples obtained from patients with HCV infection (CHCs) as well as healthy control subjects (CTLs). cholest-5-ene-3,4-diol 53-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 29279486-10 2018 Conclusion The evaluation of CYP3A4 activity by measuring 4betaHC before treatment may provide additional information that can potentially be used to select cost- and efficacy-optimized treatment of HCV. cholest-5-ene-3,4-diol 58-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 29461981-0 2018 CYP3A4 mutation causes vitamin D-dependent rickets type 3. Vitamin D 23-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29440451-5 2018 Subsequently, DME gene expression signatures were generated for known CYP3A4 inducers PF-06282999 and pazopanib. pazopanib 102-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 29352982-1 2018 The potential of the antimalarial piperaquine and its metabolites to inhibit CYP3A was investigated in pooled human liver microsomes. piperaquine 34-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 29352982-2 2018 CYP3A activity was measured by liquid chromatography-tandem mass spectrometry as the rate of 1"-hydroxymidazolam formation. 1-hydroxymethylmidazolam 93-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 29352982-3 2018 Piperaquine was found to be a reversible, potent inhibitor of CYP3A with the following parameter estimates (%CV): IC50 = 0.76 muM (29), Ki = 0.68 muM (29). piperaquine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 29672606-8 2018 DMF-culturing of HepaRG cells substantially increased hepatic differentiation; transcript levels of hepatic structural genes and hepatic transcription regulators were increased up to 15-fold (Cytochrome P450 3A4) and nuclear translocation of hepatic transcription factor CEBPalpha was stimulated. Dimethylformamide 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-211 29488691-0 2018 Sensitivity of ivacaftor to drug-drug interactions with rifampin, a cytochrome P450 3A4 inducer. ivacaftor 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-87 29488691-0 2018 Sensitivity of ivacaftor to drug-drug interactions with rifampin, a cytochrome P450 3A4 inducer. Rifampin 56-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-87 29488691-2 2018 Because it is a substrate of the cytochrome P450 system, specifically CYP3A4/5, ivacaftor is subject to significant drug-drug interactions, including due to commonly used antimicrobials such as rifampin. ivacaftor 80-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 29488691-2 2018 Because it is a substrate of the cytochrome P450 system, specifically CYP3A4/5, ivacaftor is subject to significant drug-drug interactions, including due to commonly used antimicrobials such as rifampin. Rifampin 194-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 29679912-0 2018 Effects of UGT2B7, SCN1A and CYP3A4 on the therapeutic response of sodium valproate treatment in children with generalized seizures. Valproic Acid 67-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 29679912-7 2018 CONCLUSION: In children with generalized seizures on VPA therapy, polymorphisms of UGT2B7, CYP3A4, and SCN1A genes were associated with seizure reduction. Valproic Acid 53-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 29420809-7 2018 CYP3A4 enzyme activity, however, is inhibited by propiconazole. propiconazole 49-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29461981-4 2018 In vitro, the mutant CYP3A4 oxidized 1,25-dihydroxyvitamin D with 10-fold greater activity than WT CYP3A4 and 2-fold greater activity than CYP24A1, the principal inactivator of vitamin D metabolites. 1,25-dihydroxyvitamin D 37-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 29461981-4 2018 In vitro, the mutant CYP3A4 oxidized 1,25-dihydroxyvitamin D with 10-fold greater activity than WT CYP3A4 and 2-fold greater activity than CYP24A1, the principal inactivator of vitamin D metabolites. 1,25-dihydroxyvitamin D 37-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 29461981-4 2018 In vitro, the mutant CYP3A4 oxidized 1,25-dihydroxyvitamin D with 10-fold greater activity than WT CYP3A4 and 2-fold greater activity than CYP24A1, the principal inactivator of vitamin D metabolites. Vitamin D 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 29461981-4 2018 In vitro, the mutant CYP3A4 oxidized 1,25-dihydroxyvitamin D with 10-fold greater activity than WT CYP3A4 and 2-fold greater activity than CYP24A1, the principal inactivator of vitamin D metabolites. Vitamin D 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 29461981-5 2018 As CYP3A4 mutations have not previously been linked to rickets, these findings provide insight into vitamin D metabolism and demonstrate that accelerated inactivation of vitamin D metabolites represents a mechanism for vitamin D deficiency. Vitamin D 100-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-9 29461981-5 2018 As CYP3A4 mutations have not previously been linked to rickets, these findings provide insight into vitamin D metabolism and demonstrate that accelerated inactivation of vitamin D metabolites represents a mechanism for vitamin D deficiency. Vitamin D 170-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-9 29461981-5 2018 As CYP3A4 mutations have not previously been linked to rickets, these findings provide insight into vitamin D metabolism and demonstrate that accelerated inactivation of vitamin D metabolites represents a mechanism for vitamin D deficiency. Vitamin D 170-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-9 29679509-1 2018 Docetaxel, frequently used for the treatment of breast cancer, is mainly metabolized via hepatic cytochrome P450 (CYP) 3A in humans and is also a substrate of P-glycoprotein (P-gp). Docetaxel 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-121 29615122-0 2018 Effect of CYP3 A4, CYP3 A5 and ABCB1 gene polymorphisms on the clinical efficacy of tacrolimus in the treatment of nephrotic syndrome. Tacrolimus 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-17 32309600-10 2018 In addition, administration of macimorelin with drugs that prolong QT interval and CYP3A4 inducers should be avoided. macimorelin 31-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 29634071-2 2018 There is a known pharmacological interaction between ritonavir and those corticosteroids which are metabolised by the CYP3A4 pathway. Ritonavir 53-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 29858698-6 2018 In addition, in vitro studies using human liver microsomes showed that the formation of 4beta-HC was strongly inhibited by a CYP3A inhibitor, while the inhibitory effect of the CYP3A inhibition on the formation of 25-HC was weak. cholest-5-ene-3,4-diol 88-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-130 29858698-6 2018 In addition, in vitro studies using human liver microsomes showed that the formation of 4beta-HC was strongly inhibited by a CYP3A inhibitor, while the inhibitory effect of the CYP3A inhibition on the formation of 25-HC was weak. -hc 93-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-130 29171002-10 2018 Based on PK/PD data from 1748 subjects, percent reduction in 28-day average seizure frequency from baseline and responder probability increased with increasing perampanel exposure; concomitant CYP3A-inducing AEDs lowered perampanel exposure but did not impact the slope for responder probability. perampanel 221-231 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 193-198 29117640-0 2018 Functional Characterization of 22 CYP3A4 Protein Variants to Metabolize Ibrutinib In Vitro. ibrutinib 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 29117640-3 2018 Ibrutinib is an anticancer drug and primarily metabolized by CYP3A4. ibrutinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 29155491-0 2018 Variation in the Response of Clozapine Biotransformation Pathways in Human Hepatic Microsomes to CYP1A2- and CYP3A4-selective Inhibitors. Clozapine 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 29117640-4 2018 The aim of this study was to systematically investigate the effects of 22 CYP3A4 protein variants on the metabolism of ibrutinib in vitro. ibrutinib 119-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 29155491-5 2018 To further characterize the factors underlying these interactions, we used samples from a cohort of human livers to assess variation in CLZ oxidation pathways in relation to intrinsic CYP3A4 and CYP1A2 activities and the effects of the corresponding selective inhibitors ketoconazole (0.2 and 2 muM) and fluvoxamine (1 and 10 muM). Clozapine 136-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 29117640-6 2018 As the first study of 22 CYP3A4 protein variants in ibrutinib metabolism, these comprehensive data may help in the clinical assessment of the metabolism and elimination of ibrutinib and also offer a reference to the personalized treatment of ibrutinib in clinic. ibrutinib 52-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 29155491-6 2018 The CYP3A4-selective inhibitor ketoconazole (2 muM) impaired CLZ N-oxide formation in all 14 of the livers used in inhibition studies (>=50% inhibition) while the CYP1A2-selective inhibitor fluvoxamine (10 muM) decreased norCLZ formation in nine. Ketoconazole 31-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 29117640-6 2018 As the first study of 22 CYP3A4 protein variants in ibrutinib metabolism, these comprehensive data may help in the clinical assessment of the metabolism and elimination of ibrutinib and also offer a reference to the personalized treatment of ibrutinib in clinic. ibrutinib 172-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 29155491-6 2018 The CYP3A4-selective inhibitor ketoconazole (2 muM) impaired CLZ N-oxide formation in all 14 of the livers used in inhibition studies (>=50% inhibition) while the CYP1A2-selective inhibitor fluvoxamine (10 muM) decreased norCLZ formation in nine. clozapine N-oxide 61-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 29117640-6 2018 As the first study of 22 CYP3A4 protein variants in ibrutinib metabolism, these comprehensive data may help in the clinical assessment of the metabolism and elimination of ibrutinib and also offer a reference to the personalized treatment of ibrutinib in clinic. ibrutinib 172-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 29155491-6 2018 The CYP3A4-selective inhibitor ketoconazole (2 muM) impaired CLZ N-oxide formation in all 14 of the livers used in inhibition studies (>=50% inhibition) while the CYP1A2-selective inhibitor fluvoxamine (10 muM) decreased norCLZ formation in nine. Fluvoxamine 193-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 29421559-5 2018 The CYP3A4-NeoR-EGFP iPS cells were differentiated into hepatocyte-like cells, and then the hepatocyte-like cells were treated with neomycin to concentrate the hepatocyte-like cells which strongly express CYP3A4. Neomycin 132-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 29155491-6 2018 The CYP3A4-selective inhibitor ketoconazole (2 muM) impaired CLZ N-oxide formation in all 14 of the livers used in inhibition studies (>=50% inhibition) while the CYP1A2-selective inhibitor fluvoxamine (10 muM) decreased norCLZ formation in nine. norclz 224-230 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 29155491-7 2018 Ketoconazole effectively inhibited CLZ metabolism in five of seven livers that catalysed CYP3A4-dependent testosterone 6beta-hydroxylation at or above the median rate and in four other livers with lower intrinsic CYP3A4 activity. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 29155491-7 2018 Ketoconazole effectively inhibited CLZ metabolism in five of seven livers that catalysed CYP3A4-dependent testosterone 6beta-hydroxylation at or above the median rate and in four other livers with lower intrinsic CYP3A4 activity. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 213-219 29155491-7 2018 Ketoconazole effectively inhibited CLZ metabolism in five of seven livers that catalysed CYP3A4-dependent testosterone 6beta-hydroxylation at or above the median rate and in four other livers with lower intrinsic CYP3A4 activity. Clozapine 35-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 29155491-7 2018 Ketoconazole effectively inhibited CLZ metabolism in five of seven livers that catalysed CYP3A4-dependent testosterone 6beta-hydroxylation at or above the median rate and in four other livers with lower intrinsic CYP3A4 activity. Testosterone 106-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 29166542-9 2018 The result of molecular docking further confirmed that artocarpin interacted with CYP2D6, CYP2C8 and CYP3A4 through hydrogen bonds. Hydrogen 116-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 29421559-6 2018 After the neomycin treatment, the percentage of CYP3A4-positive cells was higher than 80%. Neomycin 10-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 29302721-0 2018 Impact of ritonavir dose and schedule on CYP3A inhibition and venetoclax clinical pharmacokinetics. Ritonavir 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 29440179-9 2018 Our results indicate that SP treatment significantly attenuated PXR-mediated induction of CYP3A4 reporter activity, as well as gene expression and enzyme activity. TFF2 protein, human 26-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 29255993-5 2018 Given their lipophilicity and CYP3A4 metabolic pathway, atorvastatin and simvastatin presented a higher prevalence of drug-drug interactions while fluvastatin presented the lowest prevalence. Atorvastatin 56-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 29255993-5 2018 Given their lipophilicity and CYP3A4 metabolic pathway, atorvastatin and simvastatin presented a higher prevalence of drug-drug interactions while fluvastatin presented the lowest prevalence. Simvastatin 73-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 29302721-3 2018 The study objective was to determine the effect of different dosage regimens of ritonavir, a strong CYP3A inhibitor, on the pharmacokinetics of venetoclax in 20 healthy subjects. Ritonavir 80-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 29255993-7 2018 The second most frequent contraindicated drug-drug interaction involved CYP3A4 interaction between atorvastatin or simvastatin with either posaconazole or erythromycin. Atorvastatin 99-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 29255993-7 2018 The second most frequent contraindicated drug-drug interaction involved CYP3A4 interaction between atorvastatin or simvastatin with either posaconazole or erythromycin. Simvastatin 115-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 29302721-8 2018 Administration of 50 mg ritonavir daily saturated CYP3A inhibition and completely inhibited the formation of the major venetoclax metabolite M27. Ritonavir 24-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 29255993-7 2018 The second most frequent contraindicated drug-drug interaction involved CYP3A4 interaction between atorvastatin or simvastatin with either posaconazole or erythromycin. posaconazole 139-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 29302721-9 2018 Time-dependent CYP3A inhibition with daily 50 mg ritonavir was offset by ritonavir CYP3A induction, resulting in a limited net increase in CYP3A inhibition with multiple doses. Ritonavir 49-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-20 29255993-7 2018 The second most frequent contraindicated drug-drug interaction involved CYP3A4 interaction between atorvastatin or simvastatin with either posaconazole or erythromycin. Erythromycin 155-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 29302721-9 2018 Time-dependent CYP3A inhibition with daily 50 mg ritonavir was offset by ritonavir CYP3A induction, resulting in a limited net increase in CYP3A inhibition with multiple doses. Ritonavir 73-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 29302721-9 2018 Time-dependent CYP3A inhibition with daily 50 mg ritonavir was offset by ritonavir CYP3A induction, resulting in a limited net increase in CYP3A inhibition with multiple doses. Ritonavir 73-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 29302721-10 2018 CONCLUSION: After completion of the dose ramp-up, venetoclax dose reductions of at least 75% are recommended when administered concomitantly with strong CYP3A inhibitors to maintain venetoclax exposures within the established therapeutic window for CLL treatment. venetoclax 50-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-158 28852909-1 2018 Aim Two studies investigated the effect of gastric acid reducing agents and strong inducers/inhibitors of CYP3A4 on the pharmacokinetics of alisertib, an investigational Aurora A kinase inhibitor, in patients with advanced malignancies. MLN 8237 140-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 29239000-2 2018 However, rivaroxaban dosing in patients with mild renal impairment taking concomitant moderate inhibitors of CYP3A and P-glycoprotein is not addressed. Rivaroxaban 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-114 29031874-8 2018 Rifampicin, a potent CYP3A4 inducer, is the first-line treatment of cholestatic pruritus. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 29193123-2 2018 Gefitinib is metabolized by CYP2D6 and CYP3A4. Gefitinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 29703388-4 2018 Putative mechanisms involve inhibitory effects of GT catechins at the intestinal level on influx transporters OATP1A2 or OATP2B1 for rosuvastatin, on CYP3A for sildenafil and on both CYP3A and the efflux transporter p-glycoprotein for tacrolimus. Catechin 53-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 183-188 28355970-2 2018 Sirolimus is metabolized by cytochrome P450 3A4 and is a substrate of the P-glycoprotein (P-gp) drug efflux pump. Sirolimus 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-47 29098603-0 2018 Development of Guanfacine Extended-Release Dosing Strategies in Children and Adolescents with ADHD Using a Physiologically Based Pharmacokinetic Model to Predict Drug-Drug Interactions with Moderate CYP3A4 Inhibitors or Inducers. Guanfacine 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 199-205 29247736-0 2018 Metabolic Pathway of Icotinib In Vitro: The Differential Roles of CYP3A4, CYP3A5, and CYP1A2 on Potential Pharmacokinetic Drug-Drug Interaction. icotinib 21-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 29098603-1 2018 BACKGROUND: Guanfacine extended-release (GXR) is an orally administered, non-stimulant treatment for children and adolescents with attention-deficit/hyperactivity disorder (ADHD) and is primarily metabolized by the 3A4 isozyme of cytochrome P450 (CYP3A4). Guanfacine 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 247-253 29098603-2 2018 The results of clinical pharmacokinetic (PK) studies indicate that guanfacine is sensitive to drug-drug interactions (DDIs) perpetrated by strong inhibitors and inducers of CYP3A4. Guanfacine 67-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 29098603-5 2018 The model was validated using clinical PK data for co-administration of GXR with ketoconazole (strong CYP3A4 inhibitor) or rifampicin (strong CYP3A4 inducer). Ketoconazole 81-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 28440343-0 2018 CYP3A4 genotype is associated with sildenafil concentrations in patients with heart failure with preserved ejection fraction. Sildenafil Citrate 35-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28440343-5 2018 Hence, CYP3A4 inferred phenotype is associated with peak sildenafil dose-adjusted concentrations in patients with HFpEF receiving high doses of sildenafil. Sildenafil Citrate 144-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 29098603-5 2018 The model was validated using clinical PK data for co-administration of GXR with ketoconazole (strong CYP3A4 inhibitor) or rifampicin (strong CYP3A4 inducer). Rifampin 123-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 28440343-3 2018 In the overall population, the CYP3A4 inferred phenotype appeared associated with the dose-adjusted peak concentrations of sildenafil at week 12 and week 24 (adjusted P=0.045 for repeated measures analysis), although this P-value did not meet our corrected significance threshold of 0.0167. Sildenafil Citrate 123-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 28440343-5 2018 Hence, CYP3A4 inferred phenotype is associated with peak sildenafil dose-adjusted concentrations in patients with HFpEF receiving high doses of sildenafil. Sildenafil Citrate 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 29098603-6 2018 RESULTS: Model predictions indicated that co-administration of GXR with the moderate CYP3A4 inhibitors erythromycin 500 mg three times a day or fluconazole 200 mg daily (q.d.) Erythromycin 103-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 29098603-8 2018 The moderate CYP3A4 inducer efavirenz 400 mg or 600 mg q.d. efavirenz 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 29470228-3 2018 The long half-life of amiodarone and its active metabolite in combination with the late onset and offset of cytochrome P4503A (CYP3A4) induction by rifampicin makes this a challenging drug-drug interaction to cope with in clinical practice. Rifampin 148-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 29629825-0 2018 CYP3A pharmacogenetic association with tacrolimus pharmacokinetics differs based on route of drug administration. Tacrolimus 39-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 29629825-4 2018 In addition to CYP3A5, other pharmacogenes associated with CYP3A activity, including CYP3A4, CYP3A7 and POR have also been identified as predictors of tacrolimus exposure. Tacrolimus 151-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-20 29629825-4 2018 In addition to CYP3A5, other pharmacogenes associated with CYP3A activity, including CYP3A4, CYP3A7 and POR have also been identified as predictors of tacrolimus exposure. Tacrolimus 151-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 29606886-10 2018 CYP3A isoenzyme group activity was evaluated by determining urinary concentration of endogenous substrate of the enzyme and its metabolite (6-beta-hydroxycortisol to cortisol ratio). 6 beta-hydroxycortisol 140-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 29610665-8 2018 Physiologically based pharmacokinetic modeling (PBPK) was used to simulate the clinical consequences of rifampin induction of CYP3A4- and UGT1A4-mediated midazolam metabolism. Rifampin 104-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 29610665-10 2018 Simulations accounting for simultaneous induction of both CYP3A4 and UGT1A4 predicted a ~10-fold decrease in parent midazolam exposure with only a ~2-fold decrease in midazolam N-glucuronide metabolite exposure. Midazolam 116-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 29610665-10 2018 Simulations accounting for simultaneous induction of both CYP3A4 and UGT1A4 predicted a ~10-fold decrease in parent midazolam exposure with only a ~2-fold decrease in midazolam N-glucuronide metabolite exposure. Midazolam 167-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 29610665-10 2018 Simulations accounting for simultaneous induction of both CYP3A4 and UGT1A4 predicted a ~10-fold decrease in parent midazolam exposure with only a ~2-fold decrease in midazolam N-glucuronide metabolite exposure. n-glucuronide 177-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 29606886-10 2018 CYP3A isoenzyme group activity was evaluated by determining urinary concentration of endogenous substrate of the enzyme and its metabolite (6-beta-hydroxycortisol to cortisol ratio). Hydrocortisone 154-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 29593874-2 2018 This risk is increased with concurrent use of medications that inhibit cytochrome p450-3A4 (CYP3A4), such as macrolide antibiotics. macrolide antibiotics 109-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-90 29382727-3 2018 Testosterone (TST) hydroxylation is the prototypical CYP3A4 reaction, displaying positive homotropic cooperativity with three binding sites. Testosterone 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 29547545-1 2018 While tacrolimus and everolimus have common metabolic pathways through CYP3A4/5, tacrolimus is metabolized solely by CYP3A4 in recipients with the CYP3A5*3/*3. Tacrolimus 6-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 29547545-1 2018 While tacrolimus and everolimus have common metabolic pathways through CYP3A4/5, tacrolimus is metabolized solely by CYP3A4 in recipients with the CYP3A5*3/*3. Everolimus 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 29547545-1 2018 While tacrolimus and everolimus have common metabolic pathways through CYP3A4/5, tacrolimus is metabolized solely by CYP3A4 in recipients with the CYP3A5*3/*3. Tacrolimus 81-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 29593874-2 2018 This risk is increased with concurrent use of medications that inhibit cytochrome p450-3A4 (CYP3A4), such as macrolide antibiotics. macrolide antibiotics 109-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 29285606-10 2018 On the transcript level, highest induction up to 5.6-fold was observed for CYP3A4 by tamoxifen, (Z)-4-hydroxytamoxifen, tamoxifen bisphenol and (E)-metabolite E. Estrogen-like tamoxifen metabolites are formed in CYP-dependent reactions and are further metabolized by glucuronidation. Tamoxifen 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 29502215-0 2018 Identification of a less toxic vinca alkaloid derivative for use as a chemotherapeutic agent, based on in silico structural insights and metabolic interactions with CYP3A4 and CYP3A5. Vinca Alkaloids 31-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 29502215-2 2018 Cytochrome P450 3A5 (CYP3A5) is 9- to 14-fold more efficient at clearing vincristine than cytochrome P450 3A4 (CYP3A4) is. Vincristine 73-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-109 29502215-2 2018 Cytochrome P450 3A5 (CYP3A5) is 9- to 14-fold more efficient at clearing vincristine than cytochrome P450 3A4 (CYP3A4) is. Vincristine 73-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 29502215-8 2018 The results indicate that the addition of dimethylurea at the C20" position in vincristine may increase its binding affinity and lead to enhanced interactions with the less polymorphic CYP3A4 rather than CYP3A5. 1,3-dimethylurea 42-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 29502215-8 2018 The results indicate that the addition of dimethylurea at the C20" position in vincristine may increase its binding affinity and lead to enhanced interactions with the less polymorphic CYP3A4 rather than CYP3A5. Vincristine 79-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 29502215-10 2018 Graphical Abstract Proposed modification of Vinca alkaloid derivatives to decrease the neurotoxicity level in cancer patients exhibiting CYP3A4 gene rather than polymorphic CYP3A5 gene. Vinca Alkaloids 44-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 26910057-4 2018 Ivabradine is extensively metabolized by cytochrome P450 3A4, and its metabolism is affected by inducers and inhibitors of the 3A4 enzyme. Ivabradine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-60 29285606-10 2018 On the transcript level, highest induction up to 5.6-fold was observed for CYP3A4 by tamoxifen, (Z)-4-hydroxytamoxifen, tamoxifen bisphenol and (E)-metabolite E. Estrogen-like tamoxifen metabolites are formed in CYP-dependent reactions and are further metabolized by glucuronidation. hydroxytamoxifen 96-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 29285606-10 2018 On the transcript level, highest induction up to 5.6-fold was observed for CYP3A4 by tamoxifen, (Z)-4-hydroxytamoxifen, tamoxifen bisphenol and (E)-metabolite E. Estrogen-like tamoxifen metabolites are formed in CYP-dependent reactions and are further metabolized by glucuronidation. 1,1-bis(4-hydroxyphenyl)-2-phenylbut-1-ene 120-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 29285606-10 2018 On the transcript level, highest induction up to 5.6-fold was observed for CYP3A4 by tamoxifen, (Z)-4-hydroxytamoxifen, tamoxifen bisphenol and (E)-metabolite E. Estrogen-like tamoxifen metabolites are formed in CYP-dependent reactions and are further metabolized by glucuronidation. Tamoxifen 109-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 28945011-1 2018 Schisantherin A and schisandrin A, the most abundant active ingredients of Wuzhi capsule, are known to inhibit tacrolimus metabolism by inhibiting CYP3A4/5. schizandrer A 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 29451681-0 2018 Verification of a physiologically based pharmacokinetic model of ritonavir to estimate drug-drug interaction potential of CYP3A4 substrates. Ritonavir 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 28945011-1 2018 Schisantherin A and schisandrin A, the most abundant active ingredients of Wuzhi capsule, are known to inhibit tacrolimus metabolism by inhibiting CYP3A4/5. schizandrin A 20-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 28945011-1 2018 Schisantherin A and schisandrin A, the most abundant active ingredients of Wuzhi capsule, are known to inhibit tacrolimus metabolism by inhibiting CYP3A4/5. Tacrolimus 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 28945011-3 2018 Firstly, the inhibition mechanism of schisantherin A and schisandrin A on CYP3A4/5 was investigated. schizandrer A 37-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 28945011-3 2018 Firstly, the inhibition mechanism of schisantherin A and schisandrin A on CYP3A4/5 was investigated. schizandrin A 57-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 29451681-1 2018 Ritonavir is one of several ketoconazole alternatives used to evaluate strong CYP3A4 inhibition potential in clinical drug-drug interaction (DDI) studies. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 29451681-2 2018 In this study, four physiologically based pharmacokinetic (PBPK) models of ritonavir as an in vivo time-dependent inhibitor of CYP3A4 were created and verified for oral doses of 20, 50, 100 and 200 mg using the fraction absorbed (Fa ) and oral clearance (CLoral ) values reported in the literature, because transporter and CYP enzyme reaction phenotyping data were not available. Ritonavir 75-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 29451681-3 2018 The models were used subsequently to predict and compare the magnitude of the AUC increase in nine reference DDI studies evaluating the effect of ritonavir at steady-state on midazolam (CYP3A4 substrate) exposure. Ritonavir 146-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 186-192 29451681-3 2018 The models were used subsequently to predict and compare the magnitude of the AUC increase in nine reference DDI studies evaluating the effect of ritonavir at steady-state on midazolam (CYP3A4 substrate) exposure. Midazolam 175-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 186-192 29451681-5 2018 Simulations of the hepatic and gut CYP3A4 abundance after multiple oral dosing of ritonavir indicated that a 3-day treatment with ritonavir 100 mg twice daily is sufficient to reach maximal CYP3A4 inhibition and subsequent systemic exposure increase of a CYP3A4 substrate, resulting in the reliable estimation of fm,CYP3A4 . Ritonavir 130-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 29451681-5 2018 Simulations of the hepatic and gut CYP3A4 abundance after multiple oral dosing of ritonavir indicated that a 3-day treatment with ritonavir 100 mg twice daily is sufficient to reach maximal CYP3A4 inhibition and subsequent systemic exposure increase of a CYP3A4 substrate, resulting in the reliable estimation of fm,CYP3A4 . Ritonavir 130-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-196 29451681-5 2018 Simulations of the hepatic and gut CYP3A4 abundance after multiple oral dosing of ritonavir indicated that a 3-day treatment with ritonavir 100 mg twice daily is sufficient to reach maximal CYP3A4 inhibition and subsequent systemic exposure increase of a CYP3A4 substrate, resulting in the reliable estimation of fm,CYP3A4 . Ritonavir 130-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-196 29451681-5 2018 Simulations of the hepatic and gut CYP3A4 abundance after multiple oral dosing of ritonavir indicated that a 3-day treatment with ritonavir 100 mg twice daily is sufficient to reach maximal CYP3A4 inhibition and subsequent systemic exposure increase of a CYP3A4 substrate, resulting in the reliable estimation of fm,CYP3A4 . Ritonavir 130-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-196 29105855-0 2018 Dicloxacillin induces CYP2C19, CYP2C9 and CYP3A4 in vivo and in vitro. Dicloxacillin 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 29105855-7 2018 Additionally, other relevant pharmacokinetic parameters were affected, indicating the induction of CYP2C- and CYP3A4-mediated metabolism by dicloxacillin. Dicloxacillin 140-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 29105855-9 2018 CONCLUSIONS: Dicloxacillin is an inducer of CYP2C- and CYP3A-mediated drug metabolism, and we recommend caution when prescribing dicloxacillin to users of drugs with a narrow therapeutic window. Dicloxacillin 13-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 29105855-9 2018 CONCLUSIONS: Dicloxacillin is an inducer of CYP2C- and CYP3A-mediated drug metabolism, and we recommend caution when prescribing dicloxacillin to users of drugs with a narrow therapeutic window. Dicloxacillin 129-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 29178272-8 2018 CONCLUSIONS: These data support consideration of the risk of clinically relevant metabolic drug-drug interactions perpetrated by modafinil when this drug is co-administered with drugs that are primarily cleared by CYP2C19 (single modafinil dose or steady state modafinil dosing) or CYP3A4 (steady state modafinil dosing only) catalysed metabolic pathways. Modafinil 129-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 282-288 29223619-2 2018 CYP3A4 has a major role in the oxidation of sorafenib to its N-oxide and N-hydroxymethyl metabolites and also acts in concert with CYP2C8 to mediate imatinib N-demethylation. Sorafenib 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29474740-5 2018 In vitro studies revealed that TAK-272 was mainly metabolized by CYP3A4/5 in humans, and it was a P-glycoprotein substrate. imarikiren hydrochloride 31-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 29368050-9 2018 CONCLUSION: In patients with solid tumors, multiple doses of posaconazole, a strong CYP3A4 inhibitor, minimally affected idasanutlin PK and PD without clinical significance. posaconazole 61-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 29223619-2 2018 CYP3A4 has a major role in the oxidation of sorafenib to its N-oxide and N-hydroxymethyl metabolites and also acts in concert with CYP2C8 to mediate imatinib N-demethylation. n-oxide 61-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29223619-2 2018 CYP3A4 has a major role in the oxidation of sorafenib to its N-oxide and N-hydroxymethyl metabolites and also acts in concert with CYP2C8 to mediate imatinib N-demethylation. imatinib n 149-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29223619-9 2018 CYP3A4 has the major role in the intrinsic clearance of sorafenib but plays a secondary role to CYP2C8 in the intrinsic clearance of imatinib. Sorafenib 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29223619-9 2018 CYP3A4 has the major role in the intrinsic clearance of sorafenib but plays a secondary role to CYP2C8 in the intrinsic clearance of imatinib. Imatinib Mesylate 133-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29223619-11 2018 This information could be adapted in individualized approaches such as in vivo CYP3A4 phenotyping to optimize sorafenib safety and efficacy in cancer patients with liver dysfunction. Sorafenib 110-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 29570971-9 2018 Phenotyping also highlighted the relevance of a minor metabolic pathway for venlafaxine (CYP3A4). Venlafaxine Hydrochloride 76-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 29363349-2 2018 Fentanyl (metabolized by Cytochrome P450 3A4) and morphine (glucuronidated by UDP-glucuronosyltransferase-2B7) served as model drugs to provide insight in maturation patterns of these enzymes and provide understanding of the impact of non-maturational factors to optimize dosing in infants. Fentanyl 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-44 28278026-0 2018 7,8-benzoflavone binding to human cytochrome P450 3A4 reveals complex fluorescence quenching, suggesting binding at multiple protein sites. alpha-naphthoflavone 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-53 28967981-2 2018 In vitro data indicate that cytochrome P450 (CYP) 3A4 is the primary CYP isoenzyme involved in the metabolism of apatinib. apatinib 113-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-53 28967981-6 2018 In summary, a strong CYP3A4 inducer (rifampin) had a strong effect (>5-fold) on the clinical pharmacokinetics of apatinib, whereas a strong CYP3A inhibitor (itraconazole 100 mg once a day) had a weak effect (1.25- to 2-fold). Rifampin 37-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 28967981-6 2018 In summary, a strong CYP3A4 inducer (rifampin) had a strong effect (>5-fold) on the clinical pharmacokinetics of apatinib, whereas a strong CYP3A inhibitor (itraconazole 100 mg once a day) had a weak effect (1.25- to 2-fold). Rifampin 37-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-26 28967981-6 2018 In summary, a strong CYP3A4 inducer (rifampin) had a strong effect (>5-fold) on the clinical pharmacokinetics of apatinib, whereas a strong CYP3A inhibitor (itraconazole 100 mg once a day) had a weak effect (1.25- to 2-fold). apatinib 113-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 28967981-6 2018 In summary, a strong CYP3A4 inducer (rifampin) had a strong effect (>5-fold) on the clinical pharmacokinetics of apatinib, whereas a strong CYP3A inhibitor (itraconazole 100 mg once a day) had a weak effect (1.25- to 2-fold). apatinib 113-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-26 29102550-0 2018 A Physiologically Based Pharmacokinetic Modeling Approach to Predict Drug-Drug Interactions of Buprenorphine After Subcutaneous Administration of CAM2038 With Perpetrators of CYP3A4. Buprenorphine 95-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 29414036-0 2018 Theoretical Insights into Imidazolidine Oxidation of Imidacloprid by Cytochrome P450 3A4. Imidazolidines 26-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-88 29414036-0 2018 Theoretical Insights into Imidazolidine Oxidation of Imidacloprid by Cytochrome P450 3A4. imidacloprid 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-88 29414036-1 2018 The metabolic mechanisms for imidazolidine oxidation of imidacloprid (IMI) by cytochrome P450 3A4 (CYP3A4) have been investigated using quantum mechanical/molecular mechanical (QM/MM) calculations. Imidazolidines 29-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-97 29414036-1 2018 The metabolic mechanisms for imidazolidine oxidation of imidacloprid (IMI) by cytochrome P450 3A4 (CYP3A4) have been investigated using quantum mechanical/molecular mechanical (QM/MM) calculations. Imidazolidines 29-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 29414036-1 2018 The metabolic mechanisms for imidazolidine oxidation of imidacloprid (IMI) by cytochrome P450 3A4 (CYP3A4) have been investigated using quantum mechanical/molecular mechanical (QM/MM) calculations. imidacloprid 56-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-97 29414036-1 2018 The metabolic mechanisms for imidazolidine oxidation of imidacloprid (IMI) by cytochrome P450 3A4 (CYP3A4) have been investigated using quantum mechanical/molecular mechanical (QM/MM) calculations. imidacloprid 56-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 29414036-1 2018 The metabolic mechanisms for imidazolidine oxidation of imidacloprid (IMI) by cytochrome P450 3A4 (CYP3A4) have been investigated using quantum mechanical/molecular mechanical (QM/MM) calculations. imidacloprid 70-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-97 29414036-1 2018 The metabolic mechanisms for imidazolidine oxidation of imidacloprid (IMI) by cytochrome P450 3A4 (CYP3A4) have been investigated using quantum mechanical/molecular mechanical (QM/MM) calculations. imidacloprid 70-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 29414036-5 2018 Arg192 plays a major role in the binding of CYP3A4 with IMI based on its polarity and the hydrogen bond between the H atom in Arg192 side chain and the nitryl O atom of IMI. Hydrogen 90-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 29102550-4 2018 The strong CYP3A4 inhibitor ketoconazole was predicted to increase the buprenorphine exposure by 35% for the Q1W formulation and 34% for Q4W formulation, respectively. Ketoconazole 28-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 29102550-4 2018 The strong CYP3A4 inhibitor ketoconazole was predicted to increase the buprenorphine exposure by 35% for the Q1W formulation and 34% for Q4W formulation, respectively. Buprenorphine 71-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 29102550-5 2018 Also, the strong CYP3A4 inducer rifampin was predicted to decrease the buprenorphine exposure by 26% for both the Q1W and Q4W formulations. Buprenorphine 71-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 28316274-0 2018 Co-treatment with indole-3-carbinol and resveratrol modify porcine CYP1A and CYP3A activities and expression. indole-3-carbinol 18-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 29469606-0 2018 Detection of a rare CYP3A4 variant in a transplant patient characterized by a tacrolimus poor metabolizer phenotype. Tacrolimus 78-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 28316274-0 2018 Co-treatment with indole-3-carbinol and resveratrol modify porcine CYP1A and CYP3A activities and expression. Resveratrol 40-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 29054579-0 2018 Relevance of the CYP3A4*20 variant as a predictor of paclitaxel-induced neuropathy in the Spanish population. Paclitaxel 53-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 29440136-3 2018 Rifampicin is a common inducer of CYP3A4. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 28287022-8 2018 Recombinant cytochrome P450s (CYPs) screening showed that CYP3A4 and CYP3A5 were the primary enzymes contributing to osthole metabolism. osthol 117-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 29320849-5 2018 Finally, as an illustrative example, the relative contribution of the three primary oxidation routes of tamoxifen was rationalized through energetic barriers obtained from density functional calculations and docking experiments involving CYP3A4 and CYP2D6 isoforms. Tamoxifen 104-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 238-244 29129847-2 2018 N-dechloroethylation of CP mediated by the enzyme CYP3A4 yields nephrotoxic and neurotoxic chloroacetaldehyde (CAA) in equimolar amount to DECP. Nitrogen 0-1 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 29381358-3 2018 To this end, we have successfully found that morpholine carboxyl analogues with comparable anti-HBV activities to that of GLS4 showed decreased hERG activities, but they displayed strong CYP3A4 induction in a concentration-dependent manner, except for morpholine propionic acid analogues. morpholine 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 29129847-2 2018 N-dechloroethylation of CP mediated by the enzyme CYP3A4 yields nephrotoxic and neurotoxic chloroacetaldehyde (CAA) in equimolar amount to DECP. chloroacetaldehyde 91-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 29200287-0 2018 Drug-Drug Interactions between Atorvastatin and Dronedarone Mediated by Monomeric CYP3A4. Atorvastatin 31-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 29129847-2 2018 N-dechloroethylation of CP mediated by the enzyme CYP3A4 yields nephrotoxic and neurotoxic chloroacetaldehyde (CAA) in equimolar amount to DECP. chloroacetaldehyde 111-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 29200287-0 2018 Drug-Drug Interactions between Atorvastatin and Dronedarone Mediated by Monomeric CYP3A4. Dronedarone 48-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 29129847-2 2018 N-dechloroethylation of CP mediated by the enzyme CYP3A4 yields nephrotoxic and neurotoxic chloroacetaldehyde (CAA) in equimolar amount to DECP. 2-dechloroethylcyclophosphamide 139-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 29129847-5 2018 Our in vitro human liver microsome modeling approach suggested that KTZ inhibited CYP3A4 activity and then decreased DECP exposure. Ketoconazole 68-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 29129847-8 2018 Our results suggested that combination usage of a CYP3A4 inhibitor like KTZ may decrease CAA exposure and thus intervene against CAA-induced adverse effects in CP clinical treatment. Ketoconazole 72-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 29251928-5 2018 Selected compounds were shown to reverse paclitaxel resistance in HEK293 cells overexpressing P-gp and were selective toward P-gp over CYP3A4. Paclitaxel 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 29129847-8 2018 Our results suggested that combination usage of a CYP3A4 inhibitor like KTZ may decrease CAA exposure and thus intervene against CAA-induced adverse effects in CP clinical treatment. chloroacetaldehyde 89-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 29129847-8 2018 Our results suggested that combination usage of a CYP3A4 inhibitor like KTZ may decrease CAA exposure and thus intervene against CAA-induced adverse effects in CP clinical treatment. chloroacetaldehyde 129-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 28786218-0 2018 Response to "Impact of CYP3A4 Genotype on Voriconazole Exposure: New Insights Into the Contribution of CYP3A4*22 to Metabolism of Voriconazole". Voriconazole 42-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 29072785-0 2018 Predicting CYP3A-mediated midazolam metabolism in critically ill neonates, infants, children and adults with inflammation and organ failure. Midazolam 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-16 28786218-0 2018 Response to "Impact of CYP3A4 Genotype on Voriconazole Exposure: New Insights Into the Contribution of CYP3A4*22 to Metabolism of Voriconazole". Voriconazole 42-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 29063606-5 2018 Although CP studies are limited, meta-analysis-based reduction in CYP1A2, CYP2C19, and CYP3A4 enzyme abundances in a virtual oncology population effectively captures CP-PK for caffeine, theophylline, midazolam, simvastatin, omeprazole, and a subset of oncology compounds. Caffeine 176-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 29063606-5 2018 Although CP studies are limited, meta-analysis-based reduction in CYP1A2, CYP2C19, and CYP3A4 enzyme abundances in a virtual oncology population effectively captures CP-PK for caffeine, theophylline, midazolam, simvastatin, omeprazole, and a subset of oncology compounds. Theophylline 186-198 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 29063606-5 2018 Although CP studies are limited, meta-analysis-based reduction in CYP1A2, CYP2C19, and CYP3A4 enzyme abundances in a virtual oncology population effectively captures CP-PK for caffeine, theophylline, midazolam, simvastatin, omeprazole, and a subset of oncology compounds. Midazolam 200-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 29063606-5 2018 Although CP studies are limited, meta-analysis-based reduction in CYP1A2, CYP2C19, and CYP3A4 enzyme abundances in a virtual oncology population effectively captures CP-PK for caffeine, theophylline, midazolam, simvastatin, omeprazole, and a subset of oncology compounds. Simvastatin 211-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 29063606-5 2018 Although CP studies are limited, meta-analysis-based reduction in CYP1A2, CYP2C19, and CYP3A4 enzyme abundances in a virtual oncology population effectively captures CP-PK for caffeine, theophylline, midazolam, simvastatin, omeprazole, and a subset of oncology compounds. Omeprazole 224-234 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 28786218-0 2018 Response to "Impact of CYP3A4 Genotype on Voriconazole Exposure: New Insights Into the Contribution of CYP3A4*22 to Metabolism of Voriconazole". Voriconazole 130-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 28786218-0 2018 Response to "Impact of CYP3A4 Genotype on Voriconazole Exposure: New Insights Into the Contribution of CYP3A4*22 to Metabolism of Voriconazole". Voriconazole 130-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 28786228-0 2018 Impact of CYP3A4 Genotype on Voriconazole Exposure. Voriconazole 29-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 29117990-0 2018 Simultaneous Physiologically Based Pharmacokinetic (PBPK) Modeling of Parent and Active Metabolites to Investigate Complex CYP3A4 Drug-Drug Interaction Potential: A Case Example of Midostaurin. midostaurin 181-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 29338933-8 2018 The estimated in vivo Ki of ketoconazole for hepatic CYP3A4 (6.64 ng/mL) was consistent with the reported values. Ketoconazole 28-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 28543042-8 2018 Changes in CYP3A activity might be due to alterations in bile acid signaling. Bile Acids and Salts 57-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-16 29117990-3 2018 In vitro and clinical drug-drug interaction (DDI) studies indicated that midostaurin and its metabolites are substrates, reversible and time-dependent inhibitors, and inducers of CYP3A4. midostaurin 73-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 29117990-7 2018 The simulated midazolam area under the curve ratio of 0.54 and an accompanying observed 1.9-fold increase in the CYP3A4 activity of biomarker 4beta-hydroxycholesterol indicated a weak-to-moderate CYP3A4 induction by midostaurin and its metabolites at steady state in patients with advSM. Midazolam 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 29117990-7 2018 The simulated midazolam area under the curve ratio of 0.54 and an accompanying observed 1.9-fold increase in the CYP3A4 activity of biomarker 4beta-hydroxycholesterol indicated a weak-to-moderate CYP3A4 induction by midostaurin and its metabolites at steady state in patients with advSM. Midazolam 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 196-202 29117990-7 2018 The simulated midazolam area under the curve ratio of 0.54 and an accompanying observed 1.9-fold increase in the CYP3A4 activity of biomarker 4beta-hydroxycholesterol indicated a weak-to-moderate CYP3A4 induction by midostaurin and its metabolites at steady state in patients with advSM. cholest-5-ene-3,4-diol 142-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 29117990-7 2018 The simulated midazolam area under the curve ratio of 0.54 and an accompanying observed 1.9-fold increase in the CYP3A4 activity of biomarker 4beta-hydroxycholesterol indicated a weak-to-moderate CYP3A4 induction by midostaurin and its metabolites at steady state in patients with advSM. cholest-5-ene-3,4-diol 142-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 196-202 29117990-7 2018 The simulated midazolam area under the curve ratio of 0.54 and an accompanying observed 1.9-fold increase in the CYP3A4 activity of biomarker 4beta-hydroxycholesterol indicated a weak-to-moderate CYP3A4 induction by midostaurin and its metabolites at steady state in patients with advSM. midostaurin 216-227 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 29117990-7 2018 The simulated midazolam area under the curve ratio of 0.54 and an accompanying observed 1.9-fold increase in the CYP3A4 activity of biomarker 4beta-hydroxycholesterol indicated a weak-to-moderate CYP3A4 induction by midostaurin and its metabolites at steady state in patients with advSM. midostaurin 216-227 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 196-202 29117990-9 2018 Furthermore, endogenous biomarker data enabled evaluation of the net effect of midostaurin and its metabolites on CYP3A4 activity at steady state and increased confidence in DDI predictions. midostaurin 79-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 28782144-7 2018 The ADIs can be explained by VDS accumulation owing to inherent loss of CYP3A5 (*3/*3) function, and inhibition of CYP3A4 activity by itraconazole. Itraconazole 134-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 29305929-5 2018 The production of 11-hydroxylauric acid was mediated by CYP2E1, CYP2C9, CYP2B6, CYP1A2, CYP3A4, and CYP4A11. 11-hydroxydodecanoic acid 18-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 29256966-0 2018 Influence of donor liver CYP3A4*20 loss-of-function genotype on tacrolimus pharmacokinetics in transplanted patients. Tacrolimus 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 29134244-4 2018 Diosmin-mediated altered CYP3A enzyme activity in human and rat liver microsomes was examined using CYP3A dependent erythromycin N-demethylase assay. Diosmin 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-30 29134244-6 2018 The CYP3A enzyme activity in human and rat liver microsomes was significantly (p < 0.05) decreased by diosmin when compared to control. Diosmin 105-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-9 28800141-0 2018 Effects of Strong CYP3A Inhibition and Induction on the Pharmacokinetics of Ixazomib, an Oral Proteasome Inhibitor: Results of Drug-Drug Interaction Studies in Patients With Advanced Solid Tumors or Lymphoma and a Physiologically Based Pharmacokinetic Analysis. ixazomib 76-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-23 28800141-2 2018 However, at higher than clinical concentrations, ixazomib was metabolized by multiple CYP isoforms, with the estimated relative contribution being highest for CYP3A at 42%. ixazomib 49-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-164 28800141-3 2018 This multiarm phase 1 study (Clinicaltrials.gov identifier: NCT01454076) investigated the effect of the strong CYP3A inhibitors ketoconazole and clarithromycin and the strong CYP3A inducer rifampin on the pharmacokinetics of ixazomib. Rifampin 189-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-180 28800141-9 2018 The clinical drug-drug interaction study results were reconciled well by a physiologically based pharmacokinetic model that incorporated a minor contribution of CYP3A to overall ixazomib clearance and quantitatively considered the strength of induction of CYP3A and intestinal P-glycoprotein by rifampin. ixazomib 178-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-166 28800141-10 2018 On the basis of these study results, the ixazomib prescribing information recommends that patients should avoid concomitant administration of strong CYP3A inducers with ixazomib. ixazomib 41-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-154 28800141-10 2018 On the basis of these study results, the ixazomib prescribing information recommends that patients should avoid concomitant administration of strong CYP3A inducers with ixazomib. ixazomib 169-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-154 29362093-7 2018 A molecular dynamics analysis of the Arg376 > Lys mutation based on the CYP3A4 (a human CYP450) protein structure found that it was responsible for the increase in axis length toward the heme (active site), which is critically important for biological activity and ligand binding. Lysine 49-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 29362093-7 2018 A molecular dynamics analysis of the Arg376 > Lys mutation based on the CYP3A4 (a human CYP450) protein structure found that it was responsible for the increase in axis length toward the heme (active site), which is critically important for biological activity and ligand binding. Heme 190-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 29095797-5 2018 RESULTS: A patient with frontal lobe epilepsy and mild renal impairment [creatinine clearance (CCr): 67.7 mL/min] was taking phenytoin and 3 CYP3A4 substrates (topiramate, clobazam, and perampanel). Topiramate 160-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 29256966-2 2018 Here, we report the effect of the CYP3A4*20 frameshift allele in two Spanish liver transplant patients treated with tacrolimus. Tacrolimus 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 29256966-10 2018 CONCLUSION: This first description of CYP3A4*20 null genotype in liver-transplanted patients, supports the relevance of CYP3A genotyping in tacrolimus therapy. Tacrolimus 140-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 29256966-10 2018 CONCLUSION: This first description of CYP3A4*20 null genotype in liver-transplanted patients, supports the relevance of CYP3A genotyping in tacrolimus therapy. Tacrolimus 140-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 29310431-0 2018 Binding Specificity Determines the Cytochrome P450 3A4 Mediated Enantioselective Metabolism of Metconazole. metconazole 95-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-54 29310431-3 2018 We developed a stepwise-restrained-molecular-dynamics (MD) method to model human CYP3A4 in a complex with cis-metconazole (MEZ) isomers and performed conventional MD simulations with a total simulation time of 2.2 mus to probe the molecular interactions. metconazole 106-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 29310431-3 2018 We developed a stepwise-restrained-molecular-dynamics (MD) method to model human CYP3A4 in a complex with cis-metconazole (MEZ) isomers and performed conventional MD simulations with a total simulation time of 2.2 mus to probe the molecular interactions. metconazole 123-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 29310431-5 2018 CYP3A4 preferably metabolizes cis-RS MEZ over the cis-SR isomer, with the resultant enantiomer fraction for cis-MEZ increasing rapidly from 0.5 to 0.82. cis-rs mez 30-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29310431-5 2018 CYP3A4 preferably metabolizes cis-RS MEZ over the cis-SR isomer, with the resultant enantiomer fraction for cis-MEZ increasing rapidly from 0.5 to 0.82. cis-mez 108-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29310431-7 2018 Free-energy-perturbation calculations indicate that unfavorable van der Waals interactions between the cis-MEZ isomers and the CYP3A4 binding pocket predominantly contribute to their binding-affinity differences. cis-mez 103-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 29310431-8 2018 These results demonstrate that binding specificity determines the cytochrome P450 3A4 mediated enantioselective metabolism of cis-MEZ. cis-mez 126-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-85 29304859-2 2018 Based on in vitro data, a two-way pharmacokinetic interaction was hypothesized for KAF156 use in combination with piperaquine (PPQ) as both drugs are CYP3A4 substrates and inhibitors. piperaquine 114-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 29232137-0 2018 Inhibition of Human CYP3A4 by Rationally Designed Ritonavir-Like Compounds: Impact and Interplay of the Side Group Functionalities. Ritonavir 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 29232137-1 2018 Structure-function relationships of nine rationally designed ritonavir-like compounds were investigated to better understand the ligand binding and inhibitory mechanism in human drug-metabolizing cytochrome P450 3A4 (CYP3A4). Ritonavir 61-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 196-215 29232137-1 2018 Structure-function relationships of nine rationally designed ritonavir-like compounds were investigated to better understand the ligand binding and inhibitory mechanism in human drug-metabolizing cytochrome P450 3A4 (CYP3A4). Ritonavir 61-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-223 29801578-4 2018 For calcineurin inhibitors like cyclosporine and in particular tacrolimus however, cytochrome P450 3A4 and 3A5 variants were found to significantly affect the pharmacokinetics. Cyclosporine 32-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-102 29801578-4 2018 For calcineurin inhibitors like cyclosporine and in particular tacrolimus however, cytochrome P450 3A4 and 3A5 variants were found to significantly affect the pharmacokinetics. Tacrolimus 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-102 29314710-8 2018 Second, enzyme kinetic studies showed that the initial metabolic steps were formed by cytochrome P450 isoforms (CYP) CYP1A2, CYP2B6, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 resulting in pyrrolidine, thiophene or alkyl hydroxy metabolites depending on the length of the alkyl chain. pyrrolidine 182-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 29314710-8 2018 Second, enzyme kinetic studies showed that the initial metabolic steps were formed by cytochrome P450 isoforms (CYP) CYP1A2, CYP2B6, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 resulting in pyrrolidine, thiophene or alkyl hydroxy metabolites depending on the length of the alkyl chain. Thiophenes 195-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 29304859-2 2018 Based on in vitro data, a two-way pharmacokinetic interaction was hypothesized for KAF156 use in combination with piperaquine (PPQ) as both drugs are CYP3A4 substrates and inhibitors. piperaquine 127-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 29110626-10 2018 Sildenafil may also extend the half-life of docetaxel and some small molecule inhibitors used in lung cancer treatment by acting as an inhibitor of CYP3A4. Sildenafil Citrate 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 29055041-3 2018 It was hypothesized that cytochrome P450 (CYP)3A inhibition of the small intestine by voriconazole and P-glycoprotein (P-gp) inhibition of the small intestine by risperidone exerted a synergistic effect on the bioavailability of tacrolimus. Voriconazole 86-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-48 28833380-8 2018 Food effects, comedication with itraconazole [a cytochrome P450 (CYP) 3A4 inhibitor], fluconazole (a CYP2C19 inhibitor) and rifampicin (a CYP3A4 inducer) and formulation effects were incorporated into the base model a priori. Rifampin 124-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 29055041-3 2018 It was hypothesized that cytochrome P450 (CYP)3A inhibition of the small intestine by voriconazole and P-glycoprotein (P-gp) inhibition of the small intestine by risperidone exerted a synergistic effect on the bioavailability of tacrolimus. Risperidone 162-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-48 28834279-13 2018 One micromolar ketoconazole (CYP3A inhibitor) showed an inhibitory effect on the rates of norendoxifen formation by 45%, but 1 mum quinidine (CYP2D6 inhibitor) does not show any inhibitory effect. Ketoconazole 15-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 28834279-13 2018 One micromolar ketoconazole (CYP3A inhibitor) showed an inhibitory effect on the rates of norendoxifen formation by 45%, but 1 mum quinidine (CYP2D6 inhibitor) does not show any inhibitory effect. N,N-didesmethyl-4-hydroxytamoxifen 90-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 30347615-5 2018 METHODS: CYP1A2 and CYP3A4 were induced by omeprazole and rifampicin, respectively. Omeprazole 43-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 30347615-5 2018 METHODS: CYP1A2 and CYP3A4 were induced by omeprazole and rifampicin, respectively. Rifampin 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 30156148-12 2018 Additionally, genetic CYP3A4 variation (e.g., CYP3A4*22) is also associated with interindividual variability of exposure level to tacrolimus. Tacrolimus 130-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 28322152-8 2018 Also, GM was metabolized by various CYP isoforms, mainly CYP3A4. geissoschizine methylether 6-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 30251601-0 2018 Influence of CYP3A and ABCB1 Single Nucleotide Polymorphisms on the Pharmacokinetics/Pharmacodynamics of Tacrolimus in Pediatric Patients. Tacrolimus 105-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-18 30251601-4 2018 This article focuses on the effects of ABCB1 and CYP3A SNPs on tacrolimus in children who are undergoing organ transplantations. Tacrolimus 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 30156148-12 2018 Additionally, genetic CYP3A4 variation (e.g., CYP3A4*22) is also associated with interindividual variability of exposure level to tacrolimus. Tacrolimus 130-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 29237391-8 2018 Interestingly, elacridar, a P-gp inhibitor, suppressed metabolite formation in enterocytes for loperamide, a substrate of CYP3A4 and P-gp, suggesting that enterocytes in suspension do not have active P-gp efflux functions, and the suppression of metabolism in enterocytes is probably caused by inhibition of CYP3A4/5 by elacridar. Loperamide 95-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 29237391-3 2018 METHODS: It was found that, for CYP3A4/5 substrates such as midazolam, amprenavir and loperamide, in vitro metabolic clearance is generally lower in enterocytes compared to that of hepatocytes, which is consistent with the relative abundance of the enzyme between the intestine and liver. Midazolam 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 29237391-3 2018 METHODS: It was found that, for CYP3A4/5 substrates such as midazolam, amprenavir and loperamide, in vitro metabolic clearance is generally lower in enterocytes compared to that of hepatocytes, which is consistent with the relative abundance of the enzyme between the intestine and liver. amprenavir 71-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 29237391-3 2018 METHODS: It was found that, for CYP3A4/5 substrates such as midazolam, amprenavir and loperamide, in vitro metabolic clearance is generally lower in enterocytes compared to that of hepatocytes, which is consistent with the relative abundance of the enzyme between the intestine and liver. Loperamide 86-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 29237391-7 2018 As expected, ketoconazole inhibited CYP3A4/5-mediated metabolite formation in enterocytes for midazolam, amprenavir and loperamide, suggesting that cryopreserved enterocytes may be useful in determining intestinal CYP3A inhibition parameters. Ketoconazole 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 29237391-7 2018 As expected, ketoconazole inhibited CYP3A4/5-mediated metabolite formation in enterocytes for midazolam, amprenavir and loperamide, suggesting that cryopreserved enterocytes may be useful in determining intestinal CYP3A inhibition parameters. Midazolam 94-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 29237391-7 2018 As expected, ketoconazole inhibited CYP3A4/5-mediated metabolite formation in enterocytes for midazolam, amprenavir and loperamide, suggesting that cryopreserved enterocytes may be useful in determining intestinal CYP3A inhibition parameters. amprenavir 105-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 29357810-5 2018 mRNA expression levels and enzyme activities of CYP1A2, CYP2B6, and CYP3A in HepaRG cells treated with prototypical inducers of each CYP isoform [omeprazole (OME) for CYP1A2, phenobarbital (PB) for CYP2B6, and rifampicin (RIF) for CYP3A] were evaluated. Omeprazole 146-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 29237391-7 2018 As expected, ketoconazole inhibited CYP3A4/5-mediated metabolite formation in enterocytes for midazolam, amprenavir and loperamide, suggesting that cryopreserved enterocytes may be useful in determining intestinal CYP3A inhibition parameters. Loperamide 120-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 29357810-5 2018 mRNA expression levels and enzyme activities of CYP1A2, CYP2B6, and CYP3A in HepaRG cells treated with prototypical inducers of each CYP isoform [omeprazole (OME) for CYP1A2, phenobarbital (PB) for CYP2B6, and rifampicin (RIF) for CYP3A] were evaluated. Omeprazole 158-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 29357810-5 2018 mRNA expression levels and enzyme activities of CYP1A2, CYP2B6, and CYP3A in HepaRG cells treated with prototypical inducers of each CYP isoform [omeprazole (OME) for CYP1A2, phenobarbital (PB) for CYP2B6, and rifampicin (RIF) for CYP3A] were evaluated. Phenobarbital 175-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 29357810-5 2018 mRNA expression levels and enzyme activities of CYP1A2, CYP2B6, and CYP3A in HepaRG cells treated with prototypical inducers of each CYP isoform [omeprazole (OME) for CYP1A2, phenobarbital (PB) for CYP2B6, and rifampicin (RIF) for CYP3A] were evaluated. Phenobarbital 190-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 30117405-10 2018 CYP3A4 was inhibited by montelukast sulfoxide and triclabendazole with IC50 of 9.33 and 15.11, respectively. Montelukast sulfoxide 24-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29357810-5 2018 mRNA expression levels and enzyme activities of CYP1A2, CYP2B6, and CYP3A in HepaRG cells treated with prototypical inducers of each CYP isoform [omeprazole (OME) for CYP1A2, phenobarbital (PB) for CYP2B6, and rifampicin (RIF) for CYP3A] were evaluated. Rifampin 210-220 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 29357810-5 2018 mRNA expression levels and enzyme activities of CYP1A2, CYP2B6, and CYP3A in HepaRG cells treated with prototypical inducers of each CYP isoform [omeprazole (OME) for CYP1A2, phenobarbital (PB) for CYP2B6, and rifampicin (RIF) for CYP3A] were evaluated. Rifampin 222-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 29357810-6 2018 RESULTS: Although the activities of CYP2B6 and CYP3A were induced by treatment with PB and RIF, we found that the activity of phenacetin O-deethylase (PHOD), which is known as a marker of the activity of CYP1A2, was also enhanced by treatment with these non-CYP1A2 inducers in HepaRG cells. Phenobarbital 84-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 30117405-11 2018 Amongst the studied sulfoxide/sulfone substrates, the propensity of involvement of CY2C9 and CYP3A4 enzyme was high (approximately 56% of total) in the metabolic fate experiments. Sulfones 30-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 30117405-10 2018 CYP3A4 was inhibited by montelukast sulfoxide and triclabendazole with IC50 of 9.33 and 15.11, respectively. Triclabendazole 50-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 30117405-11 2018 Amongst the studied sulfoxide/sulfone substrates, the propensity of involvement of CY2C9 and CYP3A4 enzyme was high (approximately 56% of total) in the metabolic fate experiments. sulfoxide 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 28986606-0 2018 Effect of breviscapine on CYP3A metabolic activity in healthy volunteers. breviscapine 10-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-31 29038231-4 2018 For static and dynamic predictions, midazolam, repaglinide, and desipramine were used as probe substrates for CYP3A4/5, CYP2C8, and CYP2D6, respectively. Desipramine 64-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 29038231-7 2018 Clofazimine was predicted to be a moderate-to-strong CYP3A4/5 inhibitor and weak CYP2C8 and CYP2D6 inhibitor based on the calculated AUCR by static and PBPK modeling. Clofazimine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 28986606-7 2018 CONCLUSIONS: These findings suggest that breviscapine inhibited the metabolism of CYP3A in the volunteers, with no interaction difference among the different CYP3A5 genotypes. breviscapine 41-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-87 29963210-9 2018 From experiments using human liver microsomes and anti-CYP antibodies, it was revealed that CYP3A4 was involved in the production of nor-fentanyl, beta-hydroxy-fentanyl and (omega-1)-hydroxy-fentanyl, while CYP2D6 was partially involved in the production of 4"-hydroxy-fentanyl. beta-hydroxy-fentanyl 147-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 29038231-8 2018 Additionally, for selected antiretroviral, antitubercular, antihypertensive, antidiabetic, antileprotics, and antihyperlipidemic CYP3A4/5 substrate drugs, approximately 2- to 6-fold increases in the AUC were predicted with static modeling when coadministered with 100 mg of clofazimine. Clofazimine 274-285 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 29038231-9 2018 Therefore, the possibility of an increase in the AUC of CYP3A4/5 substrates when coadministered with clofazimine cannot be ignored. Clofazimine 101-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 29165700-6 2018 KLF11 antagonized TCDD-mediated activation of CYP3A4 gene expression and function in endometrial cells. Polychlorinated Dibenzodioxins 18-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 29963210-9 2018 From experiments using human liver microsomes and anti-CYP antibodies, it was revealed that CYP3A4 was involved in the production of nor-fentanyl, beta-hydroxy-fentanyl and (omega-1)-hydroxy-fentanyl, while CYP2D6 was partially involved in the production of 4"-hydroxy-fentanyl. norfentanyl 133-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 29963210-9 2018 From experiments using human liver microsomes and anti-CYP antibodies, it was revealed that CYP3A4 was involved in the production of nor-fentanyl, beta-hydroxy-fentanyl and (omega-1)-hydroxy-fentanyl, while CYP2D6 was partially involved in the production of 4"-hydroxy-fentanyl. (omega-1)-hydroxy-fentanyl 173-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 29963210-9 2018 From experiments using human liver microsomes and anti-CYP antibodies, it was revealed that CYP3A4 was involved in the production of nor-fentanyl, beta-hydroxy-fentanyl and (omega-1)-hydroxy-fentanyl, while CYP2D6 was partially involved in the production of 4"-hydroxy-fentanyl. 4"-hydroxy-fentanyl 258-277 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 30477963-5 2018 In addition, isavuconazole may inhibit CYP3A4. isavuconazole 13-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 29345985-1 2018 BACKGROUND: Rivaroxaban is metabolized in the liver via CYP3A4, the cytochrome involved in the metabolism of nearly 50% of all medications. Rivaroxaban 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 29345985-3 2018 METHODS: The primary goal of our research was to study the correlation between the CYP3A family activity and the safety and efficacy of anticoagulant therapy with rivaroxaban in patients with deep vein thrombosis (DVT). Rivaroxaban 163-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 29345985-6 2018 RESULTS: We found a direct statistically reliable correlation between CYP3A4 activity and both peak and trough rivaroxaban levels. Rivaroxaban 111-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 28993217-5 2018 Model predictions of oral venetoclax pharmacokinetics were verified against clinical studies of fed and fasted healthy volunteers, and clinical drug interaction studies with strong CYP3A inhibitor (ketoconazole) and inducer (rifampicin). venetoclax 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-186 30069628-10 2018 The metabolization of ruxolitinib through CYP3A4 needs to be considered particularly if co-administered with potent CYP3A4 inhibitors. ruxolitinib 22-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 29145924-2 2018 As CFZ is an inhibitor of the cytochrome P450 isoenzyme 3A4 (CYP3A4) in vitro, and BDQ a substrate of CYP3A4, there is a potential for pharmacokinetic (PK) drug-drug interaction that may result in increased BDQ exposure when co-administered with CFZ, which could increase the toxicity of BDQ. bedaquiline 83-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 29145924-2 2018 As CFZ is an inhibitor of the cytochrome P450 isoenzyme 3A4 (CYP3A4) in vitro, and BDQ a substrate of CYP3A4, there is a potential for pharmacokinetic (PK) drug-drug interaction that may result in increased BDQ exposure when co-administered with CFZ, which could increase the toxicity of BDQ. Clofazimine 3-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-59 29145924-2 2018 As CFZ is an inhibitor of the cytochrome P450 isoenzyme 3A4 (CYP3A4) in vitro, and BDQ a substrate of CYP3A4, there is a potential for pharmacokinetic (PK) drug-drug interaction that may result in increased BDQ exposure when co-administered with CFZ, which could increase the toxicity of BDQ. Clofazimine 3-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 29393278-5 2018 In general, ordonin has induced effects on the major member of CYP450s mRNA and protein expression, as well as on the enzyme activity in human HepaRG cells, especially on CYP3A4 and CYP2C9. ordonin 12-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 30069628-10 2018 The metabolization of ruxolitinib through CYP3A4 needs to be considered particularly if co-administered with potent CYP3A4 inhibitors. ruxolitinib 22-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 30270266-8 2018 In addition, these cells had the ability to induce CYP3A4 in the presence of 1alpha,25-dihydroxyvitamin D3. Calcitriol 77-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 28764083-4 2017 Assessing nitro-stilbenoids, both approaches suggested nitrostilbene to be a weaker inhibitor of CYP3A4 than resveratrol, and stronger than dimethoxy-nitrostilbene. 2-nitrostilbene 55-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 29343979-1 2018 Background: Isoenzymes CYP2D6 and CYP3A4, the activity of which varies widely, are involved in metabolism of haloperidol and may influence its profile of efficacy and safety. Haloperidol 109-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 29343979-2 2018 Objective: The primary aim of this study was to estimate the relationship between CYP3A5 gene polymorphism, activity of the CYP3A isoenzyme, and the risk of development of adverse drug reactions by haloperidol in patients with alcohol abuse. Haloperidol 198-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-87 29343979-5 2018 The activity of CYP3A was evaluated by determining the concentrations of an endogenous substrate of this isoenzyme (cortisol) and its urinary metabolite (6-beta-hydroxycortisol, 6-B-HC). Hydrocortisone 116-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-21 29343979-5 2018 The activity of CYP3A was evaluated by determining the concentrations of an endogenous substrate of this isoenzyme (cortisol) and its urinary metabolite (6-beta-hydroxycortisol, 6-B-HC). 6 beta-hydroxycortisol 154-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-21 29343979-5 2018 The activity of CYP3A was evaluated by determining the concentrations of an endogenous substrate of this isoenzyme (cortisol) and its urinary metabolite (6-beta-hydroxycortisol, 6-B-HC). 6-b-hc 178-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-21 29176011-8 2017 A midazolam PBPK model with the CYP3A4/5 ISEFs simulated the PK profiles within twofold error compared to the clinical observations. Midazolam 2-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 29263648-0 2017 Functional assessment of CYP3A4 allelic variants on lidocaine metabolism in vitro. Lidocaine 52-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 29263648-4 2017 The aim of this study was to systematically investigate the genetic polymorphisms of 23 CYP3A4 alleles and evaluate their catalytic activities on the metabolism of lidocaine in vitro. Lidocaine 164-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 29263648-6 2017 Then the insect microsomes were incubated with the CYP3A4-specific substrate lidocaine. Lidocaine 77-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 29263648-9 2017 Conclusion: As the first study of all these CYP3A4 alleles for lidocaine metabolism, our results in vitro assessment may provide novel insights into the allele-specific and substrate-specific activity of CYP3A4 and may also offer a reference to the personalized treatment of lidocaine in a clinical setting. Lidocaine 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 29263648-9 2017 Conclusion: As the first study of all these CYP3A4 alleles for lidocaine metabolism, our results in vitro assessment may provide novel insights into the allele-specific and substrate-specific activity of CYP3A4 and may also offer a reference to the personalized treatment of lidocaine in a clinical setting. Lidocaine 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 204-210 29263648-9 2017 Conclusion: As the first study of all these CYP3A4 alleles for lidocaine metabolism, our results in vitro assessment may provide novel insights into the allele-specific and substrate-specific activity of CYP3A4 and may also offer a reference to the personalized treatment of lidocaine in a clinical setting. Lidocaine 275-284 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 29263648-9 2017 Conclusion: As the first study of all these CYP3A4 alleles for lidocaine metabolism, our results in vitro assessment may provide novel insights into the allele-specific and substrate-specific activity of CYP3A4 and may also offer a reference to the personalized treatment of lidocaine in a clinical setting. Lidocaine 275-284 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 204-210 29215040-6 2017 The results from P450 reaction phenotyping using recombinant cDNA-expressed human CYPs in conjunction with specific CYP inhibitors suggested that CYP1A2 and CYP3A4 are the predominant CYPs involved in the metapristone metabolism, which were further confirmed by the enhanced protein levels of CYP1A2 and CYP3A4 induced by 1-week oral administration of metapristone to rats. metapristone 205-217 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 29215040-6 2017 The results from P450 reaction phenotyping using recombinant cDNA-expressed human CYPs in conjunction with specific CYP inhibitors suggested that CYP1A2 and CYP3A4 are the predominant CYPs involved in the metapristone metabolism, which were further confirmed by the enhanced protein levels of CYP1A2 and CYP3A4 induced by 1-week oral administration of metapristone to rats. metapristone 205-217 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 304-310 29215040-6 2017 The results from P450 reaction phenotyping using recombinant cDNA-expressed human CYPs in conjunction with specific CYP inhibitors suggested that CYP1A2 and CYP3A4 are the predominant CYPs involved in the metapristone metabolism, which were further confirmed by the enhanced protein levels of CYP1A2 and CYP3A4 induced by 1-week oral administration of metapristone to rats. metapristone 352-364 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 29215040-8 2017 The study demonstrates, for the first time, the sex-related pharmacokinetics of metapristone, and reveals that activities of liver microsomal CYP1A2 and CYP3A4 as well as the renal clearance are primarily responsible for the sex-related pharmacokinetics. metapristone 80-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 28843775-8 2017 8-Bromo-cyclic adenosine monophosphate, a membrane-permeable cAMP analog, reduced mRNA expression of CYP3A whereas the inhibitors of PI3K, NF-kappaB, PKC and PKA reversed the PTH-induced CYP3A down-regulation. 8-Bromo Cyclic Adenosine Monophosphate 0-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 28843775-8 2017 8-Bromo-cyclic adenosine monophosphate, a membrane-permeable cAMP analog, reduced mRNA expression of CYP3A whereas the inhibitors of PI3K, NF-kappaB, PKC and PKA reversed the PTH-induced CYP3A down-regulation. 8-Bromo Cyclic Adenosine Monophosphate 0-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-192 28843775-8 2017 8-Bromo-cyclic adenosine monophosphate, a membrane-permeable cAMP analog, reduced mRNA expression of CYP3A whereas the inhibitors of PI3K, NF-kappaB, PKC and PKA reversed the PTH-induced CYP3A down-regulation. Cyclic AMP 61-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 29068158-2 2017 We developed a whole-body physiologically based pharmacokinetic (PBPK) model for solithromycin in adults using PK-Sim and MoBi version 6.2, which incorporated time-dependent CYP3A4 auto-inhibition. solithromycin 81-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 29098381-0 2017 The effects of lapatinib on CYP3A metabolism of midazolam in patients with advanced cancer. Lapatinib 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 29098381-0 2017 The effects of lapatinib on CYP3A metabolism of midazolam in patients with advanced cancer. Midazolam 48-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 29098381-1 2017 PURPOSE: The potential inhibition of CYP3A4 by lapatinib was studied using midazolam as a probe substrate in patients with cancer. Lapatinib 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 29098381-8 2017 CONCLUSION: These data show that lapatinib caused weak inhibition of gastrointestinal CYP3A4 in vivo. Lapatinib 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 29098381-9 2017 This suggests that oral CYP3A4 drug substrates with a narrow therapeutic index may need dose reduction if lapatinib is to be co-prescribed. Lapatinib 106-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 28928137-2 2017 Therefore, the aim of this study was to evaluate the change in CYP3A activity measured as 4beta-hydroxycholesterol (4betaOHC) concentration after kidney transplantation. cholest-5-ene-3,4-diol 90-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 28986474-0 2017 Digging Deeper into CYP3A Testosterone Metabolism: Kinetic, Regioselectivity, and Stereoselectivity Differences between CYP3A4/5 and CYP3A7. Testosterone 26-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-25 28928137-2 2017 Therefore, the aim of this study was to evaluate the change in CYP3A activity measured as 4beta-hydroxycholesterol (4betaOHC) concentration after kidney transplantation. 4betaohc 116-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 28986474-0 2017 Digging Deeper into CYP3A Testosterone Metabolism: Kinetic, Regioselectivity, and Stereoselectivity Differences between CYP3A4/5 and CYP3A7. Testosterone 26-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 28986474-1 2017 The metabolism of testosterone to 6beta-hydroxytestosterone (6beta-OH-T) is a commonly used assay to evaluate human CYP3A enzyme activities. Testosterone 18-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 28912253-3 2017 Panobinostat was also an in vitro reversible and time-dependent inhibitor of CYP3A4/5 and a reversible inhibitor of CYP2D6 and CYP2C19. Panobinostat 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 28928137-6 2017 Linear mixed-model analysis identified a 0.16-ng/ml increase in 4betaOHC concentration per day after transplantation (P < 0.001), indicating a regain in CYP3A activity. 4betaohc 64-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-161 28912253-4 2017 Based on a previous clinical drug-drug interaction study with ketoconazole (KTZ), the contribution of CYP3A4 in vivo was estimated to be ~40%. Ketoconazole 62-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 28912253-4 2017 Based on a previous clinical drug-drug interaction study with ketoconazole (KTZ), the contribution of CYP3A4 in vivo was estimated to be ~40%. Ketoconazole 76-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 28986474-1 2017 The metabolism of testosterone to 6beta-hydroxytestosterone (6beta-OH-T) is a commonly used assay to evaluate human CYP3A enzyme activities. 6 beta-hydroxytestosterone 34-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 28928137-7 2017 Increasing estimated glomerular filtration rate after transplantation was associated with increasing 4betaOHC concentration (P < 0.001), supporting that CYP3A activity increases with recovering uremia. 4betaohc 101-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-161 28986474-1 2017 The metabolism of testosterone to 6beta-hydroxytestosterone (6beta-OH-T) is a commonly used assay to evaluate human CYP3A enzyme activities. 6beta-oh-t 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 28912253-6 2017 The model was then applied to predict the drug interaction with the strong CYP3A4 inducer rifampin (RIF) and the sensitive CYP3A4 substrate midazolam (MDZ) in lieu of clinical trials. Rifampin 90-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 28912253-6 2017 The model was then applied to predict the drug interaction with the strong CYP3A4 inducer rifampin (RIF) and the sensitive CYP3A4 substrate midazolam (MDZ) in lieu of clinical trials. Rifampin 100-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 28986474-4 2017 To this end, we performed a complete kinetic analysis of the 6beta-OH-T, 2alpha-OH-T, and 2beta-hydroxytestosterone metabolites for recombinant Supersome CYP3A4, CYP3A5, and CYP3A7 enzymes and monitored metabolism in fetal and adult human liver microsomes for comparison. 6beta-oh-t 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 28986474-8 2017 In CYP3A4, the most energetically favorable docking mode places testosterone in a position with the methyl groups directed toward the heme iron, which is more favorable for oxidation at C6beta, whereas for CYP3A7 the testosterone methyl groups are positioned away from the heme, which is more favorable for an oxidation event at C2alpha In conclusion, our data indicate an alternative binding mode for testosterone in CYP3A7 that favors the 2alpha-hydroxylation, suggesting significant structural differences in its active site compared with CYP3A4/5. Testosterone 217-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 542-548 28986474-4 2017 To this end, we performed a complete kinetic analysis of the 6beta-OH-T, 2alpha-OH-T, and 2beta-hydroxytestosterone metabolites for recombinant Supersome CYP3A4, CYP3A5, and CYP3A7 enzymes and monitored metabolism in fetal and adult human liver microsomes for comparison. 2beta-Hydroxytestosterone 90-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 28986474-7 2017 In silico docking studies revealed at least two different binding modes for testosterone between CYP3A4 and CYP3A7. Testosterone 76-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 28912253-6 2017 The model was then applied to predict the drug interaction with the strong CYP3A4 inducer rifampin (RIF) and the sensitive CYP3A4 substrate midazolam (MDZ) in lieu of clinical trials. Midazolam 140-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 28912253-6 2017 The model was then applied to predict the drug interaction with the strong CYP3A4 inducer rifampin (RIF) and the sensitive CYP3A4 substrate midazolam (MDZ) in lieu of clinical trials. Midazolam 140-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 28912253-6 2017 The model was then applied to predict the drug interaction with the strong CYP3A4 inducer rifampin (RIF) and the sensitive CYP3A4 substrate midazolam (MDZ) in lieu of clinical trials. Midazolam 151-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 28912253-6 2017 The model was then applied to predict the drug interaction with the strong CYP3A4 inducer rifampin (RIF) and the sensitive CYP3A4 substrate midazolam (MDZ) in lieu of clinical trials. Midazolam 151-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 29137842-8 2017 Extensive metabolism of cetrozole and TMD-322 was observed in the CYP2C19 expression system among the test CYP isoforms (CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4). cetrozole 24-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 28986474-8 2017 In CYP3A4, the most energetically favorable docking mode places testosterone in a position with the methyl groups directed toward the heme iron, which is more favorable for oxidation at C6beta, whereas for CYP3A7 the testosterone methyl groups are positioned away from the heme, which is more favorable for an oxidation event at C2alpha In conclusion, our data indicate an alternative binding mode for testosterone in CYP3A7 that favors the 2alpha-hydroxylation, suggesting significant structural differences in its active site compared with CYP3A4/5. Testosterone 64-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-9 28986474-8 2017 In CYP3A4, the most energetically favorable docking mode places testosterone in a position with the methyl groups directed toward the heme iron, which is more favorable for oxidation at C6beta, whereas for CYP3A7 the testosterone methyl groups are positioned away from the heme, which is more favorable for an oxidation event at C2alpha In conclusion, our data indicate an alternative binding mode for testosterone in CYP3A7 that favors the 2alpha-hydroxylation, suggesting significant structural differences in its active site compared with CYP3A4/5. Testosterone 64-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 542-548 28986474-8 2017 In CYP3A4, the most energetically favorable docking mode places testosterone in a position with the methyl groups directed toward the heme iron, which is more favorable for oxidation at C6beta, whereas for CYP3A7 the testosterone methyl groups are positioned away from the heme, which is more favorable for an oxidation event at C2alpha In conclusion, our data indicate an alternative binding mode for testosterone in CYP3A7 that favors the 2alpha-hydroxylation, suggesting significant structural differences in its active site compared with CYP3A4/5. Heme 134-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-9 28986474-8 2017 In CYP3A4, the most energetically favorable docking mode places testosterone in a position with the methyl groups directed toward the heme iron, which is more favorable for oxidation at C6beta, whereas for CYP3A7 the testosterone methyl groups are positioned away from the heme, which is more favorable for an oxidation event at C2alpha In conclusion, our data indicate an alternative binding mode for testosterone in CYP3A7 that favors the 2alpha-hydroxylation, suggesting significant structural differences in its active site compared with CYP3A4/5. Heme 134-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 542-548 28986474-8 2017 In CYP3A4, the most energetically favorable docking mode places testosterone in a position with the methyl groups directed toward the heme iron, which is more favorable for oxidation at C6beta, whereas for CYP3A7 the testosterone methyl groups are positioned away from the heme, which is more favorable for an oxidation event at C2alpha In conclusion, our data indicate an alternative binding mode for testosterone in CYP3A7 that favors the 2alpha-hydroxylation, suggesting significant structural differences in its active site compared with CYP3A4/5. Iron 139-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-9 28986474-8 2017 In CYP3A4, the most energetically favorable docking mode places testosterone in a position with the methyl groups directed toward the heme iron, which is more favorable for oxidation at C6beta, whereas for CYP3A7 the testosterone methyl groups are positioned away from the heme, which is more favorable for an oxidation event at C2alpha In conclusion, our data indicate an alternative binding mode for testosterone in CYP3A7 that favors the 2alpha-hydroxylation, suggesting significant structural differences in its active site compared with CYP3A4/5. Heme 273-277 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-9 28986474-8 2017 In CYP3A4, the most energetically favorable docking mode places testosterone in a position with the methyl groups directed toward the heme iron, which is more favorable for oxidation at C6beta, whereas for CYP3A7 the testosterone methyl groups are positioned away from the heme, which is more favorable for an oxidation event at C2alpha In conclusion, our data indicate an alternative binding mode for testosterone in CYP3A7 that favors the 2alpha-hydroxylation, suggesting significant structural differences in its active site compared with CYP3A4/5. Iron 139-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 542-548 28986474-8 2017 In CYP3A4, the most energetically favorable docking mode places testosterone in a position with the methyl groups directed toward the heme iron, which is more favorable for oxidation at C6beta, whereas for CYP3A7 the testosterone methyl groups are positioned away from the heme, which is more favorable for an oxidation event at C2alpha In conclusion, our data indicate an alternative binding mode for testosterone in CYP3A7 that favors the 2alpha-hydroxylation, suggesting significant structural differences in its active site compared with CYP3A4/5. Testosterone 217-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-9 28986474-8 2017 In CYP3A4, the most energetically favorable docking mode places testosterone in a position with the methyl groups directed toward the heme iron, which is more favorable for oxidation at C6beta, whereas for CYP3A7 the testosterone methyl groups are positioned away from the heme, which is more favorable for an oxidation event at C2alpha In conclusion, our data indicate an alternative binding mode for testosterone in CYP3A7 that favors the 2alpha-hydroxylation, suggesting significant structural differences in its active site compared with CYP3A4/5. Heme 273-277 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 542-548 28986474-8 2017 In CYP3A4, the most energetically favorable docking mode places testosterone in a position with the methyl groups directed toward the heme iron, which is more favorable for oxidation at C6beta, whereas for CYP3A7 the testosterone methyl groups are positioned away from the heme, which is more favorable for an oxidation event at C2alpha In conclusion, our data indicate an alternative binding mode for testosterone in CYP3A7 that favors the 2alpha-hydroxylation, suggesting significant structural differences in its active site compared with CYP3A4/5. Testosterone 217-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-9 28986474-8 2017 In CYP3A4, the most energetically favorable docking mode places testosterone in a position with the methyl groups directed toward the heme iron, which is more favorable for oxidation at C6beta, whereas for CYP3A7 the testosterone methyl groups are positioned away from the heme, which is more favorable for an oxidation event at C2alpha In conclusion, our data indicate an alternative binding mode for testosterone in CYP3A7 that favors the 2alpha-hydroxylation, suggesting significant structural differences in its active site compared with CYP3A4/5. Testosterone 217-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 542-548 28849250-0 2017 Effect of CYP3A4*22, CYP3A5*3, and CYP3A combined genotypes on tamoxifen metabolism. Tamoxifen 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 28849250-0 2017 Effect of CYP3A4*22, CYP3A5*3, and CYP3A combined genotypes on tamoxifen metabolism. Tamoxifen 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 28849250-2 2017 Recently, the decreased activity CYP3A4*22 allele and the loss of function CYP3A5*3 allele have been described as potential factors that could help to explain the inter-patient variability in tamoxifen metabolism. Tamoxifen 192-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 28849250-3 2017 The aim of this study is to investigate the effect of CYP3A4*22, CYP3A5*3, and CYP3A combined genotypes on tamoxifen metabolism. Tamoxifen 107-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 28849250-3 2017 The aim of this study is to investigate the effect of CYP3A4*22, CYP3A5*3, and CYP3A combined genotypes on tamoxifen metabolism. Tamoxifen 107-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-59 28849250-7 2017 RESULTS: CYP3A4*22 carriers reached significant higher concentrations of tamoxifen, N-desmethyl-tamoxifen, and 4-hydroxy-tamoxifen compared to non-carriers, whereas a tendency toward increased endoxifen levels was observed (p = 0.088). Tamoxifen 73-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 28849250-7 2017 RESULTS: CYP3A4*22 carriers reached significant higher concentrations of tamoxifen, N-desmethyl-tamoxifen, and 4-hydroxy-tamoxifen compared to non-carriers, whereas a tendency toward increased endoxifen levels was observed (p = 0.088). N-desmethyltamoxifen 84-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 28849250-7 2017 RESULTS: CYP3A4*22 carriers reached significant higher concentrations of tamoxifen, N-desmethyl-tamoxifen, and 4-hydroxy-tamoxifen compared to non-carriers, whereas a tendency toward increased endoxifen levels was observed (p = 0.088). 4'-hydroxytamoxifen 111-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 28849250-7 2017 RESULTS: CYP3A4*22 carriers reached significant higher concentrations of tamoxifen, N-desmethyl-tamoxifen, and 4-hydroxy-tamoxifen compared to non-carriers, whereas a tendency toward increased endoxifen levels was observed (p = 0.088). 4-hydroxy-N-desmethyltamoxifen 193-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 28849250-8 2017 The metabolic ratio tamoxifen/N-desmethyl-tamoxifen was significantly higher in CYP3A4*22 individuals (0.59 vs. 0.52, p < 0.001). Tamoxifen 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 28849250-8 2017 The metabolic ratio tamoxifen/N-desmethyl-tamoxifen was significantly higher in CYP3A4*22 individuals (0.59 vs. 0.52, p < 0.001). N-desmethyltamoxifen 30-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 28849250-9 2017 At the same time, CYP3A4*22 genotype contributed to improving the inter-variability [R 2 of the (log-transformed) metabolic ratio tamoxifen/N-desmethyl-tamoxifen improved from 21.8 to 23.9%, p < 0.001]. Tamoxifen 130-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 28849250-9 2017 At the same time, CYP3A4*22 genotype contributed to improving the inter-variability [R 2 of the (log-transformed) metabolic ratio tamoxifen/N-desmethyl-tamoxifen improved from 21.8 to 23.9%, p < 0.001]. N-desmethyltamoxifen 140-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 28849250-11 2017 CONCLUSION: Our data demonstrate that CYP3A genotype has a minor effect to explaining the variability between patients in tamoxifen metabolism and has no added value in addition to CYP2D6 genotype. Tamoxifen 122-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 27549341-5 2017 CYP3A4*22 was associated with a 54% greater exemestane concentration (P<0.01). exemestane 44-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 29369597-2 2017 A series of studies has shown that concurrent use of carbamazepine decreases quetiapine serum level due to induction of CYP3A enzymes by carbamazepine. Carbamazepine 53-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-125 29369597-2 2017 A series of studies has shown that concurrent use of carbamazepine decreases quetiapine serum level due to induction of CYP3A enzymes by carbamazepine. Quetiapine Fumarate 77-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-125 29369597-2 2017 A series of studies has shown that concurrent use of carbamazepine decreases quetiapine serum level due to induction of CYP3A enzymes by carbamazepine. Carbamazepine 137-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-125 29369597-7 2017 CONCLUSION: We hypothesize that induction of CYP3A lasts even after carbamazepine withdrawal. Carbamazepine 68-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-50 29369597-10 2017 The influence of carbamazepine on CYP3A enzymes lasted at least 3 weeks after carbamazepine withdrawal which is in accordance with CYP3A de-induction lasting 3 weeks. Carbamazepine 17-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-39 29369597-10 2017 The influence of carbamazepine on CYP3A enzymes lasted at least 3 weeks after carbamazepine withdrawal which is in accordance with CYP3A de-induction lasting 3 weeks. Carbamazepine 17-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-136 29369597-10 2017 The influence of carbamazepine on CYP3A enzymes lasted at least 3 weeks after carbamazepine withdrawal which is in accordance with CYP3A de-induction lasting 3 weeks. Carbamazepine 78-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-39 27549341-3 2017 The primary hypothesis was that patients carrying the low-activity CYP3A4*22 (rs35599367) single-nucleotide polymorphism (SNP) would have greater exemestane concentration. single-nucleotide 90-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 27549341-3 2017 The primary hypothesis was that patients carrying the low-activity CYP3A4*22 (rs35599367) single-nucleotide polymorphism (SNP) would have greater exemestane concentration. exemestane 146-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 28569378-8 2017 Both ketamine and CsA are CYP3A4 substrates. Ketamine 5-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 28960344-1 2017 OBJECTIVES: Ritonavir and cobicistat are strong inhibitors of human cytochrome P450-3A (CYP3A) isoforms, and are used clinically as pharmacokinetic boosting agents for other antiretroviral drugs. Ritonavir 12-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-86 28960344-1 2017 OBJECTIVES: Ritonavir and cobicistat are strong inhibitors of human cytochrome P450-3A (CYP3A) isoforms, and are used clinically as pharmacokinetic boosting agents for other antiretroviral drugs. Ritonavir 12-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-93 28960344-1 2017 OBJECTIVES: Ritonavir and cobicistat are strong inhibitors of human cytochrome P450-3A (CYP3A) isoforms, and are used clinically as pharmacokinetic boosting agents for other antiretroviral drugs. Cobicistat 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-86 28960344-1 2017 OBJECTIVES: Ritonavir and cobicistat are strong inhibitors of human cytochrome P450-3A (CYP3A) isoforms, and are used clinically as pharmacokinetic boosting agents for other antiretroviral drugs. Cobicistat 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-93 28960344-2 2017 Data reported by the manufacturer suggest that cobicistat is a more selective inhibitor of CYP3A than ritonavir. Cobicistat 47-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-96 28960344-6 2017 KEY FINDINGS: Ritonavir and cobicistat both were strong inhibitors of CYP3A4, with IC50 values of 0.014 and 0.032 mum, respectively. Ritonavir 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 28960344-6 2017 KEY FINDINGS: Ritonavir and cobicistat both were strong inhibitors of CYP3A4, with IC50 values of 0.014 and 0.032 mum, respectively. Cobicistat 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 28960344-10 2017 CONCLUSIONS: Consistent with previous reports, both ritonavir and cobicistat were highly potent inhibitors of CYP3A. Ritonavir 52-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-115 28960344-10 2017 CONCLUSIONS: Consistent with previous reports, both ritonavir and cobicistat were highly potent inhibitors of CYP3A. Cobicistat 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-115 28962866-5 2017 KEY FINDINGS: The in vitro metabolic enzyme of DCO was CYP3A4 (mediated the formation of metabolites M1-M5), CYP2C9 (mediated the formation of metabolites M1-M3, M6 and M8) and CYP2D6 (mediated the formation of metabolite M3) in HLM. 3,3-DICHLORO-2-PHOSPHONOMETHYL-ACRYLIC ACID 47-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 27378609-0 2017 Effect of ABCB1 diplotype on tacrolimus disposition in renal recipients depends on CYP3A5 and CYP3A4 genotype. Tacrolimus 29-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 29157826-6 2017 RESULTS: Transient transfection assays showed that UA effectively attenuated CYP3A4 and CYP2B6 promoter activities mediated by rifampin (RIF, human PXR agonist) and CITCO (human CAR agonist). ursolic acid 51-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 28418012-0 2017 CYP3A4 is a crosslink between vitamin D and calcineurin inhibitors in solid organ transplant recipients: implications for bone health. Vitamin D 30-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28418012-2 2017 CNIs and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) are substrates of the drug-metabolizing enzyme CYP3A4. Calcitriol 9-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 28418012-2 2017 CNIs and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) are substrates of the drug-metabolizing enzyme CYP3A4. Calcitriol 35-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 29157826-6 2017 RESULTS: Transient transfection assays showed that UA effectively attenuated CYP3A4 and CYP2B6 promoter activities mediated by rifampin (RIF, human PXR agonist) and CITCO (human CAR agonist). Rifampin 127-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 29157826-6 2017 RESULTS: Transient transfection assays showed that UA effectively attenuated CYP3A4 and CYP2B6 promoter activities mediated by rifampin (RIF, human PXR agonist) and CITCO (human CAR agonist). Rifampin 137-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 29157826-6 2017 RESULTS: Transient transfection assays showed that UA effectively attenuated CYP3A4 and CYP2B6 promoter activities mediated by rifampin (RIF, human PXR agonist) and CITCO (human CAR agonist). 6-(4-chlorophenyl)imidazo(2,1-b)(1,3)thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime 165-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 29157826-8 2017 Furthermore, the interaction of co-regulators with PXR and the transcriptional complexes in the CYP3A4 promoter activity and CYP3A4 promoter xenobiotic response element (everted repeat 6, ER6), respectively, were disrupted in the presence of UA. ursolic acid 242-244 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 29157826-8 2017 Furthermore, the interaction of co-regulators with PXR and the transcriptional complexes in the CYP3A4 promoter activity and CYP3A4 promoter xenobiotic response element (everted repeat 6, ER6), respectively, were disrupted in the presence of UA. ursolic acid 242-244 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 29157826-10 2017 Taken together, these results show that UA inhibits the transactivation effects of PXR and CAR, and reduces the expression and function of CYP3A4 and CYP2B6. ursolic acid 40-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 32454631-8 2017 In the current review, recent findings with respect to the role of mainly CYP1A1, CYP1B1, CYP2D6, CYP2E1 and CYP3A4 gene polymorphisms in response to chemotherapy and survival in patients with NSCLC have been provided, which could be useful for clinicians in the prognosis of these patients who are mainly treated with platinum-based chemotherapy. Platinum 319-327 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 28418012-5 2017 We also provide an overview of the literature on the interplay between vitamin D metabolism and CYP3A4 in experimental and clinical settings and discuss its possible implications for solid organ transplant recipients. Vitamin D 71-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 28418012-6 2017 In conclusion, there is a body of evidence on the interplay between vitamin D and the drug-metabolizing enzyme CYP3A4, which may have therapeutic implications. Vitamin D 68-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 29135906-1 2017 BACKGROUND: The interindividual variability of cyclosporin A (CsA) pharmacokinetics might be explained by heterogeneity in the cytochrome P450 3A (CYP3A) subfamily. Cyclosporine 47-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-145 29135906-1 2017 BACKGROUND: The interindividual variability of cyclosporin A (CsA) pharmacokinetics might be explained by heterogeneity in the cytochrome P450 3A (CYP3A) subfamily. Cyclosporine 47-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-152 29135906-1 2017 BACKGROUND: The interindividual variability of cyclosporin A (CsA) pharmacokinetics might be explained by heterogeneity in the cytochrome P450 3A (CYP3A) subfamily. Cyclosporine 62-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-145 29135906-1 2017 BACKGROUND: The interindividual variability of cyclosporin A (CsA) pharmacokinetics might be explained by heterogeneity in the cytochrome P450 3A (CYP3A) subfamily. Cyclosporine 62-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-152 29135906-3 2017 The aim of this study was to assess the impact of age, CYP3A5*3, CYP3A4*22, and POR*28 alleles on CsA pharmacokinetics in pediatric renal transplant recipients. Cyclosporine 98-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 27414183-10 2017 In conclusion, TAK-438 was primarily metabolized by multiple metabolizing enzymes including CYP3A4, CYP2B6, CYP2C19, CYP2D6, and a non-CYP enzyme SULT2A1, and the influence of the CYP2C19 genotype status on gastric acid suppression post TAK-438 dosing could be small. 1-(5-(2-fluorophenyl)-1-(pyridin-3-ylsulfonyl)-1H-pyrrol-3-yl)-N-methylmethanamine 15-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 28614988-5 2017 RESULTS: The results showed that DHM could inhibit the activity of CYP3A4, CYP2E1 and CYP2D6, with IC50 values of 14.75, 25.74 and 22.69 muM, respectively, but that other CYP isoforms were not affected. dihydromyricetin 33-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 28614988-6 2017 Enzyme kinetic studies showed that DHM was not only a non-competitive inhibitor of CYP3A4 but also a competitive inhibitor of CYP2E1 and CYP2D6, with Ki values of 6.06, 9.24 and 10.52 muM, respectively. dihydromyricetin 35-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 28614988-7 2017 In addition, DHM is a time-dependent inhibitor for CYP3A4 with KI/Kinact value of 12.17/0.057 min-1 muM-1. dihydromyricetin 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 28614988-8 2017 DISCUSSION AND CONCLUSION: The in vitro studies of DHM with CYP isoforms indicate that DHM has the potential to cause pharmacokinetic drug interactions with other co-administered drugs metabolized by CYP3A4, CYP2E1 and CYP2D6. dihydromyricetin 51-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 28614988-8 2017 DISCUSSION AND CONCLUSION: The in vitro studies of DHM with CYP isoforms indicate that DHM has the potential to cause pharmacokinetic drug interactions with other co-administered drugs metabolized by CYP3A4, CYP2E1 and CYP2D6. dihydromyricetin 87-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 27414183-6 2017 Furthermore, CYP3A4 mainly contributed to the metabolism of TAK-438 to M-I, M-III, and N-demethylated TAK-438, and CYP2B6, CYP2C19 and CYP2D6 partly catalyzed the metabolism of TAK-438. tak 60-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 27414183-6 2017 Furthermore, CYP3A4 mainly contributed to the metabolism of TAK-438 to M-I, M-III, and N-demethylated TAK-438, and CYP2B6, CYP2C19 and CYP2D6 partly catalyzed the metabolism of TAK-438. 1-(5-(2-fluorophenyl)-1-(pyridin-3-ylsulfonyl)-1H-pyrrol-3-yl)-N-methylmethanamine 60-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 27841077-8 2017 Out of the seven CYP isoforms in HLM, alectinib and M4 showed time-dependent inhibition (TDI) of only CYP3A4, which suggests low TDI potential due to low inactivation efficiency. alectinib 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 29493154-0 2017 [Transcriptional regulation effect of THSG and anthraquinones in tubers of Polygonum multiflorum based on human progesterone X receptor (PXR) mediated CYP3A4 rapid screening system]. thsg 38-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 27937048-0 2017 Effects of cytochrome P450 3A4 and non-genetic factors on initial voriconazole serum trough concentrations in hematological patients with different cytochrome P450 2C19 genotypes. Voriconazole 66-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-30 27937048-3 2017 Polymorphisms of CYP3A4, CYP3A5, CYP2C9 and non-genetic factors such as age, gender, body mass index (BMI), transaminase levels, concomitant medications might also affect voriconazole initial steady serum trough concentration (VICmin) in haematological patients, but the effects were not clear. Voriconazole 171-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 29493154-5 2017 The results show that the inhibitory effect of THSG, chrysophanol, emodin, rhein and aloe-emodin on CYP3A4 was inhibited by co-transfection of pcDNA3.1 and pGL4.17-CYP3A4. thsg 47-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 29493154-5 2017 The results show that the inhibitory effect of THSG, chrysophanol, emodin, rhein and aloe-emodin on CYP3A4 was inhibited by co-transfection of pcDNA3.1 and pGL4.17-CYP3A4. thsg 47-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 29493154-5 2017 The results show that the inhibitory effect of THSG, chrysophanol, emodin, rhein and aloe-emodin on CYP3A4 was inhibited by co-transfection of pcDNA3.1 and pGL4.17-CYP3A4. chrysophanic acid 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 29493154-5 2017 The results show that the inhibitory effect of THSG, chrysophanol, emodin, rhein and aloe-emodin on CYP3A4 was inhibited by co-transfection of pcDNA3.1 and pGL4.17-CYP3A4. chrysophanic acid 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 29493154-8 2017 In conclusion, the four anthraquinone compounds have an inducing effect on CYP3A4 by PXR, but emodin can directly induce CYP3A4. Anthraquinones 24-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 29493154-9 2017 THSG can inhibit CYP3A4, but plasmid can induce CYP3A4 after intervened with PXR.These results suggest that we should pay attention to the liver function and avoid liver damage in the combined administration of drugs. thsg 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 29167415-2 2017 Yet combined therapeutic regimens have the potential of pharmacological interaction with both ticagrelor and simvastatin being metabolized by CYP3A4. Ticagrelor 94-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 28919359-5 2017 CYP3A in HIM mainly catalyzed phase I metabolism of DDAs and MDAs, with polarity increased. bis(p-chlorophenyl)acetic acid 52-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 29167415-2 2017 Yet combined therapeutic regimens have the potential of pharmacological interaction with both ticagrelor and simvastatin being metabolized by CYP3A4. Simvastatin 109-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 28944677-9 2017 A strong correlation was found between CYP3A4 and CYP3A5 abundance and activity determined using midazolam and testosterone (r > 0.600, p < 0.001). Midazolam 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 29218011-5 2017 A higher proportion of novel-to-known variants for 10 genes was identified on 41 core pharmacogenomics genes related to the PK (29), PD (3), of coumarins, and coagulation proteins (9) including, CYP1A1, CYP3A4, CYP3A5, and F8, and a low proportion of novel-to-known variants on CYP2E1, VKORC1, and SULT1A1/2. Coumarins 144-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 28941798-8 2017 In human liver microsomes, shikonin was not only a mixed inhibitor of CYP1A2, CYP2B6, CYP2C9, CYP2D6 and CYP3A4, but also a competitive inhibitor of CYP2E1, with Ki values no more than 7.72muM. shikonin 27-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 28944677-9 2017 A strong correlation was found between CYP3A4 and CYP3A5 abundance and activity determined using midazolam and testosterone (r > 0.600, p < 0.001). Testosterone 111-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 28585378-0 2017 4beta-Hydroxycholesterol level significantly correlates with steady-state serum concentration of the CYP3A4 substrate quetiapine in psychiatric patients. cholest-5-ene-3,4-diol 0-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 28431455-7 2017 The results showed that CYP1A2 and CYP3A4 might be the major enzymes involved in the metabolism of cnidilin in human liver microsomes. cnidilin 99-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 29076107-10 2017 CONCLUSION: These findings confirm that amenamevir (as a cytochrome P450 3A4 substrate) can interact with ketoconazole or rifampicin, and (as a cytochrome P450 3A4 inducer) can interact with midazolam; however, no interaction between amenamevir and (S)-warfarin was observed, indicating that amenamevir is not an inducer of cytochrome P450 2C9. ASP2151 40-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-76 29076107-10 2017 CONCLUSION: These findings confirm that amenamevir (as a cytochrome P450 3A4 substrate) can interact with ketoconazole or rifampicin, and (as a cytochrome P450 3A4 inducer) can interact with midazolam; however, no interaction between amenamevir and (S)-warfarin was observed, indicating that amenamevir is not an inducer of cytochrome P450 2C9. ASP2151 40-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-163 29076107-10 2017 CONCLUSION: These findings confirm that amenamevir (as a cytochrome P450 3A4 substrate) can interact with ketoconazole or rifampicin, and (as a cytochrome P450 3A4 inducer) can interact with midazolam; however, no interaction between amenamevir and (S)-warfarin was observed, indicating that amenamevir is not an inducer of cytochrome P450 2C9. Rifampin 122-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-76 29076107-10 2017 CONCLUSION: These findings confirm that amenamevir (as a cytochrome P450 3A4 substrate) can interact with ketoconazole or rifampicin, and (as a cytochrome P450 3A4 inducer) can interact with midazolam; however, no interaction between amenamevir and (S)-warfarin was observed, indicating that amenamevir is not an inducer of cytochrome P450 2C9. Midazolam 191-200 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-163 28985999-1 2017 Discovery of potent renin inhibitors which contain a simplified alkylamino Asp-binding group and exhibit improved selectivity for renin over Cyp3A4 is described. alkylamino asp 64-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 28585378-0 2017 4beta-Hydroxycholesterol level significantly correlates with steady-state serum concentration of the CYP3A4 substrate quetiapine in psychiatric patients. Quetiapine Fumarate 118-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 28585378-1 2017 AIM: 4beta-Hydroxycholesterol (4betaOHC) is sensitive towards induction or inhibition of CYP3A4, but its potential usefulness as a dosing biomarker remains to be demonstrated. cholest-5-ene-3,4-diol 5-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 28585378-1 2017 AIM: 4beta-Hydroxycholesterol (4betaOHC) is sensitive towards induction or inhibition of CYP3A4, but its potential usefulness as a dosing biomarker remains to be demonstrated. 4betaohc 31-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 28585378-2 2017 The aim of this study was to investigate the correlation between 4betaOHC levels and steady-state concentrations (Css) of quetiapine, a CYP3A4 substrate with high presystemic metabolism, in psychiatric patients. 4betaohc 65-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 28585378-2 2017 The aim of this study was to investigate the correlation between 4betaOHC levels and steady-state concentrations (Css) of quetiapine, a CYP3A4 substrate with high presystemic metabolism, in psychiatric patients. Quetiapine Fumarate 122-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 28585378-11 2017 This supports the potential usefulness of 4betaOHC as a phenotype biomarker for individualized dosing of quetiapine and other drugs where systemic exposure is mainly determined by CYP3A4 metabolism. 4betaohc 42-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 28603840-1 2017 AIMS: The CYP3A metric 4beta-hydroxycholesterol (4betaOHC) has been shown to correlate with tacrolimus steady-state apparent oral clearance (CL/F). cholest-5-ene-3,4-diol 23-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 28603840-1 2017 AIMS: The CYP3A metric 4beta-hydroxycholesterol (4betaOHC) has been shown to correlate with tacrolimus steady-state apparent oral clearance (CL/F). 4betaohc 49-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 28603840-1 2017 AIMS: The CYP3A metric 4beta-hydroxycholesterol (4betaOHC) has been shown to correlate with tacrolimus steady-state apparent oral clearance (CL/F). Tacrolimus 92-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 28603840-1 2017 AIMS: The CYP3A metric 4beta-hydroxycholesterol (4betaOHC) has been shown to correlate with tacrolimus steady-state apparent oral clearance (CL/F). Fluorine 144-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 28603840-12 2017 CONCLUSIONS: The CYP3A metric 4betaOHC cannot be used to predict tacrolimus dose requirements in the first days after transplantation. 4betaohc 30-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-22 28887089-6 2017 In addition, the inhibitory activities of steviol and stevioside towards the major cytochrome P450 enzymes CYP3A4, CYP2C9, CYP2D6, CYP1A2 and CYP2B6 were evaluated in vitro. steviol 42-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 28835442-6 2017 When CYP3A4 was inhibited, the rate increased by 58% due to the inhibition of the subsequent sulfone formation. Sulfones 93-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 5-11 28835442-8 2017 Hence, although nominally a reduction, the deimination of AZD6738 to its sulfoxide metabolite AZ8982 is an oxidation mediated by CYP2C8, and this metabolite is subsequently oxidized to the sulfone (AZ0002) largely by CYP3A. ceralasertib 58-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-222 28835442-8 2017 Hence, although nominally a reduction, the deimination of AZD6738 to its sulfoxide metabolite AZ8982 is an oxidation mediated by CYP2C8, and this metabolite is subsequently oxidized to the sulfone (AZ0002) largely by CYP3A. az8982 94-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-222 28835442-8 2017 Hence, although nominally a reduction, the deimination of AZD6738 to its sulfoxide metabolite AZ8982 is an oxidation mediated by CYP2C8, and this metabolite is subsequently oxidized to the sulfone (AZ0002) largely by CYP3A. Sulfones 189-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-222 28846049-8 2017 Lumacaftor is a strong inducer of CYP3A while ivacaftor is a CYP3A sensitive substrate. lumacaftor 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-39 28846049-8 2017 Lumacaftor is a strong inducer of CYP3A while ivacaftor is a CYP3A sensitive substrate. ivacaftor 46-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-66 28887089-6 2017 In addition, the inhibitory activities of steviol and stevioside towards the major cytochrome P450 enzymes CYP3A4, CYP2C9, CYP2D6, CYP1A2 and CYP2B6 were evaluated in vitro. stevioside 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 28887089-7 2017 We found that steviol moderately activated the PXR and AHR, resulting in the induction of their target genes including CYP3A4 and CYP1A2 in primary human hepatocytes. steviol 14-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 28887089-8 2017 A weak inhibition of CYP3A4 and CYP2C9 with steviol was also found. steviol 44-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 28895486-8 2017 The EVG/c/TDF/FTC contains cobicistat, a strong cytochrome P450 3A4 (CYP3A4) inhibitor, which can potentiate drug interactions involving metabolizing of medications via this pathway. Cobicistat 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-67 29108449-2 2017 More rarely, it has been described in HIV-positive patients on ritonavir (RTV) while using the inhaled corticosteroid fluticasone, which is metabolized through the cytochrome P450 3A4 (CYP3A4) enzyme system. Ritonavir 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-183 29108449-2 2017 More rarely, it has been described in HIV-positive patients on ritonavir (RTV) while using the inhaled corticosteroid fluticasone, which is metabolized through the cytochrome P450 3A4 (CYP3A4) enzyme system. Ritonavir 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 29108449-2 2017 More rarely, it has been described in HIV-positive patients on ritonavir (RTV) while using the inhaled corticosteroid fluticasone, which is metabolized through the cytochrome P450 3A4 (CYP3A4) enzyme system. Ritonavir 74-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-183 29108449-2 2017 More rarely, it has been described in HIV-positive patients on ritonavir (RTV) while using the inhaled corticosteroid fluticasone, which is metabolized through the cytochrome P450 3A4 (CYP3A4) enzyme system. Ritonavir 74-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 29108449-2 2017 More rarely, it has been described in HIV-positive patients on ritonavir (RTV) while using the inhaled corticosteroid fluticasone, which is metabolized through the cytochrome P450 3A4 (CYP3A4) enzyme system. Fluticasone 118-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-183 29108449-2 2017 More rarely, it has been described in HIV-positive patients on ritonavir (RTV) while using the inhaled corticosteroid fluticasone, which is metabolized through the cytochrome P450 3A4 (CYP3A4) enzyme system. Fluticasone 118-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 29108449-3 2017 In the presence of RTV, a known CYP3A4 enzyme inhibitor, the interaction can result in impaired metabolism and systemic accumulation of inhaled fluticasone resulting in iatrogenic CS. Ritonavir 19-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 29108449-3 2017 In the presence of RTV, a known CYP3A4 enzyme inhibitor, the interaction can result in impaired metabolism and systemic accumulation of inhaled fluticasone resulting in iatrogenic CS. Fluticasone 144-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 28893623-2 2017 Abiraterone is known to inhibit several drug metabolizing cytochrome P450 enzymes including CYP1A2, CYP2D6, CYP2C8, CYP2C9, CYP2C19, CYP3A4 and CYP3A5, but its effects on steroid metabolizing P450 enzymes are not clear. abiraterone 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 28945481-7 2017 RESULTS: The alleles CYP3A5*3 and CYP3A4*18B were significantly associated with dose-adjusted tacrolimus blood trough concentrations and had a strong time-genotype interaction with tacrolimus pharmacokinetics. Tacrolimus 94-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 28945481-7 2017 RESULTS: The alleles CYP3A5*3 and CYP3A4*18B were significantly associated with dose-adjusted tacrolimus blood trough concentrations and had a strong time-genotype interaction with tacrolimus pharmacokinetics. Tacrolimus 181-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 28945481-10 2017 Thus, genotyping of the CYP3A4 and CYP3A5 genes should be considered with respect to determining tacrolimus dose regimens during the post-transplantation period. Tacrolimus 97-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 28679023-2 2017 The effect of itraconazole (a strong CYP3A inhibitor) on the pharmacokinetics of etizolam (a substrate of CYP2C19 and CYP3A) was assessed in both extensive metabolizers (EMs) and poor metabolizers (PMs) of CYP2C19. Itraconazole 14-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-42 28679023-2 2017 The effect of itraconazole (a strong CYP3A inhibitor) on the pharmacokinetics of etizolam (a substrate of CYP2C19 and CYP3A) was assessed in both extensive metabolizers (EMs) and poor metabolizers (PMs) of CYP2C19. etizolam 81-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-123 28895486-8 2017 The EVG/c/TDF/FTC contains cobicistat, a strong cytochrome P450 3A4 (CYP3A4) inhibitor, which can potentiate drug interactions involving metabolizing of medications via this pathway. Cobicistat 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 29118985-13 2017 Learning points: Drug-drug interaction between ritonavir and triamcinolone can cause Cushing syndrome.Although triamcinolone has a half-life of 3 h, an intra-articular injection may be systematically absorbed for 3 weeks after injection, and adrenal suppression may last as long as 30 days.Co-administration of ritonavir and corticosteroids may result in an increase of plasma levels of corticosteroids levels, as they are both eliminated by CYP3A metabolism, and this interaction has the potential to prolong the half-life of triamcinolone several fold.No specific guidelines are available for the management of iatrogenic Cushing syndrome secondary to ritonavir and corticosteroids.One treatment option includes replacing ritonavir with a non-protease inhibitor-based regimen.Initiating hydrocortisone replacement therapy to prevent an adrenal crisis is also an alternate option. Ritonavir 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 442-447 30227099-2 2017 DDIs with Norvir (ritonavir) and combination products (eg, Kaletra [lopinavir/ritonavir]) containing ritonavir as a PK enhancer are relevant, because these drugs could affect exposures of CYP3A4 substrates. Lopinavir 68-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-194 29118985-13 2017 Learning points: Drug-drug interaction between ritonavir and triamcinolone can cause Cushing syndrome.Although triamcinolone has a half-life of 3 h, an intra-articular injection may be systematically absorbed for 3 weeks after injection, and adrenal suppression may last as long as 30 days.Co-administration of ritonavir and corticosteroids may result in an increase of plasma levels of corticosteroids levels, as they are both eliminated by CYP3A metabolism, and this interaction has the potential to prolong the half-life of triamcinolone several fold.No specific guidelines are available for the management of iatrogenic Cushing syndrome secondary to ritonavir and corticosteroids.One treatment option includes replacing ritonavir with a non-protease inhibitor-based regimen.Initiating hydrocortisone replacement therapy to prevent an adrenal crisis is also an alternate option. Triamcinolone 111-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 442-447 29118985-13 2017 Learning points: Drug-drug interaction between ritonavir and triamcinolone can cause Cushing syndrome.Although triamcinolone has a half-life of 3 h, an intra-articular injection may be systematically absorbed for 3 weeks after injection, and adrenal suppression may last as long as 30 days.Co-administration of ritonavir and corticosteroids may result in an increase of plasma levels of corticosteroids levels, as they are both eliminated by CYP3A metabolism, and this interaction has the potential to prolong the half-life of triamcinolone several fold.No specific guidelines are available for the management of iatrogenic Cushing syndrome secondary to ritonavir and corticosteroids.One treatment option includes replacing ritonavir with a non-protease inhibitor-based regimen.Initiating hydrocortisone replacement therapy to prevent an adrenal crisis is also an alternate option. Triamcinolone 111-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 442-447 28952408-0 2017 Influence of CYP3A and ABCB1 polymorphisms on cyclosporine concentrations in renal transplant recipients. Cyclosporine 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-18 28952408-1 2017 AIM: Cyclosporine is a substrate of CYP3A and ABCB1. Cyclosporine 5-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 29118985-13 2017 Learning points: Drug-drug interaction between ritonavir and triamcinolone can cause Cushing syndrome.Although triamcinolone has a half-life of 3 h, an intra-articular injection may be systematically absorbed for 3 weeks after injection, and adrenal suppression may last as long as 30 days.Co-administration of ritonavir and corticosteroids may result in an increase of plasma levels of corticosteroids levels, as they are both eliminated by CYP3A metabolism, and this interaction has the potential to prolong the half-life of triamcinolone several fold.No specific guidelines are available for the management of iatrogenic Cushing syndrome secondary to ritonavir and corticosteroids.One treatment option includes replacing ritonavir with a non-protease inhibitor-based regimen.Initiating hydrocortisone replacement therapy to prevent an adrenal crisis is also an alternate option. Triamcinolone 61-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 442-447 29065172-2 2017 Nevirapine is a known inhibitor of cytochrome P450 3A4, which metabolizes artemether and lumefantrine. Nevirapine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-54 28759864-7 2017 Our data show that tolvaptan is metabolized to at least 20 phase I metabolites, the biotransformation reactions being catalyzed mainly by CYP3A4 and CYP3A5 isoforms. Tolvaptan 19-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 29061956-2 2017 Most oxycodone is metabolized by N-demethylation to noroxycodone by CYP3A. Oxycodone 5-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 29061956-2 2017 Most oxycodone is metabolized by N-demethylation to noroxycodone by CYP3A. Nitrogen 33-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 29061956-2 2017 Most oxycodone is metabolized by N-demethylation to noroxycodone by CYP3A. noroxycodone 52-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 29061956-3 2017 Rifampin is a strong inducer of several drug-metabolizing enzymes, including CYP3A. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 29061956-4 2017 Hence, rifampin-induced CYP3A activity may decrease the effect of oxycodone. Rifampin 7-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 29061956-4 2017 Hence, rifampin-induced CYP3A activity may decrease the effect of oxycodone. Oxycodone 66-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 29065172-2 2017 Nevirapine is a known inhibitor of cytochrome P450 3A4, which metabolizes artemether and lumefantrine. Artemether 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-54 29065172-2 2017 Nevirapine is a known inhibitor of cytochrome P450 3A4, which metabolizes artemether and lumefantrine. Lumefantrine 89-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-54 28919040-6 2017 Structure-based design led to discovery of N1-hexyl-N5-benzyl-biguanide (HBB), which bound to the CYP3A4 heme with higher affinity than metformin. Heme 105-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 28919040-9 2017 CYP3A4 AA epoxygenase inhibition by biguanides thus demonstrates convergence between eicosanoid activity in mitochondria and biguanide action in cancer, opening a new avenue for cancer drug discovery. Biguanides 36-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28919040-2 2017 CYP3A4 was unexpectedly associated with breast cancer mitochondria and synthesized arachidonic acid (AA)-derived epoxyeicosatrienoic acids (EETs), which promoted the electron transport chain/respiration and inhibited AMPKalpha. Arachidonic Acid 83-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28919040-2 2017 CYP3A4 was unexpectedly associated with breast cancer mitochondria and synthesized arachidonic acid (AA)-derived epoxyeicosatrienoic acids (EETs), which promoted the electron transport chain/respiration and inhibited AMPKalpha. epoxyeicosatrienoic acids 113-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28919040-9 2017 CYP3A4 AA epoxygenase inhibition by biguanides thus demonstrates convergence between eicosanoid activity in mitochondria and biguanide action in cancer, opening a new avenue for cancer drug discovery. Eicosanoids 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28919040-2 2017 CYP3A4 was unexpectedly associated with breast cancer mitochondria and synthesized arachidonic acid (AA)-derived epoxyeicosatrienoic acids (EETs), which promoted the electron transport chain/respiration and inhibited AMPKalpha. eets 140-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28919040-9 2017 CYP3A4 AA epoxygenase inhibition by biguanides thus demonstrates convergence between eicosanoid activity in mitochondria and biguanide action in cancer, opening a new avenue for cancer drug discovery. Biguanides 36-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28919040-2 2017 CYP3A4 was unexpectedly associated with breast cancer mitochondria and synthesized arachidonic acid (AA)-derived epoxyeicosatrienoic acids (EETs), which promoted the electron transport chain/respiration and inhibited AMPKalpha. ampkalpha 217-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28904078-5 2017 We also observed the formation of heteromeric complexes of CYP2D6 with CYP2E1 and CYP3A4, and found a significant modulation of these interactions by 3,4-methylenedioxymethylamphetamine, a widespread drug of abuse metabolized by CYP2D6. N-Methyl-3,4-methylenedioxyamphetamine 150-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 28919040-4 2017 The diabetes drug metformin inhibited CYP3A4-mediated EET biosynthesis and depleted cancer cell-intrinsic EETs. Metformin 18-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 28919040-5 2017 Metformin bound to the active-site heme of CYP3A4 in a co-crystal structure, establishing CYP3A4 as a biguanide target. Metformin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 28919040-5 2017 Metformin bound to the active-site heme of CYP3A4 in a co-crystal structure, establishing CYP3A4 as a biguanide target. Metformin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 28919040-5 2017 Metformin bound to the active-site heme of CYP3A4 in a co-crystal structure, establishing CYP3A4 as a biguanide target. Heme 35-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 28919040-5 2017 Metformin bound to the active-site heme of CYP3A4 in a co-crystal structure, establishing CYP3A4 as a biguanide target. Heme 35-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 28919040-5 2017 Metformin bound to the active-site heme of CYP3A4 in a co-crystal structure, establishing CYP3A4 as a biguanide target. Biguanides 102-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 28919040-5 2017 Metformin bound to the active-site heme of CYP3A4 in a co-crystal structure, establishing CYP3A4 as a biguanide target. Biguanides 102-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 28919040-6 2017 Structure-based design led to discovery of N1-hexyl-N5-benzyl-biguanide (HBB), which bound to the CYP3A4 heme with higher affinity than metformin. hbb 73-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 28990114-5 2017 Commonly used antimicrobials, such as macrolide antibiotics and azole antifungals, interact significantly with the CYP3A4 enzyme pathway similarly to lovastatin, simvastatin, and atorvastatin. macrolide antibiotics 38-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 28990114-5 2017 Commonly used antimicrobials, such as macrolide antibiotics and azole antifungals, interact significantly with the CYP3A4 enzyme pathway similarly to lovastatin, simvastatin, and atorvastatin. Azoles 64-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 28990114-10 2017 Macrolides and selected antifungals can significantly increase drug levels of select statins, particularly those metabolized by the CYP3A4 pathway. Macrolides 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 29023392-9 2017 All curcuminoids exhibited multiple pharmacological effects in vitro, including potent antioxidant activity as well as inhibition of CYP2C9, CYP3A4 and lipoxygenase activity without affecting the release of TNF-alpha. curcuminoids 4-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 28261841-2 2017 Propafenone (PPF) exhibits extensive saturable presystemic biotransformation (first-pass effect) resulting in two active metabolites: 5-hydroxypropafenone (5-OH PPF) formed by CYP2D6 and N-depropylpropafenone (NDP) formed by both CYP3A4 and CYP1A2 enzymes. Propafenone 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-236 29022184-1 2017 INTRODUCTION: Mifepristone, a competitive glucocorticoid receptor antagonist approved for Cushing syndrome, and ketoconazole, an antifungal and steroidogenesis inhibitor, are both inhibitors of and substrates for cytochrome P450 (CYP3A4). Mifepristone 14-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-236 29022184-1 2017 INTRODUCTION: Mifepristone, a competitive glucocorticoid receptor antagonist approved for Cushing syndrome, and ketoconazole, an antifungal and steroidogenesis inhibitor, are both inhibitors of and substrates for cytochrome P450 (CYP3A4). Ketoconazole 112-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-236 29022184-2 2017 This study evaluated the pharmacokinetic effects of concomitant ketoconazole, a strong CYP3A4 inhibitor, on mifepristone. Ketoconazole 64-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 29022184-2 2017 This study evaluated the pharmacokinetic effects of concomitant ketoconazole, a strong CYP3A4 inhibitor, on mifepristone. Mifepristone 108-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 28444958-0 2017 Role of Cytochrome P450 3A4 and 1A2 Phenotyping in Patients with Advanced Non-small-Cell Lung Cancer Receiving Erlotinib Treatment. Erlotinib Hydrochloride 111-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-35 28444958-2 2017 This study assessed CYP3A4 (midazolam) and CYP1A2 (caffeine) phenotyping in plasma and dried blood spots (DBS) for predicting the pharmacokinetics and toxicity of erlotinib in 36 patients with advanced NSCLC. Erlotinib Hydrochloride 163-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 28425104-0 2017 Inactivation kinetics and residual activity of CYP3A4 after treatment with erythromycin. Erythromycin 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 28425104-1 2017 This study aimed to characterize the inactivation kinetics of cytochrome P450 3A4 (CYP3A4) by erythromycin, which involves mechanism-based inhibition (MBI), in detail. Erythromycin 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-81 28425104-1 2017 This study aimed to characterize the inactivation kinetics of cytochrome P450 3A4 (CYP3A4) by erythromycin, which involves mechanism-based inhibition (MBI), in detail. Erythromycin 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 28425104-9 2017 In conclusion, the relatively long-term evaluation of the kinetics of CYP3A4 inactivation revealed that the enzyme was not fully inactivated by erythromycin. Erythromycin 144-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 28261841-2 2017 Propafenone (PPF) exhibits extensive saturable presystemic biotransformation (first-pass effect) resulting in two active metabolites: 5-hydroxypropafenone (5-OH PPF) formed by CYP2D6 and N-depropylpropafenone (NDP) formed by both CYP3A4 and CYP1A2 enzymes. Propafenone 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-236 28261841-2 2017 Propafenone (PPF) exhibits extensive saturable presystemic biotransformation (first-pass effect) resulting in two active metabolites: 5-hydroxypropafenone (5-OH PPF) formed by CYP2D6 and N-depropylpropafenone (NDP) formed by both CYP3A4 and CYP1A2 enzymes. 5-hydroxypropafenone 134-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-236 28261841-2 2017 Propafenone (PPF) exhibits extensive saturable presystemic biotransformation (first-pass effect) resulting in two active metabolites: 5-hydroxypropafenone (5-OH PPF) formed by CYP2D6 and N-depropylpropafenone (NDP) formed by both CYP3A4 and CYP1A2 enzymes. 5-oh ppf 156-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-236 28503781-8 2017 Ketoconazole (strong CYP3A inhibitor) increased upadacitinib Cmax and AUC by 70% and 75%, respectively. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-26 28503781-8 2017 Ketoconazole (strong CYP3A inhibitor) increased upadacitinib Cmax and AUC by 70% and 75%, respectively. upadacitinib 48-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-26 28503781-12 2017 CONCLUSIONS: Strong CYP3A inhibition and broad CYP induction result in a weak and moderate effect, respectively, on upadacitinib exposures. upadacitinib 116-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-25 28942083-4 2017 Treatment with rifampicin, a ligand of PXR, translocated PXR from the cytoplasm to nucleus and increased expression levels of CYP3A4 mRNA in HepG2 cells cultured by the hanging drop method. Rifampin 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 28236252-2 2017 Paritaprevir is primarily metabolized by cytochrome P450 (CYP) 3A4 and is administered with a low dose of ritonavir to achieve drug concentrations suitable for once-daily dosing. paritaprevir 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-66 28258380-11 2017 Furthermore, coadministration of dasabuvir with a CYP3A inducer decreased dasabuvir exposures by 55-70%. dasabuvir 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 28258380-11 2017 Furthermore, coadministration of dasabuvir with a CYP3A inducer decreased dasabuvir exposures by 55-70%. dasabuvir 74-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 28185143-1 2017 BACKGROUND AND OBJECTIVES: 1-Aminobenzotriazole, a known time-dependent inhibitor of cytochrome P450 (CYP) enzymes, and ketoconazole, a strong inhibitor of the human CYP3A4 isozyme, are used as standard probe inhibitors to characterize the CYP and/or non-CYP-mediated metabolism of xenobiotics. 1-aminobenzotriazole 27-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-172 28185143-1 2017 BACKGROUND AND OBJECTIVES: 1-Aminobenzotriazole, a known time-dependent inhibitor of cytochrome P450 (CYP) enzymes, and ketoconazole, a strong inhibitor of the human CYP3A4 isozyme, are used as standard probe inhibitors to characterize the CYP and/or non-CYP-mediated metabolism of xenobiotics. Ketoconazole 120-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-172 28949811-0 2017 Characterization of Maternal and Fetal CYP3A-Mediated Progesterone Metabolism. Progesterone 54-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 28407303-2 2017 Rifampicin, an antitubercular agent, is one of the most potent inducers of hepatic and intestinal CYP3A4 thus increasing dihydropyridine metabolism. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 28407303-2 2017 Rifampicin, an antitubercular agent, is one of the most potent inducers of hepatic and intestinal CYP3A4 thus increasing dihydropyridine metabolism. 1,4-dihydropyridine 121-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 28949811-7 2017 6beta-OHP and 16alpha-OHP were both produced by CYP3A4 (2.3 and 1.3 microL/min/pmol, respectively) to a greater extent than by CYP3A5 (0.09 and 0.003 microL/min/pmol) and CYP3A7 (0.004 and 0.003 microL/min/pmol). 6beta-ohp 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 27995989-6 2017 CYP3A4*22/CYP3A5*3 genotype was nominally associated with grade 3/4 toxicity in patients receiving docetaxel-containing chemotherapy (P=0.0175). Docetaxel 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28949811-7 2017 6beta-OHP and 16alpha-OHP were both produced by CYP3A4 (2.3 and 1.3 microL/min/pmol, respectively) to a greater extent than by CYP3A5 (0.09 and 0.003 microL/min/pmol) and CYP3A7 (0.004 and 0.003 microL/min/pmol). 16alpha-ohp 14-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 28403692-6 2017 Vinblastine is metabolized by the hepatic P450 cytochrome isoenzyme CYP3A4, therefore, concomitant administration with protease inhibitors may increase plasma levels of vinblastine. Vinblastine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 28403692-6 2017 Vinblastine is metabolized by the hepatic P450 cytochrome isoenzyme CYP3A4, therefore, concomitant administration with protease inhibitors may increase plasma levels of vinblastine. Vinblastine 169-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 28403692-9 2017 Our hypothesis is that the hypokalemia could be a result of a tenofovir-mediated tubular damage triggered by the increased vinblastine serum levels secondary to a CYP3A4 inhibition by ritonavir. Tenofovir 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 28403692-9 2017 Our hypothesis is that the hypokalemia could be a result of a tenofovir-mediated tubular damage triggered by the increased vinblastine serum levels secondary to a CYP3A4 inhibition by ritonavir. Ritonavir 184-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 28569994-6 2017 Darunavir and lopinavir PBPK models that accounted for ritonavir CYP3A inhibition effects (linked PBPK models) were developed. Darunavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 28569994-6 2017 Darunavir and lopinavir PBPK models that accounted for ritonavir CYP3A inhibition effects (linked PBPK models) were developed. Lopinavir 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 28569994-9 2017 Additional exploratory analyses predicted CYP3A inhibition effects on darunavir or lopinavir exposure in simulated hepatically impaired subjects. Darunavir 70-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 28569994-9 2017 Additional exploratory analyses predicted CYP3A inhibition effects on darunavir or lopinavir exposure in simulated hepatically impaired subjects. Lopinavir 83-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 28569994-11 2017 Exploratory simulations using the linked darunavir or lopinavir PBPK models indicated CYP3A inhibition may further increase darunavir or lopinavir exposure in patients with hepatic impairment. Darunavir 41-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 28569994-11 2017 Exploratory simulations using the linked darunavir or lopinavir PBPK models indicated CYP3A inhibition may further increase darunavir or lopinavir exposure in patients with hepatic impairment. Lopinavir 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 28569994-11 2017 Exploratory simulations using the linked darunavir or lopinavir PBPK models indicated CYP3A inhibition may further increase darunavir or lopinavir exposure in patients with hepatic impairment. Darunavir 124-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 28569994-11 2017 Exploratory simulations using the linked darunavir or lopinavir PBPK models indicated CYP3A inhibition may further increase darunavir or lopinavir exposure in patients with hepatic impairment. Lopinavir 137-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 28777242-1 2017 OBJECTIVES: Several genetic factors were identified to be responsible for interidividual variability in tacrolimus (TAC) pharmacokinetics, with the predominant role of CYP3A5 and CYP3A4 polymorphisms. Tacrolimus 104-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 28722255-0 2017 Drug-drug interactions between triazole antifungal agents used to treat invasive aspergillosis and immunosuppressants metabolized by cytochrome P450 3A4. Triazoles 31-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-152 28976264-0 2017 Epistatic interactions among CYP2C19*2, CYP3A4 and GSTP1 on the cyclophosphamide therapy in lupus nephritis patients. Cyclophosphamide 64-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 28976264-1 2017 AIM: To investigate the impact of genetic variants in CYP2C9, CYP2C19, CYP3A4, GSTT1, GSTM1 and GSTP1 on the efficacy of cyclophosphamide (CYC) therapy in patients with lupus nephritis. Cyclophosphamide 121-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 28976264-1 2017 AIM: To investigate the impact of genetic variants in CYP2C9, CYP2C19, CYP3A4, GSTT1, GSTM1 and GSTP1 on the efficacy of cyclophosphamide (CYC) therapy in patients with lupus nephritis. Cyclophosphamide 139-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 27690733-2 2017 Carbamazepine (CBZ) is an antiepileptic drug with narrow therapeutic window and administration in humans receiving long-term therapy with diosmin (DSN) may occur, which leads to CYP3A4-mediated drug interactions. Carbamazepine 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 27690733-2 2017 Carbamazepine (CBZ) is an antiepileptic drug with narrow therapeutic window and administration in humans receiving long-term therapy with diosmin (DSN) may occur, which leads to CYP3A4-mediated drug interactions. Carbamazepine 15-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 27690733-2 2017 Carbamazepine (CBZ) is an antiepileptic drug with narrow therapeutic window and administration in humans receiving long-term therapy with diosmin (DSN) may occur, which leads to CYP3A4-mediated drug interactions. Diosmin 138-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 27690733-2 2017 Carbamazepine (CBZ) is an antiepileptic drug with narrow therapeutic window and administration in humans receiving long-term therapy with diosmin (DSN) may occur, which leads to CYP3A4-mediated drug interactions. Diosmin 147-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 27690733-14 2017 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to DSN-mediated inhibition of CYP3A4 enzyme, which indicates pharmacokinetic interaction present between DSN and CBZ. Carbamazepine 84-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 27690733-14 2017 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to DSN-mediated inhibition of CYP3A4 enzyme, which indicates pharmacokinetic interaction present between DSN and CBZ. Carbamazepine 84-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 27690733-14 2017 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to DSN-mediated inhibition of CYP3A4 enzyme, which indicates pharmacokinetic interaction present between DSN and CBZ. Diosmin 111-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 27690733-14 2017 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to DSN-mediated inhibition of CYP3A4 enzyme, which indicates pharmacokinetic interaction present between DSN and CBZ. Diosmin 111-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 27690733-14 2017 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to DSN-mediated inhibition of CYP3A4 enzyme, which indicates pharmacokinetic interaction present between DSN and CBZ. Diosmin 213-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 27690733-14 2017 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to DSN-mediated inhibition of CYP3A4 enzyme, which indicates pharmacokinetic interaction present between DSN and CBZ. Diosmin 213-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 27690733-14 2017 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to DSN-mediated inhibition of CYP3A4 enzyme, which indicates pharmacokinetic interaction present between DSN and CBZ. Carbamazepine 221-224 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 27690733-14 2017 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to DSN-mediated inhibition of CYP3A4 enzyme, which indicates pharmacokinetic interaction present between DSN and CBZ. Carbamazepine 221-224 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 27819189-7 2017 The results indicated that curculigoside could inhibit the activity of CYP1A2, CYP2C8, and CYP3A4, with IC50 values of 15.26, 11.93, and 9.47 muM, respectively, but that other CYP isoforms were not affected. curculigoside 27-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 27819189-8 2017 Enzyme kinetic studies showed that curculigoside was not only a noncompetitive inhibitor of CYP1A2, but also a competitive inhibitor of CYP2C8 and CYP3A4, with Ki values of 5.43, 3.54, and 3.35 muM, respectively. curculigoside 35-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 27819189-11 2017 The in vitro studies of curculigoside with CYP isoforms suggest that curculigoside has the potential to cause pharmacokinetic drug interactions with other coadministered drugs metabolized by CYP1A2, CYP2C8, and CYP3A4. curculigoside 69-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-217 28722255-3 2017 All of these agents are inhibitors of cytochrome P450 3A4, which plays a key role in metabolizing immunosuppressant drugs such as cyclosporine, tacrolimus, and sirolimus. Cyclosporine 130-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-57 28722255-3 2017 All of these agents are inhibitors of cytochrome P450 3A4, which plays a key role in metabolizing immunosuppressant drugs such as cyclosporine, tacrolimus, and sirolimus. Tacrolimus 144-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-57 28722255-3 2017 All of these agents are inhibitors of cytochrome P450 3A4, which plays a key role in metabolizing immunosuppressant drugs such as cyclosporine, tacrolimus, and sirolimus. Sirolimus 160-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-57 28722255-5 2017 In this article, we review the evidence for the extent of inhibition of cytochrome P450 3A4 by each of these triazole antifungal drugs and assess their effects on cyclosporine, tacrolimus, and sirolimus. Triazoles 109-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-91 28951593-0 2017 MicroRNA regulation of CYP 1A2, CYP3A4 and CYP2E1 expression in acetaminophen toxicity. Acetaminophen 64-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 28787271-7 2017 CYP2D6 and CYP3A were phenotyped with HPLC-MS using the concentration of endogenous substrate of the enzyme and its urinary metabolites [6-hydroxy-1,2,3,4-tetrahydro-beta-carboline(6-HO-THBC) to pinoline ratio for CYP2D6 and 6-beta-hydroxycortisol to cortisol ratio for CYP3A]. Hydrocortisone 239-247 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-16 28787271-0 2017 Genotyping and phenotyping of CYP2D6 and CYP3A isoenzymes in patients with alcohol use disorder: correlation with haloperidol plasma concentration. Alcohols 75-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 28787271-0 2017 Genotyping and phenotyping of CYP2D6 and CYP3A isoenzymes in patients with alcohol use disorder: correlation with haloperidol plasma concentration. Haloperidol 114-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 28787271-7 2017 CYP2D6 and CYP3A were phenotyped with HPLC-MS using the concentration of endogenous substrate of the enzyme and its urinary metabolites [6-hydroxy-1,2,3,4-tetrahydro-beta-carboline(6-HO-THBC) to pinoline ratio for CYP2D6 and 6-beta-hydroxycortisol to cortisol ratio for CYP3A]. 6-hydroxy-1,2,3,4-tetrahydro-beta-carboline 137-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-16 28787271-7 2017 CYP2D6 and CYP3A were phenotyped with HPLC-MS using the concentration of endogenous substrate of the enzyme and its urinary metabolites [6-hydroxy-1,2,3,4-tetrahydro-beta-carboline(6-HO-THBC) to pinoline ratio for CYP2D6 and 6-beta-hydroxycortisol to cortisol ratio for CYP3A]. 6-ho-thbc 181-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-16 28787271-7 2017 CYP2D6 and CYP3A were phenotyped with HPLC-MS using the concentration of endogenous substrate of the enzyme and its urinary metabolites [6-hydroxy-1,2,3,4-tetrahydro-beta-carboline(6-HO-THBC) to pinoline ratio for CYP2D6 and 6-beta-hydroxycortisol to cortisol ratio for CYP3A]. 6-methoxytryptoline 195-203 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-16 28787271-7 2017 CYP2D6 and CYP3A were phenotyped with HPLC-MS using the concentration of endogenous substrate of the enzyme and its urinary metabolites [6-hydroxy-1,2,3,4-tetrahydro-beta-carboline(6-HO-THBC) to pinoline ratio for CYP2D6 and 6-beta-hydroxycortisol to cortisol ratio for CYP3A]. 6 beta-hydroxycortisol 225-247 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-16 28951593-7 2017 Collectively, the data suggest that miRNA elevations in APAP toxicity represent a regulatory response to modify CYP1A2, CYP3A4 and CYP2E1 translation due to cellular stress and injury. Acetaminophen 56-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 29075133-3 2017 CYP3A4 isoenzyme activity was determined by urine cortisol and 6-beta-hydroxycortisol levels. Hydrocortisone 50-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28915895-1 2017 BACKGROUND: Dolutegravir (DTG) is metabolized mainly by uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1), and partly by cytochrome P450 3A (CYP3A). dolutegravir 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-152 29075133-3 2017 CYP3A4 isoenzyme activity was determined by urine cortisol and 6-beta-hydroxycortisol levels. 6 beta-hydroxycortisol 63-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28915895-1 2017 BACKGROUND: Dolutegravir (DTG) is metabolized mainly by uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1), and partly by cytochrome P450 3A (CYP3A). dolutegravir 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-159 29075133-5 2017 RESULTS: Low mean 6-beta-hydroxycortisol/cortisol ratio is indicative of impaired CYP3A4 activity and was associated with higher risk of thrombosis (b coefficient=0.022, SE 0.009, p=0.021 in the linear regression model). 6 beta-hydroxycortisol 18-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 28915895-1 2017 BACKGROUND: Dolutegravir (DTG) is metabolized mainly by uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1), and partly by cytochrome P450 3A (CYP3A). dolutegravir 26-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-152 29075133-5 2017 RESULTS: Low mean 6-beta-hydroxycortisol/cortisol ratio is indicative of impaired CYP3A4 activity and was associated with higher risk of thrombosis (b coefficient=0.022, SE 0.009, p=0.021 in the linear regression model). Hydrocortisone 32-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 28915895-1 2017 BACKGROUND: Dolutegravir (DTG) is metabolized mainly by uridine diphosphate (UDP)-glucuronosyltransferase 1A1 (UGT1A1), and partly by cytochrome P450 3A (CYP3A). dolutegravir 26-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-159 28522317-5 2017 Predominantly, 17-alpha hydroxyprogesterone caproate is metabolized by CYP3A4 and CYP3A5 enzymes. 17 alpha-Hydroxyprogesterone Caproate 15-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 27692933-2 2017 The N-demethylation by CYP3A4/5 and the O-demethylation by CYP2D6 in human liver microsomes (HLM) followed Michaelis-Menten kinetics, with intrinsic clearances of 1.46muL/min/mg and 0.35muL/min/mg, respectively. Nitrogen 4-5 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 27692933-7 2017 Incubations of HLM with phase I and phase II drug probes showed that oxycodone mainly decreased the in vitro activities of CYP2D6, CYP3A4/5, UGT1A3, UGT1A6 and UGT2B subfamily with an important impact on UGT2B7. Oxycodone 69-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 28505263-2 2017 Subsequent in vitro assessment confirmed inhibition of cytochrome P450 (CYP) 2C19 and CYP3A4 by meropenem, suggesting that during meropenem treatment, narrow therapeutic index drugs metabolized by these CYPs require close monitoring. Meropenem 96-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 28388255-0 2017 Boosting axitinib exposure with a CYP3A4 inhibitor, making axitinib treatment personal. Axitinib 9-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 28388255-0 2017 Boosting axitinib exposure with a CYP3A4 inhibitor, making axitinib treatment personal. Axitinib 59-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 28522317-6 2017 OBJECTIVE: We sought to: (1) determine the relation between 17-alpha hydroxyprogesterone caproate plasma concentrations and single nucleotide polymorphisms in CYP3A4 and CYP3A5; (2) test the association between progesterone receptor single nucleotide polymorphisms and spontaneous preterm birth; and (3) test whether the association between plasma concentrations of 17-alpha hydroxyprogesterone caproate and spontaneous preterm birth varied by progesterone receptor single nucleotide polymorphisms. 17 alpha-Hydroxyprogesterone Caproate 60-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 28522317-6 2017 OBJECTIVE: We sought to: (1) determine the relation between 17-alpha hydroxyprogesterone caproate plasma concentrations and single nucleotide polymorphisms in CYP3A4 and CYP3A5; (2) test the association between progesterone receptor single nucleotide polymorphisms and spontaneous preterm birth; and (3) test whether the association between plasma concentrations of 17-alpha hydroxyprogesterone caproate and spontaneous preterm birth varied by progesterone receptor single nucleotide polymorphisms. 17 alpha-Hydroxyprogesterone Caproate 366-403 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 28370390-12 2017 CONCLUSIONS: Voriconazole pharmacokinetics is modulated by infusion rate, an autoinhibitory contribution voriconazole metabolism by CYP3A and 2C19 and to a lesser extent its main N-oxide metabolite for CYP2C19. Voriconazole 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-146 28676933-2 2017 The metabolism of temsirolimus and its active metabolite sirolimus mainly depends on cytochrome P450 3A4/5 (CYP3A4/A5) and the ABCB1 transporter. temsirolimus 18-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-106 28676933-2 2017 The metabolism of temsirolimus and its active metabolite sirolimus mainly depends on cytochrome P450 3A4/5 (CYP3A4/A5) and the ABCB1 transporter. temsirolimus 18-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 28676933-2 2017 The metabolism of temsirolimus and its active metabolite sirolimus mainly depends on cytochrome P450 3A4/5 (CYP3A4/A5) and the ABCB1 transporter. Sirolimus 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-106 28676933-2 2017 The metabolism of temsirolimus and its active metabolite sirolimus mainly depends on cytochrome P450 3A4/5 (CYP3A4/A5) and the ABCB1 transporter. Sirolimus 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 28255850-8 2017 Vemurafenib appears to be a substrate and inducer of cytochrome P450 (CYP) 3A4, a moderate inhibitor of CYP1A2 and both a substrate and inhibitor of the drug efflux transporters P-glycoprotein and breast cancer resistance protein. Vemurafenib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-78 28301096-4 2017 An open-label, phase 1 clinical study (NCT02140268) evaluated the pharmacokinetics of the CYP3A4 substrate midazolam when administered with and without tenapanor. Midazolam 107-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 28370390-1 2017 AIMS: The pharmacokinetics of voriconazole show a nonlinear dose-exposure relationship caused by inhibition of its own CYP3A-dependent metabolism. Voriconazole 30-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-124 28370390-11 2017 Concentration giving 50% CYP inhibition of voriconazole N-oxide was 146 +- 23 mumol l-1 for CYP3A4, and 40.2 +- 4.2 mumol l-1 for CYP2C19. Voriconazole N-Oxide 43-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 28370390-12 2017 CONCLUSIONS: Voriconazole pharmacokinetics is modulated by infusion rate, an autoinhibitory contribution voriconazole metabolism by CYP3A and 2C19 and to a lesser extent its main N-oxide metabolite for CYP2C19. Voriconazole 105-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-146 28610444-4 2017 Of note, midostaurin is metabolized by cytochrome P450-3A4 (CYP3A4); therefore, concomitant strong CYP3A4 inhibitors should be used with caution. midostaurin 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-58 28639119-0 2017 A pharmacokinetic drug-drug interaction study between selexipag and midazolam, a CYP3A4 substrate, in healthy male subjects. selexipag 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 28639119-0 2017 A pharmacokinetic drug-drug interaction study between selexipag and midazolam, a CYP3A4 substrate, in healthy male subjects. Midazolam 68-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 28639119-1 2017 PURPOSE: In vitro data showed that selexipag and its active metabolite (ACT-333679) have an inductive effect on CYP3A4, CYP2B6, and CYP2C9 at concentrations approximately 100-fold higher than the maximum plasma concentration (C max) measured under steady-state conditions. selexipag 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 28639119-2 2017 In order to confirm in vivo the lack of induction at the enterocyte level, we assessed the effect of selexipag on midazolam, a substrate of hepatic and intestinal CYP3A4. selexipag 101-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 28639119-2 2017 In order to confirm in vivo the lack of induction at the enterocyte level, we assessed the effect of selexipag on midazolam, a substrate of hepatic and intestinal CYP3A4. Midazolam 114-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 28610444-4 2017 Of note, midostaurin is metabolized by cytochrome P450-3A4 (CYP3A4); therefore, concomitant strong CYP3A4 inhibitors should be used with caution. midostaurin 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 28610444-4 2017 Of note, midostaurin is metabolized by cytochrome P450-3A4 (CYP3A4); therefore, concomitant strong CYP3A4 inhibitors should be used with caution. midostaurin 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 27231113-3 2017 We describe an interaction between the new anticancer agent idelalisib (CYP 3A4 inhibitor) and diazepam (CYP 3A4 substrate) that resulted in altered mental status and type II respiratory failure resulting in hospitalization. idelalisib 60-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-79 28666968-5 2017 Reaction phenotyping studies demonstrated that CYP3A mediated the metabolism of the two bufadienolides with a high specific selectivity. Bufanolides 88-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 28666968-8 2017 This study can provide important data for elucidating the phase I metabolism of GB and AB and can lead to a better understanding of the bufadienolide-CYP3A interaction which is helpful for preclinical development and rational use of bufadienolides. gamabufotalin 80-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 28666968-8 2017 This study can provide important data for elucidating the phase I metabolism of GB and AB and can lead to a better understanding of the bufadienolide-CYP3A interaction which is helpful for preclinical development and rational use of bufadienolides. bufadienolide 136-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 28666968-8 2017 This study can provide important data for elucidating the phase I metabolism of GB and AB and can lead to a better understanding of the bufadienolide-CYP3A interaction which is helpful for preclinical development and rational use of bufadienolides. Bufanolides 233-247 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 27231113-3 2017 We describe an interaction between the new anticancer agent idelalisib (CYP 3A4 inhibitor) and diazepam (CYP 3A4 substrate) that resulted in altered mental status and type II respiratory failure resulting in hospitalization. idelalisib 60-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-112 27231113-3 2017 We describe an interaction between the new anticancer agent idelalisib (CYP 3A4 inhibitor) and diazepam (CYP 3A4 substrate) that resulted in altered mental status and type II respiratory failure resulting in hospitalization. Diazepam 95-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-79 27231113-3 2017 We describe an interaction between the new anticancer agent idelalisib (CYP 3A4 inhibitor) and diazepam (CYP 3A4 substrate) that resulted in altered mental status and type II respiratory failure resulting in hospitalization. Diazepam 95-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-112 28495568-4 2017 DDIs with rifampicin and itraconazole were simulated using in vivo Rdif (ratio of diffusional uptake to active uptake) and beta (the fraction of the sum of intrinsic clearances for metabolism and biliary excretion in all possible itineraries of intracellular drugs including basolateral efflux) estimated by static analyses based on the extended clearance concept, in vivo inhibition constant (Ki) for hepatic OATPs reported previously, and in vivo Ki for CYP3A determined from DDI data with midazolam and itraconazole. Rifampin 10-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 456-461 28479356-2 2017 Repaglinide (RPG) is transported into the liver by OATP1B1 and then is metabolized by CYP2C8 and CYP3A4. repaglinide 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 28479356-2 2017 Repaglinide (RPG) is transported into the liver by OATP1B1 and then is metabolized by CYP2C8 and CYP3A4. repaglinide 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 28238899-0 2017 Estimation of the Contribution of CYP2C8 and CYP3A4 in Repaglinide Metabolism by Human Liver Microsomes Under Various Buffer Conditions. repaglinide 55-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 28238899-2 2017 In the present study, therefore, the possibility of buffer condition dependence of the fraction metabolized by CYP2C8 (fm2C8) for repaglinide, a dual substrate of CYP2C8 and CYP3A4, was estimated using human liver microsomes under various buffer conditions. repaglinide 130-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 28238899-3 2017 Montelukast and ketoconazole showed a potent and concentration-dependent inhibition of CYP2C8-mediated paclitaxel 6alpha-hydroxylation and CYP3A4-mediated triazolam alpha-hydroxylation, respectively, without dependence on the buffer condition. montelukast 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 28238899-3 2017 Montelukast and ketoconazole showed a potent and concentration-dependent inhibition of CYP2C8-mediated paclitaxel 6alpha-hydroxylation and CYP3A4-mediated triazolam alpha-hydroxylation, respectively, without dependence on the buffer condition. Ketoconazole 16-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 28238899-3 2017 Montelukast and ketoconazole showed a potent and concentration-dependent inhibition of CYP2C8-mediated paclitaxel 6alpha-hydroxylation and CYP3A4-mediated triazolam alpha-hydroxylation, respectively, without dependence on the buffer condition. Triazolam 155-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 28479356-5 2017 The time profiles of RPG and the inhibitors were analyzed by PBPK models, considering the inhibition of OATP1B1 and CYP3A4 by CsA or OATP1B1 inhibition by GEM and its glucuronide and the mechanism-based inhibition of CYP2C8 by GEM glucuronide. Cyclosporine 126-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 28817905-0 2017 Re: CYP3A4 Induction by Rifampin: An Alternative Pathway for Vitamin D Inactivation in Patients with CYP24A1 Mutations. Rifampin 24-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 28479356-5 2017 The time profiles of RPG and the inhibitors were analyzed by PBPK models, considering the inhibition of OATP1B1 and CYP3A4 by CsA or OATP1B1 inhibition by GEM and its glucuronide and the mechanism-based inhibition of CYP2C8 by GEM glucuronide. Gemfibrozil 155-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 28495568-4 2017 DDIs with rifampicin and itraconazole were simulated using in vivo Rdif (ratio of diffusional uptake to active uptake) and beta (the fraction of the sum of intrinsic clearances for metabolism and biliary excretion in all possible itineraries of intracellular drugs including basolateral efflux) estimated by static analyses based on the extended clearance concept, in vivo inhibition constant (Ki) for hepatic OATPs reported previously, and in vivo Ki for CYP3A determined from DDI data with midazolam and itraconazole. Itraconazole 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 456-461 28817905-0 2017 Re: CYP3A4 Induction by Rifampin: An Alternative Pathway for Vitamin D Inactivation in Patients with CYP24A1 Mutations. Vitamin D 61-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 28616684-0 2017 Influence of Ethanol on Darunavir Hepatic Clearance and Intracellular PK/PD in HIV-Infected Monocytes, and CYP3A4-Darunavir Interactions Using Inhibition and in Silico Binding Studies. Darunavir 114-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 28704257-0 2017 The combination of CYP3A4*22 and CYP3A5*3 single-nucleotide polymorphisms determines tacrolimus dose requirement after kidney transplantation. Tacrolimus 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 28616684-10 2017 Our docking results projected that ethanol increases the average distance between DRV and CYP3A4 heme, and alter the orientation of DRV-CYP3A4 binding. Ethanol 35-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 28616684-10 2017 Our docking results projected that ethanol increases the average distance between DRV and CYP3A4 heme, and alter the orientation of DRV-CYP3A4 binding. Ethanol 35-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 28616684-10 2017 Our docking results projected that ethanol increases the average distance between DRV and CYP3A4 heme, and alter the orientation of DRV-CYP3A4 binding. Heme 97-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 28546104-0 2017 Development of a paediatric physiologically based pharmacokinetic model to assess the impact of drug-drug interactions in tuberculosis co-infected malaria subjects: A case study with artemether-lumefantrine and the CYP3A4-inducer rifampicin. Rifampin 230-240 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-221 28546104-4 2017 The concomitant treatment of AL with tuberculosis chemotherapy, which includes the CYP3A4 inducer rifampicin, increases the risk of parasite recrudescence and malaria treatment failure. Aluminum 29-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 28546104-4 2017 The concomitant treatment of AL with tuberculosis chemotherapy, which includes the CYP3A4 inducer rifampicin, increases the risk of parasite recrudescence and malaria treatment failure. Rifampin 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 29050342-3 2017 Here, we found that CYP3A4 expression and its epoxy-product, 11,12-epoxyeicosatrienoic acid (11,12-EET) was enhanced in tamoxifen (TAM)-resistant MCF-7 (TAMR-MCF-7) breast cancer cells compared to control MCF-7 cells. Tamoxifen 131-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 28970799-6 2017 We found that proteins carrying mutations A115V, T142A located close to the FMN binding site had reduced flavin content compared to WT POR and lost almost all activity to metabolize androstenedione via CYP19A1 and showed reduced CYP3A4 activity. Androstenedione 182-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 229-235 28970799-8 2017 The mutation Q153R initially identified in a patient with disordered steroidogenesis showed remarkably increased activities of both CYP19A1 and CYP3A4 without any significant change in flavin content, indicating improved protein-protein interactions between POR Q153R and some P450 proteins. 4,6-dinitro-o-cresol 185-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 28645473-1 2017 Non-dihydropyridine calcium channel blockers (non-DHP CCBs) possess combined P-glycoprotein and moderate CYP3A4 inhibition, which may lead to increased exposure of medications that are substrates for these metabolic pathways, such as rivaroxaban. 1,4-dihydropyridine 50-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 28729056-6 2017 Docking and drug-metabolizing activity studies demonstrated that CYP3A4 was likely the main target of auriculatone, and that auriculatone elicited the hepatoprotective effect possibly through inhibiting CYP3A4"s metabolism of APAP to the toxic metabolite NAPQI. auriculatone 102-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 28729056-6 2017 Docking and drug-metabolizing activity studies demonstrated that CYP3A4 was likely the main target of auriculatone, and that auriculatone elicited the hepatoprotective effect possibly through inhibiting CYP3A4"s metabolism of APAP to the toxic metabolite NAPQI. auriculatone 102-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 28729056-6 2017 Docking and drug-metabolizing activity studies demonstrated that CYP3A4 was likely the main target of auriculatone, and that auriculatone elicited the hepatoprotective effect possibly through inhibiting CYP3A4"s metabolism of APAP to the toxic metabolite NAPQI. auriculatone 125-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 28729056-6 2017 Docking and drug-metabolizing activity studies demonstrated that CYP3A4 was likely the main target of auriculatone, and that auriculatone elicited the hepatoprotective effect possibly through inhibiting CYP3A4"s metabolism of APAP to the toxic metabolite NAPQI. Acetaminophen 226-230 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 28729056-6 2017 Docking and drug-metabolizing activity studies demonstrated that CYP3A4 was likely the main target of auriculatone, and that auriculatone elicited the hepatoprotective effect possibly through inhibiting CYP3A4"s metabolism of APAP to the toxic metabolite NAPQI. N-acetyl-4-benzoquinoneimine 255-260 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 29050342-0 2017 Role of the CYP3A4-mediated 11,12-epoxyeicosatrienoic acid pathway in the development of tamoxifen-resistant breast cancer. 11,12-epoxy-5,8,14-eicosatrienoic acid 28-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 29050342-0 2017 Role of the CYP3A4-mediated 11,12-epoxyeicosatrienoic acid pathway in the development of tamoxifen-resistant breast cancer. Tamoxifen 89-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 29050342-3 2017 Here, we found that CYP3A4 expression and its epoxy-product, 11,12-epoxyeicosatrienoic acid (11,12-EET) was enhanced in tamoxifen (TAM)-resistant MCF-7 (TAMR-MCF-7) breast cancer cells compared to control MCF-7 cells. tamr 153-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 29050342-3 2017 Here, we found that CYP3A4 expression and its epoxy-product, 11,12-epoxyeicosatrienoic acid (11,12-EET) was enhanced in tamoxifen (TAM)-resistant MCF-7 (TAMR-MCF-7) breast cancer cells compared to control MCF-7 cells. 11,12-epoxy-5,8,14-eicosatrienoic acid 61-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 29050342-3 2017 Here, we found that CYP3A4 expression and its epoxy-product, 11,12-epoxyeicosatrienoic acid (11,12-EET) was enhanced in tamoxifen (TAM)-resistant MCF-7 (TAMR-MCF-7) breast cancer cells compared to control MCF-7 cells. 11,12-epoxy-5,8,14-eicosatrienoic acid 93-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 29050342-3 2017 Here, we found that CYP3A4 expression and its epoxy-product, 11,12-epoxyeicosatrienoic acid (11,12-EET) was enhanced in tamoxifen (TAM)-resistant MCF-7 (TAMR-MCF-7) breast cancer cells compared to control MCF-7 cells. Tamoxifen 120-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 29050342-8 2017 Our findings suggest that the CYP3A4-mediated EET pathway represents a potential therapeutic target for the treatment of tamoxifen-resistant breast cancer. Tamoxifen 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 28814868-0 2017 Nano-sized cytochrome P450 3A4 inhibitors to block hepatic metabolism of docetaxel. Docetaxel 73-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-30 28786954-6 2017 Using human liver microsomes, a reversible inhibition assay revealed that Gom A was a competitive inhibitor with a KI value of 1.10 microM, and the time- and NADPH-dependent CYP3A inhibition of Gom A was observed in a time-dependent inhibition assay (KI = 0.35 microM, kinact = 1.96 min-1). NADP 158-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-179 28786954-6 2017 Using human liver microsomes, a reversible inhibition assay revealed that Gom A was a competitive inhibitor with a KI value of 1.10 microM, and the time- and NADPH-dependent CYP3A inhibition of Gom A was observed in a time-dependent inhibition assay (KI = 0.35 microM, kinact = 1.96 min-1). schizandrol B 194-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-179 28571685-0 2017 Activation of the aryl hydrocarbon receptor decreases rifampicin-induced CYP3A4 expression in primary human hepatocytes and HepaRG. Rifampin 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 28571685-6 2017 We also investigated whether knockdown of AhR using siRNA affected the basal expression of PXR and CYP3A4 and induction of CYP3A4 by rifampicin, TCDD and 3MI. Rifampin 133-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 28571685-8 2017 Moreover, in both HepaRG and PHHs, AhR activation decreased rifampicin-induced expression of CYP3A4 mRNA. Rifampin 60-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 28571685-9 2017 Knock-down of AhR in PHHs increased both basal and rifampicin-induced expression of CYP3A4 mRNA. Rifampin 51-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 28814868-7 2017 Nanoparticles of poly(lactic-co-glycolic) acid (PLGA) with a hydrodynamic diameter of 63 nm, functionalized with galactosamine, showed efficient in vitro CYP3A4 inhibition and the highest accumulation in hepatocytes. Polylactic Acid-Polyglycolic Acid Copolymer 17-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 28814868-7 2017 Nanoparticles of poly(lactic-co-glycolic) acid (PLGA) with a hydrodynamic diameter of 63 nm, functionalized with galactosamine, showed efficient in vitro CYP3A4 inhibition and the highest accumulation in hepatocytes. Galactosamine 113-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 28621555-4 2017 The model of donors" CYP3A5 rs776746 and recipients" CYP3A4 rs2242480 could predict tacrolimus metabolism at week 1 and the model of donors" CYP3A5 rs776746, recipients" CYP3A4 rs2242480, recipients" SLC28A3 rs7853758 and hemoglobin could predict tacrolimus disposition at weeks 2, 3 and 4. Tacrolimus 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 28601507-0 2017 Synthesis and pharmacological evaluation of glycine amide derivatives as novel vascular adhesion protein-1 inhibitors without CYP3A4 and CYP2C19 inhibition. glycine amide 44-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 28621555-4 2017 The model of donors" CYP3A5 rs776746 and recipients" CYP3A4 rs2242480 could predict tacrolimus metabolism at week 1 and the model of donors" CYP3A5 rs776746, recipients" CYP3A4 rs2242480, recipients" SLC28A3 rs7853758 and hemoglobin could predict tacrolimus disposition at weeks 2, 3 and 4. Tacrolimus 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 28601507-3 2017 As a result, we identified 3-chloro-4-{4-[5-(3-{[glycyl(methyl)amino]methyl}phenyl)pyrimidin-2-yl]piperazin-1-yl}benzoic acid (17h) as a novel orally active VAP-1 inhibitor, with 14-fold increased human VAP-1 inhibitory activity compared to 1, without CYP3A4 and CYP2C19 inhibition. Tetrahydrogestrinone 127-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 252-258 28050888-0 2017 A New CYP3A5*3 and CYP3A4*22 Cluster Influencing Tacrolimus Target Concentrations: A Population Approach. Tacrolimus 49-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 28280092-4 2017 Enzalutamide is a strong cytochrome P450 3A4 (CYP3A4) inducer, and ETs are commonly metabolized by CYP3A4. enzalutamide 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-44 28280092-4 2017 Enzalutamide is a strong cytochrome P450 3A4 (CYP3A4) inducer, and ETs are commonly metabolized by CYP3A4. enzalutamide 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 28050888-1 2017 BACKGROUND: Single nucleotide polymorphisms (SNPs) in the CYP3A5 and CYP3A4 genes have been reported to be an important cause of variability in the pharmacokinetics of tacrolimus in renal transplant patients. Tacrolimus 168-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 28160505-12 2017 We suggest that the mechanism underlying the effect of perazine on RIS metabolism is based on an inhibition of CYP2D6 and CYP3A4 activity. Perazine 55-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 28160505-12 2017 We suggest that the mechanism underlying the effect of perazine on RIS metabolism is based on an inhibition of CYP2D6 and CYP3A4 activity. Risperidone 67-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 28500872-10 2017 The scores for the BSID mental scale improved with increasing cord blood mercury concentrations for carriers of the most active alleles (beta[95% CI]:=2.9[1.53,4.27] for CYP3A7 rs2257401 GG+GC, 2.51[1.04,3.98] for CYP3A5 rs776746 AA+AG and 2.31[0.12,4.50] for CYP3A4 rs2740574 GG+AG). Mercury 73-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 260-266 28455946-0 2017 Response to "Pharmacogenetics of Voriconazole: CYP2C19 but Also CYP3A4 Need to Be Genotyped" - The Role of CYP3A4 and CYP3A5 Polymorphisms in Clinical Pharmacokinetics of Voriconazole. Voriconazole 33-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 28455946-0 2017 Response to "Pharmacogenetics of Voriconazole: CYP2C19 but Also CYP3A4 Need to Be Genotyped" - The Role of CYP3A4 and CYP3A5 Polymorphisms in Clinical Pharmacokinetics of Voriconazole. Voriconazole 33-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 28462502-2 2017 Quercetin is a plant-based flavonoid with inhibitory effects on P-glycoprotein (P-gp) and CYP3A4 and also antioxidant properties. Quercetin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 28050888-8 2017 CONCLUSIONS: Tacrolimus disposition in renal transplant recipients was described using a new population pharmacokinetic model that included the CYP3A5*3 and CYP3A4*22 genotype, age, and hematocrit. Tacrolimus 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 28182291-0 2017 Pharmacogenetics of Voriconazole: CYP2C19 but Also CYP3A4 Need to Be Genotyped. Voriconazole 20-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 27935260-7 2017 Studies using incubations with nicotinamide adenine dinucleotide phosphate-fortified pHLM with or without uridine 5"-diphosphoglucuronic acid and incubations with CYP-enzymes identified the main metabolic pathway of flubromazolam as hydroxylation on the alpha- and/or 4-position mediated by CYP3A4 and CYP3A5, with subsequent glucuronidation of the hydroxylated metabolites as well as of the parent drug. NADP 31-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 291-297 28462502-2 2017 Quercetin is a plant-based flavonoid with inhibitory effects on P-glycoprotein (P-gp) and CYP3A4 and also antioxidant properties. Flavonoids 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 28500872-12 2017 The interaction between the CYP3A genes and total mercury was significant (p<0.05) in European cohorts only. Mercury 50-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 27935260-7 2017 Studies using incubations with nicotinamide adenine dinucleotide phosphate-fortified pHLM with or without uridine 5"-diphosphoglucuronic acid and incubations with CYP-enzymes identified the main metabolic pathway of flubromazolam as hydroxylation on the alpha- and/or 4-position mediated by CYP3A4 and CYP3A5, with subsequent glucuronidation of the hydroxylated metabolites as well as of the parent drug. flubromazolam 216-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 291-297 28697165-3 2017 CYP3A4 and CYP3A5 enzymes of cytochrome p450 enzyme system are responsible in vincristine metabolism. Vincristine 78-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 27935260-10 2017 Based on the data presented here, flubromazolam is primarily metabolized by CYP3A4/5 with a high protein-binding and a predicted low clearance. flubromazolam 34-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 28810573-0 2017 Warfarin-induced life-threatening bleeding associated with a CYP3A4 loss-of-function mutation in an acute limb ischemia patient: Case report and review of the literature. Warfarin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 28810573-4 2017 In this patient, a cytochrome P450 3A4 loss-of-function mutation decreased the effective dose of warfarin. Warfarin 97-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-38 28462502-12 2017 Additionally, DoxQ inhibited CYP3A4 and demonstrated higher cellular uptake by MDCK-MDR cells than doxorubicin. doxq 14-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 28535410-2 2017 In vitro studies and Phase I trials indicate that perampanel is metabolized almost exclusively by CYP3A, with an elimination half-life (t1/2) averaging approximately 105h. perampanel 50-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 29050276-0 2017 A new donors" CYP3A5 and recipients" CYP3A4 cluster predicting tacrolimus disposition, and new-onset hypertension in Chinese liver transplant patients. Tacrolimus 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 28484975-2 2017 METHODS: A cocktail of subtherapeutic doses of bosentan, repaglinide, clarithromycin, darunavir, simeprevir, and midazolam (CYP3A probe) was administered orally to eight healthy volunteers. Midazolam 113-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-129 28700521-0 2017 Effect of CYP3A4 and CYP3A5 Genetic Polymorphisms on the Pharmacokinetics of Sirolimus in Healthy Chinese Volunteers. Sirolimus 77-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 28700521-3 2017 Sirolimus is primarily metabolized by cytochrome CYP3A4 and CYP3A5. Sirolimus 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 28700521-4 2017 This study aimed to clarify the effect of CYP3A genetic polymorphisms, including the CYP3A4*1G and CYP3A5*3 polymorphisms, on the pharmacokinetics of sirolimus. Sirolimus 150-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 28700521-4 2017 This study aimed to clarify the effect of CYP3A genetic polymorphisms, including the CYP3A4*1G and CYP3A5*3 polymorphisms, on the pharmacokinetics of sirolimus. Sirolimus 150-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 28700521-12 2017 CONCLUSIONS: CYP3A4 and CYP3A5 genetic polymorphisms are important factors affecting pharmacokinetic parameters of sirolimus. Sirolimus 115-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 28700521-13 2017 Our data support the monitoring of blood sirolimus concentrations, especially in CYP3A5*1 and CYP3A4*1 G carriers, to ensure accurate dosing in the clinical setting. Sirolimus 41-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 28703720-8 2017 Therapeutic drug monitoring could be clinically useful for determining the influence of AED CYP3A4 inducers on perampanel concentrations. perampanel 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 28444482-6 2017 The target and off-target affinity profiling supported the in vivo results and revealed that the hybridized pyranopyrazole dihydropyridine scaffold has delivered new moderate hits, to be optimized, for the cytochrome P450 3A4 enzymes, opening avenues for combined pharmacological activity through standard structural modification. pyranopyrazole dihydropyridine 108-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 206-225 28546420-0 2017 Alterations of Histone Modifications Contribute to Pregnane X Receptor-Mediated Induction of CYP3A4 by Rifampicin. Rifampin 103-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 28546420-3 2017 This study aims to explore the role of histone modifications in rifampicin-induced expression of CYP3A4 in LS174T cells. Rifampin 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 28546420-4 2017 We found that the induction of CYP3A4 mRNA (4- to 15-fold) by rifampicin in LS174T cells was associated with increased levels of histone H3 lysine 4 trimethylation (H3K4me3, above 1.8-fold) and H3 acetylation (above 2-fold) and a decreased level of histone H3 lysine 27 trimethylation (H3K27me3, about 50%) in the CYP3A4 promoter. Rifampin 62-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 28546420-4 2017 We found that the induction of CYP3A4 mRNA (4- to 15-fold) by rifampicin in LS174T cells was associated with increased levels of histone H3 lysine 4 trimethylation (H3K4me3, above 1.8-fold) and H3 acetylation (above 2-fold) and a decreased level of histone H3 lysine 27 trimethylation (H3K27me3, about 50%) in the CYP3A4 promoter. Rifampin 62-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 314-320 28546420-4 2017 We found that the induction of CYP3A4 mRNA (4- to 15-fold) by rifampicin in LS174T cells was associated with increased levels of histone H3 lysine 4 trimethylation (H3K4me3, above 1.8-fold) and H3 acetylation (above 2-fold) and a decreased level of histone H3 lysine 27 trimethylation (H3K27me3, about 50%) in the CYP3A4 promoter. Lysine 140-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 28546420-4 2017 We found that the induction of CYP3A4 mRNA (4- to 15-fold) by rifampicin in LS174T cells was associated with increased levels of histone H3 lysine 4 trimethylation (H3K4me3, above 1.8-fold) and H3 acetylation (above 2-fold) and a decreased level of histone H3 lysine 27 trimethylation (H3K27me3, about 50%) in the CYP3A4 promoter. Lysine 260-266 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 28546420-5 2017 Rifampicin enhanced recruitment to the CYP3A4 promoter of nuclear receptor coactivator 6 (NCOA6, above 3-fold) and histone acetyltransferase p300 (p300, above 1.6-fold). Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 28546420-9 2017 In conclusion, we show that the alterations of histone modifications contribute to the PXR-mediated induction of CYP3A4 by rifampicin. Rifampin 123-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 29062559-1 2017 Ritonavir is a powerful inhibitor of the cytochrome P450 3A4 (CYP3A4) isoenzyme. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-60 29062559-1 2017 Ritonavir is a powerful inhibitor of the cytochrome P450 3A4 (CYP3A4) isoenzyme. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 29062559-3 2017 However, when co-administered with other drugs that are metabolised via the CYP3A4 pathway, ritonavir can potentially cause serious drug-drug interactions. Ritonavir 92-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 28727815-8 2017 RESULTS: We found that CYP3A4 rs35599367 variant (CYP3A4*22 allele) carriers had higher everolimus blood concentration compared to wild type patients (P = 0.019). Everolimus 88-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 28727815-8 2017 RESULTS: We found that CYP3A4 rs35599367 variant (CYP3A4*22 allele) carriers had higher everolimus blood concentration compared to wild type patients (P = 0.019). Everolimus 88-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 28727815-11 2017 CONCLUSIONS: CYP3A4*22 allele influenced plasma concentration of everolimus and several SNPs in PI3K/AKT/mTOR pathway genes were associated with treatment toxicities and prognosis. Everolimus 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 28042936-1 2017 AIMS: Diabetes mellitus can inhibit cytochrome P450 3A4, an enzyme responsible for the metabolism of nifedipine, used for the treatment of hypertension in pregnant women. Nifedipine 101-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-55 28915658-3 2017 Since Cyp3A4 and Cyp1A2 enzymes metabolize erlotinib in the liver, the insights into the mechanisms of erlotinib effects on liver cells with maintained drug metabolizing activity are needed. Erlotinib Hydrochloride 43-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 28146606-2 2017 Tacrolimus dosing is challenged by considerable pharmacokinetic variability, both between patients and over time after transplantation, partly due to variability in cytochrome P450 3A (CYP3A) activity. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-183 28146606-2 2017 Tacrolimus dosing is challenged by considerable pharmacokinetic variability, both between patients and over time after transplantation, partly due to variability in cytochrome P450 3A (CYP3A) activity. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-190 28146606-3 2017 The aim of this study was to assess the value of the endogenous CYP3A marker 4beta-hydroxycholesterol (4betaOHC) for tacrolimus dose individualization early after kidney transplantation. cholest-5-ene-3,4-diol 77-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 28146606-3 2017 The aim of this study was to assess the value of the endogenous CYP3A marker 4beta-hydroxycholesterol (4betaOHC) for tacrolimus dose individualization early after kidney transplantation. 4betaohc 103-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 28146606-3 2017 The aim of this study was to assess the value of the endogenous CYP3A marker 4beta-hydroxycholesterol (4betaOHC) for tacrolimus dose individualization early after kidney transplantation. Tacrolimus 117-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 28146606-8 2017 4betaOHC values increased between 1 week and 2 months after transplantation (median change +57% [IQR +22-83%], P < 0.001), indicating increasing CYP3A activity. 4betaohc 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-153 27896690-1 2017 The disposition of simeprevir (SMV) in humans is characterised by cytochrome P450 3A4 metabolism and hepatic uptake by organic anion transporting polypeptide 1B1/3 (OATP1B1/3). Simeprevir 19-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-85 28067999-6 2017 Consistent with in vitro observations, lesinurad (200 mg once daily) was an inducer of CYP3A based on the effects on sildenafil exposure. lesinurad 39-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 28067999-6 2017 Consistent with in vitro observations, lesinurad (200 mg once daily) was an inducer of CYP3A based on the effects on sildenafil exposure. Sildenafil Citrate 117-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 27896690-1 2017 The disposition of simeprevir (SMV) in humans is characterised by cytochrome P450 3A4 metabolism and hepatic uptake by organic anion transporting polypeptide 1B1/3 (OATP1B1/3). Simeprevir 31-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-85 28977209-8 2017 Drug interactions can occur with azole antifungals, such as ketoconazole, by inhibiting CYP3A4 and by reducing the clearance of AIs. Azoles 33-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 28483778-4 2017 When perpetrator interactions were assessed, ritonavir was responsible for the strong increase in exposure of sensitive CYP3A substrates, whereas paritaprevir (an OATP1B1/1B3 inhibitor) greatly increased the exposure of sensitive OATP1B1/1B3 substrates. Ritonavir 45-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-125 28977209-8 2017 Drug interactions can occur with azole antifungals, such as ketoconazole, by inhibiting CYP3A4 and by reducing the clearance of AIs. Ketoconazole 60-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 28353169-2 2017 Doravirine is a substrate for cytochrome P450 (CYP) 3A and P-glycoprotein. doravirine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-54 28353169-16 2017 Long-term co-administration of rifampin or other strong CYP3A inducers with doravirine will likely reduce its efficacy. doravirine 76-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 28483778-8 2017 Plasma exposures of the 3D regimen were reduced by strong CYP3A inducers (paritaprevir and ritonavir; major CYP3A substrates) but were not affected by strong CYP3A4 inhibitors, since ritonavir (a CYP3A inhibitor) is already present in the regimen. paritaprevir 74-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 28483778-8 2017 Plasma exposures of the 3D regimen were reduced by strong CYP3A inducers (paritaprevir and ritonavir; major CYP3A substrates) but were not affected by strong CYP3A4 inhibitors, since ritonavir (a CYP3A inhibitor) is already present in the regimen. Ritonavir 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 27206429-0 2017 Monocrotophos Induces the Expression of Xenobiotic Metabolizing Cytochrome P450s (CYP2C8 and CYP3A4) and Neurotoxicity in Human Brain Cells. Monocrotophos 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 28618157-1 2017 The haem-containing mono-oxygenase cytochrome P450 3A4 (CYP3A4) and its redox partner NADPH-dependent cytochrome P450 oxidoreductase (CPR) are among the most important enzymes in human liver for metabolizing drugs and xenobiotic compounds. NADP 86-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-54 28618157-1 2017 The haem-containing mono-oxygenase cytochrome P450 3A4 (CYP3A4) and its redox partner NADPH-dependent cytochrome P450 oxidoreductase (CPR) are among the most important enzymes in human liver for metabolizing drugs and xenobiotic compounds. NADP 86-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 28618157-5 2017 Reaction kinetics were analysed using a fluorimetric assay with 7-benzyloxyquinoline as substrate for CYP3A4. 7-benzyloxyquinoline 64-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 28618157-6 2017 Full activity of the mono-oxygenase system, with electron transfer from NADPH via CPR, could only be reconstituted when CPR and CYP3A4 were colocalized within the same nanodiscs. NADP 72-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 28618157-6 2017 Full activity of the mono-oxygenase system, with electron transfer from NADPH via CPR, could only be reconstituted when CPR and CYP3A4 were colocalized within the same nanodiscs. cpr 82-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 28858450-4 2017 A small body of literature indicates that drugs that induce cytochrome P450 (CYP)2B6 and CYP3A4 will reduce exposure to ketamine and that drugs that inhibit these enzymes will increase exposure to ketamine. Ketamine 120-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 28340122-0 2017 Potential Role of Patients" CYP3A-Status in Clozapine Pharmacokinetics. Clozapine 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 28340122-3 2017 Methods: Since a potential role in clozapine metabolism is assigned to CYP1A2, CYP2C19, CYP2D6 and CYP3A enzymes, the association between the patients" CYP status (CYP genotypes, CYP expression) and clozapine clearance was evaluated in 92 psychiatric patients. Clozapine 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-104 28340122-5 2017 The functional CYP3A5*1 allele seemed to influence clozapine concentrations in those patients who expressed CYP3A4 at low levels. Clozapine 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 28340122-6 2017 The dose requirement for the therapeutic concentration of clozapine was substantially lower in low CYP3A4 expresser patients than in normal/high expressers (2.18+-0.64 vs 4.98+-1.40 mg/kg, P<.0001). Clozapine 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 28340122-7 2017 Furthermore, significantly higher plasma concentration ratios of norclozapine/clozapine and clozapine N-oxide/clozapine were observed in the patients displaying normal/high CYP3A4 expression than in the low expressers. norclozapine 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 28340122-7 2017 Furthermore, significantly higher plasma concentration ratios of norclozapine/clozapine and clozapine N-oxide/clozapine were observed in the patients displaying normal/high CYP3A4 expression than in the low expressers. Clozapine 68-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 28340122-7 2017 Furthermore, significantly higher plasma concentration ratios of norclozapine/clozapine and clozapine N-oxide/clozapine were observed in the patients displaying normal/high CYP3A4 expression than in the low expressers. clozapine N-oxide 92-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 28340122-7 2017 Furthermore, significantly higher plasma concentration ratios of norclozapine/clozapine and clozapine N-oxide/clozapine were observed in the patients displaying normal/high CYP3A4 expression than in the low expressers. Clozapine 78-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 28340122-8 2017 Conclusion: Prospective assaying of CYP3A-status (CYP3A4 expression, CYP3A5 genotype) may better identify the patients with higher risk of inefficiency or adverse reactions and may facilitate the improvement of personalized clozapine therapy; however, further clinical studies are required to prove the benefit of CYP3A testing for patients under clozapine therapy. Clozapine 224-233 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 28340122-8 2017 Conclusion: Prospective assaying of CYP3A-status (CYP3A4 expression, CYP3A5 genotype) may better identify the patients with higher risk of inefficiency or adverse reactions and may facilitate the improvement of personalized clozapine therapy; however, further clinical studies are required to prove the benefit of CYP3A testing for patients under clozapine therapy. Clozapine 224-233 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 28340122-8 2017 Conclusion: Prospective assaying of CYP3A-status (CYP3A4 expression, CYP3A5 genotype) may better identify the patients with higher risk of inefficiency or adverse reactions and may facilitate the improvement of personalized clozapine therapy; however, further clinical studies are required to prove the benefit of CYP3A testing for patients under clozapine therapy. Clozapine 347-356 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 28194792-0 2017 Semisimultaneous Midazolam Administration to Evaluate the Time Course of CYP3A Activation by a Single Oral Dose of Efavirenz. Midazolam 17-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 28194792-2 2017 In 12 healthy participants individual CYP3A activity was quantified using a semisimultaneous methodology (midazolam orally and 6 hours later intravenously) both alone and during a period of 22 days after a single oral dose of 400 mg efavirenz. Midazolam 106-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 28194792-2 2017 In 12 healthy participants individual CYP3A activity was quantified using a semisimultaneous methodology (midazolam orally and 6 hours later intravenously) both alone and during a period of 22 days after a single oral dose of 400 mg efavirenz. efavirenz 233-242 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 28194792-5 2017 At least on day 1, the midazolam clearance increase is consistent with the in vitro observed CYP3A activation. Midazolam 23-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 28408657-8 2017 The decrease in hPXR expression by the miR-18a-5p mimic was associated with a reduction in the extent of hPXR target gene (CYP3A4) induction by rifampin and rilpivirine. Rifampin 144-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 28408657-8 2017 The decrease in hPXR expression by the miR-18a-5p mimic was associated with a reduction in the extent of hPXR target gene (CYP3A4) induction by rifampin and rilpivirine. Rilpivirine 157-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 27206429-3 2017 To address this issue, we investigated the expression and inducibility of CYP2C8 and CYP3A4 and their responsiveness against cyclophosphamide (CPA) and organophosphorus pesticide monocrotophos (MCP), a known developmental neurotoxicant in human neural (SH-SY5Y) and glial (U373-MG) cell lines. Cyclophosphamide 125-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 27206429-3 2017 To address this issue, we investigated the expression and inducibility of CYP2C8 and CYP3A4 and their responsiveness against cyclophosphamide (CPA) and organophosphorus pesticide monocrotophos (MCP), a known developmental neurotoxicant in human neural (SH-SY5Y) and glial (U373-MG) cell lines. Cyclophosphamide 143-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 27206429-4 2017 CPA induced significant expression of CYP2C8 and CYP3A4 in both types of cells in a time-dependent manner. Cyclophosphamide 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 28747995-10 2017 Due to the inhibition of the particular intestinal CYP3A4, the obtained Ki values of 14 microM of propiverine (30 mg daily, IR) resulted in a predicted doubling of the AUC for midazolam (CYP3A4 substrate). propiverine 98-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 27993531-8 2017 A possible interpretation proposes a slight inducing effect of smoking on risperidone metabolism most likely via CYP3A4. Risperidone 74-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 28442602-7 2017 Utilizing a HPH-HepG2 coculture model, we demonstrate that inclusion of HPH converts PK11195 from an antagonist to an agonist of hCAR, and such conversion was attenuated by potent CYP3A4 inhibitor ketoconazole. Ketoconazole 197-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 27485383-5 2017 Using azamulin as a specific CYP3A4 MBI, we demonstrated the proof of concept that CYP3A4 can be totally, specifically (even against 3A5) and permanently (at least for six years) inhibited by our process. azamulin 6-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 27485383-5 2017 Using azamulin as a specific CYP3A4 MBI, we demonstrated the proof of concept that CYP3A4 can be totally, specifically (even against 3A5) and permanently (at least for six years) inhibited by our process. azamulin 6-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 27499416-0 2017 Oxidative metabolism of koumine is mainly catalyzed by microsomal CYP3A4/3A5. koumine 24-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 27499416-11 2017 Chemical inhibition study showed that the inhibitor of CYP3A4/3A5 significantly decreased (93%) the formation of koumine metabolites. koumine 113-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 27499416-12 2017 Further, CYP3A4/3A5 was shown as the most efficient isoform in biotransformation of koumine, among a series of CYP isoforms tested. koumine 84-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 27499416-15 2017 And CYP3A4/3A5 was probably the main contributor to the hepatic oxidative metabolism of koumine. koumine 88-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 28590129-0 2017 High-Level Production and Properties of the Cysteine-Depleted Cytochrome P450 3A4. Cysteine 44-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-81 28590129-3 2017 This study was undertaken to engineer a well-expressed and functionally active cysteine-depleted CYP3A4 that can be used in biochemical and biophysical studies. Cysteine 79-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 28590129-4 2017 cDNA codon optimization and screening mutagenesis were utilized to boost the level of bacterial expression of CYP3A4 and identify the least harmful substitutions for all six non-heme-ligating cysteines. Cysteine 192-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 28590129-5 2017 The C58A/C64M/C98A/C239T/C377A/C468S (Cys-less) mutant was found to be expressed as highly as the optimized wild-type (opt-WT) CYP3A4. Cysteine 38-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 28590129-6 2017 The high-resolution X-ray structures of opt-WT and Cys-less CYP3A4 revealed that gene optimization leads to a different folding in the Phe108 and Phe189 regions and promotes binding of the active site glycerol that interlocks Ser119 and Arg212, critical for ligand association, and the hydrophobic cluster adjacent to Phe108. Cysteine 51-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 28590129-6 2017 The high-resolution X-ray structures of opt-WT and Cys-less CYP3A4 revealed that gene optimization leads to a different folding in the Phe108 and Phe189 regions and promotes binding of the active site glycerol that interlocks Ser119 and Arg212, critical for ligand association, and the hydrophobic cluster adjacent to Phe108. Glycerol 201-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 28590129-7 2017 Crowding and decreased flexibility of the active site, as well as structural alterations observed at the C64M, C239T, and C468S mutational sites, might be responsible for the distinct ligand binding behavior of opt-WT and Cys-less CYP3A4. Cysteine 222-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 231-237 28747995-10 2017 Due to the inhibition of the particular intestinal CYP3A4, the obtained Ki values of 14 microM of propiverine (30 mg daily, IR) resulted in a predicted doubling of the AUC for midazolam (CYP3A4 substrate). propiverine 98-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 28747995-10 2017 Due to the inhibition of the particular intestinal CYP3A4, the obtained Ki values of 14 microM of propiverine (30 mg daily, IR) resulted in a predicted doubling of the AUC for midazolam (CYP3A4 substrate). Midazolam 176-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 28747995-10 2017 Due to the inhibition of the particular intestinal CYP3A4, the obtained Ki values of 14 microM of propiverine (30 mg daily, IR) resulted in a predicted doubling of the AUC for midazolam (CYP3A4 substrate). Midazolam 176-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 28324194-8 2017 Since the blood concentration of tacrolimus in patients with CYP3A5*3/*3 varies depending on sex and age, these factors should be considered when studying the difference of sex in CYP3A. Tacrolimus 33-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-66 28588200-6 2017 Midazolam metabolism by CYP3A4 in these HepLCs was comparable to that in wild-type HepLCs. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 28642710-0 2017 Tacrolimus Updated Guidelines through popPK Modeling: How to Benefit More from CYP3A Pre-emptive Genotyping Prior to Kidney Transplantation. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-84 28642710-4 2017 The integration of CYP3A4 and CY3A5 genotype in tacrolimus population-based PK (PopPK) modeling approaches has been proven to accurately predict the dose requirement to reach the therapeutic window. Tacrolimus 48-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 28642710-10 2017 Our model estimated that tacrolimus concentrations were 33% IC95%[20-26%], 41% IC95%[36-45%] lower in CYP3A IM and EM when compared to PM, respectively. Tacrolimus 25-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 28008657-0 2017 Bodyweight-adjustments introduce significant correlations between CYP3A metrics and tacrolimus clearance. Tacrolimus 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 28400237-6 2017 The hepatotoxic potential of tacrine derivatives was evaluated using recombinant cytochrome (CYP) P450 CYP1A2 and CYP3A4 enzymes. Tacrine 29-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 28044353-2 2017 METHODS: The contribution of the CYP3A4/5 genotype in paediatric liver transplant recipients and donors to the tacrolimus blood trough concentrations (C0 ) and the tacrolimus concentration/weight-adjusted dose ratio on day 1 was evaluated in 67 liver-transplanted children: 33 boys and 34 girls, mean age 4.5 years. Tacrolimus 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 28374426-0 2017 Response to: "Response to: Bodyweight-adjustments introduce significant correlations between CYP3A metrics and tacrolimus clearance". Tacrolimus 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 28168728-0 2017 Response to: "Bodyweight-adjustments introduce significant correlations between CYP3A metrics and tacrolimus clearance". Tacrolimus 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-85 27722854-3 2017 This study evaluated the pharmacokinetic profile of simvastatin (a CYP3A4 substrate) before and 1 week after a single dose of sarilumab (a human monoclonal antibody [mAb] blocking the IL-6Ralpha) in patients with RA, to assess potential interaction. Simvastatin 52-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 28484907-4 2017 MAM-2201 potently inhibited CYP2C9-catalyzed diclofenac 4"-hydroxylation, CYP3A4-catalyzed midazolam 1"-hydroxylation, and UGT1A3-catalyzed chenodeoxycholic acid 24-acyl-glucuronidation, with K i values of 5.6, 5.4 and 5.0 microM, respectively. Midazolam 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 28035588-8 2017 Naloxegol is a sensitive substrate of cytochrome P450 (CYP) 3A4 and its exposure can be significantly altered by strong or moderate CYP3A modulators. naloxegol 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-63 28283499-8 2017 In addition to NGMN, we have also elucidated the biotransformation of norgestrel (NG), a downstream norgestimate and NGMN metabolite, and found that CYP3A4 and UGT1A1 have a major contribution to the elimination of NG with a combined fm value of 1. Norgestrel 70-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 28229376-1 2017 INTRODUCTION: Tacrolimus is a calcineurin inhibitor used as an immunosuppressant drug in solid organ transplantation, and is mainly metabolized by cytochrome P450 (CYP) 3A4 and CYP3A5. Tacrolimus 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-172 28229376-3 2017 Variants in the genes PPARA, POR and CYP3A4 have recently been shown to influence tacrolimus metabolism. Tacrolimus 82-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 28495029-0 2017 The Pharmacokinetics of the CYP3A Substrate Midazolam After Steady-state Dosing of Delafloxacin. Midazolam 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 28495029-0 2017 The Pharmacokinetics of the CYP3A Substrate Midazolam After Steady-state Dosing of Delafloxacin. delafloxacin 83-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 28495029-2 2017 The objective of this study was to evaluate the effects of delafloxacin on the pharmacokinetics of midazolam, a cytochrome P450 (CYP) 3A substrate. delafloxacin 59-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-136 28495029-2 2017 The objective of this study was to evaluate the effects of delafloxacin on the pharmacokinetics of midazolam, a cytochrome P450 (CYP) 3A substrate. Midazolam 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-136 28495029-3 2017 METHODS: CYP3A activity using midazolam as a probe was assessed before and after multiple doses of delafloxacin to reach steady state. Midazolam 30-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-14 28229376-5 2017 In the present study, we investigated a potential association between CYP3A5*3, PPARA c.209-1003G>A, POR*28 and CYP3A4*22 and dose-adjusted tacrolimus trough concentrations in a primarily corticosteroid-free (>85%) population of Danish pediatric and adult kidney transplant recipients. Tacrolimus 143-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 28283499-8 2017 In addition to NGMN, we have also elucidated the biotransformation of norgestrel (NG), a downstream norgestimate and NGMN metabolite, and found that CYP3A4 and UGT1A1 have a major contribution to the elimination of NG with a combined fm value of 1. norgestimate 100-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 28283499-9 2017 The data presented in this paper will lead to better understanding and management of NGMN-based drug-drug interactions when norgestimate is coadministered with CYP3A4 modulators. ngmn 85-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 27317395-5 2017 METHODS: Metabolism data for tramadol and for the probe substrates midazolam (CYP3A4) and dextromethorphan (CYP2D6) were gathered in human liver microsomes (HLM) and recombinant human enzyme systems (rhCYP). Midazolam 67-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 27904973-0 2017 Platelet reactivity and clinical outcomes in patients using CYP3A4-metabolized statins with clopidogrel in percutaneous coronary intervention. Clopidogrel 92-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 27904973-1 2017 Statins are primarily metabolized by cytochrome P450 3A4 (CYP3A4), which reduces clopidogrel to its active metabolite. Clopidogrel 81-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-56 27904973-1 2017 Statins are primarily metabolized by cytochrome P450 3A4 (CYP3A4), which reduces clopidogrel to its active metabolite. Clopidogrel 81-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 27904973-2 2017 Recent studies suggest that CYP3A4-metabolized statins attenuate clopidogrel"s anti-aggregatory effect on platelets. Clopidogrel 65-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 27904973-10 2017 CYP3A4-metabolized statins slightly inhibit the antiplatelet activity of clopidogrel during dual antiplatelet therapy. Clopidogrel 73-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 27820970-1 2017 Due to Cytochrome P450 3A (CYP3A) metabolism, clinical trials of ibrutinib-treated chronic lymphocytic leukemia (CLL) patients prohibited concurrent medications metabolized by CYP3A. ibrutinib 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-25 28344076-2 2017 However, the potential herb-drug interactions (HDI) between these lignans and other drugs through inhibiting human cytochrome P450 3A4 (CYP3A4) and CYP3A5 remains unclear. Lignans 66-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-134 28344076-2 2017 However, the potential herb-drug interactions (HDI) between these lignans and other drugs through inhibiting human cytochrome P450 3A4 (CYP3A4) and CYP3A5 remains unclear. Lignans 66-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 28344076-3 2017 In the present study, the inhibitory action of GC and GG on CYP3A4 and CYP3A5 were investigated. schizandrer A 47-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 28344076-3 2017 In the present study, the inhibitory action of GC and GG on CYP3A4 and CYP3A5 were investigated. schizandrer A 54-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 28344076-5 2017 Notably, the inhibitory intensity of GC towards CYP3A4 was stronger than CYP3A5 when using midazolam and nifedipine as substrates. Midazolam 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 28344076-5 2017 Notably, the inhibitory intensity of GC towards CYP3A4 was stronger than CYP3A5 when using midazolam and nifedipine as substrates. Nifedipine 105-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 28344076-6 2017 While inhibition of GC towards CYP3A5 was weaker than CYP3A4 when using testosterone as substrate. Testosterone 72-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 28026013-2 2017 As a substrate for CYP3A-mediated metabolism, doravirine could potentially be affected by liver-function changes. doravirine 46-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-24 28052338-3 2017 The PBPK model was independently verified against clinical studies of the strong CYP3A inhibitor ketoconazole, the strong CYP3A inducer, multiple-dose rifampin, and the steady-state venetoclax PK in chronic lymphocytic leukemia (CLL) subjects by comparing predicted to observed ratios of the venetoclax maximum concentration (Cmax R) and area under the curve from time 0 to infinity (AUC R) from these studies. Ketoconazole 97-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 28052338-7 2017 Model simulations indicated no effect of weak CYP3A inhibitors or inducers on Cmax or AUC , while both moderate and strong CYP3A inducers were estimated to decrease venetoclax exposure. venetoclax 166-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-129 28052338-9 2017 The recommended venetoclax dose reductions of at least 50% and 75% when coadministered with moderate and strong CYP3A inhibitors, respectively, maintain venetoclax exposures between therapeutic and maximally administered safe doses. venetoclax 16-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-117 28052338-9 2017 The recommended venetoclax dose reductions of at least 50% and 75% when coadministered with moderate and strong CYP3A inhibitors, respectively, maintain venetoclax exposures between therapeutic and maximally administered safe doses. venetoclax 153-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-117 28674221-5 2017 In addition, we also determined the allele frequencies of CYP3A4*1A and CYP3A4*1H were 82.29% and 28.13%, respectively. Hydrogen 79-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 26921085-5 2017 Results Coadministration of aprepitant with antineoplastics or opiods may result in significant elevations in the serum levels of the agents metabolized via CYP3A4, with the best documentation for cyclophosphamide, ifosfamide, erlotinib and oxycodone. Erlotinib Hydrochloride 227-236 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 26921085-5 2017 Results Coadministration of aprepitant with antineoplastics or opiods may result in significant elevations in the serum levels of the agents metabolized via CYP3A4, with the best documentation for cyclophosphamide, ifosfamide, erlotinib and oxycodone. Oxycodone 241-250 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 28344076-0 2017 Inhibition of human CYP3A4 and CYP3A5 enzymes by gomisin C and gomisin G, two lignan analogs derived from Schisandra chinensis. Lignans 78-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 27820970-1 2017 Due to Cytochrome P450 3A (CYP3A) metabolism, clinical trials of ibrutinib-treated chronic lymphocytic leukemia (CLL) patients prohibited concurrent medications metabolized by CYP3A. ibrutinib 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 27820970-1 2017 Due to Cytochrome P450 3A (CYP3A) metabolism, clinical trials of ibrutinib-treated chronic lymphocytic leukemia (CLL) patients prohibited concurrent medications metabolized by CYP3A. ibrutinib 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-181 28087064-1 2017 AIM OF THE STUDY: Propafenone (PPF) is an antiarrhythmic drug, metabolized mainly by CYP2D6 to 5-hydroxypropafenone (5OH-PPF) and by CYP3A4 to norpropafenone (NOR-PPF). Propafenone 18-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 28440407-1 2017 The present study aimed to investigate the association between the genetic polymorphism of cytochrome P450 family 3 subfamily A member 5 (CYP3A5) and the activity of CYP3A and plasma concentrations of daunorubicin (DNR) in patients with acute leukemia. Daunorubicin 201-213 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-143 28440407-1 2017 The present study aimed to investigate the association between the genetic polymorphism of cytochrome P450 family 3 subfamily A member 5 (CYP3A5) and the activity of CYP3A and plasma concentrations of daunorubicin (DNR) in patients with acute leukemia. Daunorubicin 215-218 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-143 28383355-2 2017 During chronic use of imatinib, CYP2C8 becomes an important metabolizing enzyme because of cytochrome P450 3A4 (CYP3A4) autoinhibition. Imatinib Mesylate 22-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-110 28383355-2 2017 During chronic use of imatinib, CYP2C8 becomes an important metabolizing enzyme because of cytochrome P450 3A4 (CYP3A4) autoinhibition. Imatinib Mesylate 22-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 28238727-4 2017 Testosterone, the standard compound for characterization of the human CYP3A4, was used to characterize the newly expressed equine CYPs. Testosterone 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 28238727-8 2017 Ketoconazole inhibited 2-OH-TES in the human CYP3A4 and the equine CYP3A94 and CYP3A97 completely, whereas a 70% inhibition was found in CYP3A95. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 28288941-6 2017 Carnosic acid, carnosol, and ursolic acid, but not rosmarinic acid, increased hPXR target gene expression, as shown by an increase in CYP3A4, UGT1A3, and ABCB1 mRNA expression in LS180 human colon adenocarcinoma cells. salvin 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 28288941-6 2017 Carnosic acid, carnosol, and ursolic acid, but not rosmarinic acid, increased hPXR target gene expression, as shown by an increase in CYP3A4, UGT1A3, and ABCB1 mRNA expression in LS180 human colon adenocarcinoma cells. carnosol 15-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 28288941-6 2017 Carnosic acid, carnosol, and ursolic acid, but not rosmarinic acid, increased hPXR target gene expression, as shown by an increase in CYP3A4, UGT1A3, and ABCB1 mRNA expression in LS180 human colon adenocarcinoma cells. ursolic acid 29-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 28238727-8 2017 Ketoconazole inhibited 2-OH-TES in the human CYP3A4 and the equine CYP3A94 and CYP3A97 completely, whereas a 70% inhibition was found in CYP3A95. 2-oh-tes 23-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 28087064-1 2017 AIM OF THE STUDY: Propafenone (PPF) is an antiarrhythmic drug, metabolized mainly by CYP2D6 to 5-hydroxypropafenone (5OH-PPF) and by CYP3A4 to norpropafenone (NOR-PPF). Propafenone 31-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 28087064-1 2017 AIM OF THE STUDY: Propafenone (PPF) is an antiarrhythmic drug, metabolized mainly by CYP2D6 to 5-hydroxypropafenone (5OH-PPF) and by CYP3A4 to norpropafenone (NOR-PPF). N-depropylpropafenone 143-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 28087064-1 2017 AIM OF THE STUDY: Propafenone (PPF) is an antiarrhythmic drug, metabolized mainly by CYP2D6 to 5-hydroxypropafenone (5OH-PPF) and by CYP3A4 to norpropafenone (NOR-PPF). N-depropylpropafenone 159-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 28368100-6 2017 Analysis of existing structures suggests that halogen-pi interactions may be unique to the CYP2B enzymes within CYP family 2 but are also important for CYP3A enzymes. Halogens 46-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-157 29450233-9 2017 Pharmacogenetic testing revealed that the patient exhibited a cytochrome P450 3A4 ultrarapid metabolizer phenotype, which necessitated a higher than recommended daily dose of buprenorphine (32 mg) for adequate OUD management. Buprenorphine 175-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-81 28399110-6 2017 Midazolam was administered as phenotyping probe for cytochrome P450 isoenzyme 3A (CYP3A). Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-80 28399110-6 2017 Midazolam was administered as phenotyping probe for cytochrome P450 isoenzyme 3A (CYP3A). Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-87 28399110-10 2017 CONCLUSIONS: Metabolic phenotyping of CYP3A using midazolam is a promising strategy to individualise cabazitaxel dosing. Midazolam 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 28399110-10 2017 CONCLUSIONS: Metabolic phenotyping of CYP3A using midazolam is a promising strategy to individualise cabazitaxel dosing. cabazitaxel 101-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 27743401-0 2017 Bile acids and their oxo derivatives: Potential inhibitors of carbonic anhydrase I and II, androgen receptor antagonists and CYP3A4 substrates. Bile Acids and Salts 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 28341123-0 2017 Acetaminophen analog N-acetyl-m-aminophenol, but not its reactive metabolite, N-acetyl-p-benzoquinone imine induces CYP3A activity via inhibition of protein degradation. Acetaminophen 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 28341123-0 2017 Acetaminophen analog N-acetyl-m-aminophenol, but not its reactive metabolite, N-acetyl-p-benzoquinone imine induces CYP3A activity via inhibition of protein degradation. 3-hydroxyacetanilide 21-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 28341123-3 2017 We previously reported that acetaminophen (APAP) induces CYP3A activity via inhibition of protein degradation and proposed a novel DDI concept. Acetaminophen 28-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 28341123-3 2017 We previously reported that acetaminophen (APAP) induces CYP3A activity via inhibition of protein degradation and proposed a novel DDI concept. Acetaminophen 43-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 28476838-2 2017 Taxanes are metabolized in human liver by the cytochrome CYP3A and are substrate of ATP-binding cassette multidrug transporters ABCB1. Taxoids 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 27545757-2 2017 Alectinib is mainly metabolized by cytochrome P450 3A (CYP3A) to a major similarly active metabolite, M4. alectinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-53 28173639-3 2017 In this study, the effects of bosentan and rifampin on the expression and activities of organic anion-transporting peptide (OATP) and cytochrome P450 (CYP450) 2C9 and CYP3A4 were investigated in vitro. Bosentan 30-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 167-173 28173639-3 2017 In this study, the effects of bosentan and rifampin on the expression and activities of organic anion-transporting peptide (OATP) and cytochrome P450 (CYP450) 2C9 and CYP3A4 were investigated in vitro. Rifampin 43-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 167-173 28173639-5 2017 In primary human hepatocytes, CYP2C9 and CYP3A4 gene expression and activities decreased upon treatment with 20 muM bosentan+200 muM rifampin. Bosentan 116-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 28173639-5 2017 In primary human hepatocytes, CYP2C9 and CYP3A4 gene expression and activities decreased upon treatment with 20 muM bosentan+200 muM rifampin. Rifampin 133-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 28155129-2 2017 This study evaluated the inhibitory effect of osilodrostat on the pharmacokinetics of probe substrates of the cytochrome P450 (CYP) enzymes CYP1A2, CYP2C19, CYP2D6, and CYP3A4. Osilodrostat 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 28155129-9 2017 CONCLUSIONS: Osilodrostat is a moderate inhibitor of CYP1A2 and CYP2C19 and a weak inhibitor of CYP2D6 and the most clinically important CYP enzyme, CYP3A4. Osilodrostat 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 27734291-6 2017 Cabozantinib AUC was increased by 63-81 % or 7-30 % in subjects with mild/moderate hepatic or renal impairment, respectively; by 34-38 % with concomitant cytochrome P450 3A4 inhibitor ketoconazole; and by 57 % following a high-fat meal. cabozantinib 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-173 27734291-7 2017 Cabozantinib AUC was decreased by 76-77 % with concomitant cytochrome P450 3A4 inducer rifampin, and was unaffected following administration of proton pump inhibitor esomeprazole. cabozantinib 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-78 28482130-4 2017 Associations between CYP3A4*22 or CYP3A5*3 and cholesterol response were not detected in either race, and no significant race-gene or gene-gene interactions were detected. Cholesterol 47-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 28254951-1 2017 The propensity for CYP3A4 induction by 2-(6-(5-chloro-2-methoxyphenyl)-4-oxo-2-thioxo-3,4-dihydropyrimidin-1(2H)-yl)acetamide (PF-06282999), an irreversible inactivator of myeloperoxidase, was examined in the present study. 2-(6-(5-chloro-2-methoxyphenyl)-4-oxo-2-thioxo-3,4-dihydropyrimidin-1(2H)-yl)acetamide 39-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 28254951-1 2017 The propensity for CYP3A4 induction by 2-(6-(5-chloro-2-methoxyphenyl)-4-oxo-2-thioxo-3,4-dihydropyrimidin-1(2H)-yl)acetamide (PF-06282999), an irreversible inactivator of myeloperoxidase, was examined in the present study. 2-(6-(5-chloro-2-methoxyphenyl)-4-oxo-2-thioxo-3,4-dihydropyrimidin-1(2H)-yl)acetamide 127-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 28254951-3 2017 At the highest tested concentration of 300 muM, PF-06282999 caused maximal induction in CYP3A4 mRNA and enzyme activity ranging from 56% to 86% and 47% t0 72%, respectively, of rifampicin response across the three hepatocyte donor pools. pyrazofurin 48-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 28254951-3 2017 At the highest tested concentration of 300 muM, PF-06282999 caused maximal induction in CYP3A4 mRNA and enzyme activity ranging from 56% to 86% and 47% t0 72%, respectively, of rifampicin response across the three hepatocyte donor pools. Rifampin 177-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 28270565-12 2017 Because midostaurin, CGP52421, and CGP62221 are metabolized mainly by CYP3A4 and are inhibitors/inducers for CYP3A, potential drug-drug interactions with mainly CYP3A4 modulators/CYP3A substrates could be expected. midostaurin 8-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 28270565-12 2017 Because midostaurin, CGP52421, and CGP62221 are metabolized mainly by CYP3A4 and are inhibitors/inducers for CYP3A, potential drug-drug interactions with mainly CYP3A4 modulators/CYP3A substrates could be expected. midostaurin 8-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-75 28270565-12 2017 Because midostaurin, CGP52421, and CGP62221 are metabolized mainly by CYP3A4 and are inhibitors/inducers for CYP3A, potential drug-drug interactions with mainly CYP3A4 modulators/CYP3A substrates could be expected. midostaurin 8-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 28270565-12 2017 Because midostaurin, CGP52421, and CGP62221 are metabolized mainly by CYP3A4 and are inhibitors/inducers for CYP3A, potential drug-drug interactions with mainly CYP3A4 modulators/CYP3A substrates could be expected. midostaurin 8-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-114 28436563-6 2017 Yeast microsomes containing human CYP3A4, but not those that do not contain CYP3A4, were active in hydroxylation of diclofenac, a known CYP3A4 substrate drug, a result confirming CYP3A4 activity in the recombinant yeast strain. Diclofenac 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 28436563-8 2017 Expression of CYP3A4 also conferred sensitivity in rad4 rad51 mutants exposed to colon carcinogen, 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx). 2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline 99-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 28436563-8 2017 Expression of CYP3A4 also conferred sensitivity in rad4 rad51 mutants exposed to colon carcinogen, 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx). 2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline 146-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 28436563-9 2017 These data confirm the ability of human CYP3A4 to mediate the genotoxicity of AFB1 , and illustrate the usefulness of the CYP3A4-expressing, DNA-repair mutant yeast strain for screening other chemical compounds that are CYP3A4 substrates, for potential genotoxicity. Aflatoxin B1 78-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 28436563-9 2017 These data confirm the ability of human CYP3A4 to mediate the genotoxicity of AFB1 , and illustrate the usefulness of the CYP3A4-expressing, DNA-repair mutant yeast strain for screening other chemical compounds that are CYP3A4 substrates, for potential genotoxicity. Aflatoxin B1 78-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 28436563-9 2017 These data confirm the ability of human CYP3A4 to mediate the genotoxicity of AFB1 , and illustrate the usefulness of the CYP3A4-expressing, DNA-repair mutant yeast strain for screening other chemical compounds that are CYP3A4 substrates, for potential genotoxicity. Aflatoxin B1 78-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 28157069-3 2017 To clarify the time courses of deinduction of CYP2C9 and -CYP3A activities after rifampicin withdrawal, we monitored these enzyme activities in 2 patients over time after discontinuing rifampicin. Rifampin 81-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 28157069-7 2017 We monitored CYP2C9 and CYP3A activities over their clinical courses by measuring the metabolic clearance of S-warfarin to S-7-hydroxywarfarin and that of cortisol to 6beta-hydroxycortisol, respectively. Warfarin 109-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 28157069-7 2017 We monitored CYP2C9 and CYP3A activities over their clinical courses by measuring the metabolic clearance of S-warfarin to S-7-hydroxywarfarin and that of cortisol to 6beta-hydroxycortisol, respectively. 7-hydroxywarfarin 123-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 28157069-7 2017 We monitored CYP2C9 and CYP3A activities over their clinical courses by measuring the metabolic clearance of S-warfarin to S-7-hydroxywarfarin and that of cortisol to 6beta-hydroxycortisol, respectively. Hydrocortisone 155-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 28157069-7 2017 We monitored CYP2C9 and CYP3A activities over their clinical courses by measuring the metabolic clearance of S-warfarin to S-7-hydroxywarfarin and that of cortisol to 6beta-hydroxycortisol, respectively. 6 beta-hydroxycortisol 167-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 28301431-3 2017 Our aim was to elucidate the activity of CYP3A4 and P-gp in subjects with Crohn"s disease (CD) and to evaluate their influence on budesonide pharmacokinetics. Budesonide 130-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 28301431-4 2017 METHODS: A detailed pharmacokinetic assessment was conducted in 8 individuals diagnosed with CD on stable doses of oral budesonide, a putative shared CYP3A4, and P-gp substrate, where hepatic and intestinal CYP3A4 activity were also assessed using intravenous and oral midazolam. Budesonide 120-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 28301431-4 2017 METHODS: A detailed pharmacokinetic assessment was conducted in 8 individuals diagnosed with CD on stable doses of oral budesonide, a putative shared CYP3A4, and P-gp substrate, where hepatic and intestinal CYP3A4 activity were also assessed using intravenous and oral midazolam. Budesonide 120-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 28468305-5 2017 Dimethyllirioresinol weakly inhibited CYP2C19 and CYP2C8 with IC50 values of 55.1 and 85.0 muM, respectively, without inhibition of CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2D6, and CYP3A4 activities at 100 muM. dimethyllirioresinol 0-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 28324001-0 2017 CYP3A4 Induction by Rifampin: An Alternative Pathway for Vitamin D Inactivation in Patients With CYP24A1 Mutations. Rifampin 20-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28324001-0 2017 CYP3A4 Induction by Rifampin: An Alternative Pathway for Vitamin D Inactivation in Patients With CYP24A1 Mutations. Vitamin D 57-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28324001-4 2017 CYP3A4 is a P450 enzyme that inactivates many drugs and xenobiotics and may represent an alternative pathway for inactivation of vitamin D metabolites. Vitamin D 129-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28324001-5 2017 Objective: Our goal was to determine if rifampin, a potent inducer of CYP3A4, can normalize mineral metabolism in patients with IIH due to mutations in CYP24A1. Rifampin 40-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 28324001-5 2017 Objective: Our goal was to determine if rifampin, a potent inducer of CYP3A4, can normalize mineral metabolism in patients with IIH due to mutations in CYP24A1. 4-(7-Chloro-1,3-Benzoxazol-2-Yl)-2,6-Diiodophenol 128-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 28324001-10 2017 Conclusion: These observations suggest that rifampin-induced overexpression of CYP3A4 provides an alternative pathway for inactivation of vitamin D metabolites in patients who lack CYP24A1 function. Rifampin 44-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 28324001-10 2017 Conclusion: These observations suggest that rifampin-induced overexpression of CYP3A4 provides an alternative pathway for inactivation of vitamin D metabolites in patients who lack CYP24A1 function. Vitamin D 138-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 28341759-2 2017 In this study to treat KS, sorafenib was poorly tolerated at doses less than those approved by the U.S. Food and Drug Administration for hepatocellular carcinoma and other cancers, and showed only modest activity.Sorafenib"s metabolism occurs via the CYP3A4 pathway, which is inhibited by ritonavir, a commonly used antiretroviral agent used by most patients in this study. Sorafenib 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 251-257 28341759-2 2017 In this study to treat KS, sorafenib was poorly tolerated at doses less than those approved by the U.S. Food and Drug Administration for hepatocellular carcinoma and other cancers, and showed only modest activity.Sorafenib"s metabolism occurs via the CYP3A4 pathway, which is inhibited by ritonavir, a commonly used antiretroviral agent used by most patients in this study. Sorafenib 213-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 251-257 28341759-3 2017 Strong CYP3A4 inhibition by ritonavir may contribute to the observed sorafenib toxicity.Alternate antiretroviral agents without predicted interactions are preferred for co-administration in patients with HIV and cancers for which sorafenib is indicated. Ritonavir 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 28341759-3 2017 Strong CYP3A4 inhibition by ritonavir may contribute to the observed sorafenib toxicity.Alternate antiretroviral agents without predicted interactions are preferred for co-administration in patients with HIV and cancers for which sorafenib is indicated. Sorafenib 69-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 28341759-3 2017 Strong CYP3A4 inhibition by ritonavir may contribute to the observed sorafenib toxicity.Alternate antiretroviral agents without predicted interactions are preferred for co-administration in patients with HIV and cancers for which sorafenib is indicated. Sorafenib 230-239 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 28341759-5 2017 We evaluated drug-drug interactions between sorafenib and ritonavir, an HIV medication with strong CYP3A4 inhibitory activity. Sorafenib 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 28341759-5 2017 We evaluated drug-drug interactions between sorafenib and ritonavir, an HIV medication with strong CYP3A4 inhibitory activity. Ritonavir 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 28341759-14 2017 Steady-state area under the curve of the dosing interval (AUCTAU) of sorafenib was not significantly affected by ritonavir; however, a trend for decreased AUCTAU of the CYP3A4 metabolite sorafenib-N-oxide (3.8-fold decrease; p = .08) suggests other metabolites may be increased. Sorafenib 187-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 28341759-16 2017 Strong CYP3A4 inhibitors may contribute to sorafenib toxicity, and ritonavir has previously been shown to be a CYP3A4 inhibitor. Sorafenib 43-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 28341759-16 2017 Strong CYP3A4 inhibitors may contribute to sorafenib toxicity, and ritonavir has previously been shown to be a CYP3A4 inhibitor. Ritonavir 67-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 28060049-2 2017 We describe a case of symptomatic Cushing"s syndrome in an adolescent male with sight-threatening vernal keratoconjunctivitis on antiretroviral therapy for HIV-1 infection that included ritonavir, a potent cytochrome p450 CYP3A4 inhibitor. Ritonavir 186-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 222-228 28060049-3 2017 CYP3A4 inhibition reduces the metabolism of exogenous corticosteroids leading to suppression of endogenous steroid production and Cushing"s syndrome. Steroids 61-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28073119-4 2017 The apparent Ki value for CYP2C9 was 50.60 microM and those for CYP3A4/5 were 48.71 microM and 31.25 microM using two different probe substrates, nifedipine and midazolam, respectively. Nifedipine 146-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 28073119-4 2017 The apparent Ki value for CYP2C9 was 50.60 microM and those for CYP3A4/5 were 48.71 microM and 31.25 microM using two different probe substrates, nifedipine and midazolam, respectively. Midazolam 161-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 28073119-5 2017 The apparent KI, kinact, and kinact/KI ratio for the mechanism-based inhibition of CYP3A4/5 were 6.40 microM, 0.037 min-1, and 5.78 mL min-1 micromol-1, respectively, by examining nifedipine oxidation, and 31.53 microM, 0.049 min-1, and 1.55 mL min-1 micromol-1, respectively, by examining midazolam 1"-hydroxylation. Nifedipine 182-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 28073119-5 2017 The apparent KI, kinact, and kinact/KI ratio for the mechanism-based inhibition of CYP3A4/5 were 6.40 microM, 0.037 min-1, and 5.78 mL min-1 micromol-1, respectively, by examining nifedipine oxidation, and 31.53 microM, 0.049 min-1, and 1.55 mL min-1 micromol-1, respectively, by examining midazolam 1"-hydroxylation. Midazolam 294-303 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 28329820-5 2017 In HepaRG cells, cytotoxicity started at 20 and 100 microM for posaconazole and ketoconazole, respectively, and was slightly accentuated by cytochrome P450 3A4 induction with rifampicin and 1A2 with 3-methylcholantrene. Rifampin 175-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-159 28329820-5 2017 In HepaRG cells, cytotoxicity started at 20 and 100 microM for posaconazole and ketoconazole, respectively, and was slightly accentuated by cytochrome P450 3A4 induction with rifampicin and 1A2 with 3-methylcholantrene. 3-methylcholantrene 199-218 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-159 28339191-0 2017 Allosteric Activation of Cytochrome P450 3A4 via Progesterone Bioconjugation. Progesterone 49-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-44 28339191-6 2017 CYP3A4 mutants were created and covalently modified with various small molecules including progesterone. Progesterone 91-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28232125-0 2017 In vitro inhibition of human CYP2E1 and CYP3A by quercetin and myricetin in hepatic microsomes is not gender dependent. Quercetin 49-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 28232125-0 2017 In vitro inhibition of human CYP2E1 and CYP3A by quercetin and myricetin in hepatic microsomes is not gender dependent. myricetin 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 28232125-2 2017 Activities of CYP2E1 and CYP3A were measured in the presence of quercetin, myricetin, or isorhamnetin in hepatic microsomal pools from male and female donors. Quercetin 64-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-30 28232125-2 2017 Activities of CYP2E1 and CYP3A were measured in the presence of quercetin, myricetin, or isorhamnetin in hepatic microsomal pools from male and female donors. myricetin 75-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-30 28232125-2 2017 Activities of CYP2E1 and CYP3A were measured in the presence of quercetin, myricetin, or isorhamnetin in hepatic microsomal pools from male and female donors. 3-methylquercetin 89-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-30 28232125-6 2017 Quercetin inhibited BFC activity in human recombinant cDNA-expressed CYP3A4 competitively with the Ki=15.4+-1.52muM, and myricetin - noncompetitively with the Ki=74.6+-7.99muM. Quercetin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 28232125-10 2017 We concluded that observed inhibition of CYP2E1 and CYP3A by some flavonols were not gender-dependent. Flavonols 66-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-57 28446877-0 2017 Exploring the Role of CYP3A4 Mediated Drug Metabolism in the Pharmacological Modulation of Nitric Oxide Production. Nitric Oxide 91-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 28446877-6 2017 Our results suggested that for some macrolide compounds, the cytochrome P450 3A4 derived drug metabolites have an important effect on nitric oxide production and might critically contribute to the pharmacological immunomodulatory activity observed. Macrolides 36-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-80 28446877-6 2017 Our results suggested that for some macrolide compounds, the cytochrome P450 3A4 derived drug metabolites have an important effect on nitric oxide production and might critically contribute to the pharmacological immunomodulatory activity observed. Nitric Oxide 134-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-80 28520384-2 2012 Risperidone is metabolized to the active metabolite 9-hydroxyrisperidone by the enzyme CYP2D6 and to a lesser extent by CYP3A4. Risperidone 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 28458904-6 2017 Pharmacogenetic analysis revealed that the pediatric patient carried the CYP3A4 *1B/*1G and CYP3A5 *3/*3 genotype (associated with a partial and complete loss of enzyme activity, respectively) which is associated with the development of iatrogenic Cushing"s syndrome in patients treated for HIV due to the strong inhibition of CYP3 enzymes by Ritonavir. Ritonavir 343-352 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 28458904-8 2017 LEARNING POINTS: Fluticasone therapy may induce iatrogenic Cushing"s syndrome in a patient treated with anti-retroviral therapy.Pharmacogenetic analysis, in particular CYP3A genotyping, provides useful information in patients treated for HIV with respect to possible future steroid treatment.Fluticasone furoate is not detected in the Siemens Immulite cortisol binding assay. Fluticasone 17-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-173 28458904-8 2017 LEARNING POINTS: Fluticasone therapy may induce iatrogenic Cushing"s syndrome in a patient treated with anti-retroviral therapy.Pharmacogenetic analysis, in particular CYP3A genotyping, provides useful information in patients treated for HIV with respect to possible future steroid treatment.Fluticasone furoate is not detected in the Siemens Immulite cortisol binding assay. Steroids 274-281 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-173 28458904-8 2017 LEARNING POINTS: Fluticasone therapy may induce iatrogenic Cushing"s syndrome in a patient treated with anti-retroviral therapy.Pharmacogenetic analysis, in particular CYP3A genotyping, provides useful information in patients treated for HIV with respect to possible future steroid treatment.Fluticasone furoate is not detected in the Siemens Immulite cortisol binding assay. fluticasone furoate 292-311 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-173 28520383-4 2012 Propafenone is metabolized by CYP2D6, CYP3A4, and CYP1A2 enzymes. Propafenone 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 28520383-7 2012 In addition, drugs that inhibit CYP2D6, CYP3A4, and CYP1A2 may also increase propafenone levels, which may lead to cardiac arrhythmia episodes. Propafenone 77-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 27173987-6 2017 In vitro investigation of 8-arm-poly(ethylene glycol) against CYP3A4-catalyzed felodipine metabolism employing human liver microsomes compared closely with naringenin, a typical grapefruit flavonoid, yielding IC50 values of 7.22 and 121.97 muM, respectively. 8-arm-poly(ethylene glycol) 26-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 27173987-6 2017 In vitro investigation of 8-arm-poly(ethylene glycol) against CYP3A4-catalyzed felodipine metabolism employing human liver microsomes compared closely with naringenin, a typical grapefruit flavonoid, yielding IC50 values of 7.22 and 121.97 muM, respectively. Felodipine 79-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 27173987-9 2017 The outcome of this research presents a novel CYP3A4 inhibitor, 8-arm-poly(ethylene glycol) for oral bioavailability enhancement. 8-arm-poly(ethylene glycol) 64-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 27859472-0 2017 Effect of ketoconazole, a strong CYP3A inhibitor, on the pharmacokinetics of venetoclax, a BCL-2 inhibitor, in patients with non-Hodgkin lymphoma. Ketoconazole 10-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 27859472-1 2017 AIMS: To examine the effect of a strong cytochrome P450 (CYP) 3A inhibitor, ketoconazole, on the pharmacokinetics, safety and tolerability of venetoclax. Ketoconazole 76-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-64 27859472-1 2017 AIMS: To examine the effect of a strong cytochrome P450 (CYP) 3A inhibitor, ketoconazole, on the pharmacokinetics, safety and tolerability of venetoclax. venetoclax 142-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-64 27859472-7 2017 CONCLUSIONS: Coadministration of venetoclax with multiple doses of ketoconazole resulted in a significant increase of venetoclax exposures, strongly suggesting that CYP3A plays a major role in elimination of venetoclax in patients. venetoclax 33-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-170 27859472-7 2017 CONCLUSIONS: Coadministration of venetoclax with multiple doses of ketoconazole resulted in a significant increase of venetoclax exposures, strongly suggesting that CYP3A plays a major role in elimination of venetoclax in patients. Ketoconazole 67-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-170 27859472-7 2017 CONCLUSIONS: Coadministration of venetoclax with multiple doses of ketoconazole resulted in a significant increase of venetoclax exposures, strongly suggesting that CYP3A plays a major role in elimination of venetoclax in patients. venetoclax 118-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-170 27859472-7 2017 CONCLUSIONS: Coadministration of venetoclax with multiple doses of ketoconazole resulted in a significant increase of venetoclax exposures, strongly suggesting that CYP3A plays a major role in elimination of venetoclax in patients. venetoclax 118-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-170 27859472-9 2017 For patients who have completed the ramp-up phase, a modification in venetoclax dose for use with strong and moderate inhibitors or inducers of CYP3A is recommended. venetoclax 69-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-149 28340451-3 2017 Drug-drug interactions (DDIs) may occur in prostate cancer patients due to inhibition by abiraterone of liver cytochrome P450 (CYP)-dependent enzymes CYP2C8 and 2D6, which are involved in the metabolism of approximately 25% of all drugs, and induction by enzalutamide of CYP3A4, 2C9 and 2C19, which metabolize up to 50% of medications. abiraterone 89-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 271-277 28340451-7 2017 Enzalutamide may decrease plasma levels of CYP3A4, 2C9 and 2C19 substrates including disopiramide, quetiapine, quinidine and warfarin. enzalutamide 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 28340451-7 2017 Enzalutamide may decrease plasma levels of CYP3A4, 2C9 and 2C19 substrates including disopiramide, quetiapine, quinidine and warfarin. UNII-4HB8OU08NH 85-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 28340451-7 2017 Enzalutamide may decrease plasma levels of CYP3A4, 2C9 and 2C19 substrates including disopiramide, quetiapine, quinidine and warfarin. Quetiapine Fumarate 99-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 28340451-7 2017 Enzalutamide may decrease plasma levels of CYP3A4, 2C9 and 2C19 substrates including disopiramide, quetiapine, quinidine and warfarin. Quinidine 111-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 28063163-1 2017 OBJECTIVE: Mitotane induces hepatic CYP3A4 activity, resulting in accelerated cortisol inactivation, and also increases cortisol binding globulin (CBG). Mitotane 11-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 27599706-4 2017 METHODS: This study predicted the magnitude of the DDI between efavirenz, an inducer of CYP3A4 and inhibitor of CYP2C8, and dual CYP3A4/CYP2C8 substrates (repaglinide, montelukast, pioglitazone, paclitaxel) using a physiologically based pharmacokinetic (PBPK) modeling approach integrating concurrent effects on CYPs. efavirenz 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 27599706-4 2017 METHODS: This study predicted the magnitude of the DDI between efavirenz, an inducer of CYP3A4 and inhibitor of CYP2C8, and dual CYP3A4/CYP2C8 substrates (repaglinide, montelukast, pioglitazone, paclitaxel) using a physiologically based pharmacokinetic (PBPK) modeling approach integrating concurrent effects on CYPs. efavirenz 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 27599706-4 2017 METHODS: This study predicted the magnitude of the DDI between efavirenz, an inducer of CYP3A4 and inhibitor of CYP2C8, and dual CYP3A4/CYP2C8 substrates (repaglinide, montelukast, pioglitazone, paclitaxel) using a physiologically based pharmacokinetic (PBPK) modeling approach integrating concurrent effects on CYPs. repaglinide 155-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 27599706-4 2017 METHODS: This study predicted the magnitude of the DDI between efavirenz, an inducer of CYP3A4 and inhibitor of CYP2C8, and dual CYP3A4/CYP2C8 substrates (repaglinide, montelukast, pioglitazone, paclitaxel) using a physiologically based pharmacokinetic (PBPK) modeling approach integrating concurrent effects on CYPs. montelukast 168-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 27599706-4 2017 METHODS: This study predicted the magnitude of the DDI between efavirenz, an inducer of CYP3A4 and inhibitor of CYP2C8, and dual CYP3A4/CYP2C8 substrates (repaglinide, montelukast, pioglitazone, paclitaxel) using a physiologically based pharmacokinetic (PBPK) modeling approach integrating concurrent effects on CYPs. Pioglitazone 181-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 27599706-4 2017 METHODS: This study predicted the magnitude of the DDI between efavirenz, an inducer of CYP3A4 and inhibitor of CYP2C8, and dual CYP3A4/CYP2C8 substrates (repaglinide, montelukast, pioglitazone, paclitaxel) using a physiologically based pharmacokinetic (PBPK) modeling approach integrating concurrent effects on CYPs. Paclitaxel 195-205 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 28167538-2 2017 Bosutinib is predominantly metabolized by CYP3A4 as the primary clearance mechanism. bosutinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 28183147-1 2017 1beta-hydroxydeoxycholic acid in unlabeled and stable isotope labeled forms was required for use as a biomarker for Cytochrome P450 3A4/5 activity. 1beta-hydroxydeoxycholic acid 0-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-135 26864621-5 2017 With higher bioavailability of recently FDA-approved posaconazole delayed release tablets, this azole may be a therapeutic option for transplant patients who need to remain on CYP3A4-metabolized immunosuppressive agents. posaconazole 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 28616429-2 2017 It can increase blood concentrations of other medications including cyclosporine A (CsA) which are substrates for cytochrome P450 3A4. Cyclosporine 68-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-133 28616429-2 2017 It can increase blood concentrations of other medications including cyclosporine A (CsA) which are substrates for cytochrome P450 3A4. Cyclosporine 84-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-133 28350522-0 2017 The influences of SLCO1B1 and ABCB1 genotypes on the pharmacokinetics of simvastatin, in relation to CYP3A4 inhibition. Simvastatin 73-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 28350522-1 2017 AIM: To investigate the combined effects of SLCO1B1 and ABCB1 genotypes on the pharmacokinetics of simvastatin and its active metabolite simvastatin acid, in relation to CYP3A4 inhibition. Simvastatin 99-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 28350522-1 2017 AIM: To investigate the combined effects of SLCO1B1 and ABCB1 genotypes on the pharmacokinetics of simvastatin and its active metabolite simvastatin acid, in relation to CYP3A4 inhibition. simvastatin acid 137-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 28350522-7 2017 SLCO1B1 genotyping may be particularly beneficial in simvastatin users who are co-administered CYP3A4 inhibitors. Simvastatin 53-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 27939799-4 2017 The selective P-gp inhibitors (CP100356 and PSC833) enhanced 3-hydroxy-quinidine (3OH-Qi) in jejunum and ileum, while dual inhibitors of P-gp and CYP3A4 (verapamil and ketoconazole) decreased the 3OH-Qi production, despite of the increased intracellular Qi concentration, due to inhibition of CYP3A4. CP 100356 31-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 293-299 27939799-4 2017 The selective P-gp inhibitors (CP100356 and PSC833) enhanced 3-hydroxy-quinidine (3OH-Qi) in jejunum and ileum, while dual inhibitors of P-gp and CYP3A4 (verapamil and ketoconazole) decreased the 3OH-Qi production, despite of the increased intracellular Qi concentration, due to inhibition of CYP3A4. valspodar 44-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 27939799-4 2017 The selective P-gp inhibitors (CP100356 and PSC833) enhanced 3-hydroxy-quinidine (3OH-Qi) in jejunum and ileum, while dual inhibitors of P-gp and CYP3A4 (verapamil and ketoconazole) decreased the 3OH-Qi production, despite of the increased intracellular Qi concentration, due to inhibition of CYP3A4. valspodar 44-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 293-299 27939799-4 2017 The selective P-gp inhibitors (CP100356 and PSC833) enhanced 3-hydroxy-quinidine (3OH-Qi) in jejunum and ileum, while dual inhibitors of P-gp and CYP3A4 (verapamil and ketoconazole) decreased the 3OH-Qi production, despite of the increased intracellular Qi concentration, due to inhibition of CYP3A4. Verapamil 154-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 27939799-4 2017 The selective P-gp inhibitors (CP100356 and PSC833) enhanced 3-hydroxy-quinidine (3OH-Qi) in jejunum and ileum, while dual inhibitors of P-gp and CYP3A4 (verapamil and ketoconazole) decreased the 3OH-Qi production, despite of the increased intracellular Qi concentration, due to inhibition of CYP3A4. Ketoconazole 168-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 28067989-4 2017 The observed drug interaction occurred on two separate hospital admissions, during both of which the patient exhibited therapeutic TAC concentrations prior to exposure to NAF, a CYP3A4 inducer. Nafcillin 171-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 27226420-10 2017 CYP3A4-related drug-drug interactions with panobinostat have been documented with ketoconazole (inhibitor) and dexamethasone (inducer). Panobinostat 43-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 27226420-10 2017 CYP3A4-related drug-drug interactions with panobinostat have been documented with ketoconazole (inhibitor) and dexamethasone (inducer). Ketoconazole 82-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 27226420-10 2017 CYP3A4-related drug-drug interactions with panobinostat have been documented with ketoconazole (inhibitor) and dexamethasone (inducer). Dexamethasone 111-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 27312150-5 2017 The most potent inhibitors were genistein and daidzein inhibiting noncompetitively the CYP2C9 with Ki of 35.95 +- 6.96 and 60.56 +- 3.53 mumol/l and CYP3A4 (inhibited by genistein with Ki of 23.25 +- 5.85 mumol/l also by a noncompetitive mechanism). Genistein 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 27312150-5 2017 The most potent inhibitors were genistein and daidzein inhibiting noncompetitively the CYP2C9 with Ki of 35.95 +- 6.96 and 60.56 +- 3.53 mumol/l and CYP3A4 (inhibited by genistein with Ki of 23.25 +- 5.85 mumol/l also by a noncompetitive mechanism). daidzein 46-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 27312150-5 2017 The most potent inhibitors were genistein and daidzein inhibiting noncompetitively the CYP2C9 with Ki of 35.95 +- 6.96 and 60.56 +- 3.53 mumol/l and CYP3A4 (inhibited by genistein with Ki of 23.25 +- 5.85 mumol/l also by a noncompetitive mechanism). Genistein 170-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 27312150-8 2017 Genistein and daidzein inhibit noncompetitively CYP3A4 and CYP2C9. Genistein 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 27312150-8 2017 Genistein and daidzein inhibit noncompetitively CYP3A4 and CYP2C9. daidzein 14-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 27324291-5 2017 The exposure of primary hepatocytes to luseogliflozin for 72 hrs weakly induced CYP3A4 at a concentration of 10 muM, whereas it did not induce CYP1A2 or CYP2B6 at concentrations of 0.1-10 muM. 1,5-anhydro-1-(5-(4-ethoxybenzyl)-2-methoxy-4-methylphenyl)-1-thioglucitol 39-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 28408884-0 2017 Effect of CYP3A4*1G and CYP3A5*3 Polymorphisms on Pharmacokinetics and Pharmacodynamics of Ticagrelor in Healthy Chinese Subjects. Ticagrelor 91-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 28408884-4 2017 The metabolism of ticagrelor to AR-C124910XX involves CYP3A4 and CYP3A5. Argon 32-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 28408884-6 2017 Genetic differences in CYP3A4 and CYP3A5 expression in human volunteers and patients might affect the clearance of ticagrelor or AR-C124910XX in vivo resulting in subsequent variable patient response. Ticagrelor 115-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 28408884-7 2017 Thus, this study is designed to explore the effects of CYP3A4*1G and CYP3A5*3 polymorphisms on the pharmacokinetics and pharmcodynamics of ticagrelor in healthy Chinese subjects. Ticagrelor 139-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 28408884-8 2017 The results indicated that the CYP3A4*1G polymorphism significantly influenced the pharmacokinetics of AR-C124910XX, and it may be more important than CYP3A5*3 with respect to influencing ticagrelor pharmacokinetics by increasing CYP3A4 activity. Ticagrelor 188-198 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 28408884-8 2017 The results indicated that the CYP3A4*1G polymorphism significantly influenced the pharmacokinetics of AR-C124910XX, and it may be more important than CYP3A5*3 with respect to influencing ticagrelor pharmacokinetics by increasing CYP3A4 activity. Ticagrelor 188-198 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-236 28221037-7 2017 Our results revealed that the binding mode of progesterone (PGS), a substrate of CYP3A4, in the crystal structure was not stable and underwent a significant conformational change. Progesterone 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 28338641-7 2017 The results indicate that acyclic sesquiterpenes might affect CYP1A, CYP2B and CYP3A mediated metabolism of concurrently administered drugs and other xenobiotics. Sesquiterpenes 34-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-84 28469859-1 2017 Nilotinib, a BCR-ABL tyrosine kinase inhibitor, is a known inhibitor of CYP3A4 and could increase the concentration of drugs metabolized by CYP3A4. nilotinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 28469859-1 2017 Nilotinib, a BCR-ABL tyrosine kinase inhibitor, is a known inhibitor of CYP3A4 and could increase the concentration of drugs metabolized by CYP3A4. nilotinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 28352156-11 2017 An increase in Cmax and AUC for atorvastatin in fed subjects was attributed to extended transit along the gut lumen and reduced atorvastatin metabolism due to lower CYP3A4 expression at more distal small intestine absorption sites. Atorvastatin 32-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 28257661-13 2017 ABA also induced the expression of endogenous CYP3A4 mRNA in both cultured hPXR-overexpressing hepatoma cells and human primary hepatocytes. alisol B 23-acetate 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 28287454-6 2017 These in vitro results indicate that AM-2201 needs to be examined for potential pharmacokinetic drug interactions in vivo due to its potent inhibition of CYP2C8, CYP2C9, CYP3A4, UGT1A3, and UGT2B7 enzyme activities. 1-(5-fluoropentyl)-3-(1-naphthoyl)indole 37-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 28414290-6 2017 The SPR-based experiments have shown that a high concentration of isatin (270 mM) increases Kd values for complexes CYB5A/CYP3A5 and CYB5A/CYP3A4 (twofold and threefold, respectively), but has no influence on complex formation between CYB5A and other CYP (including indol-metabolizing CYP2C19 and CYP2E1). Isatin 66-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 28414290-7 2017 Isatin injection to the optical biosensor chip with the preformed molecular complex CYB5A/CYP3A4 caused a 30%-increase in its dissociation rate. Isatin 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 28414290-8 2017 Molecular docking manipulations have shown that isatin can influence interaction of CYP3A5 or CYP3A4 with CYB5A acting at the contact region of CYB5A/CYP. Isatin 48-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 27928738-0 2017 Effect of Multiple Oral Doses of the Potent CYP3A4 Inhibitor Clarithromycin on the Pharmacokinetics of a Single Oral Dose of Vonoprazan: A Phase I, Open-Label, Sequential Design Study. Clarithromycin 61-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 27928738-0 2017 Effect of Multiple Oral Doses of the Potent CYP3A4 Inhibitor Clarithromycin on the Pharmacokinetics of a Single Oral Dose of Vonoprazan: A Phase I, Open-Label, Sequential Design Study. 1-(5-(2-fluorophenyl)-1-(pyridin-3-ylsulfonyl)-1H-pyrrol-3-yl)-N-methylmethanamine 125-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 27928738-11 2017 CONCLUSIONS: Modest increases in plasma concentrations of the potent CYP3A4 inhibitor clarithromycin and vonoprazan were observed during coadministration, however these differences were not considered clinically significant. Clarithromycin 86-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 27928738-11 2017 CONCLUSIONS: Modest increases in plasma concentrations of the potent CYP3A4 inhibitor clarithromycin and vonoprazan were observed during coadministration, however these differences were not considered clinically significant. 1-(5-(2-fluorophenyl)-1-(pyridin-3-ylsulfonyl)-1H-pyrrol-3-yl)-N-methylmethanamine 105-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 27648490-5 2017 Clinical DDIs of montelukast were evaluated using physiologically based pharmacokinetic modeling; and simulation of the interactions with gemfibrozil-CYP2C8 and OATP1B1/1B3 inhibitor, clarithromycin-CYP3A and OATP1B1/1B3 inhibitor, and itraconazole-CYP3A inhibitor, implicated OATPs-CYP2C8-CYP2C8 interplay as the primary determinant of montelukast pharmacokinetics. montelukast 17-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 199-204 27648490-5 2017 Clinical DDIs of montelukast were evaluated using physiologically based pharmacokinetic modeling; and simulation of the interactions with gemfibrozil-CYP2C8 and OATP1B1/1B3 inhibitor, clarithromycin-CYP3A and OATP1B1/1B3 inhibitor, and itraconazole-CYP3A inhibitor, implicated OATPs-CYP2C8-CYP2C8 interplay as the primary determinant of montelukast pharmacokinetics. montelukast 17-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 249-254 28263461-6 2017 Initial in vitro studies identified CYP3A4 as metabolizing methadone. Methadone 59-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 28263461-7 2017 Subsequently, by extrapolation, CYP3A4 was long assumed to be responsible for clinical methadone disposition. Methadone 87-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 27974381-0 2017 Difference in Mechanism-Based Inhibition of Cytochrome P450 3A4 and 3A5 by a Series of Fluoroquinolone Antibacterial Agents. Fluoroquinolones 87-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-63 27974381-1 2017 A series of fluoroquinolone antibacterial compounds were found to be irreversible (compounds 1-5) and quasi-irreversible (compounds 6-9) inhibitors of CYP3A4. Fluoroquinolones 12-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 27974381-6 2017 The homology modeling of CYP3A5 suggests that four residues around the nitroso intermediate of compound 6 in the substrate-binding pocket of CYP3A4 correspond with the bulkier residues in CYP3A5-especially Phe210 in CYP3A5-which might contribute to the steric hindrance with the nitroso intermediate of compound 6. nitroso 71-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 27974381-6 2017 The homology modeling of CYP3A5 suggests that four residues around the nitroso intermediate of compound 6 in the substrate-binding pocket of CYP3A4 correspond with the bulkier residues in CYP3A5-especially Phe210 in CYP3A5-which might contribute to the steric hindrance with the nitroso intermediate of compound 6. nitroso 279-286 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 28053220-2 2017 Studies have revealed that the clearance of rivaroxaban is largely attributed to CYP3A4, CYP2J2 metabolism, and P-glycoprotein (P-gp) efflux pathways. Rivaroxaban 44-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 28053220-4 2017 Amiodarone, dronedarone, and their major metabolites, N-desethylamiodarone (NDEA) and N-desbutyldronedarone (NDBD), demonstrate inhibitory effects on CYP3A4 and CYP2J2 with U.S. Food and Drug Administration-recommended probe substrates. Amiodarone 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 28053220-4 2017 Amiodarone, dronedarone, and their major metabolites, N-desethylamiodarone (NDEA) and N-desbutyldronedarone (NDBD), demonstrate inhibitory effects on CYP3A4 and CYP2J2 with U.S. Food and Drug Administration-recommended probe substrates. Dronedarone 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 28053220-4 2017 Amiodarone, dronedarone, and their major metabolites, N-desethylamiodarone (NDEA) and N-desbutyldronedarone (NDBD), demonstrate inhibitory effects on CYP3A4 and CYP2J2 with U.S. Food and Drug Administration-recommended probe substrates. desethylamiodarone 54-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 28053220-4 2017 Amiodarone, dronedarone, and their major metabolites, N-desethylamiodarone (NDEA) and N-desbutyldronedarone (NDBD), demonstrate inhibitory effects on CYP3A4 and CYP2J2 with U.S. Food and Drug Administration-recommended probe substrates. desethylamiodarone 76-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 28053220-4 2017 Amiodarone, dronedarone, and their major metabolites, N-desethylamiodarone (NDEA) and N-desbutyldronedarone (NDBD), demonstrate inhibitory effects on CYP3A4 and CYP2J2 with U.S. Food and Drug Administration-recommended probe substrates. N-desbutyldronedarone 86-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 28053220-4 2017 Amiodarone, dronedarone, and their major metabolites, N-desethylamiodarone (NDEA) and N-desbutyldronedarone (NDBD), demonstrate inhibitory effects on CYP3A4 and CYP2J2 with U.S. Food and Drug Administration-recommended probe substrates. N-desbutyldronedarone 109-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 28053220-8 2017 In this study, in vitro inhibition assays using rivaroxaban as the probe substrate demonstrated that both dronedarone and NDBD produced reversible inhibition as well as irreversible mechanism-based inactivation of CYP3A4- and CYP2J2-mediated metabolism of rivaroxaban. Rivaroxaban 48-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 214-220 28053220-8 2017 In this study, in vitro inhibition assays using rivaroxaban as the probe substrate demonstrated that both dronedarone and NDBD produced reversible inhibition as well as irreversible mechanism-based inactivation of CYP3A4- and CYP2J2-mediated metabolism of rivaroxaban. Dronedarone 106-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 214-220 28053220-8 2017 In this study, in vitro inhibition assays using rivaroxaban as the probe substrate demonstrated that both dronedarone and NDBD produced reversible inhibition as well as irreversible mechanism-based inactivation of CYP3A4- and CYP2J2-mediated metabolism of rivaroxaban. N-desbutyldronedarone 122-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 214-220 28053220-8 2017 In this study, in vitro inhibition assays using rivaroxaban as the probe substrate demonstrated that both dronedarone and NDBD produced reversible inhibition as well as irreversible mechanism-based inactivation of CYP3A4- and CYP2J2-mediated metabolism of rivaroxaban. Rivaroxaban 256-267 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 214-220 28053220-9 2017 However, amiodarone and NDEA were observed to cause reversible inhibition as well as mechanism-based inactivation of CYP3A4 but not CYP2J2. Amiodarone 9-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 28053220-9 2017 However, amiodarone and NDEA were observed to cause reversible inhibition as well as mechanism-based inactivation of CYP3A4 but not CYP2J2. desethylamiodarone 24-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 28069721-2 2017 Atorvastatin (ATV), a substrate for CYP3A and human OATP1B1, is likely to be coadministered with LB in patients with the metabolic syndrome. Atorvastatin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 28069721-2 2017 Atorvastatin (ATV), a substrate for CYP3A and human OATP1B1, is likely to be coadministered with LB in patients with the metabolic syndrome. Atorvastatin 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 28074333-7 2017 The CYP2C8 (69 +- 20%), CYP2C9 (42 +- 10%), CYP3A4 (52 +- 23%), and CEP2E1 (41 +- 13%) inhibitors all significantly inhibited rosiglitazone metabolism. Rosiglitazone 126-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 28074333-8 2017 CONCLUSION: The results suggest that other cytochrome P450 enzymes, including CYP2C9, CYP3A4, and CEP2E1, in addition to CYP28, also play an important role in the metabolism of rosiglitazone. Rosiglitazone 177-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 28012672-5 2017 We herein evaluated five commonly used triazole fungicides including bitertanol, hexaconazole, penconazole, tebuconazole and uniconazole for the androgenic and anti-androgenic activity using two-hybrid recombinant human androgen receptor (AR) yeast bioassay and comparatively evaluated their effects on enzymatic activity of CYP3A4 by P450-Glo CYP3A4 bioassay. uniconazole 125-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 325-331 28012672-5 2017 We herein evaluated five commonly used triazole fungicides including bitertanol, hexaconazole, penconazole, tebuconazole and uniconazole for the androgenic and anti-androgenic activity using two-hybrid recombinant human androgen receptor (AR) yeast bioassay and comparatively evaluated their effects on enzymatic activity of CYP3A4 by P450-Glo CYP3A4 bioassay. uniconazole 125-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 345-351 28012672-8 2017 These fungicides significantly inhibited the activity of CYP3A4 at the environmental relevant concentrations and the potency ranks as tebuconazole > uniconazole > hexaconazole > penconazole > bitertanol with the corresponding IC50 of 0.81 muM, 0.93 muM, 1.27 muM, 2.22 muM, and 2.74 muM, respectively. tebuconazole 134-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 28012672-8 2017 These fungicides significantly inhibited the activity of CYP3A4 at the environmental relevant concentrations and the potency ranks as tebuconazole > uniconazole > hexaconazole > penconazole > bitertanol with the corresponding IC50 of 0.81 muM, 0.93 muM, 1.27 muM, 2.22 muM, and 2.74 muM, respectively. uniconazole 152-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 28012672-8 2017 These fungicides significantly inhibited the activity of CYP3A4 at the environmental relevant concentrations and the potency ranks as tebuconazole > uniconazole > hexaconazole > penconazole > bitertanol with the corresponding IC50 of 0.81 muM, 0.93 muM, 1.27 muM, 2.22 muM, and 2.74 muM, respectively. hexaconazole 169-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 28012672-8 2017 These fungicides significantly inhibited the activity of CYP3A4 at the environmental relevant concentrations and the potency ranks as tebuconazole > uniconazole > hexaconazole > penconazole > bitertanol with the corresponding IC50 of 0.81 muM, 0.93 muM, 1.27 muM, 2.22 muM, and 2.74 muM, respectively. penconazole 187-198 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 28012672-8 2017 These fungicides significantly inhibited the activity of CYP3A4 at the environmental relevant concentrations and the potency ranks as tebuconazole > uniconazole > hexaconazole > penconazole > bitertanol with the corresponding IC50 of 0.81 muM, 0.93 muM, 1.27 muM, 2.22 muM, and 2.74 muM, respectively. bitertanol 204-214 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 27975131-1 2017 PURPOSE: Individual variability in the endogenous CYP3A metabolite 4beta-hydroxycholesterol (4betaOHC) is substantial, but to which extent this is determined by genetic and nongenetic factors remains unclear. cholest-5-ene-3,4-diol 67-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 27975131-1 2017 PURPOSE: Individual variability in the endogenous CYP3A metabolite 4beta-hydroxycholesterol (4betaOHC) is substantial, but to which extent this is determined by genetic and nongenetic factors remains unclear. 4betaohc 93-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 27975131-7 2017 CONCLUSIONS: These findings suggest that the CYP3A4*22, CYP3A5*3, and POR*28 variant alleles are of limited importance for overall individual variability in 4betaOHC levels compared to nongenetic factors. 4betaohc 157-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 27822915-4 2017 Multiple regression analysis showed that concomitant use of oral itraconazole or voriconazole significantly increased the (C/Dpo)/(C/Div) of tacrolimus (p = 0.002), probably owing to the inhibition of enterohepatic cytochrome P450 3A4. Itraconazole 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-234 27822915-4 2017 Multiple regression analysis showed that concomitant use of oral itraconazole or voriconazole significantly increased the (C/Dpo)/(C/Div) of tacrolimus (p = 0.002), probably owing to the inhibition of enterohepatic cytochrome P450 3A4. Voriconazole 81-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-234 27822915-4 2017 Multiple regression analysis showed that concomitant use of oral itraconazole or voriconazole significantly increased the (C/Dpo)/(C/Div) of tacrolimus (p = 0.002), probably owing to the inhibition of enterohepatic cytochrome P450 3A4. Tacrolimus 141-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-234 28249055-4 2017 The trigger for our patient"s statin-induced rhabdomyolysis was fluconazole, a known moderate inhibitor of CYP3A4, which is comparatively weaker than certain potent azoles like itraconazole or ketoconazole. Fluconazole 64-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 28291036-7 2017 Formation of N-desmethylclozapine is correlated with activity of the cytochrome P450 enzymes 1A2 and 3A4 (CYP1A2 and CYP3A4). norclozapine 13-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 27545757-0 2017 Clinical Drug-Drug Interactions Through Cytochrome P450 3A (CYP3A) for the Selective ALK Inhibitor Alectinib. alectinib 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-58 27545757-0 2017 Clinical Drug-Drug Interactions Through Cytochrome P450 3A (CYP3A) for the Selective ALK Inhibitor Alectinib. alectinib 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 27545757-2 2017 Alectinib is mainly metabolized by cytochrome P450 3A (CYP3A) to a major similarly active metabolite, M4. alectinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 27545757-3 2017 Alectinib and M4 show evidence of weak time-dependent inhibition and small induction of CYP3A in vitro. alectinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-93 28248857-13 2017 The patients with CC genotype of CYP2D610 polymorphism and 3/3 genotype of CYP3A53 polymorphism exhibited higher scores of >ASAS20, >BASDAI50%, and effective rate. asas20 127-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 27545757-4 2017 We present results from 3 fixed-sequence studies evaluating drug-drug interactions for alectinib through CYP3A. alectinib 87-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-110 27545757-5 2017 Studies NP28990 and NP29042 enrolled 17 and 24 healthy subjects, respectively, and investigated potent CYP3A inhibition with posaconazole and potent CYP3A induction through rifampin, respectively, on the single oral dose pharmacokinetics (PK) of alectinib. posaconazole 125-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 27545757-5 2017 Studies NP28990 and NP29042 enrolled 17 and 24 healthy subjects, respectively, and investigated potent CYP3A inhibition with posaconazole and potent CYP3A induction through rifampin, respectively, on the single oral dose pharmacokinetics (PK) of alectinib. Rifampin 173-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-154 27545757-6 2017 A substudy of the global phase 2 NP28673 study enrolled 15 patients with ALK+ NSCLC to determine the effect of multiple doses of alectinib on the single oral dose PK of midazolam, a sensitive substrate of CYP3A. Midazolam 169-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 205-210 27545757-7 2017 Potent CYP3A inhibition or induction resulted in only minor effects on the combined exposure of alectinib and M4. alectinib 96-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-12 27665573-2 2017 Etravirine is primarily metabolized by cytochrome P450 (CYP) 2C9, CYP2C19, and CYP3A. etravirine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-84 27995413-9 2017 Stromal cells isolated from ovarian endometriotic lesions expressed CYP3A4 and their exposure to luteal phase-mimicking hormones (estradiol + progesterone) reduced CYP3A4 mRNA in parallel with a diminished expression of the corresponding receptors, estrogen receptor alpha and progesterone receptor. Estradiol 130-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 27995413-9 2017 Stromal cells isolated from ovarian endometriotic lesions expressed CYP3A4 and their exposure to luteal phase-mimicking hormones (estradiol + progesterone) reduced CYP3A4 mRNA in parallel with a diminished expression of the corresponding receptors, estrogen receptor alpha and progesterone receptor. Estradiol 130-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 27995413-9 2017 Stromal cells isolated from ovarian endometriotic lesions expressed CYP3A4 and their exposure to luteal phase-mimicking hormones (estradiol + progesterone) reduced CYP3A4 mRNA in parallel with a diminished expression of the corresponding receptors, estrogen receptor alpha and progesterone receptor. Progesterone 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 27995413-9 2017 Stromal cells isolated from ovarian endometriotic lesions expressed CYP3A4 and their exposure to luteal phase-mimicking hormones (estradiol + progesterone) reduced CYP3A4 mRNA in parallel with a diminished expression of the corresponding receptors, estrogen receptor alpha and progesterone receptor. Progesterone 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 28152547-9 2017 Neratinib-resistant cells were more aggressive than their drug-sensitive counterparts, with increased CYP3A4 activity identified as a novel mechanism of neratinib resistance. neratinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 27995413-10 2017 Our findings suggest that steroid hormones are able to regulate CYP3A4 mRNA expression, although the circulating levels of these hormones can only regulate control endometrium and not endometriosis tissues, probably because of dysregulated local steroid concentration in these latter samples. Steroids 26-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 27995413-10 2017 Our findings suggest that steroid hormones are able to regulate CYP3A4 mRNA expression, although the circulating levels of these hormones can only regulate control endometrium and not endometriosis tissues, probably because of dysregulated local steroid concentration in these latter samples. Steroids 26-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 28219593-2 2017 Tacrolimus, an immunosuppressant that protects against organ rejection in transplant recipients, not only is mainly metabolized by CYP3A enzymes but also has a narrow therapeutic range. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-136 28454244-4 2017 Sphere-forming PLC/PRF/5 cells were more resistant to sorafenib, as compared with control cells, exhibiting higher expression levels of CYP3A4. Sorafenib 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 28152547-9 2017 Neratinib-resistant cells were more aggressive than their drug-sensitive counterparts, with increased CYP3A4 activity identified as a novel mechanism of neratinib resistance. neratinib 153-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 28152547-10 2017 CONCLUSIONS: The potential of increased CYP3A4 activity as a biomarker and/or target to add value to neratinib warrants investigation. neratinib 101-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 27530469-7 2017 DDI are more likely to occur with 3D regimen, daclatasvir, simeprevir and ledipasvir, as they are all both substrates and inhibitors of P-gp and/or CYP3A4, than with sofosbuvir. daclatasvir 46-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 28078726-7 2017 The most stable binding modes in CYP3A4 favor the formation of the 3alpha-hydroxylated and 8,9-exo-epoxide metabolites. 8,9-exo-epoxide 91-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 28231276-9 2017 Furthermore, CYP3A4, MRP1 and MDR1 protein levels were significantly induced in treatment groups which included ethanol compared to those with no treatment. Ethanol 112-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 27966929-6 2017 We studied the structure of human estrogen metabolizing enzymes (CYP1A1, CYP1A2, CYP1B1, and CYP3A4) in complex with estrone using docking and investigated the susceptibility of estrone, equilin, and equilenin (which only differ in the unsaturation of ring B) to undergo 2- and 4-hydroxylation using several models of CYP enzymes (Compound I, methoxy, and phenoxy radical). Estrone 117-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 27966929-6 2017 We studied the structure of human estrogen metabolizing enzymes (CYP1A1, CYP1A2, CYP1B1, and CYP3A4) in complex with estrone using docking and investigated the susceptibility of estrone, equilin, and equilenin (which only differ in the unsaturation of ring B) to undergo 2- and 4-hydroxylation using several models of CYP enzymes (Compound I, methoxy, and phenoxy radical). Estrone 178-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 27966929-6 2017 We studied the structure of human estrogen metabolizing enzymes (CYP1A1, CYP1A2, CYP1B1, and CYP3A4) in complex with estrone using docking and investigated the susceptibility of estrone, equilin, and equilenin (which only differ in the unsaturation of ring B) to undergo 2- and 4-hydroxylation using several models of CYP enzymes (Compound I, methoxy, and phenoxy radical). Equilin 187-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 27966929-6 2017 We studied the structure of human estrogen metabolizing enzymes (CYP1A1, CYP1A2, CYP1B1, and CYP3A4) in complex with estrone using docking and investigated the susceptibility of estrone, equilin, and equilenin (which only differ in the unsaturation of ring B) to undergo 2- and 4-hydroxylation using several models of CYP enzymes (Compound I, methoxy, and phenoxy radical). Equilenin 200-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 27966929-6 2017 We studied the structure of human estrogen metabolizing enzymes (CYP1A1, CYP1A2, CYP1B1, and CYP3A4) in complex with estrone using docking and investigated the susceptibility of estrone, equilin, and equilenin (which only differ in the unsaturation of ring B) to undergo 2- and 4-hydroxylation using several models of CYP enzymes (Compound I, methoxy, and phenoxy radical). 7-methoxy-6-(2'-methoxy-3'-hydroxy-3'-methyl butyl) 343-350 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 27966929-6 2017 We studied the structure of human estrogen metabolizing enzymes (CYP1A1, CYP1A2, CYP1B1, and CYP3A4) in complex with estrone using docking and investigated the susceptibility of estrone, equilin, and equilenin (which only differ in the unsaturation of ring B) to undergo 2- and 4-hydroxylation using several models of CYP enzymes (Compound I, methoxy, and phenoxy radical). phenoxy radical 356-371 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 27664690-7 2017 Studies with baculosomes further demonstrated that CYP2D6 and CYP3A4 could transform tyrosol into hydroxytyrosol. 4-hydroxyphenylethanol 85-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 27664690-7 2017 Studies with baculosomes further demonstrated that CYP2D6 and CYP3A4 could transform tyrosol into hydroxytyrosol. 3,4-dihydroxyphenylethanol 98-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 27611887-1 2017 Pantoprazole is a proton pump inhibitor that is commonly used in the treatment of peptic ulcer disease (PUD) and metabolized by cytochrome P450 (CYP) enzymes CYP2C19 and CYP3A4. Pantoprazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 27611887-3 2017 Single nucleotide polymorphisms (SNPs) in CYP2C19, CYP3A4 and MDR1 affect enzyme activity or gene expression of proteins and may alter plasma pantoprazole concentrations and treatment success in PUD. Pantoprazole 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 27611887-4 2017 In this study, we aimed to investigate the association between genetic polymorphisms in CYP2C19, CYP3A4 and MDR1 and pharmacokinetics of pantoprazole and therapeutic outcome in patients with either Helicobacter pylori-associated [H.P. Pantoprazole 137-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 28111961-1 2017 AIM: Midazolam is a commonly used marker substrate for the in vivo assessment of CYP3A activity. Midazolam 5-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 28111961-6 2017 The validated method was utilized successfully for the sample assay during a midazolam microdosing study for the evaluation of CYP3A4 activity of a clinical candidate. Midazolam 77-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 27530469-7 2017 DDI are more likely to occur with 3D regimen, daclatasvir, simeprevir and ledipasvir, as they are all both substrates and inhibitors of P-gp and/or CYP3A4, than with sofosbuvir. ledipasvir 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 27530469-7 2017 DDI are more likely to occur with 3D regimen, daclatasvir, simeprevir and ledipasvir, as they are all both substrates and inhibitors of P-gp and/or CYP3A4, than with sofosbuvir. Simeprevir 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 28243904-1 2017 The possibility of interactions between warfarin and dasatinib and their interactions with other drugs metabolized by cytochrome P450 isoform CYP3A4 was demonstrated using a previously created cytochrome P450 substrate-inhibitor panel for preclinical in vitro studies of drug biotransformation on a 3D histotypical microfluidic cell model of human liver (liver-on-a-chip technology). Warfarin 40-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 28243904-1 2017 The possibility of interactions between warfarin and dasatinib and their interactions with other drugs metabolized by cytochrome P450 isoform CYP3A4 was demonstrated using a previously created cytochrome P450 substrate-inhibitor panel for preclinical in vitro studies of drug biotransformation on a 3D histotypical microfluidic cell model of human liver (liver-on-a-chip technology). Dasatinib 53-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 28161120-1 2017 PURPOSE: The effect of posaconazole, a strong cytochrome P450 3A (CYP3A) inhibitor and commonly used antifungal agent, on the pharmacokinetic properties of venetoclax, a CYP3A substrate, was evaluated in patients with acute myeloid leukemia to determine the dose adjustments needed to manage this potential interaction. posaconazole 23-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-64 28161120-1 2017 PURPOSE: The effect of posaconazole, a strong cytochrome P450 3A (CYP3A) inhibitor and commonly used antifungal agent, on the pharmacokinetic properties of venetoclax, a CYP3A substrate, was evaluated in patients with acute myeloid leukemia to determine the dose adjustments needed to manage this potential interaction. posaconazole 23-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 28161120-1 2017 PURPOSE: The effect of posaconazole, a strong cytochrome P450 3A (CYP3A) inhibitor and commonly used antifungal agent, on the pharmacokinetic properties of venetoclax, a CYP3A substrate, was evaluated in patients with acute myeloid leukemia to determine the dose adjustments needed to manage this potential interaction. posaconazole 23-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-175 28161120-1 2017 PURPOSE: The effect of posaconazole, a strong cytochrome P450 3A (CYP3A) inhibitor and commonly used antifungal agent, on the pharmacokinetic properties of venetoclax, a CYP3A substrate, was evaluated in patients with acute myeloid leukemia to determine the dose adjustments needed to manage this potential interaction. venetoclax 156-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-64 27798496-4 2017 RAL and DTG are not metabolized via cytochrome P450 (CYP) resulting in fewer drug interactions and less toxicity risk in patients receiving direct-acting antivirals and other coadministered medications.EVG is currently available as a single tablet regimen and requires cobisistat, a pharmacokinetic booster and CYP3A inhibitor to allow QD dosing. elvitegravir 202-205 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 311-316 28161120-1 2017 PURPOSE: The effect of posaconazole, a strong cytochrome P450 3A (CYP3A) inhibitor and commonly used antifungal agent, on the pharmacokinetic properties of venetoclax, a CYP3A substrate, was evaluated in patients with acute myeloid leukemia to determine the dose adjustments needed to manage this potential interaction. venetoclax 156-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 28161120-8 2017 IMPLICATIONS: The results are consistent with inhibition of CYP3A-mediated metabolism of venetoclax. venetoclax 89-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 27934636-4 2017 The RAF value for CYP3A4 or CYP2C9 derived from a particular P450-selective probe reaction was applied to calculate RAF-scaled CLint for other probe reactions of the same P450 isoform in a crossover manner and compared with the measured HLM CLint When RAF derived from midazolam or nifedipine was used for CYP3A4, the ICR for testosterone 6beta-hydroxylation was 31 and 25, respectively, suggesting significantly diverse interactions of CYP3A4 probes with the testing systems. Midazolam 269-278 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 27718639-0 2017 Perspective: 4beta-hydroxycholesterol as an emerging endogenous biomarker of hepatic CYP3A. cholest-5-ene-3,4-diol 13-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-90 27718639-3 2017 Plasma 4beta-hydroxycholesterol (4beta-HC) is considered as an emerging endogenous biomarker for cytochrome P450 3A (CYP3A), one of the major drug metabolizing enzymes. cholest-5-ene-3,4-diol 7-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-115 27718639-3 2017 Plasma 4beta-hydroxycholesterol (4beta-HC) is considered as an emerging endogenous biomarker for cytochrome P450 3A (CYP3A), one of the major drug metabolizing enzymes. cholest-5-ene-3,4-diol 7-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-122 27718639-3 2017 Plasma 4beta-hydroxycholesterol (4beta-HC) is considered as an emerging endogenous biomarker for cytochrome P450 3A (CYP3A), one of the major drug metabolizing enzymes. cholest-5-ene-3,4-diol 33-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-115 27718639-3 2017 Plasma 4beta-hydroxycholesterol (4beta-HC) is considered as an emerging endogenous biomarker for cytochrome P450 3A (CYP3A), one of the major drug metabolizing enzymes. cholest-5-ene-3,4-diol 33-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-122 27718639-5 2017 Herein, we review the biology of 4beta-HC, its response to treatment with CYP3A inducers, inhibitors and mixed inducer/inhibitors in healthy volunteers and patients, the association of 4beta-HC with other probes of CYP3A activity (e.g. midazolam, urinary cortisol ratios), and present predictive pharmacokinetic models. cholest-5-ene-3,4-diol 33-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-79 27934636-7 2017 Only using the RAF derived from testosterone for CYP3A4 produced the expected CYP2C9 contribution of 72%-87% and 47%-69% for metabolism of losartan and meloxicam, respectively. Meloxicam 152-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 27934636-4 2017 The RAF value for CYP3A4 or CYP2C9 derived from a particular P450-selective probe reaction was applied to calculate RAF-scaled CLint for other probe reactions of the same P450 isoform in a crossover manner and compared with the measured HLM CLint When RAF derived from midazolam or nifedipine was used for CYP3A4, the ICR for testosterone 6beta-hydroxylation was 31 and 25, respectively, suggesting significantly diverse interactions of CYP3A4 probes with the testing systems. Midazolam 269-278 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 306-312 27934636-4 2017 The RAF value for CYP3A4 or CYP2C9 derived from a particular P450-selective probe reaction was applied to calculate RAF-scaled CLint for other probe reactions of the same P450 isoform in a crossover manner and compared with the measured HLM CLint When RAF derived from midazolam or nifedipine was used for CYP3A4, the ICR for testosterone 6beta-hydroxylation was 31 and 25, respectively, suggesting significantly diverse interactions of CYP3A4 probes with the testing systems. Midazolam 269-278 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 306-312 27934636-4 2017 The RAF value for CYP3A4 or CYP2C9 derived from a particular P450-selective probe reaction was applied to calculate RAF-scaled CLint for other probe reactions of the same P450 isoform in a crossover manner and compared with the measured HLM CLint When RAF derived from midazolam or nifedipine was used for CYP3A4, the ICR for testosterone 6beta-hydroxylation was 31 and 25, respectively, suggesting significantly diverse interactions of CYP3A4 probes with the testing systems. Nifedipine 282-292 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 27934636-4 2017 The RAF value for CYP3A4 or CYP2C9 derived from a particular P450-selective probe reaction was applied to calculate RAF-scaled CLint for other probe reactions of the same P450 isoform in a crossover manner and compared with the measured HLM CLint When RAF derived from midazolam or nifedipine was used for CYP3A4, the ICR for testosterone 6beta-hydroxylation was 31 and 25, respectively, suggesting significantly diverse interactions of CYP3A4 probes with the testing systems. Nifedipine 282-292 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 306-312 27934636-4 2017 The RAF value for CYP3A4 or CYP2C9 derived from a particular P450-selective probe reaction was applied to calculate RAF-scaled CLint for other probe reactions of the same P450 isoform in a crossover manner and compared with the measured HLM CLint When RAF derived from midazolam or nifedipine was used for CYP3A4, the ICR for testosterone 6beta-hydroxylation was 31 and 25, respectively, suggesting significantly diverse interactions of CYP3A4 probes with the testing systems. Nifedipine 282-292 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 306-312 27934636-4 2017 The RAF value for CYP3A4 or CYP2C9 derived from a particular P450-selective probe reaction was applied to calculate RAF-scaled CLint for other probe reactions of the same P450 isoform in a crossover manner and compared with the measured HLM CLint When RAF derived from midazolam or nifedipine was used for CYP3A4, the ICR for testosterone 6beta-hydroxylation was 31 and 25, respectively, suggesting significantly diverse interactions of CYP3A4 probes with the testing systems. testosterone 6beta 326-344 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 27934636-4 2017 The RAF value for CYP3A4 or CYP2C9 derived from a particular P450-selective probe reaction was applied to calculate RAF-scaled CLint for other probe reactions of the same P450 isoform in a crossover manner and compared with the measured HLM CLint When RAF derived from midazolam or nifedipine was used for CYP3A4, the ICR for testosterone 6beta-hydroxylation was 31 and 25, respectively, suggesting significantly diverse interactions of CYP3A4 probes with the testing systems. testosterone 6beta 326-344 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 306-312 27934636-4 2017 The RAF value for CYP3A4 or CYP2C9 derived from a particular P450-selective probe reaction was applied to calculate RAF-scaled CLint for other probe reactions of the same P450 isoform in a crossover manner and compared with the measured HLM CLint When RAF derived from midazolam or nifedipine was used for CYP3A4, the ICR for testosterone 6beta-hydroxylation was 31 and 25, respectively, suggesting significantly diverse interactions of CYP3A4 probes with the testing systems. testosterone 6beta 326-344 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 306-312 27934636-7 2017 Only using the RAF derived from testosterone for CYP3A4 produced the expected CYP2C9 contribution of 72%-87% and 47%-69% for metabolism of losartan and meloxicam, respectively. Testosterone 32-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 27934636-7 2017 Only using the RAF derived from testosterone for CYP3A4 produced the expected CYP2C9 contribution of 72%-87% and 47%-69% for metabolism of losartan and meloxicam, respectively. Losartan 139-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 27889832-0 2017 Effects of cytochrome P450 (CYP3A4 and CYP2C19) inhibition and induction on the exposure of selumetinib, a MEK1/2 inhibitor, in healthy subjects: results from two clinical trials. AZD 6244 92-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 26874845-4 2017 RESULTS: The results showed that triptolide inhibited the activity of CYP1A2 and CYP3A4, with 50 % inhibitory concentration (IC50) values of 14.18 and 8.36 muM, respectively, but that other CYP isoforms were not affected. triptolide 33-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 26874845-5 2017 Enzyme kinetic studies showed that triptolide was not only a non-competitive inhibitor of CYP1A2, but also a competitive inhibitor of CYP3A4, with inhibition constant (K i) values of 7.32 and 5.67 muM, respectively. triptolide 35-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 26874845-8 2017 CONCLUSIONS: The in vitro studies of triptolide with CYP isoforms and P-gp indicate that triptolide has the potential to cause pharmacokinetic drug interactions with other co-administered drugs metabolized by CYP1A2 and CYP3A4. triptolide 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 26874845-8 2017 CONCLUSIONS: The in vitro studies of triptolide with CYP isoforms and P-gp indicate that triptolide has the potential to cause pharmacokinetic drug interactions with other co-administered drugs metabolized by CYP1A2 and CYP3A4. triptolide 89-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 26891871-0 2017 Impact of CYP3A4*1G Allele on Clinical Pharmacokinetics and Pharmacodynamics of Clopidogrel. Clopidogrel 80-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 27889832-8 2017 CONCLUSIONS: Co-administration of CYP3A4/CYP2C19 inhibitors will likely increase exposure to selumetinib, while CYP3A4 inducers will likely reduce its exposure. AZD 6244 93-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 26891871-3 2017 The aim of this study was to evaluate the influence of CYP3A4*1G (IVS10+12G>A, rs2242480) on the pharmacokinetics and pharmacodynamics of clopidogrel. Clopidogrel 141-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 26891871-4 2017 METHODS: CYP3A4*1G polymorphism was determined in a group of 82 patients undergoing percutaneous coronary intervention and taking 75 mg of clopidogrel daily. Clopidogrel 139-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 28038962-1 2017 Bedaquiline and its metabolite M2 are metabolised by CYP3A4. bedaquiline 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 28038962-2 2017 The antiretrovirals ritonavir-boosted lopinavir (LPV/r) and nevirapine inhibit and induce CYP3A4, respectively. Ritonavir 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 28038962-2 2017 The antiretrovirals ritonavir-boosted lopinavir (LPV/r) and nevirapine inhibit and induce CYP3A4, respectively. Lopinavir 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 27402157-6 2017 Using this final PBPK model, it was predicted that weak CYP3A inhibitors (fluoxetine and fluvoxamine) are anticipated to have negligible DDI risk with palbociclib, whereas moderate CYP3A inhibitors (diltiazem and verapamil) may increase plasma palbociclib AUC by ~40%. Fluoxetine 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 27841150-0 2017 CYP3A4*1G and CYP3A5*3 genetic polymorphisms alter the antihypertensive efficacy of amlodipine in patients with hypertension following renal transplantation : . Amlodipine 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 27841150-1 2017 OBJECTIVE: Previous studies have determined that CYP3A and multidrug resistance protein 1 (MDR1) polymorphisms can affect the pharmacokinetics and pharmacodynamics of amlodipine in both healthy subjects and those with early hypertensive renal disease. Amlodipine 167-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 27841150-2 2017 In the current study, our objective was to analyze the association between the CYP3A4*1G, CYP3A5*3, and MDR1 C3435T gene polymorphisms and the antihypertensive efficacy of amlodipine in hypertensive patients after renal transplantation. Amlodipine 172-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 27798211-2 2017 When combined with the CYP3A4 substrate daclatasvir, the daclatasvir dosage should be reduced from 60 to 30 mg once daily. daclatasvir 57-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 27432796-1 2017 Voriconazole, a broad-spectrum triazole antifungal agent, is metabolized by cytochrome P450 (CYP) 2C19 and, to a lesser extent, by CYP3A. Voriconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-136 27432796-1 2017 Voriconazole, a broad-spectrum triazole antifungal agent, is metabolized by cytochrome P450 (CYP) 2C19 and, to a lesser extent, by CYP3A. Triazoles 31-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-136 27402157-6 2017 Using this final PBPK model, it was predicted that weak CYP3A inhibitors (fluoxetine and fluvoxamine) are anticipated to have negligible DDI risk with palbociclib, whereas moderate CYP3A inhibitors (diltiazem and verapamil) may increase plasma palbociclib AUC by ~40%. Fluvoxamine 89-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 27402157-6 2017 Using this final PBPK model, it was predicted that weak CYP3A inhibitors (fluoxetine and fluvoxamine) are anticipated to have negligible DDI risk with palbociclib, whereas moderate CYP3A inhibitors (diltiazem and verapamil) may increase plasma palbociclib AUC by ~40%. Verapamil 213-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 27893182-6 2017 Rivaroxaban is metabolized by cytochrome P450 A4 (CYP3A4). Rivaroxaban 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 27893182-18 2017 Coadministration of a P-gp/CYP3A4 inhibitor with dabigatran or rivaroxaban may warrant caution in patients at risk of overexposure. Dabigatran 49-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 27893182-18 2017 Coadministration of a P-gp/CYP3A4 inhibitor with dabigatran or rivaroxaban may warrant caution in patients at risk of overexposure. Rivaroxaban 63-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 27836570-0 2017 Metabolic-induced cytotoxicity of diosbulbin B in CYP3A4-expressing cells. diosbulbin B 34-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 28226339-5 2017 Clinicians should appreciate that since fentanyl is metabolized mainly via CYP3A4, potential adverse effects can occur with concomitant use of any drug which affects CYP3A4 activity. Fentanyl 40-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 28226339-5 2017 Clinicians should appreciate that since fentanyl is metabolized mainly via CYP3A4, potential adverse effects can occur with concomitant use of any drug which affects CYP3A4 activity. Fentanyl 40-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-172 28226339-6 2017 Discontinuation of CYP3A4 inducers can also result in an increase in fentanyl plasma concentration. Fentanyl 69-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 27794450-6 2017 We further showed that hepatospheroids convert phenacetin (by CYP1A2) and testosterone (by CYP3A4) to their human-specific metabolites acetaminophen and 6beta-hydroxytestosterone with a predictive clearance rate of 0.011ml/h/106 cells and 0.021ml/h/106 cells respectively, according to first-order kinetics. hepatospheroids 23-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 27794450-6 2017 We further showed that hepatospheroids convert phenacetin (by CYP1A2) and testosterone (by CYP3A4) to their human-specific metabolites acetaminophen and 6beta-hydroxytestosterone with a predictive clearance rate of 0.011ml/h/106 cells and 0.021ml/h/106 cells respectively, according to first-order kinetics. Testosterone 74-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 27836570-2 2017 DB is mainly metabolized by CYP3A4 in vitro and in vivo, but the cytotoxicity and anti-tumor mechanisms of DB have yet to be clarified. diosbulbin B 0-2 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 27836570-3 2017 This study aimed to determine whether the cytotoxicity and anti-tumor effects of DB are related to the metabolism-induced activation of CYP3A4 in various cell models, including CYP-free NIH3T3 cells, primary rat hepatocytes, HepG2 and L02 cells of high CYP3A4 expression and wild-type. diosbulbin B 81-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 27836570-3 2017 This study aimed to determine whether the cytotoxicity and anti-tumor effects of DB are related to the metabolism-induced activation of CYP3A4 in various cell models, including CYP-free NIH3T3 cells, primary rat hepatocytes, HepG2 and L02 cells of high CYP3A4 expression and wild-type. diosbulbin B 81-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 253-259 27836570-10 2017 Ketoconazole, however, could restrain DB induced cytotoxicity on primary rat hepatocytes and in CYP3A4 transfected HepG2 and L02 cells. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 27836570-11 2017 Therefore, the cytotoxicity of DB was closely related to CYP3A4-metabolized reactive DB metabolites. diosbulbin B 31-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 27836570-11 2017 Therefore, the cytotoxicity of DB was closely related to CYP3A4-metabolized reactive DB metabolites. diosbulbin B 85-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 27890698-7 2017 Thus, inhibition of CYP3A4 is presumably the underlying reason for the observed increase in the concentrations of the CYP3A4 substrate tacrolimus in the patient. Tacrolimus 135-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 28194109-8 2017 All of the neurokinin-1 receptor antagonists with the exception of rolapitant inhibit or induce cytochrome P450 3A4 (CYP3A4), and a reduced dose of dexamethasone (a CYP3A4 substrate) should be administered with aprepitant or netupitant; by contrast, this is not necessary with rolapitant. Dexamethasone 148-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 27872069-3 2017 While doravirine is a cytochrome P450 3A4 (CYP3A4) substrate, efavirenz induces CYP3A4; therefore, the pharmacokinetics of both drugs following a switch from efavirenz to doravirine were assessed. doravirine 6-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-41 27872069-3 2017 While doravirine is a cytochrome P450 3A4 (CYP3A4) substrate, efavirenz induces CYP3A4; therefore, the pharmacokinetics of both drugs following a switch from efavirenz to doravirine were assessed. doravirine 6-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 27872069-3 2017 While doravirine is a cytochrome P450 3A4 (CYP3A4) substrate, efavirenz induces CYP3A4; therefore, the pharmacokinetics of both drugs following a switch from efavirenz to doravirine were assessed. efavirenz 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 27872071-4 2017 Atorvastatin is subject to drug-drug interactions with cytochrome P450 3A4 (CYP3A4) inhibitors. Atorvastatin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-74 27872071-4 2017 Atorvastatin is subject to drug-drug interactions with cytochrome P450 3A4 (CYP3A4) inhibitors. Atorvastatin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 28031486-0 2017 Structural basis for regiospecific midazolam oxidation by human cytochrome P450 3A4. Midazolam 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-83 28031486-4 2017 Despite the vast variety of drugs undergoing metabolism, only the sedative midazolam (MDZ) serves as a marker substrate for the in vivo activity assessment because it is preferentially and regioselectively oxidized by CYP3A4. Midazolam 75-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 218-224 28031486-4 2017 Despite the vast variety of drugs undergoing metabolism, only the sedative midazolam (MDZ) serves as a marker substrate for the in vivo activity assessment because it is preferentially and regioselectively oxidized by CYP3A4. Midazolam 86-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 218-224 27890698-7 2017 Thus, inhibition of CYP3A4 is presumably the underlying reason for the observed increase in the concentrations of the CYP3A4 substrate tacrolimus in the patient. Tacrolimus 135-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 27822600-2 2017 Administered concomitantly, clarithromycin causes drug-drug interactions (DDI) with the victim drugs midazolam (CYP3A4 substrate) and digoxin (P-gp substrate). Clarithromycin 28-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 28069789-7 2017 The concomitant use of calcium-channel blockers and macrolide antibiotics increases the levels of calcium-channel blockers in the blood as they are metabolised by cytochrome P450 3A4 (CYP3A4), which is inhibited by macrolide antibiotics. macrolide antibiotics 52-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-182 28069789-7 2017 The concomitant use of calcium-channel blockers and macrolide antibiotics increases the levels of calcium-channel blockers in the blood as they are metabolised by cytochrome P450 3A4 (CYP3A4), which is inhibited by macrolide antibiotics. macrolide antibiotics 52-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 28069789-7 2017 The concomitant use of calcium-channel blockers and macrolide antibiotics increases the levels of calcium-channel blockers in the blood as they are metabolised by cytochrome P450 3A4 (CYP3A4), which is inhibited by macrolide antibiotics. macrolide antibiotics 215-236 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-182 28069789-7 2017 The concomitant use of calcium-channel blockers and macrolide antibiotics increases the levels of calcium-channel blockers in the blood as they are metabolised by cytochrome P450 3A4 (CYP3A4), which is inhibited by macrolide antibiotics. macrolide antibiotics 215-236 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 27822600-2 2017 Administered concomitantly, clarithromycin causes drug-drug interactions (DDI) with the victim drugs midazolam (CYP3A4 substrate) and digoxin (P-gp substrate). Midazolam 101-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 27285124-9 2017 Drug metabolite profiling of phenacetin (CYP1A2) and testosterone (CYP3A4) using LC-MS/MS and HPLC, respectively, revealed that HepaRGs had more intact (Phase I-II) metabolism profile. hepargs 128-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 28049954-2 2017 It is rapidly absorbed and partly metabolized to the active metabolite AR-C124910XX by CYP3A4 and CYP3A5. AR C124910XX 71-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 28049954-3 2017 Three genetic loci (SLCO1B1, CYP3A4, and UGT2B7) were reported to affect ticagrelor pharmacokinetics. Ticagrelor 73-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 28674251-0 2017 Co-administration of Fluvastatin and CYP3A4 and CYP2C8 Inhibitors May Increase the Exposure to Fluvastatin in Carriers of CYP2C9 Genetic Variants. Fluvastatin 95-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 28674251-1 2017 Fluvastatin, which is one of the hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors (statins), is primarily metabolized by CYP2C9 and to a lesser extent by CYP3A4 and CYP2C8. Fluvastatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 28674251-4 2017 Since CYP2C9 is a polymorphic enzyme, we investigated the effect of DDI via CYP2C9, CYP3A4, and CYP2C8 on fluvastatin pharmacokinetics by using a validated prediction method in relation to CYP2C9 variants. Fluvastatin 106-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 28674251-6 2017 Our in silico model predicted that administration of fluvastatin in conjunction with the potent inhibitors that completely inhibited CYP3A4 and CYP2C8 in carriers with the CYP2C9*3/*3 variant would cause a 3.23- and 2.60-fold increase in the AUC ratios, respectively, when compared to that for the carriers with the CYP2C9*1/*1 taking fluvastatin alone. Fluvastatin 53-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 28674251-6 2017 Our in silico model predicted that administration of fluvastatin in conjunction with the potent inhibitors that completely inhibited CYP3A4 and CYP2C8 in carriers with the CYP2C9*3/*3 variant would cause a 3.23- and 2.60-fold increase in the AUC ratios, respectively, when compared to that for the carriers with the CYP2C9*1/*1 taking fluvastatin alone. Fluvastatin 335-346 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 28966237-9 2017 CYP3A4 activity was markedly inhibited by trimebutine, papaverine, and oxethazaine. Trimebutine 42-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28867739-3 2017 Various flavonoids in vegetables, such as kaempferol and quercetin, possess inhibitory effects, and some vegetable and fruit juices have also been found to inhibit CYP3A4 activity. Flavonoids 8-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 28966237-9 2017 CYP3A4 activity was markedly inhibited by trimebutine, papaverine, and oxethazaine. Papaverine 55-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28867739-3 2017 Various flavonoids in vegetables, such as kaempferol and quercetin, possess inhibitory effects, and some vegetable and fruit juices have also been found to inhibit CYP3A4 activity. kaempferol 42-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 28867739-3 2017 Various flavonoids in vegetables, such as kaempferol and quercetin, possess inhibitory effects, and some vegetable and fruit juices have also been found to inhibit CYP3A4 activity. Quercetin 57-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 28966237-9 2017 CYP3A4 activity was markedly inhibited by trimebutine, papaverine, and oxethazaine. oxethazaine 71-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28867739-7 2017 Metabolism to 6beta-hydroxytestosterone by recombinant CYP3A4 was strongly inhibited by cabbage, onion, and green pepper juices, and cabbage and green pepper juices significantly inhibited CYP3A4 activity in a preincubation time-dependent manner. 6 beta-hydroxytestosterone 14-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 28867739-7 2017 Metabolism to 6beta-hydroxytestosterone by recombinant CYP3A4 was strongly inhibited by cabbage, onion, and green pepper juices, and cabbage and green pepper juices significantly inhibited CYP3A4 activity in a preincubation time-dependent manner. 6 beta-hydroxytestosterone 14-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 27942916-4 2017 However, the efficacy of this combination may be confounded by lapatinib, a potent inactivator of CYP3A4/5 which could negate the bioactivation of tamoxifen to the active metabolite endoxifen. Lapatinib 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 27942916-4 2017 However, the efficacy of this combination may be confounded by lapatinib, a potent inactivator of CYP3A4/5 which could negate the bioactivation of tamoxifen to the active metabolite endoxifen. Tamoxifen 147-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 27942916-4 2017 However, the efficacy of this combination may be confounded by lapatinib, a potent inactivator of CYP3A4/5 which could negate the bioactivation of tamoxifen to the active metabolite endoxifen. 4-hydroxy-N-desmethyltamoxifen 182-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 28875044-15 2017 Phenytoin is a combined CYP3A4 and P-glycoprotein inducer, which might reduce rivaroxaban levels. Phenytoin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 28875044-15 2017 Phenytoin is a combined CYP3A4 and P-glycoprotein inducer, which might reduce rivaroxaban levels. Rivaroxaban 78-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 27138546-0 2017 An Exposure-Response Modeling Approach to Examine the Relationship Between Potency of CYP3A Inducer and Plasma 4beta-Hydroxycholesterol in Healthy Subjects. cholest-5-ene-3,4-diol 111-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 27273461-0 2017 Pharmacokinetic Evaluation of CYP3A4-Mediated Drug-Drug Interactions of Isavuconazole With Rifampin, Ketoconazole, Midazolam, and Ethinyl Estradiol/Norethindrone in Healthy Adults. isavuconazole 72-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 27273461-0 2017 Pharmacokinetic Evaluation of CYP3A4-Mediated Drug-Drug Interactions of Isavuconazole With Rifampin, Ketoconazole, Midazolam, and Ethinyl Estradiol/Norethindrone in Healthy Adults. Rifampin 91-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 27273461-0 2017 Pharmacokinetic Evaluation of CYP3A4-Mediated Drug-Drug Interactions of Isavuconazole With Rifampin, Ketoconazole, Midazolam, and Ethinyl Estradiol/Norethindrone in Healthy Adults. Ketoconazole 101-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 27273461-0 2017 Pharmacokinetic Evaluation of CYP3A4-Mediated Drug-Drug Interactions of Isavuconazole With Rifampin, Ketoconazole, Midazolam, and Ethinyl Estradiol/Norethindrone in Healthy Adults. Midazolam 115-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 28655393-0 2017 The role of single nucleotide polymorphisms of CYP3A and ABCB1 on tacrolimus predose concentration in kidney transplant recipients. Tacrolimus 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 27273461-0 2017 Pharmacokinetic Evaluation of CYP3A4-Mediated Drug-Drug Interactions of Isavuconazole With Rifampin, Ketoconazole, Midazolam, and Ethinyl Estradiol/Norethindrone in Healthy Adults. Ethinyl Estradiol 130-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 27273461-0 2017 Pharmacokinetic Evaluation of CYP3A4-Mediated Drug-Drug Interactions of Isavuconazole With Rifampin, Ketoconazole, Midazolam, and Ethinyl Estradiol/Norethindrone in Healthy Adults. Norethindrone 148-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 27273461-1 2017 This report describes the phase 1 trials that evaluated the metabolism of the novel triazole antifungal isavuconazole by cytochrome P450 3A4 (CYP3A4) and isavuconazole"s effects on CYP3A4-mediated metabolism in healthy adults. Triazoles 84-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-140 27273461-1 2017 This report describes the phase 1 trials that evaluated the metabolism of the novel triazole antifungal isavuconazole by cytochrome P450 3A4 (CYP3A4) and isavuconazole"s effects on CYP3A4-mediated metabolism in healthy adults. Triazoles 84-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 27273461-1 2017 This report describes the phase 1 trials that evaluated the metabolism of the novel triazole antifungal isavuconazole by cytochrome P450 3A4 (CYP3A4) and isavuconazole"s effects on CYP3A4-mediated metabolism in healthy adults. Triazoles 84-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-187 27273461-1 2017 This report describes the phase 1 trials that evaluated the metabolism of the novel triazole antifungal isavuconazole by cytochrome P450 3A4 (CYP3A4) and isavuconazole"s effects on CYP3A4-mediated metabolism in healthy adults. isavuconazole 104-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-140 27273461-1 2017 This report describes the phase 1 trials that evaluated the metabolism of the novel triazole antifungal isavuconazole by cytochrome P450 3A4 (CYP3A4) and isavuconazole"s effects on CYP3A4-mediated metabolism in healthy adults. isavuconazole 104-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 27273461-1 2017 This report describes the phase 1 trials that evaluated the metabolism of the novel triazole antifungal isavuconazole by cytochrome P450 3A4 (CYP3A4) and isavuconazole"s effects on CYP3A4-mediated metabolism in healthy adults. isavuconazole 104-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-187 27273461-1 2017 This report describes the phase 1 trials that evaluated the metabolism of the novel triazole antifungal isavuconazole by cytochrome P450 3A4 (CYP3A4) and isavuconazole"s effects on CYP3A4-mediated metabolism in healthy adults. isavuconazole 154-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-187 27273461-2 2017 Coadministration of oral isavuconazole (100 mg once daily) with oral rifampin (600 mg once daily; CYP3A4 inducer) decreased isavuconazole area under the concentration-time curve (AUCtau ) during a dosing interval by 90% and maximum concentration (Cmax ) by 75%. isavuconazole 25-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 27273461-2 2017 Coadministration of oral isavuconazole (100 mg once daily) with oral rifampin (600 mg once daily; CYP3A4 inducer) decreased isavuconazole area under the concentration-time curve (AUCtau ) during a dosing interval by 90% and maximum concentration (Cmax ) by 75%. Rifampin 69-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 27273461-2 2017 Coadministration of oral isavuconazole (100 mg once daily) with oral rifampin (600 mg once daily; CYP3A4 inducer) decreased isavuconazole area under the concentration-time curve (AUCtau ) during a dosing interval by 90% and maximum concentration (Cmax ) by 75%. isavuconazole 124-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 28655393-8 2017 On the other hand, less than 1% of our transplant recipients possess the <italic>CYP3A</italic> genotype, which requires high daily tacrolimus dose. Tacrolimus 144-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 27273461-3 2017 Conversely, coadministration of isavuconazole (200 mg single dose) with oral ketoconazole (200 mg twice daily; CYP3A4 inhibitor) increased isavuconazole AUC from time 0 to infinity (AUC0- ) and Cmax by 422% and 9%, respectively. isavuconazole 32-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 27273461-3 2017 Conversely, coadministration of isavuconazole (200 mg single dose) with oral ketoconazole (200 mg twice daily; CYP3A4 inhibitor) increased isavuconazole AUC from time 0 to infinity (AUC0- ) and Cmax by 422% and 9%, respectively. Ketoconazole 77-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 28412920-7 2017 CONCLUSION: THC and CBD are metabolized mainly in the liver by cytochrome P-450 isoenzymes (mainly CYP2Cs and CYP3A4). Dronabinol 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 27273461-3 2017 Conversely, coadministration of isavuconazole (200 mg single dose) with oral ketoconazole (200 mg twice daily; CYP3A4 inhibitor) increased isavuconazole AUC from time 0 to infinity (AUC0- ) and Cmax by 422% and 9%, respectively. isavuconazole 139-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 27273461-4 2017 Isavuconazole was coadministered (200 mg 3 times daily for 2 days, then 200 mg once daily) with single doses of oral midazolam (3 mg; CYP3A4 substrate) or ethinyl estradiol/norethindrone (35 mug/1 mg; CYP3A4 substrate). isavuconazole 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 27273461-4 2017 Isavuconazole was coadministered (200 mg 3 times daily for 2 days, then 200 mg once daily) with single doses of oral midazolam (3 mg; CYP3A4 substrate) or ethinyl estradiol/norethindrone (35 mug/1 mg; CYP3A4 substrate). isavuconazole 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-207 27273461-7 2017 These results indicate that isavuconazole is a sensitive substrate and moderate inhibitor of CYP3A4. isavuconazole 28-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 27317415-5 2017 Conversely, EVG metabolism occurs primarily via CYP3A4 and requires pharmacokinetic boosting to achieve systemic exposures amenable to once-daily dosing. elvitegravir 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 27991741-2 2017 We determined 4beta-hydroxycholesterol (4betaOHC), an endogenous CYP3A4 metabolite, in patients with rheumatoid arthritis (RA) before and after treatment with biological disease-modifying antirheumatic drugs (bDMARDs). cholest-5-ene-3,4-diol 14-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 27991741-2 2017 We determined 4beta-hydroxycholesterol (4betaOHC), an endogenous CYP3A4 metabolite, in patients with rheumatoid arthritis (RA) before and after treatment with biological disease-modifying antirheumatic drugs (bDMARDs). 4betaohc 40-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 28412920-7 2017 CONCLUSION: THC and CBD are metabolized mainly in the liver by cytochrome P-450 isoenzymes (mainly CYP2Cs and CYP3A4). Cannabidiol 20-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 28412920-8 2017 In vitro studies indicate that THC and CBD both inhibit CYP1A1, 1A2 and 1B1 enzymes, and recent studies have indicated that CBD is also a potent inhibitor of CYP2C19 and CYP3A4. Cannabidiol 124-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 27776366-10 2017 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to PIP mediated inhibition of CYP3A4 enzyme. Carbamazepine 84-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 27821435-5 2017 When NMEs were considered as victim drugs, 21 NMEs had at least one positive clinical DDI, with three NMEs shown to be sensitive substrates of CYP3A (AUC ratio >= 5 when coadministered with strong inhibitors): cobimetinib, isavuconazole (the active metabolite of prodrug isavuconazonium sulfate), and ivabradine. cobimetinib 213-224 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 27821435-5 2017 When NMEs were considered as victim drugs, 21 NMEs had at least one positive clinical DDI, with three NMEs shown to be sensitive substrates of CYP3A (AUC ratio >= 5 when coadministered with strong inhibitors): cobimetinib, isavuconazole (the active metabolite of prodrug isavuconazonium sulfate), and ivabradine. isavuconazole 226-239 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 27821435-5 2017 When NMEs were considered as victim drugs, 21 NMEs had at least one positive clinical DDI, with three NMEs shown to be sensitive substrates of CYP3A (AUC ratio >= 5 when coadministered with strong inhibitors): cobimetinib, isavuconazole (the active metabolite of prodrug isavuconazonium sulfate), and ivabradine. isavuconazole 274-297 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 27821435-5 2017 When NMEs were considered as victim drugs, 21 NMEs had at least one positive clinical DDI, with three NMEs shown to be sensitive substrates of CYP3A (AUC ratio >= 5 when coadministered with strong inhibitors): cobimetinib, isavuconazole (the active metabolite of prodrug isavuconazonium sulfate), and ivabradine. Ivabradine 304-314 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 27821435-7 2017 The most significant changes for inhibition and induction were observed with rolapitant, a moderate inhibitor of CYP2D6 and lumacaftor, a strong inducer of CYP3A. lumacaftor 124-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-161 27821437-4 2017 SC-mediated inhibition of CYP3A4 was found to rank in the order of CAP (IC50 1.84 +- 0.71 microM) ~ PIP (2.12 +- 0.45 microM) > CUR (11.93 +- 3.49 microM), while CYP2C9 inhibition was in the order of CAP (11.95 +- 4.24 microM) ~ CUR (14.58 +- 4.57 microM) > PIP (89.62 +- 9.17 microM). piperine 100-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 27821437-4 2017 SC-mediated inhibition of CYP3A4 was found to rank in the order of CAP (IC50 1.84 +- 0.71 microM) ~ PIP (2.12 +- 0.45 microM) > CUR (11.93 +- 3.49 microM), while CYP2C9 inhibition was in the order of CAP (11.95 +- 4.24 microM) ~ CUR (14.58 +- 4.57 microM) > PIP (89.62 +- 9.17 microM). piperine 264-267 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 27743791-0 2017 Benzotriazole UV 328 and UV-P showed distinct antiandrogenic activity upon human CYP3A4-mediated biotransformation. benzotriazole 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 27718000-2 2017 Bosutinib is primarily metabolized by cytochrome P450 (CYP) 3A4, suggesting drug interaction potential with other CYP3A4 modulators. bosutinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-63 27718000-2 2017 Bosutinib is primarily metabolized by cytochrome P450 (CYP) 3A4, suggesting drug interaction potential with other CYP3A4 modulators. bosutinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 27776366-10 2017 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to PIP mediated inhibition of CYP3A4 enzyme. Carbamazepine 84-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 27777246-6 2017 The sensitive CYP3A biomarker 4beta-hydroxycholesterol is built into the early clinical phase I studies for all candidates since rare cases of in vivo induction have been found without any induction alerts from the currently used in vitro methods. cholest-5-ene-3,4-diol 30-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 28674358-0 2017 Acute Kidney Injury from Excessive Potentiation of Calcium-channel Blocker via Synergistic CYP3A4 Inhibition by Clarithromycin Plus Voriconazole. Clarithromycin 112-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 28674358-0 2017 Acute Kidney Injury from Excessive Potentiation of Calcium-channel Blocker via Synergistic CYP3A4 Inhibition by Clarithromycin Plus Voriconazole. Voriconazole 132-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 28674358-6 2017 The combination of CYP3A4-inhibitors such as clarithromycin plus voriconazole can synergistically potentiate calcium-channel blockers. Clarithromycin 45-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 28674358-6 2017 The combination of CYP3A4-inhibitors such as clarithromycin plus voriconazole can synergistically potentiate calcium-channel blockers. Voriconazole 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 27821711-2 2017 Initial enzyme phenotyping studies indicated that CYP3A4/5 dominates basimglurant metabolism and highlights a risk for drug-drug interactions when it is comedicated with strong CYP3A4/5 inhibitors or inactivators; however, a clinical drug-drug interaction (DDI) study using the potent and selective CYP3A4/5 inhibitor ketoconazole resulted in an area under the curve (AUC) AUCi/AUC ratio of only 1.24. Ketoconazole 318-330 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 27321774-1 2017 This open-label 2-period study assessed the effect of multiple-dose administration of rifampin, a strong cytochrome P450 3A (CYP3A) and P-glycoprotein inducer, on the pharmacokinetics of odanacatib, a cathepsin K inhibitor. Rifampin 86-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-123 27321774-1 2017 This open-label 2-period study assessed the effect of multiple-dose administration of rifampin, a strong cytochrome P450 3A (CYP3A) and P-glycoprotein inducer, on the pharmacokinetics of odanacatib, a cathepsin K inhibitor. Rifampin 86-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-130 27821711-3 2017 A further study using the CYP3A4 inducer carbamazepine resulted in an AUCi/AUC ratio of 0.69. Carbamazepine 41-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 28079798-6 2017 From the 96 SNPs analyzed, VKORC1 rs9923231, CYP1A2 rs2069514, CYP3A4 rs28371759, and APOE rs7412 were associated with higher average warfarin maintenance doses, whereas CYP2C9 rs1057910, EPHX1 rs2260863, and CYP4F2 rs2189784 were associated with lower warfarin doses (P < 0.05). Warfarin 134-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 27030208-2 2017 These plants and their phytomolecules, such as andrographolide, bacoside A and asiaticoside, were studied for their inhibition potential on pooled CYP450 as well as human CYP3A4, CYP2D6, CYP2C9 and CYP1A2 by CYP-CO complex assay and fluorogenic assay respectively followed by IC50 determination. asiaticoside 79-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 29457079-14 2017 When warfarin and methadone are used together, we have to consider their interaction by comparing the competitive inhibition of CYP2C9 to the induction of CYP3A4 by methadone, because CYP3A4 metabolize various drugs including oxycodone. Warfarin 5-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 29457079-14 2017 When warfarin and methadone are used together, we have to consider their interaction by comparing the competitive inhibition of CYP2C9 to the induction of CYP3A4 by methadone, because CYP3A4 metabolize various drugs including oxycodone. Warfarin 5-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 29457079-14 2017 When warfarin and methadone are used together, we have to consider their interaction by comparing the competitive inhibition of CYP2C9 to the induction of CYP3A4 by methadone, because CYP3A4 metabolize various drugs including oxycodone. Methadone 18-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 29457079-14 2017 When warfarin and methadone are used together, we have to consider their interaction by comparing the competitive inhibition of CYP2C9 to the induction of CYP3A4 by methadone, because CYP3A4 metabolize various drugs including oxycodone. Methadone 18-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 29457079-14 2017 When warfarin and methadone are used together, we have to consider their interaction by comparing the competitive inhibition of CYP2C9 to the induction of CYP3A4 by methadone, because CYP3A4 metabolize various drugs including oxycodone. Methadone 165-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 29457079-14 2017 When warfarin and methadone are used together, we have to consider their interaction by comparing the competitive inhibition of CYP2C9 to the induction of CYP3A4 by methadone, because CYP3A4 metabolize various drugs including oxycodone. Methadone 165-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 29457079-14 2017 When warfarin and methadone are used together, we have to consider their interaction by comparing the competitive inhibition of CYP2C9 to the induction of CYP3A4 by methadone, because CYP3A4 metabolize various drugs including oxycodone. Oxycodone 226-235 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 29457079-14 2017 When warfarin and methadone are used together, we have to consider their interaction by comparing the competitive inhibition of CYP2C9 to the induction of CYP3A4 by methadone, because CYP3A4 metabolize various drugs including oxycodone. Oxycodone 226-235 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 28121959-0 2017 Patients with CYP3A4*1G genetic polymorphism consumed significantly lower amount of sufentanil in general anesthesia during lung resection. Sufentanil 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 28121959-3 2017 Sufentanil, a synthetic opioid commonly used for the induction and maintenance of general anesthesia, analgesia, and sedation, is mainly metabolized by CYP3A4. Sufentanil 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 28121959-4 2017 So far, the impact of CYP3A4*1G on sufentanil metabolism has not been investigated. Sufentanil 35-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 28079798-9 2017 In the limited sample set, we also found that novel genetic predictors (CYP1A2, CYP3A4, APOE, EPHX1, CYP4F2, and VKORC1 rs2884737) may be associated with warfarin dosing. Warfarin 154-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 27678410-0 2017 Differential effects of the enantiomers of tamsulosin and tolterodine on P-glycoprotein and cytochrome P450 3A4. Tamsulosin 43-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-111 28121959-10 2017 Significantly lower amount of sufentanil was consumed in mutant patients compared with wild type subjects, likely a result of impaired CYP3A4 activity due to the point mutation. Sufentanil 30-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 28121959-11 2017 These findings suggest genotyping of CYP3A4 might be of value in providing guidance for the use of sufentanil. Sufentanil 99-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 29104319-0 2017 Cytochrome b5 plays a dual role in the reaction cycle of cytochrome P450 3A4 during oxidation of the anticancer drug ellipticine. ellipticine 117-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-76 28221736-8 2017 CYP3A4-activity was mesured using the Erythromycin Breath Test (ERMBT). Erythromycin 38-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28221736-8 2017 CYP3A4-activity was mesured using the Erythromycin Breath Test (ERMBT). ermbt 64-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28244811-2 2017 MATERIALS & METHODS: The promoter and exons of CYP3A4 gene in 1114 unrelated, healthy Han Chinese subjects were amplified and genotyped by direct sequencing. Adenosine Monophosphate 11-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 29104319-1 2017 Abstract: Ellipticine is an anticancer agent that forms covalent DNA adducts after enzymatic activation by cytochrome P450 (CYP) enzymes, mainly by CYP3A4. ellipticine 10-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 29104319-5 2017 Using HPLC analysis we detected up to five ellipticine metabolites, which were formed by human hepatic microsomes and human CYP3A4 in the presence of NADPH or NADH. ellipticine 43-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 29104319-5 2017 Using HPLC analysis we detected up to five ellipticine metabolites, which were formed by human hepatic microsomes and human CYP3A4 in the presence of NADPH or NADH. NAD 159-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 27678410-0 2017 Differential effects of the enantiomers of tamsulosin and tolterodine on P-glycoprotein and cytochrome P450 3A4. Tolterodine Tartrate 58-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-111 27678410-11 2017 Taken together, tamsulosin and tolterodine are demonstrated to interfere with P-gp and CYP3A4 regulation in an enantiomer-specific way. Tamsulosin 16-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 27678410-11 2017 Taken together, tamsulosin and tolterodine are demonstrated to interfere with P-gp and CYP3A4 regulation in an enantiomer-specific way. Tolterodine Tartrate 31-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 28215696-11 2017 CONCLUSION: The combination of DOACs with carbamazepine, an inducer of P-gp and CYP3A4-activity, should be avoided since the anticoagulant effect is decreased. doacs 31-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 29104319-7 2017 Human CYP3A4 in Supersomes generated only three metabolic products, 9-hydroxy-, 12-hydroxy-, and 13-hydroxyellipticine. 9-hydroxy-, 12-hydroxy-, and 13-hydroxyellipticine 69-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 29104319-8 2017 Using the 32P-postlabeling method two ellipticine-derived DNA adducts were generated by microsomes and the CYP3A4-Supersome system, both in the presence of NADPH and NADH. Phosphorus-32 10-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 29104319-8 2017 Using the 32P-postlabeling method two ellipticine-derived DNA adducts were generated by microsomes and the CYP3A4-Supersome system, both in the presence of NADPH and NADH. ellipticine 38-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 29104319-8 2017 Using the 32P-postlabeling method two ellipticine-derived DNA adducts were generated by microsomes and the CYP3A4-Supersome system, both in the presence of NADPH and NADH. NAD 166-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 29104319-10 2017 In the presence of NADPH or NADH, cytochrome b5 stimulated the CYP3A4-mediated oxidation of ellipticine, but the stimulation effect differed for individual ellipticine metabolites. NAD 28-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 29104319-10 2017 In the presence of NADPH or NADH, cytochrome b5 stimulated the CYP3A4-mediated oxidation of ellipticine, but the stimulation effect differed for individual ellipticine metabolites. ellipticine 92-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 29104319-10 2017 In the presence of NADPH or NADH, cytochrome b5 stimulated the CYP3A4-mediated oxidation of ellipticine, but the stimulation effect differed for individual ellipticine metabolites. ellipticine 156-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 29104319-12 2017 The results demonstrate that cytochrome b5 plays a dual role in the CYP3A4-catalyzed oxidation of ellipticine: (1) cytochrome b5 mediates CYP3A4 catalytic activities by donating the first and second electron to this enzyme in its catalytic cycle, indicating that NADH:cytochrome b5 reductase can substitute NADPH-dependent POR in this enzymatic reaction and (2) cytochrome b5 can act as an allosteric modifier of the CYP3A4 oxygenase. ellipticine 98-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 29104319-12 2017 The results demonstrate that cytochrome b5 plays a dual role in the CYP3A4-catalyzed oxidation of ellipticine: (1) cytochrome b5 mediates CYP3A4 catalytic activities by donating the first and second electron to this enzyme in its catalytic cycle, indicating that NADH:cytochrome b5 reductase can substitute NADPH-dependent POR in this enzymatic reaction and (2) cytochrome b5 can act as an allosteric modifier of the CYP3A4 oxygenase. ellipticine 98-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 29104319-12 2017 The results demonstrate that cytochrome b5 plays a dual role in the CYP3A4-catalyzed oxidation of ellipticine: (1) cytochrome b5 mediates CYP3A4 catalytic activities by donating the first and second electron to this enzyme in its catalytic cycle, indicating that NADH:cytochrome b5 reductase can substitute NADPH-dependent POR in this enzymatic reaction and (2) cytochrome b5 can act as an allosteric modifier of the CYP3A4 oxygenase. ellipticine 98-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 29104319-12 2017 The results demonstrate that cytochrome b5 plays a dual role in the CYP3A4-catalyzed oxidation of ellipticine: (1) cytochrome b5 mediates CYP3A4 catalytic activities by donating the first and second electron to this enzyme in its catalytic cycle, indicating that NADH:cytochrome b5 reductase can substitute NADPH-dependent POR in this enzymatic reaction and (2) cytochrome b5 can act as an allosteric modifier of the CYP3A4 oxygenase. NAD 263-267 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 29104319-12 2017 The results demonstrate that cytochrome b5 plays a dual role in the CYP3A4-catalyzed oxidation of ellipticine: (1) cytochrome b5 mediates CYP3A4 catalytic activities by donating the first and second electron to this enzyme in its catalytic cycle, indicating that NADH:cytochrome b5 reductase can substitute NADPH-dependent POR in this enzymatic reaction and (2) cytochrome b5 can act as an allosteric modifier of the CYP3A4 oxygenase. NAD 263-267 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 29104319-12 2017 The results demonstrate that cytochrome b5 plays a dual role in the CYP3A4-catalyzed oxidation of ellipticine: (1) cytochrome b5 mediates CYP3A4 catalytic activities by donating the first and second electron to this enzyme in its catalytic cycle, indicating that NADH:cytochrome b5 reductase can substitute NADPH-dependent POR in this enzymatic reaction and (2) cytochrome b5 can act as an allosteric modifier of the CYP3A4 oxygenase. NAD 263-267 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 28215696-2 2017 Absorption and elimination of DOACs are dependent on the permeability glycoprotein (P-gp) efflux transporter protein system, and DOACs are substrates of the hepatic cytochrome P 450 3A4 (CYP3A4) enzymes. doacs 30-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-185 28215696-2 2017 Absorption and elimination of DOACs are dependent on the permeability glycoprotein (P-gp) efflux transporter protein system, and DOACs are substrates of the hepatic cytochrome P 450 3A4 (CYP3A4) enzymes. doacs 30-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 28215696-2 2017 Absorption and elimination of DOACs are dependent on the permeability glycoprotein (P-gp) efflux transporter protein system, and DOACs are substrates of the hepatic cytochrome P 450 3A4 (CYP3A4) enzymes. doacs 129-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-185 28215696-2 2017 Absorption and elimination of DOACs are dependent on the permeability glycoprotein (P-gp) efflux transporter protein system, and DOACs are substrates of the hepatic cytochrome P 450 3A4 (CYP3A4) enzymes. doacs 129-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 28215696-3 2017 Therefore, drug-interactions may occur when DOACs are administered with drugs affecting the activity of P-gp or CYP3A4 systems. doacs 44-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 28215696-4 2017 Several antiepileptic drugs like carbamazepine are known to affect P-gp and CYP3A4-activity. Carbamazepine 33-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 28215696-11 2017 CONCLUSION: The combination of DOACs with carbamazepine, an inducer of P-gp and CYP3A4-activity, should be avoided since the anticoagulant effect is decreased. Carbamazepine 42-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 27679675-0 2017 Effect of CYP3A4 genetic polymorphisms on the genotoxicity of 4,4"-methylene-bis(2-chloroaniline)-exposed workers. Methylenebis(chloroaniline) 62-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 26810136-0 2017 Sunitinib-induced hypertension in CYP3A4 rs4646437 A-allele carriers with metastatic renal cell carcinoma. Sunitinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 26810136-7 2017 In conclusion, hypertension is more likely to occur in A-allele carriers of the CYP3A4 rs4646437 variant in our cohort of mRCC patients treated with sunitinib. Sunitinib 149-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 26810136-1 2017 The single nucleotide polymorphism (SNP) rs4646437G>A in CYP3A4 was suggested to be related to sunitinib toxicity. Sunitinib 98-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 28110334-0 2017 Muscone Induces CYP1A2 and CYP3A4 Enzyme Expression in L02 Human Liver Cells and CYP1A2 and CYP3A11 Enzyme Expression in Kunming Mice. muscone 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 27967318-0 2017 Effect of polymorphisms in CYP3A4, PPARA, NR1I2, NFKB1, ABCG2 and SLCO1B1 on the pharmacokinetics of lovastatin in healthy Chinese volunteers. Lovastatin 101-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 27967318-1 2017 AIM: This study examined whether gene polymorphisms (CYP3A4, ABCG2, SLCO1B1, NR1I2, PPARA and NFKB1) influenced the pharmacokinetics of lovastatin in Chinese healthy subjects. Lovastatin 136-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 28110334-1 2017 AIM: To examine the effect of synthetic muscone on the expression of CYP1A2 and CYP3A4 enzymes in human liver L02 cells and in the liver tissue of Kunming mice. muscone 40-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 28110334-5 2017 RESULTS: Muscone induced the expression of CYP1A2 (middle and low concentrations) and of CYP3A4 (high concentration) enzymes in L02 cells. muscone 9-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 28110334-11 2017 CONCLUSIONS: Muscone induces CYP1A2 and CYP3A4 expression in liver cells in vitro and in vivo. muscone 13-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 27838152-8 2017 The cytotoxicity of sibutramine to HepG2 and Chang Liver cells was remarkably augmented by inhibition and knockdown of CYP3A4. sibutramine 20-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 30730634-11 2017 Olaparib is metabolised in the liver, mainly by cytochrome P450 isoenzymes CYP3A4 and CYP3A5. olaparib 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 27838152-9 2017 This study also suggests an inverse relationship between sibutramine cytotoxicity and CYP3A4-mediated metabolism into the N-desmethyl metabolites. sibutramine 57-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 27639091-0 2016 Optimization of Clonazepam Therapy Adjusted to Patient"s CYP3A Status and NAT2 Genotype. Clonazepam 16-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 29911787-1 2017 This study was designed to investigate effects of pargyline on histone methylation in the promoter and enhancer regions and transcription of cytochrome P450 3A4/3A7 (CYP3A4/3A7) gene. Pargyline 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-176 27967330-5 2017 MiR-628-3p and miR-641 repressed the 3"-UTR luciferase activity of CYP3A4. mir-628-3p 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 27967330-6 2017 Overexpression of miR-628-3p and miR-641 showed significant decrease of CYP3A4 mRNA level as well as CYP3A4 induction by rifampin. Rifampin 121-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 27967330-7 2017 CONCLUSION: miR-628-3p and miR-641 could directly target CYP3A4 and are negatively regulated in CYP3A4 induction by rifampin. Rifampin 116-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 27967330-7 2017 CONCLUSION: miR-628-3p and miR-641 could directly target CYP3A4 and are negatively regulated in CYP3A4 induction by rifampin. Rifampin 116-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 28966261-2 2017 The furanocoumarin derivatives Paradisin A and bergamottin, which are present in GFJ, are potent mechanism-based inhibitors of CYP3A4. Furocoumarins 4-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 28966261-3 2017 The primary aim of this work was to synthesize a series of furanocoumarin derivatives with a view to determining the relationship between the structure of the inhibitors and their inhibitory CYP3A4 activity. Furocoumarins 59-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-197 28966261-4 2017 Furanocoumarin derivatives that were more stable and accessible than the furanocoumarin derivatives in GFJ were prepared, and their ability to inhibit CYP3A4 was examined. Furocoumarins 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 28966261-5 2017 Synthesized furanocoumarin monomers showed strong mechanism-based inhibition of CYP3A4. Furocoumarins 12-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 28966261-6 2017 The furanocoumarin dimers are also mechanism-based inhibitors of CYP3A4. Furocoumarins 4-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 29911787-11 2017 The level of CYP3A7 was markedly enhanced in human primary fetal liver cells by treatment with 1.2, 2.4 mmol L(-1) of pargyline (P < 0.05, P < 0.01) and the levels of CYP3A4/3A7 were remarkably enhanced by treatment with 3 mmol L(-1) of pargyline in HepG2 cells (P < 0.001) compared with solvent control. Pargyline 118-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 29911787-14 2017 In conclusion, the enriched H3K4me2 in the promoter and enhancer regions was induced by pargyline with HNF4A or GR binding site in CYP3A4/3A7 gene to activate the corresponding genes. Pargyline 88-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 27639091-4 2016 RESULTS: The patients" CYP3A4 expression was found to be the major determinant of clonazepam plasma concentrations normalized by the dose and bodyweight (1263.5+-482.9 and 558.5+-202.4ng/mL per mg/kg bodyweight in low and normal expressers, respectively, P<.0001). Clonazepam 82-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 27639091-5 2016 Consequently, the dose requirement for the therapeutic concentration of clonazepam was substantially lower in low-CYP3A4 expresser patients than in normal expressers (0.029+-0.011 vs 0.058+-0.024mg/kg bodyweight, P<.0001). Clonazepam 72-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 27639091-6 2016 Furthermore, significantly higher (about 2-fold) plasma concentration ratio of 7-amino-clonazepam and clonazepam was observed in the patients displaying normal CYP3A4 expression and slower N-acetylation than all the others. 7-aminoclonazepam 79-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 27639091-6 2016 Furthermore, significantly higher (about 2-fold) plasma concentration ratio of 7-amino-clonazepam and clonazepam was observed in the patients displaying normal CYP3A4 expression and slower N-acetylation than all the others. Clonazepam 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 27639091-7 2016 CONCLUSION: Prospective assaying of CYP3A4 expression and N-acetyl transferase 2 acetylator phenotype can better identify the patients with higher risk of adverse reactions and can facilitate the improvement of personalized clonazepam therapy and withdrawal regimen. Clonazepam 224-234 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 27530188-12 2016 CONCLUSIONS: Administration of dual inhibitors of P-gp and CYP3A4 increased edoxaban exposure by less than two-fold. edoxaban 76-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 28008998-9 2016 However hepatic impairment of expected in chronic cholestasis downregulation of CYP7A1 and upregulation of CYP3A4 may promote BA-induced liver injury in PSC. Bile Acids and Salts 126-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 28723497-9 2016 In the sunitinib cohort, the CYP3A4 rs464637 AG variant was associated with a lower risk of high-grade AEs (odds ratio 0.27, 95% confidence interval 0.08-0.88; p=0.03), but no SNPs were associated with hypertension. Sunitinib 7-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 28723497-11 2016 CONCLUSIONS: We observed an association between CYP3A4 polymorphisms and toxicity outcomes in mRCC patients treated with sunitinib, but not with everolimus or temsirolimus. Sunitinib 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 28723497-13 2016 PATIENT SUMMARY: We found that variants of CYP3A4, a gene involved in drug metabolism, are associated with sunitinib toxicity. Sunitinib 107-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 27994580-2 2016 Rifabutin (RFB) is an alternative to rifampin (RIF) for TB regimens and is recommended for HIV patients concurrently receiving protease inhibitors because of reduced induction of CYP3A4. Rifabutin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 27501475-1 2016 AIMS: We compared the CYP3A4 metrics weight-corrected midazolam apparent oral clearance (MDZ Cl/F/W) and plasma 4beta-hydroxycholesterol/cholesterol (4beta-OHC/C) as they relate to tacrolimus (TAC) Cl/F/W in renal transplant recipients. Midazolam 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 28006013-6 2016 Aflatoxin B1 and benzo(a)pyrene were predominantly detected by the CYP3A4 + RAD54 system, while N-nitrosodimethylamine only moderately activated the CYP2B6 + RAD54 reporter system and none of them was identified by the CYP2D6 + RAD54 system. Aflatoxin B1 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 28006013-6 2016 Aflatoxin B1 and benzo(a)pyrene were predominantly detected by the CYP3A4 + RAD54 system, while N-nitrosodimethylamine only moderately activated the CYP2B6 + RAD54 reporter system and none of them was identified by the CYP2D6 + RAD54 system. Benzo(a)pyrene 17-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 28263536-0 2016 Effectiveness of human cytochrome P450 3A4 present in liposomal and microsomal nanoparticles in formation of covalent DNA adducts by ellipticine. ellipticine 133-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-42 28263536-6 2016 However, since its anticancer efficiency depends on the CYP3A4-mediated metabolism in cancer cells, the aim of our research is to develop nanoparticles containing this enzyme that can be transported to tumor cells, thereby potentiating ellipticine cytotoxicity. ellipticine 236-247 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 28263536-7 2016 METHODS: The CYP3A4 enzyme encapsulated into two nanoparticle forms, liposomes and microsomes, was tested to activate ellipticine to its reactive species forming covalent DNA adducts. ellipticine 118-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 28263536-9 2016 RESULTS: The CYP3A4 enzyme both in the liposome and microsome nanoparticle forms was efficient to activate ellipticine to species forming DNA adducts. ellipticine 107-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 28263536-10 2016 Two DNA adducts, which are formed from ellipticine metabolites 12-hydroxy- and 13-hydroxyellipticine generated by its oxidation by CYP3A4, were formed by both CYP3A4 nanoparticle systems. ellipticine 39-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 28263536-10 2016 Two DNA adducts, which are formed from ellipticine metabolites 12-hydroxy- and 13-hydroxyellipticine generated by its oxidation by CYP3A4, were formed by both CYP3A4 nanoparticle systems. ellipticine 39-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 28263536-10 2016 Two DNA adducts, which are formed from ellipticine metabolites 12-hydroxy- and 13-hydroxyellipticine generated by its oxidation by CYP3A4, were formed by both CYP3A4 nanoparticle systems. 12-hydroxy- and 13-hydroxyellipticine 63-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 28263536-10 2016 Two DNA adducts, which are formed from ellipticine metabolites 12-hydroxy- and 13-hydroxyellipticine generated by its oxidation by CYP3A4, were formed by both CYP3A4 nanoparticle systems. 12-hydroxy- and 13-hydroxyellipticine 63-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 28263536-11 2016 A higher effectiveness of CYP3A4 in microsomal than in liposomal nanoparticles to form ellipticine-DNA adducts was found. ellipticine 87-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 28263536-12 2016 CONCLUSION: Further testing in a suitable cancer cell model is encouraged to investigate whether the DNA-damaging effects of ellipticine after its activation by CYP3A4 nanoparticle forms are appropriate for active targeting of this enzyme to specific cancer cells. ellipticine 125-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 27749250-5 2016 Treatment by rutin significantly inhibited protein expressions of cytochrome P450-dependent CYP3A4 (75.3 %, p < 0.0001), elevated CYP1A1 enzymes (1.7-fold, p = 0.0084) and increased protein expressions of antioxidant and phase II reaction catalyzing enzymes, NQO1 (2.42-fold, p < 0.0001) and GSTP1 (2.03-fold, p < 0.0001). Rutin 13-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 27749250-6 2016 Besides, rutin treatment significantly inhibited mRNA expression of CYP3A4 (73.2 %, p=0.0014). Rutin 9-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 27855510-0 2016 UHPLC-MS/MS bioanalysis of urinary DHEA, cortisone and their hydroxylated metabolites as potential biomarkers for CYP3A-mediated drug-drug interactions. Dehydroepiandrosterone 35-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 27855510-0 2016 UHPLC-MS/MS bioanalysis of urinary DHEA, cortisone and their hydroxylated metabolites as potential biomarkers for CYP3A-mediated drug-drug interactions. Cortisone 41-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 27855510-5 2016 It is also suitable for future drug-drug interaction studies to continue evaluating the potential of these steroids as biomarkers for CYP3A inhibition and induction. Steroids 107-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-139 27501475-1 2016 AIMS: We compared the CYP3A4 metrics weight-corrected midazolam apparent oral clearance (MDZ Cl/F/W) and plasma 4beta-hydroxycholesterol/cholesterol (4beta-OHC/C) as they relate to tacrolimus (TAC) Cl/F/W in renal transplant recipients. mdz cl 89-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 27530188-1 2016 AIMS: Edoxaban, a novel factor Xa inhibitor, is a substrate of cytochrome P450 3 A4 (CYP3A4) and the efflux transporter P-glycoprotein (P-gp). edoxaban 6-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-83 27530188-1 2016 AIMS: Edoxaban, a novel factor Xa inhibitor, is a substrate of cytochrome P450 3 A4 (CYP3A4) and the efflux transporter P-glycoprotein (P-gp). edoxaban 6-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 27454549-4 2016 In addition, the study revealed iridoid glycosides inhibited the activity of cytochrome CYP3A4 enzyme. Iridoid Glycosides 32-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 27909995-20 2016 Because solithromycin is a possible substrate and inhibitor of both CYP3A4 and P-glycoprotein (P-gp), it may display drug interactions similar to macrolides such as clarithromycin. solithromycin 8-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 27621203-9 2016 This change in CYP3A4 activity decreased the half-life and area under the curve up to the last measurable concentration (AUClast) of the small molecule CYP3A4 substrate simvastatin hydroxy acid, measured before and after tocilizumab treatment. simvastatin hydroxyacid 169-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 27621203-9 2016 This change in CYP3A4 activity decreased the half-life and area under the curve up to the last measurable concentration (AUClast) of the small molecule CYP3A4 substrate simvastatin hydroxy acid, measured before and after tocilizumab treatment. simvastatin hydroxyacid 169-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 27236320-0 2016 Dose-Dependent Bioavailability and CYP3A Inhibition Contribute to Non-Linear Pharmacokinetics of Voriconazole. Voriconazole 97-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-40 27236320-1 2016 Voriconazole is both a substrate and a potent inhibitor of cytochrome P450 (CYP) 3A. Voriconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-83 27236320-4 2016 Concurrently, we determined systemic and presystemic CYP3A activity with microdosed midazolam. Midazolam 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 27236320-8 2016 Dose-dependent autoinhibition of CYP3A-dependent first-pass metabolism and systemic metabolism is a possible explanation for the dose-dependent bioavailability and elimination of voriconazole, either as additional mechanism to, or instead of, saturation of presystemic metabolism. Voriconazole 179-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 27236320-9 2016 Higher bioavailability and non-linear pharmacokinetics are expected to be a common property of drugs that are substrates and inhibitors of CYP3A, e.g. clarithromycin. Clarithromycin 151-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-144 27286724-8 2016 (S)-methadone clearance was influenced by cytochrome P450 (CYP) 2B6 activity, ABCB1 3435C>T, and alpha-1 acid glycoprotein level, while (R)-methadone clearance was influenced by CYP2B6 activity, POR*28, and CYP3A4*22. Methadone 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 210-216 27566315-12 2016 CONCLUSIONS: Cancer cachexia raised the plasma exposure of oxycodone through the reduction of CYP3A metabolic pathway. Oxycodone 59-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-99 27414036-5 2016 Diethyldithiocarbamate-copper complex revealed inconsistent and rather modulatory effect on the expression of CYP1A2 and CYP3A4 in several cultures of human hepatocytes. Ditiocarb 0-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 27414036-5 2016 Diethyldithiocarbamate-copper complex revealed inconsistent and rather modulatory effect on the expression of CYP1A2 and CYP3A4 in several cultures of human hepatocytes. Copper 23-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 27764027-4 2016 The aim of this study was to develop and validate a simplified but sensitive method for the simultaneous quantification of 5 probe drugs [caffeine (CYP1A2), metoprolol (CYP2D6), midazolam (CYP3A4), omeprazole (CYP2C19), and S-warfarin (CYP2C9)] in a previously validated cocktail using a liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. Omeprazole 198-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 27196064-4 2016 It was concluded that 2-oxo-clopidogrel was formed via CYP3A oxidation. 2-oxo-clopidogrel 22-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 27196064-11 2016 Clopidogrel is therefore now considered to be primarily a CYP3A4/5 substrate. Clopidogrel 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 27764027-4 2016 The aim of this study was to develop and validate a simplified but sensitive method for the simultaneous quantification of 5 probe drugs [caffeine (CYP1A2), metoprolol (CYP2D6), midazolam (CYP3A4), omeprazole (CYP2C19), and S-warfarin (CYP2C9)] in a previously validated cocktail using a liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. Warfarin 224-234 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 26928326-13 2016 In conclusion, C-1305 inhibited human recombinant CYP1A2 and CYP3A4 isoenzymes by mechanism-based inactivation. C 1305 15-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 26928326-7 2016 The objective of this study was to investigate the mechanism of the observed C-1305-mediated inactivation of CYP1A2 and CYP3A4. C 1305 77-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 26936324-2 2016 Carbamazepine is an antiepileptic drug which is metabolized by CYP3A4 into carbamazepine-10,11-epoxide. Carbamazepine 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 26928326-9 2016 Our findings indicated that C-1305 produced a time- and concentration-dependent decrease in 7-ethoxycoumarin O-deethylation (CYP1A2, KI = 10.8 +- 2.14 muM) and testosterone 6beta-hydroxylation (CYP3A4, KI = 9.1 +- 2.82 muM). C 1305 28-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 26936324-2 2016 Carbamazepine is an antiepileptic drug which is metabolized by CYP3A4 into carbamazepine-10,11-epoxide. carbamazepine epoxide 75-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 27876007-6 2016 The enzyme activity of CYP3A4 was evaluated by measuring the plasma ratio of 1"-hydroxymidazolam to midazolam 1 h after intravenous administration of 0.1 mg/kg midazolam. 1-hydroxymethylmidazolam 77-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 27809336-4 2016 Granisetron is primarily metabolized by the cytochrome P450 (CYP) enzymes CYP1A1 and CYP3A and is likely a substrate of the ABCB1 transporter. Granisetron 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-90 27809336-5 2016 Single-nucleotide polymorphisms (SNPs) in CYP3A, CYP1A1, and ABCB1 can alter drug metabolism. single-nucleotide 0-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 27876007-6 2016 The enzyme activity of CYP3A4 was evaluated by measuring the plasma ratio of 1"-hydroxymidazolam to midazolam 1 h after intravenous administration of 0.1 mg/kg midazolam. Midazolam 87-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 27876007-6 2016 The enzyme activity of CYP3A4 was evaluated by measuring the plasma ratio of 1"-hydroxymidazolam to midazolam 1 h after intravenous administration of 0.1 mg/kg midazolam. Midazolam 100-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 27917125-3 2016 Under non-induced conditions, all CYP activities could be determined in 3D-PHH, CYP2B6, CYP2C19, CYP2D6, and CYP3A4 in 2D-PHH and HepaRG, and CYP2C19 and CYP3A4 in HepG2 cells. 4,5,6,7-tetrachlorophthalide 75-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 27917125-3 2016 Under non-induced conditions, all CYP activities could be determined in 3D-PHH, CYP2B6, CYP2C19, CYP2D6, and CYP3A4 in 2D-PHH and HepaRG, and CYP2C19 and CYP3A4 in HepG2 cells. heparg 130-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 27917125-3 2016 Under non-induced conditions, all CYP activities could be determined in 3D-PHH, CYP2B6, CYP2C19, CYP2D6, and CYP3A4 in 2D-PHH and HepaRG, and CYP2C19 and CYP3A4 in HepG2 cells. heparg 130-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 27917125-6 2016 After treatment with 20 muM rifampicin, mRNA increased 3- to 50-fold for all CYPs except CYP1A2 and 2D6 for HepaRG and 3D-PHH, 4-fold (CYP2B6) and 17-fold (CYP3A4) for 2D-PHH and four-fold (CYP3A4) for HepG2. Rifampin 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 27917125-6 2016 After treatment with 20 muM rifampicin, mRNA increased 3- to 50-fold for all CYPs except CYP1A2 and 2D6 for HepaRG and 3D-PHH, 4-fold (CYP2B6) and 17-fold (CYP3A4) for 2D-PHH and four-fold (CYP3A4) for HepG2. Rifampin 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-196 27732883-9 2016 Tested CCBs inhibited enzyme activities of CYP3A4 (benidipine (+)>(-); felodipine (-)>(+); isradipine (-)-(+)) and CYP2C9 (benidipine (-)>(+); felodipine (+)>(-); isradipine (-)>(+)). benidipine 51-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 27732883-9 2016 Tested CCBs inhibited enzyme activities of CYP3A4 (benidipine (+)>(-); felodipine (-)>(+); isradipine (-)-(+)) and CYP2C9 (benidipine (-)>(+); felodipine (+)>(-); isradipine (-)>(+)). Felodipine 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 27782404-6 2016 Melting temperatures (Tm), heat capacities (DeltaCp), and calorimetric enthalpies (DeltaHcal) for denaturation of CYP3A4 each increased with an increasing fraction of DMPC, with a maximum at 50% DMPC, before decreasing at 75% DMPC. Dimyristoylphosphatidylcholine 167-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 27782404-6 2016 Melting temperatures (Tm), heat capacities (DeltaCp), and calorimetric enthalpies (DeltaHcal) for denaturation of CYP3A4 each increased with an increasing fraction of DMPC, with a maximum at 50% DMPC, before decreasing at 75% DMPC. Dimyristoylphosphatidylcholine 195-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 27782404-6 2016 Melting temperatures (Tm), heat capacities (DeltaCp), and calorimetric enthalpies (DeltaHcal) for denaturation of CYP3A4 each increased with an increasing fraction of DMPC, with a maximum at 50% DMPC, before decreasing at 75% DMPC. Dimyristoylphosphatidylcholine 195-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 27732883-9 2016 Tested CCBs inhibited enzyme activities of CYP3A4 (benidipine (+)>(-); felodipine (-)>(+); isradipine (-)-(+)) and CYP2C9 (benidipine (-)>(+); felodipine (+)>(-); isradipine (-)>(+)). Isradipine 97-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 27732883-9 2016 Tested CCBs inhibited enzyme activities of CYP3A4 (benidipine (+)>(-); felodipine (-)>(+); isradipine (-)-(+)) and CYP2C9 (benidipine (-)>(+); felodipine (+)>(-); isradipine (-)>(+)). benidipine 129-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 27732883-9 2016 Tested CCBs inhibited enzyme activities of CYP3A4 (benidipine (+)>(-); felodipine (-)>(+); isradipine (-)-(+)) and CYP2C9 (benidipine (-)>(+); felodipine (+)>(-); isradipine (-)>(+)). Felodipine 152-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 27732883-9 2016 Tested CCBs inhibited enzyme activities of CYP3A4 (benidipine (+)>(-); felodipine (-)>(+); isradipine (-)-(+)) and CYP2C9 (benidipine (-)>(+); felodipine (+)>(-); isradipine (-)>(+)). Isradipine 175-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 27665849-1 2016 AIM: Iloperidone is an atypical antipsychotic drug that is mainly metabolized by CYP2D6, CYP3A4, and cytosolic enzymes. iloperidone 5-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 27782404-3 2016 Here, circular dichroism and differential scanning calorimetry were used to compare the stability of CYP3A4 in lipid bilayer nanodiscs with varying ratios of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine to 1,2-dimyristoyl-sn-glycero-3-phosphocholine (DMPC). Lipid Bilayers 111-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 27723344-3 2016 Using microsecond-long molecular dynamics simulations, we analyzed interaction of CYP3A4 with bilayers composed of lipids differing in their polar head groups, i.e., phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and phosphatidylglycerol. Phosphatidylcholines 166-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 27723344-3 2016 Using microsecond-long molecular dynamics simulations, we analyzed interaction of CYP3A4 with bilayers composed of lipids differing in their polar head groups, i.e., phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and phosphatidylglycerol. Phosphatidylserines 213-231 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 27723344-3 2016 Using microsecond-long molecular dynamics simulations, we analyzed interaction of CYP3A4 with bilayers composed of lipids differing in their polar head groups, i.e., phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and phosphatidylglycerol. Phosphatidylglycerols 237-257 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 27664109-4 2016 DCV may be the object of a DDI via the induction or inhibition of cytochrome P450 (CYP) 3A4 and/or P-glycoprotein (P-gp) by the concomitant medication, or the precipitant of a DDI via DCV-based induction/inhibition of CYP 3A4 or inhibition of P-gp, organic anion transporting polypeptide 1B1/B3, and/or breast cancer resistance protein. daclatasvir 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-91 27664109-4 2016 DCV may be the object of a DDI via the induction or inhibition of cytochrome P450 (CYP) 3A4 and/or P-glycoprotein (P-gp) by the concomitant medication, or the precipitant of a DDI via DCV-based induction/inhibition of CYP 3A4 or inhibition of P-gp, organic anion transporting polypeptide 1B1/B3, and/or breast cancer resistance protein. daclatasvir 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 218-225 27723344-4 2016 In the negatively charged lipids, CYP3A4 was immersed more deeply and was more inclined toward the membrane because of favorable electrostatic and hydrogen bonding interactions between the CYP catalytic domain and lipid polar head groups. Hydrogen 147-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 27538919-2 2016 Since substrate specificity of CYP3A often overlaps that of P-gp, and estimation of their saturability in the intestine is difficult, dose-dependent FaFg (fraction of the administered drugs that reach the portal blood) of substrate drugs and the relative importance of CYP3A and P-gp have not been clarified in many cases. fafg 149-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-36 28097004-13 2016 This can be mainly explained by an enhancement of CYP3A-mediated first-pass metabolism, which sublingual buprenorphine only partially bypasses. Buprenorphine 105-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 27225997-2 2016 A clinical drug-drug interaction (DDI) study with the potent CYP3A4 inhibitor itraconazole resulted in an approximately sevenfold increase in cobimetinib exposure. Itraconazole 78-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 27225997-2 2016 A clinical drug-drug interaction (DDI) study with the potent CYP3A4 inhibitor itraconazole resulted in an approximately sevenfold increase in cobimetinib exposure. cobimetinib 142-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 27225997-3 2016 The DDI risk for cobimetinib with other CYP3A4 inhibitors and inducers needs to be assessed in order to provide dosing instructions. cobimetinib 17-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 27225997-6 2016 The contribution of CYP3A4 to the clearance of cobimetinib in humans was confirmed using sensitivity analysis in a retrospective simulation of itraconazole-cobimetinib DDI data. cobimetinib 47-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 27225997-7 2016 The verified PBPK model was then used to predict the effect of other CYP3A4 inhibitors and inducers on cobimetinib pharmacokinetics. cobimetinib 103-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 27225997-9 2016 Sensitivity analysis suggested that CYP3A4 contributes ~78 % of the total clearance of cobimetinib. cobimetinib 87-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 27225997-11 2016 Similarly, cobimetinib exposure in the presence of strong (rifampicin) and moderate (efavirenz) CYP3A inducers was predicted to decrease by 83 and 72 %, respectively. cobimetinib 11-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-101 25719441-2 2016 Omeprazole is an acid suppressant and CYP2C9, CYP3A4, and CYP2C19 substrate and inhibitor, as well as inhibitor of transporters (like P-gp). Omeprazole 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 27367453-0 2016 Ibrutinib Dosing Strategies Based on Interaction Potential of CYP3A4 Perpetrators Using Physiologically Based Pharmacokinetic Modeling. ibrutinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 27367453-1 2016 Based on ibrutinib pharmacokinetics and potential sensitivity towards CYP3A4-mediated drug-drug interactions (DDIs), a physiologically based pharmacokinetic approach was developed to mechanistically describe DDI with various CYP3A4 perpetrators in healthy men under fasting conditions. ibrutinib 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 27367453-1 2016 Based on ibrutinib pharmacokinetics and potential sensitivity towards CYP3A4-mediated drug-drug interactions (DDIs), a physiologically based pharmacokinetic approach was developed to mechanistically describe DDI with various CYP3A4 perpetrators in healthy men under fasting conditions. ibrutinib 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 225-231 27367453-4 2016 The ibrutinib dose should be reduced to 140 mg (quarter of maximal prescribed dose) when coadministered with moderate CYP3A4 inhibitors so that exposures remain within observed ranges at therapeutic doses. ibrutinib 4-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 27367453-5 2016 Thus, dose recommendations for CYP3A4 perpetrator use during ibrutinib treatment were developed and approved for labeling. ibrutinib 61-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 27538915-0 2016 Rifampin-Mediated Induction of Tamoxifen Metabolism in a Humanized PXR-CAR-CYP3A4/3A7-CYP2D6 Mouse Model. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 27538915-3 2016 In humans, tamoxifen is metabolized primarily by CYP3A4 and CYP2D6, and multiple-day treatment with rifampin decreased tamoxifen exposure by 6.2-fold. Tamoxifen 11-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 27538915-3 2016 In humans, tamoxifen is metabolized primarily by CYP3A4 and CYP2D6, and multiple-day treatment with rifampin decreased tamoxifen exposure by 6.2-fold. Rifampin 100-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 27538915-8 2016 In vitro kinetics determined in microsomes prepared from livers of the Tg-composite animals showed that, although Km values were not different between vehicle- and rifampin-treated groups, rifampin increased the Vmax for the CYP3A4-mediated pathways. Rifampin 189-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 225-231 27538919-2 2016 Since substrate specificity of CYP3A often overlaps that of P-gp, and estimation of their saturability in the intestine is difficult, dose-dependent FaFg (fraction of the administered drugs that reach the portal blood) of substrate drugs and the relative importance of CYP3A and P-gp have not been clarified in many cases. fafg 149-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 269-274 27538919-5 2016 The SFs of Vmax for CYP3A (SFCYP3A) and P-gp (SFP-gp) were simultaneously optimized to explain the FaFg of CYP3A and/or P-gp substrate drugs. fafg 99-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-25 27538919-5 2016 The SFs of Vmax for CYP3A (SFCYP3A) and P-gp (SFP-gp) were simultaneously optimized to explain the FaFg of CYP3A and/or P-gp substrate drugs. fafg 99-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 27538919-6 2016 The best predictability of FaFg was achieved when considering both SFCYP3A and SFP-gp The simulation also clarified the relative importance of CYP3A and P-gp in determining FaFg In particular, the nonlinear intestinal absorption of verapamil was caused by the saturation of intestinal CYP3A, whereas that of quinidine was governed by the saturation of both CYP3A and P-gp. fafg 27-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 27538919-6 2016 The best predictability of FaFg was achieved when considering both SFCYP3A and SFP-gp The simulation also clarified the relative importance of CYP3A and P-gp in determining FaFg In particular, the nonlinear intestinal absorption of verapamil was caused by the saturation of intestinal CYP3A, whereas that of quinidine was governed by the saturation of both CYP3A and P-gp. fafg 27-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 27538919-6 2016 The best predictability of FaFg was achieved when considering both SFCYP3A and SFP-gp The simulation also clarified the relative importance of CYP3A and P-gp in determining FaFg In particular, the nonlinear intestinal absorption of verapamil was caused by the saturation of intestinal CYP3A, whereas that of quinidine was governed by the saturation of both CYP3A and P-gp. fafg 27-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 27538919-6 2016 The best predictability of FaFg was achieved when considering both SFCYP3A and SFP-gp The simulation also clarified the relative importance of CYP3A and P-gp in determining FaFg In particular, the nonlinear intestinal absorption of verapamil was caused by the saturation of intestinal CYP3A, whereas that of quinidine was governed by the saturation of both CYP3A and P-gp. fafg 173-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 27538919-6 2016 The best predictability of FaFg was achieved when considering both SFCYP3A and SFP-gp The simulation also clarified the relative importance of CYP3A and P-gp in determining FaFg In particular, the nonlinear intestinal absorption of verapamil was caused by the saturation of intestinal CYP3A, whereas that of quinidine was governed by the saturation of both CYP3A and P-gp. fafg 173-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 27538919-6 2016 The best predictability of FaFg was achieved when considering both SFCYP3A and SFP-gp The simulation also clarified the relative importance of CYP3A and P-gp in determining FaFg In particular, the nonlinear intestinal absorption of verapamil was caused by the saturation of intestinal CYP3A, whereas that of quinidine was governed by the saturation of both CYP3A and P-gp. Verapamil 232-241 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 27538919-6 2016 The best predictability of FaFg was achieved when considering both SFCYP3A and SFP-gp The simulation also clarified the relative importance of CYP3A and P-gp in determining FaFg In particular, the nonlinear intestinal absorption of verapamil was caused by the saturation of intestinal CYP3A, whereas that of quinidine was governed by the saturation of both CYP3A and P-gp. Verapamil 232-241 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 27538919-6 2016 The best predictability of FaFg was achieved when considering both SFCYP3A and SFP-gp The simulation also clarified the relative importance of CYP3A and P-gp in determining FaFg In particular, the nonlinear intestinal absorption of verapamil was caused by the saturation of intestinal CYP3A, whereas that of quinidine was governed by the saturation of both CYP3A and P-gp. Verapamil 232-241 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 27538919-7 2016 In addition, the dose-dependent FaFg of selective and dual CYP3A and/or P-gp substrates was well predicted. fafg 32-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 27500989-5 2016 Clinical history, liver histology and genetic assessment (sequence analysis) of cytochrome P3A4 (CYP3A4) and uridine diphosphate-glucuronosyltransferase 1A9 (UGT1A9) involved in regorafenib metabolization were here reported for patients with severe hepatotoxicity. regorafenib 178-189 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-95 26686945-3 2016 We therefore conducted a literature review to identify reports of statistically significant associations between single nucleotide polymorphisms (SNP) in 11 vitamin D pathway genes (DHCR7, CYP2R1, CYP3A4, CYP27A1, DBP, LRP2, CUB, CYP27B1, CYP24A1, VDR and RXRA) and non-bone health outcomes and circulating levels of 25-hydroxyvitamin D (25[OH]D and 1,25-dihydroxyvitamin D (1,25[OH]2D). Vitamin D 157-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 27858915-0 2016 Genetic polymorphisms of CYP3A4 among Chinese patients with steroid-induced osteonecrosis of the femoral head. Steroids 60-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 27858915-3 2016 The aim of this study was to investigate the associations of polymorphisms of cytochrome P4503A4 (CYP3A4) gene with steroid-induced ONFH in Chinese patients. Steroids 116-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-96 27858915-3 2016 The aim of this study was to investigate the associations of polymorphisms of cytochrome P4503A4 (CYP3A4) gene with steroid-induced ONFH in Chinese patients. Steroids 116-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 27858915-6 2016 RESULTS: We identified rs2242480 in the CYP3A4 gene that was potentially associated with an increased risk of steroid-induced ONFH in the allele model (P = 0.023; odds ratio [OR]: 1.47; 95% confidence intervals [CI]: 1.05-2.04) and in the additive model (P = 0.028; OR: 1.44; 95% CI: 1.04-1.99) adjusted age + gender. Steroids 110-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 26953185-0 2016 Evaluation of Rifampin"s Transporter Inhibitory and CYP3A Inductive Effects on the Pharmacokinetics of Venetoclax, a BCL-2 Inhibitor: Results of a Single- and Multiple-Dose Study. venetoclax 103-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-57 26953185-2 2016 A single-dose and multiple-dose rifampin study was conducted to evaluate the effect of CYP3A induction and transporter inhibition on the pharmacokinetics of venetoclax. venetoclax 157-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 27794414-1 2016 Erlotinib, a substrate drug metabolized by the CYP3A4 enzyme, is an epidermal growth factor receptor tyrosine kinase inhibitor used to treat nonsmall cell lung cancer (NSCLC). Erlotinib Hydrochloride 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 27794414-2 2016 Concomitant use of erlotinib and the antiepileptic drug phenytoin, an inducer of CYP3A4, may result in a drug-drug interaction accompanied by changes in the blood concentrations of both drugs. Erlotinib Hydrochloride 19-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 27794414-6 2016 The present case revealed that blood phenytoin increased and blood erlotinib decreased subsequent to the interaction of the 2 drugs in the CYP3A4 metabolic enzyme system. Phenytoin 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 27794414-6 2016 The present case revealed that blood phenytoin increased and blood erlotinib decreased subsequent to the interaction of the 2 drugs in the CYP3A4 metabolic enzyme system. Erlotinib Hydrochloride 67-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 27500989-5 2016 Clinical history, liver histology and genetic assessment (sequence analysis) of cytochrome P3A4 (CYP3A4) and uridine diphosphate-glucuronosyltransferase 1A9 (UGT1A9) involved in regorafenib metabolization were here reported for patients with severe hepatotoxicity. regorafenib 178-189 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 26899628-5 2016 The primary isoforms involved in the elimination of tivantinib were CYP2C19 and CYP3A4/5. ARQ 197 52-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 27858915-8 2016 CONCLUSION: These findings suggested that polymorphisms of CYP3A4 gene may be associated with susceptibility to steroid-induced ONFH. Steroids 112-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 27634100-9 2016 Finally, the MRM-MS quantification of CYP3A4 in homogenates also correlated (r = 0.44; p < 0.05) with the level of enzyme activity in the same samples, as determined by measuring the chenodeoxycholic to hyocholic acid conversion. chenodeoxycholic 186-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 27634100-9 2016 Finally, the MRM-MS quantification of CYP3A4 in homogenates also correlated (r = 0.44; p < 0.05) with the level of enzyme activity in the same samples, as determined by measuring the chenodeoxycholic to hyocholic acid conversion. muricholic acid 206-220 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 26899628-12 2016 In conclusion, CYP2C19, CYP3A4/5, UGT1A9 and ADH4 were the primary drug metabolizing enzymes involved in the in vitro metabolism of tivantinib and its metabolites. ARQ 197 132-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 27626107-1 2016 Unexplored electrochemical behavior of abiraterone, a recent and widely used prostate cancer drug, in interaction with cytochrome P450 3A4 (CYP3A4) enzyme and multiwalled carbon nanotubes (MWCNTs) is investigated in this work. abiraterone 39-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-138 27843352-10 2016 Therefore, isoenzyms different from CYP3A4 are supposed to be less affected by cobicistat, and thus fewer drug-drug interactions are expected. Cobicistat 79-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 27541626-9 2016 Further phenotyping experiment proved that CYP3A4 was the most active enzyme responsible for the biotransformation of pyrotinib, implying the vital necessity of the assessment of the potential CYP3A-mediated drug-drug interactions in humans. pyrotinib 118-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 27565568-0 2016 Rapid LC-MS/MS method for the determination of 4-hydroxycholesterol/cholesterol ratio in serum as endogenous biomarker for CYP3A activity in human and foals. cholest-5-ene-3,4-diol 47-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-128 27565568-0 2016 Rapid LC-MS/MS method for the determination of 4-hydroxycholesterol/cholesterol ratio in serum as endogenous biomarker for CYP3A activity in human and foals. Cholesterol 56-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-128 27565568-2 2016 Thus, it was the aim of this study to develop and validate an analytical method allowing estimation of the hepatic CYP3A enzyme activity using the 4-hydroxycholesterol to cholesterol ratio as an endogenous biomarker in serum. cholest-5-ene-3,4-diol 147-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 27565568-2 2016 Thus, it was the aim of this study to develop and validate an analytical method allowing estimation of the hepatic CYP3A enzyme activity using the 4-hydroxycholesterol to cholesterol ratio as an endogenous biomarker in serum. Cholesterol 156-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 27565568-11 2016 Finally, the validated assay was applied to measure 4-hydroxycholesterol and cholesterol in serum samples of clinical studies in humans and foals that could verify induction of hepatic CYP3A4 (human) and CYP3A89 (foals) after premedication with the known enzyme inducer rifampicin. cholest-5-ene-3,4-diol 52-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 27565568-11 2016 Finally, the validated assay was applied to measure 4-hydroxycholesterol and cholesterol in serum samples of clinical studies in humans and foals that could verify induction of hepatic CYP3A4 (human) and CYP3A89 (foals) after premedication with the known enzyme inducer rifampicin. Cholesterol 61-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 27565568-11 2016 Finally, the validated assay was applied to measure 4-hydroxycholesterol and cholesterol in serum samples of clinical studies in humans and foals that could verify induction of hepatic CYP3A4 (human) and CYP3A89 (foals) after premedication with the known enzyme inducer rifampicin. Rifampin 270-280 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 27626107-1 2016 Unexplored electrochemical behavior of abiraterone, a recent and widely used prostate cancer drug, in interaction with cytochrome P450 3A4 (CYP3A4) enzyme and multiwalled carbon nanotubes (MWCNTs) is investigated in this work. abiraterone 39-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 27650703-0 2016 Correction to Concurrent Cooperativity and Substrate Inhibition in the Epoxidation of Carbamazepine by Cytochrome P450 3A4 Active Site Mutants Inspired by Molecular Dynamics Simulations. Carbamazepine 86-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-122 27287938-6 2016 Regarding CYP450 inhibition, the cell viability of SC-iHeps and p-Heps was increased by ketoconazole, a CYP3A4 inhibitor. Ketoconazole 88-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 27006091-0 2016 An evaluation of the CYP2D6 and CYP3A4 inhibition potential of metoprolol metabolites and their contribution to drug-drug and drug-herb interaction by LC-ESI/MS/MS. Metoprolol 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 27006091-1 2016 The aim of the present study was to evaluate the contribution of metabolites to drug-drug interaction and drug-herb interaction using the inhibition of CYP2D6 and CYP3A4 by metoprolol (MET) and its metabolites. Metoprolol 173-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 27745744-1 2016 PURPOSE: The metabolism of olaparib, a potent inhibitor of poly(ADP-ribose) polymerase (PARP) with demonstrated efficacy in patients with BRCA-mutated ovarian cancer, is mediated by cytochrome P450 (CYP) enzymes (predominantly CYP3A4/5). olaparib 27-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 227-233 27697800-1 2016 Ritonavir and cobicistat, used as pharmacokinetic enhancers in combination with some antiretrovirals (ARVs) for the treatment of HIV, are potent inhibitors of the CYP3A4 isoenzyme. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 27697800-1 2016 Ritonavir and cobicistat, used as pharmacokinetic enhancers in combination with some antiretrovirals (ARVs) for the treatment of HIV, are potent inhibitors of the CYP3A4 isoenzyme. Cobicistat 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 27697800-2 2016 Most glucocorticoids are metabolised via the CYP3A4 pathway and iatrogenic Cushing"s syndrome (ICS), with possible secondary adrenal insufficiency (SAI), is a recognised complication following co-administration with ritonavir or cobicistat. Ritonavir 216-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 27697800-2 2016 Most glucocorticoids are metabolised via the CYP3A4 pathway and iatrogenic Cushing"s syndrome (ICS), with possible secondary adrenal insufficiency (SAI), is a recognised complication following co-administration with ritonavir or cobicistat. Cobicistat 229-239 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 27745744-2 2016 We assessed the potential of a CYP3A4 inhibitor (itraconazole) and inducer (rifampin) to alter the pharmacokinetic (PK) profile of olaparib following single oral tablet doses. olaparib 131-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 27745744-13 2016 IMPLICATIONS: Exposure to olaparib was significantly increased when co-administered with the potent CYP3A4 inhibitor itraconazole, and significantly decreased when co-administered with the potent CYP3A4 inducer rifampin, compared with olaparib alone. olaparib 26-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 27745744-13 2016 IMPLICATIONS: Exposure to olaparib was significantly increased when co-administered with the potent CYP3A4 inhibitor itraconazole, and significantly decreased when co-administered with the potent CYP3A4 inducer rifampin, compared with olaparib alone. olaparib 26-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 196-202 27745744-13 2016 IMPLICATIONS: Exposure to olaparib was significantly increased when co-administered with the potent CYP3A4 inhibitor itraconazole, and significantly decreased when co-administered with the potent CYP3A4 inducer rifampin, compared with olaparib alone. Rifampin 211-219 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 196-202 27745744-14 2016 Potent CYP3A4 enzyme inhibitors and inducers should be avoided during olaparib treatment. olaparib 70-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 27469000-0 2016 Analysis of Mechanism-Based Inhibition of CYP 3A4 by a Series of Fluoroquinolone Antibacterial Agents. Fluoroquinolones 65-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-49 27450182-2 2016 The objective of this study was to examine the roles of CYP3A4 and CYP3A5 in lapatinib bioactivation leading to a reactive, potentially toxic quinoneimine. Lapatinib 77-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 27469000-4 2016 Representative quasi-irreversible inhibitors form a metabolite-intermediate (MI) complex with the heme of CYP3A4 according to absorption analysis. Heme 98-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 27450182-2 2016 The objective of this study was to examine the roles of CYP3A4 and CYP3A5 in lapatinib bioactivation leading to a reactive, potentially toxic quinoneimine. quinoneimine 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 27450182-5 2016 A screen of cDNA-expressed P450s confirmed that CYP3A4 and CYP3A5 are the primary enzymes responsible for quinoneimine-GSH adduct formation using lapatinib or O-dealkylated lapatinib as the substrate. quinoneimine 106-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 27469000-5 2016 Metabolite profiling identified the cyclopropane ring-opened metabolites from representative irreversible inhibitors, suggesting irreversible binding of the carbon-centered radical species with CYP3A4. cyclopropane 36-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 27450182-5 2016 A screen of cDNA-expressed P450s confirmed that CYP3A4 and CYP3A5 are the primary enzymes responsible for quinoneimine-GSH adduct formation using lapatinib or O-dealkylated lapatinib as the substrate. Glutathione 119-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 27450182-5 2016 A screen of cDNA-expressed P450s confirmed that CYP3A4 and CYP3A5 are the primary enzymes responsible for quinoneimine-GSH adduct formation using lapatinib or O-dealkylated lapatinib as the substrate. Lapatinib 146-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 27469000-5 2016 Metabolite profiling identified the cyclopropane ring-opened metabolites from representative irreversible inhibitors, suggesting irreversible binding of the carbon-centered radical species with CYP3A4. Carbon 157-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 27450182-5 2016 A screen of cDNA-expressed P450s confirmed that CYP3A4 and CYP3A5 are the primary enzymes responsible for quinoneimine-GSH adduct formation using lapatinib or O-dealkylated lapatinib as the substrate. Lapatinib 173-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 27469000-8 2016 The docking study with CYP3A4 suggested that a methyl moiety introduced at the carbon atom at the root of the primary amine disrupts formation of the MI complex between the heme and the nitroso intermediate because of steric hindrance. Carbon 79-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 27450182-6 2016 The mean kinetic parameters (Km and kcat) of lapatinib O-dealkylation revealed that CYP3A4 was 5.2-fold more efficient than CYP3A5 at lapatinib O-dealkylation (CYP3A4 kcat/Km = 6.8 muM(-1) min(-1) versus CYP3A5 kcat/Km = 1.3 muM(-1) min(-1)). Lapatinib 45-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 27450182-6 2016 The mean kinetic parameters (Km and kcat) of lapatinib O-dealkylation revealed that CYP3A4 was 5.2-fold more efficient than CYP3A5 at lapatinib O-dealkylation (CYP3A4 kcat/Km = 6.8 muM(-1) min(-1) versus CYP3A5 kcat/Km = 1.3 muM(-1) min(-1)). Lapatinib 45-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 27469000-8 2016 The docking study with CYP3A4 suggested that a methyl moiety introduced at the carbon atom at the root of the primary amine disrupts formation of the MI complex between the heme and the nitroso intermediate because of steric hindrance. Amines 118-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 27450182-6 2016 The mean kinetic parameters (Km and kcat) of lapatinib O-dealkylation revealed that CYP3A4 was 5.2-fold more efficient than CYP3A5 at lapatinib O-dealkylation (CYP3A4 kcat/Km = 6.8 muM(-1) min(-1) versus CYP3A5 kcat/Km = 1.3 muM(-1) min(-1)). Lapatinib 134-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 27469000-8 2016 The docking study with CYP3A4 suggested that a methyl moiety introduced at the carbon atom at the root of the primary amine disrupts formation of the MI complex between the heme and the nitroso intermediate because of steric hindrance. Heme 173-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 27450182-6 2016 The mean kinetic parameters (Km and kcat) of lapatinib O-dealkylation revealed that CYP3A4 was 5.2-fold more efficient than CYP3A5 at lapatinib O-dealkylation (CYP3A4 kcat/Km = 6.8 muM(-1) min(-1) versus CYP3A5 kcat/Km = 1.3 muM(-1) min(-1)). Lapatinib 134-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 27469000-8 2016 The docking study with CYP3A4 suggested that a methyl moiety introduced at the carbon atom at the root of the primary amine disrupts formation of the MI complex between the heme and the nitroso intermediate because of steric hindrance. nitroso 186-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 27450182-7 2016 Kinetic analysis of GSH adduct formation indicated that CYP3A4 was also 4-fold more efficient at quinoneimine-GSH adduct formation as measured by kcat (maximum relative GSH adduct levels)/Km (CYP3A4 = 0.0082 vs. CYP3A5 = 0.0021). Glutathione 20-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 27450182-7 2016 Kinetic analysis of GSH adduct formation indicated that CYP3A4 was also 4-fold more efficient at quinoneimine-GSH adduct formation as measured by kcat (maximum relative GSH adduct levels)/Km (CYP3A4 = 0.0082 vs. CYP3A5 = 0.0021). Glutathione 20-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-198 27530708-0 2016 Increased inhibition of cytochrome P450 3A4 with the tablet formulation of posaconazole. posaconazole 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-43 27450182-7 2016 Kinetic analysis of GSH adduct formation indicated that CYP3A4 was also 4-fold more efficient at quinoneimine-GSH adduct formation as measured by kcat (maximum relative GSH adduct levels)/Km (CYP3A4 = 0.0082 vs. CYP3A5 = 0.0021). quinoneimine 97-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 27450182-7 2016 Kinetic analysis of GSH adduct formation indicated that CYP3A4 was also 4-fold more efficient at quinoneimine-GSH adduct formation as measured by kcat (maximum relative GSH adduct levels)/Km (CYP3A4 = 0.0082 vs. CYP3A5 = 0.0021). quinoneimine 97-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-198 27450182-7 2016 Kinetic analysis of GSH adduct formation indicated that CYP3A4 was also 4-fold more efficient at quinoneimine-GSH adduct formation as measured by kcat (maximum relative GSH adduct levels)/Km (CYP3A4 = 0.0082 vs. CYP3A5 = 0.0021). Glutathione 110-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 27450182-7 2016 Kinetic analysis of GSH adduct formation indicated that CYP3A4 was also 4-fold more efficient at quinoneimine-GSH adduct formation as measured by kcat (maximum relative GSH adduct levels)/Km (CYP3A4 = 0.0082 vs. CYP3A5 = 0.0021). Glutathione 110-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-198 27450182-7 2016 Kinetic analysis of GSH adduct formation indicated that CYP3A4 was also 4-fold more efficient at quinoneimine-GSH adduct formation as measured by kcat (maximum relative GSH adduct levels)/Km (CYP3A4 = 0.0082 vs. CYP3A5 = 0.0021). Glutathione 110-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 27450182-7 2016 Kinetic analysis of GSH adduct formation indicated that CYP3A4 was also 4-fold more efficient at quinoneimine-GSH adduct formation as measured by kcat (maximum relative GSH adduct levels)/Km (CYP3A4 = 0.0082 vs. CYP3A5 = 0.0021). Glutathione 110-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-198 27450182-8 2016 In human liver microsomal (HLM) incubations, CYP3A4-selective inhibitors SR-9186 and CYP3cide reduced formation of GSH adducts by 78% and 72%, respectively, compared with >90% inhibition by the pan-CYP3A inhibitor ketoconazole. 1-(4-imidazopyridinyl-7-phenyl)-3-(4'-cyanobiphenyl)urea 73-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 27530708-1 2016 Being a substrate of the cytochrome P450 3A4 (CYP3A4) isoenzyme, sirolimus metabolism is decreased when posaconazole is administered concomitantly. Sirolimus 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-44 27450182-8 2016 In human liver microsomal (HLM) incubations, CYP3A4-selective inhibitors SR-9186 and CYP3cide reduced formation of GSH adducts by 78% and 72%, respectively, compared with >90% inhibition by the pan-CYP3A inhibitor ketoconazole. 1-(4-imidazopyridinyl-7-phenyl)-3-(4'-cyanobiphenyl)urea 73-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-50 27450182-8 2016 In human liver microsomal (HLM) incubations, CYP3A4-selective inhibitors SR-9186 and CYP3cide reduced formation of GSH adducts by 78% and 72%, respectively, compared with >90% inhibition by the pan-CYP3A inhibitor ketoconazole. Glutathione 115-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 27450182-8 2016 In human liver microsomal (HLM) incubations, CYP3A4-selective inhibitors SR-9186 and CYP3cide reduced formation of GSH adducts by 78% and 72%, respectively, compared with >90% inhibition by the pan-CYP3A inhibitor ketoconazole. Glutathione 115-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-50 27450182-8 2016 In human liver microsomal (HLM) incubations, CYP3A4-selective inhibitors SR-9186 and CYP3cide reduced formation of GSH adducts by 78% and 72%, respectively, compared with >90% inhibition by the pan-CYP3A inhibitor ketoconazole. Ketoconazole 217-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 27530708-1 2016 Being a substrate of the cytochrome P450 3A4 (CYP3A4) isoenzyme, sirolimus metabolism is decreased when posaconazole is administered concomitantly. Sirolimus 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 27450182-8 2016 In human liver microsomal (HLM) incubations, CYP3A4-selective inhibitors SR-9186 and CYP3cide reduced formation of GSH adducts by 78% and 72%, respectively, compared with >90% inhibition by the pan-CYP3A inhibitor ketoconazole. Ketoconazole 217-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-50 27450182-9 2016 The 16%-22% difference between CYP3A- and CYP3A4-selective inhibition indicates the involvement of remaining CYP3A5 activity in generating reactive metabolites from lapatinib in pooled HLMs. Lapatinib 165-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-36 27530708-1 2016 Being a substrate of the cytochrome P450 3A4 (CYP3A4) isoenzyme, sirolimus metabolism is decreased when posaconazole is administered concomitantly. posaconazole 104-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-44 27450182-9 2016 The 16%-22% difference between CYP3A- and CYP3A4-selective inhibition indicates the involvement of remaining CYP3A5 activity in generating reactive metabolites from lapatinib in pooled HLMs. Lapatinib 165-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 27530708-1 2016 Being a substrate of the cytochrome P450 3A4 (CYP3A4) isoenzyme, sirolimus metabolism is decreased when posaconazole is administered concomitantly. posaconazole 104-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 27450182-10 2016 Collectively, these findings support the conclusion that both CYP3A4 and CYP3A5 are quantitatively important contributors to lapatinib bioactivation. Lapatinib 125-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 27530708-2 2016 However, because of the poor bioavailability of the oral suspension of posaconazole with which low plasma concentrations are obtained, CYP3A4 inhibition is weak and a 50-75% dose reduction of sirolimus is sufficient to avoid sirolimus overdosage. posaconazole 71-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 27530708-8 2016 The clinicians and pharmacologists must be warned that the use of posaconazole tablets may result in an inhibition of CYP3A4 of greater magnitude than with the oral suspension. posaconazole 66-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 27457783-10 2016 NAC and selective inhibitors of CYP2B6 and CYP3A4 significantly reduced TMP covalent binding. Acetylcysteine 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 27450623-7 2016 Carbamazepine, oxcarbazepine, phenytoin, phenobarbital and topiramate might decrease the effect of NOACs by inducing CYP3A4 activity. Carbamazepine 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 27457783-10 2016 NAC and selective inhibitors of CYP2B6 and CYP3A4 significantly reduced TMP covalent binding. Trimethoprim 72-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 27457784-9 2016 Further, incubations of M11 with recombinant P450s showed that M12 is formed via N-dealkylation of M11 by CYP3A4, CYP2C19, and CYP1A2. Nitrogen 81-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 27450623-7 2016 Carbamazepine, oxcarbazepine, phenytoin, phenobarbital and topiramate might decrease the effect of NOACs by inducing CYP3A4 activity. Oxcarbazepine 15-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 27450623-7 2016 Carbamazepine, oxcarbazepine, phenytoin, phenobarbital and topiramate might decrease the effect of NOACs by inducing CYP3A4 activity. Phenytoin 30-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 27450623-7 2016 Carbamazepine, oxcarbazepine, phenytoin, phenobarbital and topiramate might decrease the effect of NOACs by inducing CYP3A4 activity. Phenobarbital 41-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 27450623-7 2016 Carbamazepine, oxcarbazepine, phenytoin, phenobarbital and topiramate might decrease the effect of NOACs by inducing CYP3A4 activity. Topiramate 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 27450623-7 2016 Carbamazepine, oxcarbazepine, phenytoin, phenobarbital and topiramate might decrease the effect of NOACs by inducing CYP3A4 activity. noacs 99-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 27450623-8 2016 Controversial data - inhibition as well as induction of CYP3A4 - were found about valproic acid. Valproic Acid 82-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 27430348-0 2016 Rhabdomyolysis caused by the moderate CYP3A4 inhibitor fluconazole in a patient on stable atorvastatin therapy: a case report and literature review. Fluconazole 55-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 26829173-1 2016 Ketoconazole is a potent CYP3A inhibitor in vivo, and frequently serves as an index CYP3A inhibitor in drug-drug interaction (DDI) studies with healthy volunteers. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-30 26829173-1 2016 Ketoconazole is a potent CYP3A inhibitor in vivo, and frequently serves as an index CYP3A inhibitor in drug-drug interaction (DDI) studies with healthy volunteers. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-89 27430348-0 2016 Rhabdomyolysis caused by the moderate CYP3A4 inhibitor fluconazole in a patient on stable atorvastatin therapy: a case report and literature review. Atorvastatin 90-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 27430348-6 2016 WHAT IS NEW AND CONCLUSION: Our case demonstrates that in some subjects even a moderate CYP3A4 inhibitor such as fluconazole may lead to rhabdomyolysis in subjects receiving a statin. Fluconazole 113-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 27511886-0 2016 Associations of the CYP3A5*3 and CYP3A4*1G polymorphisms with the pharmacokinetics of oral midazolam and the urinary 6beta-hydroxycortisol/cortisol ratio as markers of CYP3A activity in healthy male Chinese. Midazolam 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 27417180-5 2016 The CYP3A4 assay was evaluated using two long t1/2 compounds, carbamazepine and antipyrine (t1/2 > 30 minutes); one moderate t1/2 compound, ketoconazole (10 < t1/2 < 30 minutes); and two short t1/2 compounds, loperamide and buspirone (t1/2 < 10 minutes). Carbamazepine 62-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 27511886-0 2016 Associations of the CYP3A5*3 and CYP3A4*1G polymorphisms with the pharmacokinetics of oral midazolam and the urinary 6beta-hydroxycortisol/cortisol ratio as markers of CYP3A activity in healthy male Chinese. Midazolam 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-25 27511886-0 2016 Associations of the CYP3A5*3 and CYP3A4*1G polymorphisms with the pharmacokinetics of oral midazolam and the urinary 6beta-hydroxycortisol/cortisol ratio as markers of CYP3A activity in healthy male Chinese. Hydrocortisone 130-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-25 27417180-5 2016 The CYP3A4 assay was evaluated using two long t1/2 compounds, carbamazepine and antipyrine (t1/2 > 30 minutes); one moderate t1/2 compound, ketoconazole (10 < t1/2 < 30 minutes); and two short t1/2 compounds, loperamide and buspirone (t1/2 < 10 minutes). Antipyrine 80-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 27511886-1 2016 WHAT IS KNOWN AND OBJECTIVE: The oral plasma clearance of midazolam and the ratio of 6beta-hydroxycortisol (6beta-OHF) to cortisol (F) in urine are two potential markers for evaluating CYP3A activity in vivo. Midazolam 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-190 27450182-0 2016 Cytochrome P450 3A4 and CYP3A5-Catalyzed Bioactivation of Lapatinib. Lapatinib 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 27450182-1 2016 Metabolic activation of the dual-tyrosine kinase inhibitor lapatinib by cytochromes CYP3A4 and CYP3A5 has been implicated in lapatinib-induced idiosyncratic hepatotoxicity; however, the relative enzyme contributions have not been established. Lapatinib 59-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 27450182-1 2016 Metabolic activation of the dual-tyrosine kinase inhibitor lapatinib by cytochromes CYP3A4 and CYP3A5 has been implicated in lapatinib-induced idiosyncratic hepatotoxicity; however, the relative enzyme contributions have not been established. Lapatinib 125-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 27511886-2 2016 We assessed the influence of two common CYP3A polymorphisms on the pharmacokinetics of oral midazolam and urinary ratio of 6beta-OHF/F in healthy Chinese. Midazolam 92-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 27511886-3 2016 METHODS: Single oral 15 mg doses of midazolam were given to 20 healthy male Chinese subjects who were genotyped for the CYP3A5*3 and CYP3A4*1G polymorphisms. Midazolam 36-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 27482056-3 2016 Here, we investigated the role of the lipid- and glucose-modulating hormone fibroblast growth factor 21 (FGF21) in the molecular mechanism regulating CYP3A4 expression in NAFLD. Glucose 49-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 27695181-0 2016 Hemopericardium with tamponade following rivaroxaban administration and its attenuation by CYP3A4 inhibitors. Rivaroxaban 41-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 27399255-10 2016 Everolimus and tacrolimus are two immunosuppressive drugs metabolized by CYP3A4. Everolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 27399255-10 2016 Everolimus and tacrolimus are two immunosuppressive drugs metabolized by CYP3A4. Tacrolimus 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 30645821-14 2016 Ruxolitinib is mainly metabolised by cytochrome P450 isoenzymes CYP3A4 and CYP2C9, creating a risk of multiple drug interactions. ruxolitinib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 30645828-5 2016 In particular, they showed that the risk was higher with doses greater than 30 mg per day or with concomitant use of inhibitors of the cytochrome P450 isoenzyme CYP3A4, which reduce domperidone clearance. Domperidone 182-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 27695181-4 2016 A review of the patient"s medications revealed a total of seven agents known to be metabolized through cytochrome P450 3A4 (CYP3A4), the major pathway for rivaroxaban metabolism. Rivaroxaban 155-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-122 27695181-4 2016 A review of the patient"s medications revealed a total of seven agents known to be metabolized through cytochrome P450 3A4 (CYP3A4), the major pathway for rivaroxaban metabolism. Rivaroxaban 155-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 27714268-7 2016 Similarly, two methoxy-substituted biphenyl ureas 5d and 5e also displayed potent and selective inhibition of CYP1B1 with IC50 values of 69 and 58 nM, respectively, showing >62 and >98-fold selectivity over CYP1A1, CYP1A2, CYP3A4 and CYP2D6 enzymes. methoxy-substituted biphenyl ureas 15-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 229-235 27310200-8 2016 Cyclosporine predominantly inhibited CYP3A4 (half maximal inhibitory concentration = 0.71 microM) rather than CYP3A5 (>5 microM), whereas tacrolimus showed similar inhibition for CYP3A4 (0.29 microM) and CYP3A5 (0.41 microM). Cyclosporine 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 27310200-8 2016 Cyclosporine predominantly inhibited CYP3A4 (half maximal inhibitory concentration = 0.71 microM) rather than CYP3A5 (>5 microM), whereas tacrolimus showed similar inhibition for CYP3A4 (0.29 microM) and CYP3A5 (0.41 microM). Tacrolimus 141-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 182-188 26796435-10 2016 Using recombinantly expressed human cytochrome P450 (CYP) isoenzymes, dydrogesterone was shown to be metabolically transformed by CYP3A4 and CYP2C19. Dydrogesterone 70-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 26796435-12 2016 A clear contribution of CYP3A4 to microsomal metabolism of dydrogesterone was demonstrated with HLM and isoenzyme-specific CYP inhibitors, and confirmed by a significant correlation between dydrogesterone clearance and CYP3A4 activity. Dydrogesterone 59-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 26796435-12 2016 A clear contribution of CYP3A4 to microsomal metabolism of dydrogesterone was demonstrated with HLM and isoenzyme-specific CYP inhibitors, and confirmed by a significant correlation between dydrogesterone clearance and CYP3A4 activity. Dydrogesterone 59-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 26796435-12 2016 A clear contribution of CYP3A4 to microsomal metabolism of dydrogesterone was demonstrated with HLM and isoenzyme-specific CYP inhibitors, and confirmed by a significant correlation between dydrogesterone clearance and CYP3A4 activity. Dydrogesterone 190-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 26796435-12 2016 A clear contribution of CYP3A4 to microsomal metabolism of dydrogesterone was demonstrated with HLM and isoenzyme-specific CYP inhibitors, and confirmed by a significant correlation between dydrogesterone clearance and CYP3A4 activity. Dydrogesterone 190-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 26796435-17 2016 In conclusion, dydrogesterone metabolism in the liver is dominated primarily by cytosolic enzymes (particularly AKR1C) and secondarily by CYP3A4, with the former exclusively responsible for 20alpha-DHD formation. Dydrogesterone 15-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 26796435-17 2016 In conclusion, dydrogesterone metabolism in the liver is dominated primarily by cytosolic enzymes (particularly AKR1C) and secondarily by CYP3A4, with the former exclusively responsible for 20alpha-DHD formation. 20-alpha-dihydrodydrogesterone 190-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 26864332-12 2016 In vitro, suvorexant demonstrated reversible inhibition of CYP3A4 and 2C19 (IC50 ~ 4-5 muM), and weak time-dependent inhibition of CYP3A4 (KI = 12 muM, kinact = 0.14 min(-1)). suvorexant 10-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-74 26864332-12 2016 In vitro, suvorexant demonstrated reversible inhibition of CYP3A4 and 2C19 (IC50 ~ 4-5 muM), and weak time-dependent inhibition of CYP3A4 (KI = 12 muM, kinact = 0.14 min(-1)). suvorexant 10-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 26864332-13 2016 Suvorexant was also a weak inducer of CYP3A4, 1A2 and 2B6. suvorexant 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 27506419-6 2016 Moreover, there was significant up-regulation of CYP3A4 expression via PXR activation for TBB and TBPH and their metabolites. 2-ethylhexyl 2,3,4,5-tetrabromobenzoate 90-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 27506419-6 2016 Moreover, there was significant up-regulation of CYP3A4 expression via PXR activation for TBB and TBPH and their metabolites. bis(2-ethylhexyl) 2,3,4,5-tetrabromophthalate 98-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 27458223-2 2016 Three studies were conducted to evaluate the potential drug-drug interactions between delamanid and antiretroviral drugs, including ritonavir, a strong inhibitor of CYP3A4, and selected anti-TB drugs, including rifampin, a strong inducer of cytochrome P450 (CYP) isozymes. OPC-67683 86-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 27458223-2 2016 Three studies were conducted to evaluate the potential drug-drug interactions between delamanid and antiretroviral drugs, including ritonavir, a strong inhibitor of CYP3A4, and selected anti-TB drugs, including rifampin, a strong inducer of cytochrome P450 (CYP) isozymes. Ritonavir 132-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 27695358-1 2016 BACKGROUND: Today, it is proved that isoenzymes CYP2D6 and CYP3A4 are involved in metabolism of haloperidol. Haloperidol 96-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 27624558-8 2016 In HepG2 cells, up-regulations of CYP3A4 and SLCO1B1 potentiated hepatotoxicity and ROS generation, whereas knockdowns of CYP3A4 and SLCO1B1 as well as CYP3A4/SLCO1B1 inhibitions showed the opposite effects. ros 84-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 27713827-7 2016 Induction of CYP3A4 by PB, artemisinin, and phenytoin was also much reduced in PXR-KO cells, while the response to CITCO was maintained. Phenobarbital 23-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 27713827-7 2016 Induction of CYP3A4 by PB, artemisinin, and phenytoin was also much reduced in PXR-KO cells, while the response to CITCO was maintained. artemisinin 27-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 27713827-7 2016 Induction of CYP3A4 by PB, artemisinin, and phenytoin was also much reduced in PXR-KO cells, while the response to CITCO was maintained. Phenytoin 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 27325500-3 2016 When investigating the proteasome inhibitors bortezomib, carfilzomib, and ixazomib, we observed increased luminescence for bortezomib and ixazomib, but not for carfilzomib, in a pregnane-X-receptor (PXR) reporter gene assay, which was inconsistent with the mRNA expression levels of the main PXR target gene CYP3A4. Bortezomib 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 308-314 27325500-3 2016 When investigating the proteasome inhibitors bortezomib, carfilzomib, and ixazomib, we observed increased luminescence for bortezomib and ixazomib, but not for carfilzomib, in a pregnane-X-receptor (PXR) reporter gene assay, which was inconsistent with the mRNA expression levels of the main PXR target gene CYP3A4. carfilzomib 57-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 308-314 27325500-3 2016 When investigating the proteasome inhibitors bortezomib, carfilzomib, and ixazomib, we observed increased luminescence for bortezomib and ixazomib, but not for carfilzomib, in a pregnane-X-receptor (PXR) reporter gene assay, which was inconsistent with the mRNA expression levels of the main PXR target gene CYP3A4. ixazomib 74-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 308-314 27325500-3 2016 When investigating the proteasome inhibitors bortezomib, carfilzomib, and ixazomib, we observed increased luminescence for bortezomib and ixazomib, but not for carfilzomib, in a pregnane-X-receptor (PXR) reporter gene assay, which was inconsistent with the mRNA expression levels of the main PXR target gene CYP3A4. Bortezomib 123-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 308-314 27325500-3 2016 When investigating the proteasome inhibitors bortezomib, carfilzomib, and ixazomib, we observed increased luminescence for bortezomib and ixazomib, but not for carfilzomib, in a pregnane-X-receptor (PXR) reporter gene assay, which was inconsistent with the mRNA expression levels of the main PXR target gene CYP3A4. ixazomib 138-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 308-314 27695358-2 2016 In our previous investigation, we found a medium correlation between the efficacy and safety of haloperidol and the activity of CYP3A4 in patients with alcohol abuse. Haloperidol 96-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 27233802-5 2016 The terminal half-life in cancer subjects was estimated to be approximately 26 h. Moderate and strong CYP3A inhibitors decreased venetoclax apparent clearance by 19% and 84%, respectively, while weak CYP3A inhibitors and inducers did not affect clearance. venetoclax 129-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 27233802-12 2016 In conclusion, the concomitant administration of moderate and strong CYP3A inhibitors and rituximab as well as food were the main factors impacting venetoclax pharmacokinetics, while patient characteristics had only minimal impact. venetoclax 148-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 27317471-8 2016 Our results suggest that the urinary 6beta-hydroxycortisol/cortisol ratio is the best predictor of hepatic CYP3A activity under both maximal inhibition and maximal induction. 6 beta-hydroxycortisol 37-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-112 27317471-0 2016 Urinary 6beta-Hydroxycortisol/Cortisol Ratio Most Highly Correlates With Midazolam Clearance Under Hepatic CYP3A Inhibition and Induction in Females: A Pharmacometabolomics Approach. 6 beta-hydroxycortisol 8-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-112 27317471-8 2016 Our results suggest that the urinary 6beta-hydroxycortisol/cortisol ratio is the best predictor of hepatic CYP3A activity under both maximal inhibition and maximal induction. Hydrocortisone 50-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-112 27317471-9 2016 Furthermore, the predictive model including 6beta-hydroxycortisol/cortisol as a covariate could be applied to predict the magnitude of CYP3A-mediated drug interactions. 6 beta-hydroxycortisol 44-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-140 27317471-0 2016 Urinary 6beta-Hydroxycortisol/Cortisol Ratio Most Highly Correlates With Midazolam Clearance Under Hepatic CYP3A Inhibition and Induction in Females: A Pharmacometabolomics Approach. Hydrocortisone 30-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-112 27317471-0 2016 Urinary 6beta-Hydroxycortisol/Cortisol Ratio Most Highly Correlates With Midazolam Clearance Under Hepatic CYP3A Inhibition and Induction in Females: A Pharmacometabolomics Approach. Midazolam 73-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-112 27317471-9 2016 Furthermore, the predictive model including 6beta-hydroxycortisol/cortisol as a covariate could be applied to predict the magnitude of CYP3A-mediated drug interactions. Hydrocortisone 57-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-140 27317471-5 2016 A statistical model was generated to predict midazolam clearance using measurements of endogenous metabolites associated with the inhibition and induction of CYP3A. Midazolam 45-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-163 27317471-7 2016 Of the urine and plasma metabolites measured, the 6beta-hydroxycortisol/cortisol ratio was most significantly correlated with midazolam clearance during hepatic CYP3A inhibition and induction. 6 beta-hydroxycortisol 50-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-166 27350147-0 2016 Recommendations on the Development of a Bioanalytical Assay for 4beta-Hydroxycholesterol, an Emerging Endogenous Biomarker of CYP3A Activity. cholest-5-ene-3,4-diol 64-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-131 27317471-7 2016 Of the urine and plasma metabolites measured, the 6beta-hydroxycortisol/cortisol ratio was most significantly correlated with midazolam clearance during hepatic CYP3A inhibition and induction. Hydrocortisone 63-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-166 27350147-1 2016 The availability of reliable assays for measuring 4beta-hydroxycholesterol (4beta-HC), a CYP3A metabolite of cholesterol, is an important step in qualifying this endogenous moiety as a biomarker of CYP3A activity. cholest-5-ene-3,4-diol 50-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-94 27350147-1 2016 The availability of reliable assays for measuring 4beta-hydroxycholesterol (4beta-HC), a CYP3A metabolite of cholesterol, is an important step in qualifying this endogenous moiety as a biomarker of CYP3A activity. cholest-5-ene-3,4-diol 50-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 198-203 27317471-7 2016 Of the urine and plasma metabolites measured, the 6beta-hydroxycortisol/cortisol ratio was most significantly correlated with midazolam clearance during hepatic CYP3A inhibition and induction. Midazolam 126-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-166 27350147-1 2016 The availability of reliable assays for measuring 4beta-hydroxycholesterol (4beta-HC), a CYP3A metabolite of cholesterol, is an important step in qualifying this endogenous moiety as a biomarker of CYP3A activity. cholest-5-ene-3,4-diol 76-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-94 27605198-5 2016 Three commonly used statins-simvastatin, atorvastatin and lovastatin-are metabolised by the liver enzyme CYP3A4. Simvastatin 28-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 27138968-2 2016 Tofacitinib metabolism is primarily mediated by cytochrome P450 3A4. tofacitinib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-67 27605198-5 2016 Three commonly used statins-simvastatin, atorvastatin and lovastatin-are metabolised by the liver enzyme CYP3A4. Atorvastatin 41-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 27605198-5 2016 Three commonly used statins-simvastatin, atorvastatin and lovastatin-are metabolised by the liver enzyme CYP3A4. Lovastatin 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 27350147-1 2016 The availability of reliable assays for measuring 4beta-hydroxycholesterol (4beta-HC), a CYP3A metabolite of cholesterol, is an important step in qualifying this endogenous moiety as a biomarker of CYP3A activity. cholest-5-ene-3,4-diol 76-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 198-203 27350147-1 2016 The availability of reliable assays for measuring 4beta-hydroxycholesterol (4beta-HC), a CYP3A metabolite of cholesterol, is an important step in qualifying this endogenous moiety as a biomarker of CYP3A activity. Cholesterol 63-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-94 27350147-1 2016 The availability of reliable assays for measuring 4beta-hydroxycholesterol (4beta-HC), a CYP3A metabolite of cholesterol, is an important step in qualifying this endogenous moiety as a biomarker of CYP3A activity. Cholesterol 63-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 198-203 27323294-1 2016 Cytochrome P450 (P450) 3A (CYP3A) is an enzyme responsible for the metabolism of therapeutic drugs such as midazolam, nifedipine, testosterone and triazolam. Midazolam 107-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 27323294-1 2016 Cytochrome P450 (P450) 3A (CYP3A) is an enzyme responsible for the metabolism of therapeutic drugs such as midazolam, nifedipine, testosterone and triazolam. Nifedipine 118-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 27323294-1 2016 Cytochrome P450 (P450) 3A (CYP3A) is an enzyme responsible for the metabolism of therapeutic drugs such as midazolam, nifedipine, testosterone and triazolam. Testosterone 130-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 27323294-1 2016 Cytochrome P450 (P450) 3A (CYP3A) is an enzyme responsible for the metabolism of therapeutic drugs such as midazolam, nifedipine, testosterone and triazolam. Triazolam 147-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 27323294-8 2016 It involves the employment of a CYP3A substrate cocktail (including midazolam, testosterone and nifedipine). Testosterone 79-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-37 27323294-9 2016 The concentration of each CYP3A probe substrate in vitro was optimized (0.1 mum for midazolam, 2 mum for testosterone and 2 mum for nifedipine) to minimize mutual drug interactions among probe substrates. Midazolam 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-31 27323294-9 2016 The concentration of each CYP3A probe substrate in vitro was optimized (0.1 mum for midazolam, 2 mum for testosterone and 2 mum for nifedipine) to minimize mutual drug interactions among probe substrates. Testosterone 105-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-31 27323294-9 2016 The concentration of each CYP3A probe substrate in vitro was optimized (0.1 mum for midazolam, 2 mum for testosterone and 2 mum for nifedipine) to minimize mutual drug interactions among probe substrates. Nifedipine 132-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-31 27314545-2 2016 We sought to determine the singular and combined impact of CYP3A4*22 and CYP3A5*3 variants on tacrolimus drug disposition in adult heart transplant recipients. Tacrolimus 94-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 27314545-8 2016 When combined CYP3A genotypes were evaluated, tacrolimus C0 /D was 1.8-fold lower in EMs vs IMs (P<.001) and EMs vs PMs (P=.001). Tacrolimus 46-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 27314545-10 2016 CONCLUSION: Combined CYP3A genotype was associated with tacrolimus drug disposition in adult heart transplant recipients, but the effect was largely driven by CYP3A5*3. Tacrolimus 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-26 27028535-4 2016 It undergoes oxidative metabolism, mainly to norketamine by cytochrome P450 (CYP) 3A and CYP2B6 enzymes. norketamine 45-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-84 27435452-6 2016 This current article assesses the interactions that do or may occur with the DOACs, particularly with respect to the P-gp and CYP3A4 systems. doacs 77-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 27627192-1 2016 The objectives were to estimate and compare, in silico and in vivo, the effects of a strong and a moderate CYP3A4 inhibitor on AZD1305 pharmacokinetics. tert-butyl (2-(7-(2-(4-cyano-2-fluorophenoxy)ethyl)-9-oxa-3,7-diazabicyclo(3.3.1)non3-yl)ethyl)carbamate 127-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 27627192-8 2016 Simcyp predicted the effects of ketoconazole and verapamil on the sensitive CYP3A4 substrate AZD1305 pharmacokinetics well. Ketoconazole 32-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 27627192-8 2016 Simcyp predicted the effects of ketoconazole and verapamil on the sensitive CYP3A4 substrate AZD1305 pharmacokinetics well. Verapamil 49-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 27627192-8 2016 Simcyp predicted the effects of ketoconazole and verapamil on the sensitive CYP3A4 substrate AZD1305 pharmacokinetics well. tert-butyl (2-(7-(2-(4-cyano-2-fluorophenoxy)ethyl)-9-oxa-3,7-diazabicyclo(3.3.1)non3-yl)ethyl)carbamate 93-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 27402728-0 2016 CYP3A Specifically Catalyzes 1beta-Hydroxylation of Deoxycholic Acid: Characterization and Enzymatic Synthesis of a Potential Novel Urinary Biomarker for CYP3A Activity. 1,2-Di(anthracen-9-yl)ethyne 29-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 27402728-0 2016 CYP3A Specifically Catalyzes 1beta-Hydroxylation of Deoxycholic Acid: Characterization and Enzymatic Synthesis of a Potential Novel Urinary Biomarker for CYP3A Activity. 1,2-Di(anthracen-9-yl)ethyne 29-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-159 27402728-0 2016 CYP3A Specifically Catalyzes 1beta-Hydroxylation of Deoxycholic Acid: Characterization and Enzymatic Synthesis of a Potential Novel Urinary Biomarker for CYP3A Activity. Deoxycholic Acid 52-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 27474842-3 2016 The aim of this study is to describe the distribution of CYP2C9*2, CYP2C9*3, CYP3A4*22 and CYP3A5*3 defective alleles, according to losartan tolerance in paediatric Marfan patients. Losartan 132-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 27572875-4 2016 PXR agonists, phthalate and pregnenolone had significant positive effects on cytochrome P450 (CYP) 3A4 expression and PXR-mediated transcription through the CYP3A4 promoter, whereas MDR1 expression and PXR-mediated transcription though the MDR1 promoter were significantly increased in the presence of paclitaxel or cisplatin. phthalic acid 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 27402728-0 2016 CYP3A Specifically Catalyzes 1beta-Hydroxylation of Deoxycholic Acid: Characterization and Enzymatic Synthesis of a Potential Novel Urinary Biomarker for CYP3A Activity. Deoxycholic Acid 52-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-159 27402728-1 2016 The endogenous bile acid metabolite 1beta-hydroxy-deoxycholic acid (1beta-OH-DCA) excreted in human urine may be used as a sensitive CYP3A biomarker in drug development reflecting in vivo CYP3A activity. Bile Acids and Salts 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-138 27402728-1 2016 The endogenous bile acid metabolite 1beta-hydroxy-deoxycholic acid (1beta-OH-DCA) excreted in human urine may be used as a sensitive CYP3A biomarker in drug development reflecting in vivo CYP3A activity. Bile Acids and Salts 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-193 27402728-1 2016 The endogenous bile acid metabolite 1beta-hydroxy-deoxycholic acid (1beta-OH-DCA) excreted in human urine may be used as a sensitive CYP3A biomarker in drug development reflecting in vivo CYP3A activity. 1beta-hydroxy-deoxycholic acid 36-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-138 27402728-1 2016 The endogenous bile acid metabolite 1beta-hydroxy-deoxycholic acid (1beta-OH-DCA) excreted in human urine may be used as a sensitive CYP3A biomarker in drug development reflecting in vivo CYP3A activity. 1beta-hydroxy-deoxycholic acid 36-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-193 27402728-1 2016 The endogenous bile acid metabolite 1beta-hydroxy-deoxycholic acid (1beta-OH-DCA) excreted in human urine may be used as a sensitive CYP3A biomarker in drug development reflecting in vivo CYP3A activity. 1beta-oh-dca 68-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-138 27402728-1 2016 The endogenous bile acid metabolite 1beta-hydroxy-deoxycholic acid (1beta-OH-DCA) excreted in human urine may be used as a sensitive CYP3A biomarker in drug development reflecting in vivo CYP3A activity. 1beta-oh-dca 68-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-193 27402728-5 2016 Its formation was strongly inhibited by CYP3A inhibitor ketoconazole. Ketoconazole 56-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 27402728-7 2016 This indicated that 1beta-hydroxylation of DCA may be a useful marker reaction for CYP3A activity in vitro. 1,2-Di(anthracen-9-yl)ethyne 20-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 27402728-7 2016 This indicated that 1beta-hydroxylation of DCA may be a useful marker reaction for CYP3A activity in vitro. Deoxycholic Acid 43-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 27402728-9 2016 The potential utility of 1beta-hydroxylation of DCA as a urinary CYP3A biomarker was illustrated by comparing the ratio of 1beta-OH-DCA:DCA in a pooled spot urine sample from six healthy control subjects to a sample from one patient treated with carbamazepine, a potent CYP3A inducer; 1beta-OH-DCA:DCA was considerably higher in the patient versus controls (ratio 2.8 vs. 0.4). 1,2-Di(anthracen-9-yl)ethyne 25-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 27402728-9 2016 The potential utility of 1beta-hydroxylation of DCA as a urinary CYP3A biomarker was illustrated by comparing the ratio of 1beta-OH-DCA:DCA in a pooled spot urine sample from six healthy control subjects to a sample from one patient treated with carbamazepine, a potent CYP3A inducer; 1beta-OH-DCA:DCA was considerably higher in the patient versus controls (ratio 2.8 vs. 0.4). 1,2-Di(anthracen-9-yl)ethyne 25-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 270-275 27402728-9 2016 The potential utility of 1beta-hydroxylation of DCA as a urinary CYP3A biomarker was illustrated by comparing the ratio of 1beta-OH-DCA:DCA in a pooled spot urine sample from six healthy control subjects to a sample from one patient treated with carbamazepine, a potent CYP3A inducer; 1beta-OH-DCA:DCA was considerably higher in the patient versus controls (ratio 2.8 vs. 0.4). Deoxycholic Acid 48-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 27402728-9 2016 The potential utility of 1beta-hydroxylation of DCA as a urinary CYP3A biomarker was illustrated by comparing the ratio of 1beta-OH-DCA:DCA in a pooled spot urine sample from six healthy control subjects to a sample from one patient treated with carbamazepine, a potent CYP3A inducer; 1beta-OH-DCA:DCA was considerably higher in the patient versus controls (ratio 2.8 vs. 0.4). Deoxycholic Acid 48-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 270-275 27402728-9 2016 The potential utility of 1beta-hydroxylation of DCA as a urinary CYP3A biomarker was illustrated by comparing the ratio of 1beta-OH-DCA:DCA in a pooled spot urine sample from six healthy control subjects to a sample from one patient treated with carbamazepine, a potent CYP3A inducer; 1beta-OH-DCA:DCA was considerably higher in the patient versus controls (ratio 2.8 vs. 0.4). 1beta-oh-dca 123-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 27402728-9 2016 The potential utility of 1beta-hydroxylation of DCA as a urinary CYP3A biomarker was illustrated by comparing the ratio of 1beta-OH-DCA:DCA in a pooled spot urine sample from six healthy control subjects to a sample from one patient treated with carbamazepine, a potent CYP3A inducer; 1beta-OH-DCA:DCA was considerably higher in the patient versus controls (ratio 2.8 vs. 0.4). Deoxycholic Acid 132-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 27402728-9 2016 The potential utility of 1beta-hydroxylation of DCA as a urinary CYP3A biomarker was illustrated by comparing the ratio of 1beta-OH-DCA:DCA in a pooled spot urine sample from six healthy control subjects to a sample from one patient treated with carbamazepine, a potent CYP3A inducer; 1beta-OH-DCA:DCA was considerably higher in the patient versus controls (ratio 2.8 vs. 0.4). Carbamazepine 246-259 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 27402728-9 2016 The potential utility of 1beta-hydroxylation of DCA as a urinary CYP3A biomarker was illustrated by comparing the ratio of 1beta-OH-DCA:DCA in a pooled spot urine sample from six healthy control subjects to a sample from one patient treated with carbamazepine, a potent CYP3A inducer; 1beta-OH-DCA:DCA was considerably higher in the patient versus controls (ratio 2.8 vs. 0.4). 1beta-oh-dca 285-297 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 27402728-9 2016 The potential utility of 1beta-hydroxylation of DCA as a urinary CYP3A biomarker was illustrated by comparing the ratio of 1beta-OH-DCA:DCA in a pooled spot urine sample from six healthy control subjects to a sample from one patient treated with carbamazepine, a potent CYP3A inducer; 1beta-OH-DCA:DCA was considerably higher in the patient versus controls (ratio 2.8 vs. 0.4). Deoxycholic Acid 132-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 27402728-10 2016 Our results highlight the potential of 1beta-OH-DCA as a urinary biomarker in clinical CYP3A DDI studies. 1beta-oh-dca 39-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 26724677-8 2016 Furthermore, catalytic activities of cytochrome P450 3A4 were modified by omeprazole and rifampicin in the 3D-cultured HepaRG spheroids. Omeprazole 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-56 26724677-8 2016 Furthermore, catalytic activities of cytochrome P450 3A4 were modified by omeprazole and rifampicin in the 3D-cultured HepaRG spheroids. Rifampin 89-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-56 27572875-4 2016 PXR agonists, phthalate and pregnenolone had significant positive effects on cytochrome P450 (CYP) 3A4 expression and PXR-mediated transcription through the CYP3A4 promoter, whereas MDR1 expression and PXR-mediated transcription though the MDR1 promoter were significantly increased in the presence of paclitaxel or cisplatin. Pregnenolone 28-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 27572875-4 2016 PXR agonists, phthalate and pregnenolone had significant positive effects on cytochrome P450 (CYP) 3A4 expression and PXR-mediated transcription through the CYP3A4 promoter, whereas MDR1 expression and PXR-mediated transcription though the MDR1 promoter were significantly increased in the presence of paclitaxel or cisplatin. Paclitaxel 302-312 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 27572875-4 2016 PXR agonists, phthalate and pregnenolone had significant positive effects on cytochrome P450 (CYP) 3A4 expression and PXR-mediated transcription through the CYP3A4 promoter, whereas MDR1 expression and PXR-mediated transcription though the MDR1 promoter were significantly increased in the presence of paclitaxel or cisplatin. Cisplatin 316-325 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 29767595-2 2016 Our results draw attention to the impact of CYP3A4*1B on the clinical effect of clopidogrel during dual antiplatelet therapy after PCI. Clopidogrel 80-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 27582887-10 2016 Naloxegol is metabolised through CYP3A4 to six metabolites, with the majority of the dose (68%) excreted with faeces and less (16%) with urine. naloxegol 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 27556885-0 2016 Plasma miR-142 accounting for the missing heritability of CYP3A4/5 functionality is associated with pharmacokinetics of clopidogrel. Clopidogrel 120-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 27556885-1 2016 AIM: To investigate whether plasma miRNAs targeting CYP3A4/5 have an impact on the variance of pharmacokinetics of clopidogrel. Clopidogrel 115-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 27556885-3 2016 The association between plasma miRNAs targeting CYP3A4/5 mRNA and clopidogrel pharmacokinetics was analyzed in 31 patients with coronary heart disease who received 300 mg loading dose of clopidogrel. Clopidogrel 66-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 27556885-6 2016 CONCLUSION: miR-142 could account for a part of missing heritability of CYP3A4/5 functionality related to clopidogrel activation. Clopidogrel 106-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 26711482-2 2016 Auto-induction potentials of oxcarbazepine, its pharmacologically active metabolite 10-hydroxyoxcarbazepine and carbamazepine were evaluated by cytochrome P450 (CYP) 1A2, CYP2B6 and CYP3A4 mRNA levels and primary metabolic rates using human hepatocytes and HepaRG cells. Oxcarbazepine 29-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 182-188 26711482-5 2016 The fold change for CYP3A4 induction level by oxcarbazepine, 10-hydroxyoxcarbazepine and carbamazepine was 3.5 (1.2-7.4), 2.7 (0.8-5.7) and 8.3 (3.5-14.5), respectively. Oxcarbazepine 46-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 26711482-5 2016 The fold change for CYP3A4 induction level by oxcarbazepine, 10-hydroxyoxcarbazepine and carbamazepine was 3.5 (1.2-7.4), 2.7 (0.8-5.7) and 8.3 (3.5-14.5), respectively. 10-hydroxyoxcarbazepine 61-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 26711482-5 2016 The fold change for CYP3A4 induction level by oxcarbazepine, 10-hydroxyoxcarbazepine and carbamazepine was 3.5 (1.2-7.4), 2.7 (0.8-5.7) and 8.3 (3.5-14.5), respectively. Carbamazepine 89-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 27574448-0 2016 Polymorphism of CYP3A4 and ABCB1 genes increase the risk of neuropathy in breast cancer patients treated with paclitaxel and docetaxel. Paclitaxel 110-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 27561272-2 2016 Here we describe the preclinical and clinical results of a translational drug development effort to create a next-generation nitric oxide donor with improved pharmacokinetic properties and a unique mechanism of nitric oxide release through CYP3A4 metabolism that was designed to circumvent the development of tolerance. Nitric Oxide 125-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 240-246 27561272-2 2016 Here we describe the preclinical and clinical results of a translational drug development effort to create a next-generation nitric oxide donor with improved pharmacokinetic properties and a unique mechanism of nitric oxide release through CYP3A4 metabolism that was designed to circumvent the development of tolerance. Nitric Oxide 211-223 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 240-246 27563870-4 2016 Moreover, ticagrelor is a cytochrome P450 3A4 substrate/inhibitor and, therefore, caution should be exercised when it is used concomitantly with strong CYP3A4 inducers/inhibitors. Ticagrelor 10-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 27519420-10 2016 The pharmacological interaction between vinflunine and cyclosporine, both metabolized by CYP 3A4, may explain the excellent result and the concomitant severe toxicity. vinflunine 40-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-96 27519420-10 2016 The pharmacological interaction between vinflunine and cyclosporine, both metabolized by CYP 3A4, may explain the excellent result and the concomitant severe toxicity. Cyclosporine 55-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-96 29924509-5 2016 Genetic polymorphisms of CYP2D6 and CYP3A4 will influence the plasma concentrations of active TAM metabolites and clinical outcomes for breast cancer patients treated with TAM. Tamoxifen 94-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 29924509-5 2016 Genetic polymorphisms of CYP2D6 and CYP3A4 will influence the plasma concentrations of active TAM metabolites and clinical outcomes for breast cancer patients treated with TAM. Tamoxifen 172-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 27561272-7 2016 However, despite a unique mechanism of nitric oxide release mediated by CYP3A4 metabolism, tolerance developed over 28 days, suggesting that tolerance to nitric oxide donors is multifactorial and cannot be overcome solely through altered in vivo release of nitric oxide. Nitric Oxide 39-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 27530542-1 2016 Many dietary compounds, including resveratrol, are potent inhibitors of CYP3A4. Resveratrol 34-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 27530542-3 2016 Mono, di, and tri-acetoxy resveratrol were synthesized, a cell line of human intestine origin and microsomes from rat liver served to determine their in vitro inhibition of CYP3A4, and compared to that of resveratrol. mono, di, and tri-acetoxy resveratrol 0-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 27530542-8 2016 The simulation demonstrated exclusion of all interactions between tri-acetoxy resveratrol and the heme due to distal binding, highlighting the complexity of the CYP3A4 binding site, which may allow simultaneous accommodation of two molecules. tri-acetoxy resveratrol 66-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 27530542-8 2016 The simulation demonstrated exclusion of all interactions between tri-acetoxy resveratrol and the heme due to distal binding, highlighting the complexity of the CYP3A4 binding site, which may allow simultaneous accommodation of two molecules. Heme 98-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 27574448-0 2016 Polymorphism of CYP3A4 and ABCB1 genes increase the risk of neuropathy in breast cancer patients treated with paclitaxel and docetaxel. Docetaxel 125-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 27208383-0 2016 Establishment of In Silico Prediction Models for CYP3A4 and CYP2B6 Induction in Human Hepatocytes by Multiple Regression Analysis Using Azole Compounds. Azoles 136-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 27441453-6 2016 Using menadione as the redox-cycling chemical, we discovered that this enzymatic reaction blocks metabolic activation of parathion in rat and human liver microsomes and in recombinant CYPs important to parathion metabolism, including CYP1A2, CYP2B6, and CYP3A4. Vitamin K 3 6-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 254-260 27441453-6 2016 Using menadione as the redox-cycling chemical, we discovered that this enzymatic reaction blocks metabolic activation of parathion in rat and human liver microsomes and in recombinant CYPs important to parathion metabolism, including CYP1A2, CYP2B6, and CYP3A4. Parathion 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 254-260 27501453-6 2016 CYP3A-dependent sirolimus metabolite formation changed in a similar fashion. Sirolimus 16-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 27179126-12 2016 Cytochrome P450 profiling indicated that dasabuvir was mainly metabolized by CYP2C8, followed by CYP3A4. dasabuvir 41-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 26626330-10 2016 Both compounds induced several drug metabolizing genes (including CYP2B6, CYP3A4 and UGT1A1), mediated by CAR activation in Nevirapine and PXR in Ritonavir. Nevirapine 124-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 26626330-10 2016 Both compounds induced several drug metabolizing genes (including CYP2B6, CYP3A4 and UGT1A1), mediated by CAR activation in Nevirapine and PXR in Ritonavir. Ritonavir 146-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 26360322-6 2016 Incubations of UR-144 and XLR-11 with recombinant CYP enzymes revealed that UR-144 and XLR-11 are extensively metabolized by CYP3A4 at the tetramethylcyclopropyl (TMCP) moiety, but also CYP1A2 and CYP2C19 showed activity. Urea 15-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 26360322-6 2016 Incubations of UR-144 and XLR-11 with recombinant CYP enzymes revealed that UR-144 and XLR-11 are extensively metabolized by CYP3A4 at the tetramethylcyclopropyl (TMCP) moiety, but also CYP1A2 and CYP2C19 showed activity. Urea 76-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 26360322-6 2016 Incubations of UR-144 and XLR-11 with recombinant CYP enzymes revealed that UR-144 and XLR-11 are extensively metabolized by CYP3A4 at the tetramethylcyclopropyl (TMCP) moiety, but also CYP1A2 and CYP2C19 showed activity. tmcp 163-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 26360322-7 2016 Inhibition of CYP3A4 in HLM attenuated the metabolism of UR-144 and XLR-11, while inhibition of the other CYP enzymes in HLM had only minor effects. Urea 57-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 27197997-6 2016 Activation of CAR and PXR in cells treated with a high dose of CITCO [6-(4-chlorophenyl)-imidazo(2,1-b)thiazole-5-carbaldehyde] or cotreated with rifampicin and tetracycline resulted in synergistic enhancement of CYP3A4, but not CYP2B6, CYP2C9, or UGT1A1, mRNA expression in HepTR/hCAR/hPXR cells. 6-(4-chlorophenyl)imidazo(2,1-b)(1,3)thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime 63-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 213-219 27208383-3 2016 In this study, we have established regression models for CYP3A4 and CYP2B6 induction in human hepatocytes using several physicochemical parameters for a set of azole compounds with different P450 induction as characteristics as model compounds. Azoles 160-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 26360322-8 2016 Thus, CYP3A4 is the major contributor to the CYP mediated metabolism of UR-144 and XLR-11 with minor contributions from CYP1A2. Urea 72-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 27197997-6 2016 Activation of CAR and PXR in cells treated with a high dose of CITCO [6-(4-chlorophenyl)-imidazo(2,1-b)thiazole-5-carbaldehyde] or cotreated with rifampicin and tetracycline resulted in synergistic enhancement of CYP3A4, but not CYP2B6, CYP2C9, or UGT1A1, mRNA expression in HepTR/hCAR/hPXR cells. 6-(4-chlorophenyl)-imidazo(2,1-b)thiazole 70-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 213-219 26360322-9 2016 Users of UR-144 and XLR-11 are thus subject to the influence of potential drug-drug interactions, if they are concomitantly medicated with CYP3A4 inducers (e.g. some antiepileptics) or inhibitors (e.g. some antifungal drugs). (1-pentyl-1H-indol-3-yl)(2,2,3,3-tetramethylcyclopropyl)methanone 9-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 27208383-4 2016 To obtain a well-correlated regression model, the compounds for CYP3A4 or CYP2B6 induction were independently selected from the tested azole compounds using principal component analysis with fold-induction data. Azoles 135-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 27226351-4 2016 Osimertinib, AZ5104, and AZ7550 were predominantly metabolized by CYP3A. osimertinib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 27208383-7 2016 The fold-induction of the validation compounds, another set of 12 azole-containing compounds, were predicted within twofold limits for both CYP3A4 and CYP2B6. Azoles 66-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 27226351-4 2016 Osimertinib, AZ5104, and AZ7550 were predominantly metabolized by CYP3A. Ro 21-5104 13-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 25737032-4 2016 Pazopanib can be well docked into the activity cavity of CYP3A4, and the interaction structure in pazopanib was methyl group located besides nitrogen in the five-membered ring. pazopanib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 27226351-4 2016 Osimertinib, AZ5104, and AZ7550 were predominantly metabolized by CYP3A. AZ7550 25-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 27298338-0 2016 VX-509 (Decernotinib)-Mediated CYP3A Time-Dependent Inhibition: An Aldehyde Oxidase Metabolite as a Perpetrator of Drug-Drug Interactions. 2-((2-(1H-pyrrolo(2,3-b)pyridin-3-yl)pyrimidin-4-yl)amino)-2-methyl-N-(2,2,2-trifluoroethyl)butanamide 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-36 27298338-0 2016 VX-509 (Decernotinib)-Mediated CYP3A Time-Dependent Inhibition: An Aldehyde Oxidase Metabolite as a Perpetrator of Drug-Drug Interactions. 2-((2-(1H-pyrrolo(2,3-b)pyridin-3-yl)pyrimidin-4-yl)amino)-2-methyl-N-(2,2,2-trifluoroethyl)butanamide 8-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-36 25737032-7 2016 Furthermore, both pazopanib and ketoconazole were docked into the activity cavity of CYP3A4 to compare their binding potential. Ketoconazole 32-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 25737032-8 2016 The distance between ketoconazole and activity center (2.10 A) is closer than the distance between pazopanib and activity center of CYP3A4, indicating the easy influence of CYP3A4 inhibitor toward the metabolism of pazopanib. Ketoconazole 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 27278961-4 2016 The exception was C-7, a hydroxylated metabolite, largely formed by CYP2B6 and CYP3A4/5. Carbon 18-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 25737032-4 2016 Pazopanib can be well docked into the activity cavity of CYP3A4, and the interaction structure in pazopanib was methyl group located besides nitrogen in the five-membered ring. pazopanib 98-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 25737032-8 2016 The distance between ketoconazole and activity center (2.10 A) is closer than the distance between pazopanib and activity center of CYP3A4, indicating the easy influence of CYP3A4 inhibitor toward the metabolism of pazopanib. pazopanib 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 25737032-4 2016 Pazopanib can be well docked into the activity cavity of CYP3A4, and the interaction structure in pazopanib was methyl group located besides nitrogen in the five-membered ring. Nitrogen 141-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 25737032-8 2016 The distance between ketoconazole and activity center (2.10 A) is closer than the distance between pazopanib and activity center of CYP3A4, indicating the easy influence of CYP3A4 inhibitor toward the metabolism of pazopanib. pazopanib 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 25737032-8 2016 The distance between ketoconazole and activity center (2.10 A) is closer than the distance between pazopanib and activity center of CYP3A4, indicating the easy influence of CYP3A4 inhibitor toward the metabolism of pazopanib. pazopanib 215-224 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 25737032-7 2016 Furthermore, both pazopanib and ketoconazole were docked into the activity cavity of CYP3A4 to compare their binding potential. pazopanib 18-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 25737032-8 2016 The distance between ketoconazole and activity center (2.10 A) is closer than the distance between pazopanib and activity center of CYP3A4, indicating the easy influence of CYP3A4 inhibitor toward the metabolism of pazopanib. pazopanib 215-224 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 27141088-4 2016 In vitro, the NNRTI rilpivirine is both a pregnane X receptor agonist and cytochrome P450 (CYP) 3A inhibitor. Rilpivirine 20-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-98 27191770-8 2016 DISCUSSION: Because suvorexant is metabolized by CYP3A4, next-day somnolence could have occurred as a result of increased plasma suvorexant concentration due to CYP3A4 inhibition by diltiazem. suvorexant 20-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 27191770-8 2016 DISCUSSION: Because suvorexant is metabolized by CYP3A4, next-day somnolence could have occurred as a result of increased plasma suvorexant concentration due to CYP3A4 inhibition by diltiazem. suvorexant 20-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 27191770-8 2016 DISCUSSION: Because suvorexant is metabolized by CYP3A4, next-day somnolence could have occurred as a result of increased plasma suvorexant concentration due to CYP3A4 inhibition by diltiazem. suvorexant 129-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 27191770-8 2016 DISCUSSION: Because suvorexant is metabolized by CYP3A4, next-day somnolence could have occurred as a result of increased plasma suvorexant concentration due to CYP3A4 inhibition by diltiazem. Diltiazem 182-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 27141088-5 2016 Clinical data concerning the potential effects of rilpivirine coadministration on the pharmacokinetics of the CYP3A substrate tadalafil are lacking. Rilpivirine 50-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-115 27251417-10 2016 CONCLUSIONS AND LIMITATIONS: Our data show a potential pharmacokinetic interaction, most likely via CYP3A4 between amlodipine and RIS, reflected in significantly different C/Ds for RIS, 9-OH-RIS and AM. Amlodipine 115-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 26678015-0 2016 Effects of CYP3A Modulators on the Pharmacokinetics of Naloxegol. naloxegol 55-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-16 26678015-2 2016 This study evaluated the effects of CYP3A inhibition and induction on the pharmacokinetics, safety, and tolerability of naloxegol. naloxegol 120-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 26678015-5 2016 Naloxegol was generally safe and well tolerated when given alone or coadministered with the respective CYP3A modulators; 1 subject discontinued because of elevations in liver enzymes attributed to rifampin. naloxegol 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 26678015-6 2016 The exposure of naloxegol was affected substantially by ketoconazole, diltiazem, and rifampin, suggesting that it is a sensitive in vivo substrate of CYP3A4. naloxegol 16-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 26678015-6 2016 The exposure of naloxegol was affected substantially by ketoconazole, diltiazem, and rifampin, suggesting that it is a sensitive in vivo substrate of CYP3A4. Rifampin 85-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 27251417-10 2016 CONCLUSIONS AND LIMITATIONS: Our data show a potential pharmacokinetic interaction, most likely via CYP3A4 between amlodipine and RIS, reflected in significantly different C/Ds for RIS, 9-OH-RIS and AM. Risperidone 130-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 27469576-3 2016 Haloperidol is mainly metabolized by Phase I CYP2D6 and to the lesser extent by CYP3A4 and by Phase II UGT2B7 enzymes. Haloperidol 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 26968126-3 2016 Cellular CYP3A4 activity was significantly enhanced when 20% HAp macroporous carrier was used, reaching 1.49+-0.28 pmol/10(6) cells/min of benzyloxyresorufin-O-dealkylation activity, which is comparable to that of primary human hepatocytes from livers of adult donors. benzyloxyresorufin-o 139-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 27559961-6 2016 TB co-infection, low Karnofsky score, high viral load, and high CYP3A activity as measured by plasma 4beta-hydroxycholesterol/cholesterol ratios were significant predictors of low 25 (OH)D3 levels at baseline. 4beta 101-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 27559961-6 2016 TB co-infection, low Karnofsky score, high viral load, and high CYP3A activity as measured by plasma 4beta-hydroxycholesterol/cholesterol ratios were significant predictors of low 25 (OH)D3 levels at baseline. Hydroxycholesterols 107-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 27559961-6 2016 TB co-infection, low Karnofsky score, high viral load, and high CYP3A activity as measured by plasma 4beta-hydroxycholesterol/cholesterol ratios were significant predictors of low 25 (OH)D3 levels at baseline. Cholesterol 114-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 27110874-3 2016 The present work aimed to identify the mechanism of the observed C-1311-mediated inactivation of CYP1A2 and CYP3A4. C 1311 65-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 27110874-5 2016 CYP isoenzyme activities were determined using the CYP-specific reactions, 7-ethoxycoumarin O-deethylation (CYP1A2) and testosterone 6beta-hydroxylation (CYP3A4). Testosterone 120-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 27110874-11 2016 CONCLUSIONS: Our results indicated that C-1311 is a potent mechanism-based inactivator of CYP1A2 and CYP3A4. C 1311 40-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 27469576-5 2016 Of the CYPs, haloperidol is metabolized by CYP2D6 and CYP3A4 primarily. Haloperidol 13-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 27469576-6 2016 It was the introduction of ciprofloxacin which was a trigger for the development of adverse drug reaction due to inhibition of CYP3A4, which was in presented patient main metabolic pathway for haloperidol since he was CYP2D6 poor metabolizer. Ciprofloxacin 27-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 27469576-6 2016 It was the introduction of ciprofloxacin which was a trigger for the development of adverse drug reaction due to inhibition of CYP3A4, which was in presented patient main metabolic pathway for haloperidol since he was CYP2D6 poor metabolizer. Haloperidol 193-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 27133299-3 2016 The goal of this study was to investigate the associations of polymorphisms of CYP3A4, NR1I2, CYP2C19 and P2RY12 genes with CR in Chinese patients with ischemic stroke. Chromium 124-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 27161631-5 2016 Furthermore, VT-1129 weakly inhibited human CYP2C9, CYP2C19, and CYP3A4, suggesting a low drug-drug interaction potential. VT-1129 13-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 27133299-0 2016 Associations of CYP3A4, NR1I2, CYP2C19 and P2RY12 polymorphisms with clopidogrel resistance in Chinese patients with ischemic stroke. Clopidogrel 69-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 26796541-3 2016 OBJECTIVES: To prospectively study the relationship between inflammation, organ failure, and midazolam clearance as a validated marker of CYP3A-mediated drug metabolism in critically ill children. Midazolam 93-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-143 26796541-9 2016 CONCLUSIONS: Inflammation and organ failure strongly reduce midazolam clearance, a surrogate marker of CYP3A-mediated drug metabolism, in critically ill children. Midazolam 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 27261575-9 2016 Our data demonstrate that HP or AR treatment in light or dark PDT conditions had an inhibitory effect on the activity of individual membrane transport proteins and significantly decreased CYP3A4 activity in HT-29 cells. hyperforin 26-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-194 26302866-2 2016 Our early work demonstrated that tetrandrine produced acute pulmonary toxicity and that tetrandrine was biotransformed to a quinone methide-derived metabolite mediated by CYP3A enzymes. tetrandrine 88-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-176 26302866-2 2016 Our early work demonstrated that tetrandrine produced acute pulmonary toxicity and that tetrandrine was biotransformed to a quinone methide-derived metabolite mediated by CYP3A enzymes. quinone methide 124-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-176 27261575-0 2016 Drug membrane transporters and CYP3A4 are affected by hypericin, hyperforin or aristoforin in colon adenocarcinoma cells. hypericin 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 27261575-0 2016 Drug membrane transporters and CYP3A4 are affected by hypericin, hyperforin or aristoforin in colon adenocarcinoma cells. hyperforin 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 27261575-0 2016 Drug membrane transporters and CYP3A4 are affected by hypericin, hyperforin or aristoforin in colon adenocarcinoma cells. Aristoforin 79-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 27138133-0 2016 Compelling Relationship of CYP3A Induction to Levels of the Putative Biomarker 4beta-Hydroxycholesterol and Changes in Midazolam Exposure. cholest-5-ene-3,4-diol 79-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 27138133-0 2016 Compelling Relationship of CYP3A Induction to Levels of the Putative Biomarker 4beta-Hydroxycholesterol and Changes in Midazolam Exposure. Midazolam 119-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 26772622-0 2016 Dynamics of Cytosine Methylation in the Proximal Promoters of CYP3A4 and CYP3A7 in Pediatric and Prenatal Livers. Cytosine 12-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 26772622-4 2016 The objective of this study was to investigate changes in cytosine methylation of the CYP3A4 and CYP3A7 genes in human pediatric and prenatal livers. Cytosine 58-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 26772622-8 2016 In contrast, a cytosine 383 base pair upstream of CYP3A4 is hypermethylated in liver samples from neonates compared with adolescents (P = 0.00001). Cytosine 15-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 26772622-9 2016 Developmental changes in methylation of cytosines in the proximal promoters of CYP3A4 and CYP3A7 in pediatric livers were confirmed by bisulfite sequencing. Cytosine 40-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 26772622-9 2016 Developmental changes in methylation of cytosines in the proximal promoters of CYP3A4 and CYP3A7 in pediatric livers were confirmed by bisulfite sequencing. hydrogen sulfite 135-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 26772622-10 2016 In addition, the methylation status of cytosine in the CYP3A4 and CYP3A7 proximal promoters correlated with changes in developmental expression of mRNA for the two enzymes. Cytosine 39-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 27037683-6 2016 The CYP3A4 midazolam metabolism was maintained in biochips after 13 days of culture, whereas it was almost undetectable in Petri dishes. Midazolam 11-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 27052878-7 2016 CYP2E1 and CYP3A contributed to 4-OH-ATX formation in livers with CYP2D6 intermediate and poor metabolizer status. 4-oh-atx 32-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-16 27261575-9 2016 Our data demonstrate that HP or AR treatment in light or dark PDT conditions had an inhibitory effect on the activity of individual membrane transport proteins and significantly decreased CYP3A4 activity in HT-29 cells. Aristoforin 32-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-194 27261575-11 2016 These results suggest that HY, HP and AR might affect the efficiency of anti-cancer drugs, through interaction with membrane transporters and CYP3A4. hyperforin 31-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 27261575-11 2016 These results suggest that HY, HP and AR might affect the efficiency of anti-cancer drugs, through interaction with membrane transporters and CYP3A4. Aristoforin 38-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 27216294-7 2016 CONCLUSION: A short-term hypercaloric high fat diet increases exposure to midazolam and omeprazole, possibly reflecting modulation of CYP3A4 and CYP2C19. Midazolam 74-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 27313275-3 2016 Bosentan is mainly metabolized by cytochrome P450 (CYP) 3A4 and 2C9 enzymes with the involvement of multiple transporters that control its hepatic uptake and biliary excretion. Bosentan 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-67 27313275-5 2016 While bosentan exhibits high protein binding restricting the drug from extensive distribution and significant urinary excretion, bosentan induces its own metabolism by an increased expression of CYP3A4 on repeated dosing. Bosentan 129-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 27045668-3 2016 Bosentan is mainly metabolized by cytochrome P450 (CYP) 3A4 and 2C9 enzymes with the involvement of multiple transporters that control its hepatic uptake and biliary excretion. Bosentan 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-67 27045668-5 2016 While bosentan exhibits high protein binding restricting the drug from extensive distribution and significant urinary excretion, bosentan induces its own metabolism by an increased expression of CYP3A4 on repeated dosing. Bosentan 129-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 26918544-3 2016 Rilpivirine is metabolized by CYP3A4. Rilpivirine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 27216294-7 2016 CONCLUSION: A short-term hypercaloric high fat diet increases exposure to midazolam and omeprazole, possibly reflecting modulation of CYP3A4 and CYP2C19. Omeprazole 88-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 29736470-7 2016 We speculate a significant interference on adverse events (mainly atrial fibrillation and consequently acute coronary syndromes) and on the outcome of unfavorable interactions between ivabradine and diltiazem, verapamil and strong inhibitors of CYP3A4 (4.6% of the total population). Ivabradine 184-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 245-251 27126611-2 2016 Herein we describe a spectroscopic investigation of the interaction of CYP3A4 with N-methylritonavir, an analog of ritonavir, widely used as a pharmacoenhancer. n-methylritonavir 83-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 27126611-2 2016 Herein we describe a spectroscopic investigation of the interaction of CYP3A4 with N-methylritonavir, an analog of ritonavir, widely used as a pharmacoenhancer. Ritonavir 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 27126611-3 2016 In contrast to ritonavir, the binding affinity of N-methylritonavir for CYP3A4 is pH-dependent. n-methylritonavir 50-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 27126611-8 2016 This mechanism is supported by time-dependent density functional theory with an active site model that accurately reproduces distinguishing features of the experimental UV-visible spectra of N-methylritonavir bound to CYP3A4. n-methylritonavir 191-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 218-224 27130197-6 2016 However, the two-step bioactivation to DF-2,5-QI appears to be catalyzed with highest activity by two different CYPs: 5-hydroxylation of DF is predominantly catalyzed by CYP3A4, whereas its subsequent bioactivation to DF-2,5-QI is catalyzed with 14-fold higher intrinsic clearance by CYP2C9. df-2,5-qi 39-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 27130197-6 2016 However, the two-step bioactivation to DF-2,5-QI appears to be catalyzed with highest activity by two different CYPs: 5-hydroxylation of DF is predominantly catalyzed by CYP3A4, whereas its subsequent bioactivation to DF-2,5-QI is catalyzed with 14-fold higher intrinsic clearance by CYP2C9. df-2,5-qi 218-227 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 27113703-0 2016 The role of CYP 3A4 and 1A1 in amiodarone-induced hepatocellular toxicity. Amiodarone 31-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-27 27113703-3 2016 Significantly higher cytotoxicity of amiodarone was observed in HepG2 cells overexpressing CYP3A4 or CYP1A1, compared with that observed in empty vector transduced control cells. Amiodarone 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 27113703-4 2016 Further, higher levels of the more potent hepatotoxic metabolite desethylamiodarone were detected in CYP3A4 or CYP1A1 expressed cells. desethylamiodarone 65-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 27113703-5 2016 The CYP3A4 inhibitor ketoconazole and the CYP1A1 inhibitor alpha-naphthoflavone drastically inhibited the metabolism of amiodarone to desethylamiodarone. Ketoconazole 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 27113703-5 2016 The CYP3A4 inhibitor ketoconazole and the CYP1A1 inhibitor alpha-naphthoflavone drastically inhibited the metabolism of amiodarone to desethylamiodarone. Amiodarone 120-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 27113703-5 2016 The CYP3A4 inhibitor ketoconazole and the CYP1A1 inhibitor alpha-naphthoflavone drastically inhibited the metabolism of amiodarone to desethylamiodarone. desethylamiodarone 134-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 27113703-6 2016 Along with the inhibition of CYP1A1 or CYP3A4, the cytotoxicity of amiodarone was significantly reduced. Amiodarone 67-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 27113703-7 2016 These data indicate that the metabolism of amiodarone to desethylamiodarone by CYP1A1 or CYP3A4 plays an important role in the hepatocellular toxicity of amiodarone. Amiodarone 43-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 27113703-7 2016 These data indicate that the metabolism of amiodarone to desethylamiodarone by CYP1A1 or CYP3A4 plays an important role in the hepatocellular toxicity of amiodarone. desethylamiodarone 57-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 27113703-7 2016 These data indicate that the metabolism of amiodarone to desethylamiodarone by CYP1A1 or CYP3A4 plays an important role in the hepatocellular toxicity of amiodarone. Amiodarone 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 27311637-5 2016 Moreover, berberine inhibits expressions of CAR and its target genes CYP2B6 and CYP3A4. Berberine 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 27514549-0 2016 [Toxic effect of trichloroethylene on liver cells with CYP3A4 gene defect]. Trichloroethylene 17-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 27514549-1 2016 OBJECTIVE: To investigate the toxic effect of trichloroethylene on liver cells with CYP3A4 gene defect. Trichloroethylene 46-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 27514549-2 2016 METHODS: The normal human liver cells (L02 cells) and liver cells with CYP3A4 gene defect were exposed to trichloroethylene at different doses (0.0, 0.4, 0.8, 1.6, 3.2, and 6.4 mmol/L). Trichloroethylene 106-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 27514549-4 2016 RESULTS: After being exposed to trichloroethylene at doses of 1.6, 3.2, and 6.4 mmol/L, the liver cells with CYP3A4 gene defect showed significantly higher cell viability than L02 cells (0.91+-0.06/0.89+-0.05/0.85+-0.07 vs 0.80+-0.04/0.73+-0.06/0.67+-0.07, P<0.05). Trichloroethylene 32-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 27329697-5 2016 In humans, plumbagin was not only a mixed inhibitor of CYP2B6, CYP2C9, CYP2D6, CYP2E1 and CYP3A4, but also a non-competitive inhibitor of CYP1A2, with Ki values no more than 2.16 muM. plumbagin 11-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 27514549-7 2016 CONCLUSION: Trichloroethylene exposure has a less effect on the expression of apoptosis genes and oncogenes in liver cells with CYP3A4 gene defect than in normal human liver cells, suggesting that CYP3A4 gene defect reduces the inductive effect of trichloroethylene on apoptosis genes and oncogenes. Trichloroethylene 12-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 27514549-7 2016 CONCLUSION: Trichloroethylene exposure has a less effect on the expression of apoptosis genes and oncogenes in liver cells with CYP3A4 gene defect than in normal human liver cells, suggesting that CYP3A4 gene defect reduces the inductive effect of trichloroethylene on apoptosis genes and oncogenes. Trichloroethylene 12-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 27514549-7 2016 CONCLUSION: Trichloroethylene exposure has a less effect on the expression of apoptosis genes and oncogenes in liver cells with CYP3A4 gene defect than in normal human liver cells, suggesting that CYP3A4 gene defect reduces the inductive effect of trichloroethylene on apoptosis genes and oncogenes. Trichloroethylene 248-265 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 27514549-7 2016 CONCLUSION: Trichloroethylene exposure has a less effect on the expression of apoptosis genes and oncogenes in liver cells with CYP3A4 gene defect than in normal human liver cells, suggesting that CYP3A4 gene defect reduces the inductive effect of trichloroethylene on apoptosis genes and oncogenes. Trichloroethylene 248-265 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 27311637-6 2016 Furthermore, berberine enhances DNA methylation level in whole genome but reduces that in promoter regions CpG sites of CYP2B6 and CYP3A4 genes under the presence of CAR condition. Berberine 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 27177772-9 2016 Expression of SXR target genes (tsukushi, matrilin-2, and CYP3A4) and SXR response element-luciferase activity were increased by bisphenol A treatment in normal osteoblasts transfected with SXR (hFOB/SXR) and in osteoblast-like cells (MG-63). bisphenol A 129-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 27107807-0 2016 In vitro effects of the citrus flavonoids diosmin, naringenin and naringin on the hepatic drug-metabolizing CYP3A enzyme in human, pig, mouse and fish. Flavonoids 31-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 27107807-0 2016 In vitro effects of the citrus flavonoids diosmin, naringenin and naringin on the hepatic drug-metabolizing CYP3A enzyme in human, pig, mouse and fish. Diosmin 42-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 27107807-0 2016 In vitro effects of the citrus flavonoids diosmin, naringenin and naringin on the hepatic drug-metabolizing CYP3A enzyme in human, pig, mouse and fish. naringenin 51-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 27107807-0 2016 In vitro effects of the citrus flavonoids diosmin, naringenin and naringin on the hepatic drug-metabolizing CYP3A enzyme in human, pig, mouse and fish. naringin 66-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 27107807-3 2016 Therefore, the effects of several naturally occurring flavonoids on the activity of CYP3A-dependent 7-benzyloxy-4-trifluoromethylcoumarin O-debenzylase (BFCOD) were evaluated in human, pig, mouse, and juvenile rainbow trout sources of hepatic microsomes. Flavonoids 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-89 27153105-0 2016 An ultra-high performance liquid chromatography-tandem mass spectrometric assay for quantifying 3-ketocholanoic acid: Application to the human liver microsomal CYP3A-dependent lithocholic acid 3-oxidation assay. 3-ketocholanoic acid 96-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-165 27153105-0 2016 An ultra-high performance liquid chromatography-tandem mass spectrometric assay for quantifying 3-ketocholanoic acid: Application to the human liver microsomal CYP3A-dependent lithocholic acid 3-oxidation assay. Lithocholic Acid 176-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-165 27153105-1 2016 Lithocholic acid (LCA), a hepatotoxic and carcinogenic bile acid, is metabolized to 3-ketocholanoic acid (3-KCA) by cytochrome P450 3A (CYP3A). Lithocholic Acid 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-134 27153105-1 2016 Lithocholic acid (LCA), a hepatotoxic and carcinogenic bile acid, is metabolized to 3-ketocholanoic acid (3-KCA) by cytochrome P450 3A (CYP3A). Lithocholic Acid 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-141 27153105-1 2016 Lithocholic acid (LCA), a hepatotoxic and carcinogenic bile acid, is metabolized to 3-ketocholanoic acid (3-KCA) by cytochrome P450 3A (CYP3A). Lithocholic Acid 18-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-134 27153105-1 2016 Lithocholic acid (LCA), a hepatotoxic and carcinogenic bile acid, is metabolized to 3-ketocholanoic acid (3-KCA) by cytochrome P450 3A (CYP3A). Lithocholic Acid 18-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-141 27153105-1 2016 Lithocholic acid (LCA), a hepatotoxic and carcinogenic bile acid, is metabolized to 3-ketocholanoic acid (3-KCA) by cytochrome P450 3A (CYP3A). Bile Acids and Salts 55-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-134 27153105-1 2016 Lithocholic acid (LCA), a hepatotoxic and carcinogenic bile acid, is metabolized to 3-ketocholanoic acid (3-KCA) by cytochrome P450 3A (CYP3A). Bile Acids and Salts 55-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-141 27153105-1 2016 Lithocholic acid (LCA), a hepatotoxic and carcinogenic bile acid, is metabolized to 3-ketocholanoic acid (3-KCA) by cytochrome P450 3A (CYP3A). 3-ketocholanoic acid 84-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-134 27153105-1 2016 Lithocholic acid (LCA), a hepatotoxic and carcinogenic bile acid, is metabolized to 3-ketocholanoic acid (3-KCA) by cytochrome P450 3A (CYP3A). 3-ketocholanoic acid 84-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-141 27049867-2 2016 In order to investigate profoundly the relationship between DFDPT with human CYP3A4 proteaset and anticancer molecular mechanism of DFDPT, the intercalative mode of binding of DFDPT with CYP3A4 under physiological conditions were comprehensively evaluated using steady state, synchronous, three-dimensional fluorescence spectroscopy,circular dichroism and molecular docking. dfdpt 60-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 27049867-2 2016 In order to investigate profoundly the relationship between DFDPT with human CYP3A4 proteaset and anticancer molecular mechanism of DFDPT, the intercalative mode of binding of DFDPT with CYP3A4 under physiological conditions were comprehensively evaluated using steady state, synchronous, three-dimensional fluorescence spectroscopy,circular dichroism and molecular docking. dfdpt 60-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 27049867-2 2016 In order to investigate profoundly the relationship between DFDPT with human CYP3A4 proteaset and anticancer molecular mechanism of DFDPT, the intercalative mode of binding of DFDPT with CYP3A4 under physiological conditions were comprehensively evaluated using steady state, synchronous, three-dimensional fluorescence spectroscopy,circular dichroism and molecular docking. dfdpt 132-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 27049867-2 2016 In order to investigate profoundly the relationship between DFDPT with human CYP3A4 proteaset and anticancer molecular mechanism of DFDPT, the intercalative mode of binding of DFDPT with CYP3A4 under physiological conditions were comprehensively evaluated using steady state, synchronous, three-dimensional fluorescence spectroscopy,circular dichroism and molecular docking. dfdpt 132-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 27049867-2 2016 In order to investigate profoundly the relationship between DFDPT with human CYP3A4 proteaset and anticancer molecular mechanism of DFDPT, the intercalative mode of binding of DFDPT with CYP3A4 under physiological conditions were comprehensively evaluated using steady state, synchronous, three-dimensional fluorescence spectroscopy,circular dichroism and molecular docking. dfdpt 132-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 27049867-2 2016 In order to investigate profoundly the relationship between DFDPT with human CYP3A4 proteaset and anticancer molecular mechanism of DFDPT, the intercalative mode of binding of DFDPT with CYP3A4 under physiological conditions were comprehensively evaluated using steady state, synchronous, three-dimensional fluorescence spectroscopy,circular dichroism and molecular docking. dfdpt 132-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 27049867-3 2016 Fluorescence emission data showed that CYP3A4 fluorescence affected by DFDPT was a static quenching procedure, which implied that DFDPT-CYP3A4 complex had been formed. dfdpt 71-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 27049867-3 2016 Fluorescence emission data showed that CYP3A4 fluorescence affected by DFDPT was a static quenching procedure, which implied that DFDPT-CYP3A4 complex had been formed. dfdpt 71-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 27049867-3 2016 Fluorescence emission data showed that CYP3A4 fluorescence affected by DFDPT was a static quenching procedure, which implied that DFDPT-CYP3A4 complex had been formed. dfdpt 130-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 27049867-3 2016 Fluorescence emission data showed that CYP3A4 fluorescence affected by DFDPT was a static quenching procedure, which implied that DFDPT-CYP3A4 complex had been formed. dfdpt 130-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 27049867-6 2016 The thermodynamic parameters DeltaH and DeltaS of the DFDPT-CYP3A4 complex were negative, which indicated that their interaction was driven mainly by hydrogen bonding and van der Waals force. Hydrogen 150-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 27049867-8 2016 The synchronous results showed DFDPT induced conformational changes of CYP3A4 protein. dfdpt 31-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 27049867-9 2016 Three-dimensional fluorescence and circular dichroism spectra results also revealed conformation of CYP3A4 protein had been possible changed in the presence of DFDPT. dfdpt 160-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 27049867-10 2016 Molecular docking was used to study the interaction orientation between DFDPT and CYP3A4 protease. dfdpt 72-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 27049867-11 2016 The results indicated that DFDPT interacted with a panel of amino acids in the active sites of CYP3A4 protein mainly through formation of hydrogen bond. dfdpt 27-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 27049867-11 2016 The results indicated that DFDPT interacted with a panel of amino acids in the active sites of CYP3A4 protein mainly through formation of hydrogen bond. Hydrogen 138-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 27049867-12 2016 Furthermore, the predicted binding mode of DFDPT into CYP3A4 appeared to adopt an orientation with interactions among Arg105, Ser119 and Thr309. dfdpt 43-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 27350760-2 2016 There has been a concern that statins that are metabolized by cytochrome P450 3A4 may interfere with clopidogrel metabolism at high doses. Clopidogrel 101-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-81 27296832-1 2016 BACKGROUND: To investigate the associations between atorvastatin-induced liver injury (AILI) and polymorphisms in eight genes possibly involved in the hepatic metabolism (CYP2C9, CYP2C19, CYP3A4, CYP3A5 and UGT1A1) and membrane transport (ABCB1, ABCG2 and SLCO1B1) of atorvastatin, we genotyped 30 AILI and 414 non-AILI patients recruited at BioBank Japan for 15 single nucleotide polymorphisms (SNPs). Atorvastatin 52-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-194 27013400-1 2016 Tolvaptan is a selective V2-receptor antagonist primarily metabolized by CYP3A. Tolvaptan 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 26617265-1 2016 The endogenous oxysterol 4beta-hydroxycholesterol may be used as a marker for the drug-metabolizing enzymes cytochrome P450 3A (CYP3A). oxysterol 4beta-hydroxycholesterol 15-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-126 26617265-1 2016 The endogenous oxysterol 4beta-hydroxycholesterol may be used as a marker for the drug-metabolizing enzymes cytochrome P450 3A (CYP3A). oxysterol 4beta-hydroxycholesterol 15-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-133 26943346-3 2016 Furthermore, 5 %(v/v) PEG (20 or 35 kDa) added to Leibovitz-15 medium was optimal for microencapsulated C3A cells, enhancing cell viability and liver-specific functions, including albumin and urea synthesis as well as CYP1A2 and CYP3A4 activities. Polyethylene Glycols 22-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 229-235 27098526-1 2016 Since many drugs are cytochrome P450 (CYP)-3A4 substrates, it has become common practice to assess drug-drug interaction (DDI) potential with a CYP3A4 inhibitor (ketoconazole) or inducer (rifampicin) in early drug development. Rifampin 188-198 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 27098526-5 2016 We hypothesized that DDIs between anticancer drugs and rifampicin were primarily driven by CYP3A4 induction. Rifampin 55-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 27098526-7 2016 The hypothesis that CYP3A4 induction would decrease drug exposure appeared paradoxical for intravenous romidepsin and-to a somewhat lesser extent-for cabazitaxel. cabazitaxel 150-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 27098526-9 2016 Given the complexity and paradoxical effects arising with DDIs with rifampicin, the continued preference for rifampicin as CYP3A4 inducer needs immediate re-appraisal. Rifampin 109-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 26952092-1 2016 PURPOSE: The purpose of the study is to evaluate whether donepezil (D) plasma concentrations and activity of CYP2D6 and CYP3A4 are associated with the therapeutic response of patients with mild to moderate Alzheimer"s disease (AD). Donepezil 57-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 26965514-1 2016 PURPOSE: Cyclosporine A (CsA) and imatinib are both CYP3A4 and P-glycoprotein substrates. Imatinib Mesylate 34-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 26932749-4 2016 We aimed to study the association of known variations in SLCO1B1, CYP3A4, ABCB1, CYP3A5, ABCG5 and CYP7A1 genes with lipid levels in response to atorvastatin therapy. Atorvastatin 145-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 26932749-10 2016 WHAT IS NEW AND CONCLUSION: The variable response to atorvastatin therapy in terms of LDL-cholesterol lowering due to genetic variations in CYP7A1, CYP3A4, SLCO1B1 and ABCB1 is a promising finding. Atorvastatin 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 27149910-0 2016 Significant impacts of CYP3A4*1G and CYP3A5*3 genetic polymorphisms on the pharmacokinetics of diltiazem and its main metabolites in Chinese adult kidney transplant patients. Diltiazem 95-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 27149910-3 2016 This study was carried out to investigate the impacts of the CYP3A4*1G and CYP3A5*3 genetic polymorphisms on the trough concentration/dose ratios and pharmacokinetics of diltiazem and its main metabolites in Chinese adult renal transplant patients. Diltiazem 170-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 27098526-1 2016 Since many drugs are cytochrome P450 (CYP)-3A4 substrates, it has become common practice to assess drug-drug interaction (DDI) potential with a CYP3A4 inhibitor (ketoconazole) or inducer (rifampicin) in early drug development. Ketoconazole 162-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-46 27098526-1 2016 Since many drugs are cytochrome P450 (CYP)-3A4 substrates, it has become common practice to assess drug-drug interaction (DDI) potential with a CYP3A4 inhibitor (ketoconazole) or inducer (rifampicin) in early drug development. Ketoconazole 162-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 27161454-8 2016 The mRNA expression of CYP3A4 was markedly induced by 1alpha,25-dihydroxyvitamin D3. Calcitriol 54-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 26898568-1 2016 PURPOSE: Dolutegravir (DTG) is primarily metabolized by UGT1A1 with CYP3A as a minor route. dolutegravir 9-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 26898568-1 2016 PURPOSE: Dolutegravir (DTG) is primarily metabolized by UGT1A1 with CYP3A as a minor route. dolutegravir 23-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 26381054-1 2016 Macitentan, a dual endothelin receptor antagonist used in pulmonary arterial hypertension, induces cytochrome P450 (CYP) 3A at supratherapeutic concentrations in vitro. macitentan 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-123 27149910-10 2016 WHAT IS NEW AND CONCLUSION: The CYP3A4*1G and CYP3A5*3 genetic polymorphisms are closely related to the trough concentration/dose ratios and pharmacokinetics of diltiazem and its main metabolites in Chinese adult renal transplant patients. Diltiazem 161-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 27149910-7 2016 RESULTS AND DISCUSSION: The dose-adjusted concentrations and pharmacokinetics of diltiazem and its main metabolites were significantly affected by CYP3A4 *1G and CYP3A5*3 alleles. Diltiazem 81-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 27149910-8 2016 Patients with a CYP3A4*1/*1 genotype were found to have a higher dose-adjusted trough concentration and AUC of diltiazem and its main metabolites compared with those with CYP3A4*1G*1G(P<0 05). Diltiazem 111-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 26956883-0 2016 Modulation of CYP3A4 activity alters the cytotoxicity of lipophilic phycotoxins in human hepatic HepaRG cells. phycotoxins 68-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 25998320-3 2016 In vitro data suggest that NETU inhibits CYP3A4 and is a substrate for and weak inhibitor of P-glycoprotein (P-gp). netupitant 27-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 25998320-4 2016 This review evaluates potential drug-drug interactions between NETU or NEPA and CYP3A4 substrates/inducers/inhibitors or P-gp substrates in healthy subjects. netupitant 63-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 25998320-12 2016 Coadministration of NETU or NEPA with CYP3A4 inducers/inhibitors/substrates should be done with caution. netupitant 20-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 26956883-5 2016 Moreover, we found that inhibition of CYP3A4 activity by ketoconazole enhances the toxic effects of OA, DTX-1, DTX-2, and PTX-2 in HepaRG cells. Ketoconazole 57-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 27274257-6 2016 Carbamazepine and other antiepileptic drugs can enhance its metabolism via induction of CYP3A4. Carbamazepine 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 26956883-5 2016 Moreover, we found that inhibition of CYP3A4 activity by ketoconazole enhances the toxic effects of OA, DTX-1, DTX-2, and PTX-2 in HepaRG cells. pectenotoxin 2 122-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 26956883-6 2016 Taken together, these results suggest that CYP3A4-mediated metabolism of some lipophilic phycotoxins decreases their in vitro toxicity. phycotoxins 89-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 26927871-6 2016 Hence enzalutamide, a strong Cyp3A4 inductor, has the potential to substantially decrease plasma concentrations and the effects of many co-medications in this patient population, whereas abiraterone acetate, a strong Cyp2D6 inhibitor, is less of a concern with respect to Cyp450 inhibition, since the Cyp2D6-mediated metabolism is much smaller and Cyp2D6 substrates are prescribed to a lesser extent in patients with prostate cancer. enzalutamide 6-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 26371436-3 2016 On the basis of our investigations of analogs of ritonavir, a potent CYP3A4 inactivator and pharmacoenhancer, we have built a pharmacophore model for a CYP3A4-specific inhibitor. Ritonavir 49-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 27211076-4 2016 CYP3A activity was a unique independent predictor of variability of atorvastatin metabolism, explaining the majority of the variance in reduction of atorvastatin (60.0%) and formation of ortho-hydroxy atorvastatin (78.8%) and para-hydroxy atorvastatin (83.9%). Atorvastatin 68-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 27211076-4 2016 CYP3A activity was a unique independent predictor of variability of atorvastatin metabolism, explaining the majority of the variance in reduction of atorvastatin (60.0%) and formation of ortho-hydroxy atorvastatin (78.8%) and para-hydroxy atorvastatin (83.9%). Atorvastatin 149-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 27211076-4 2016 CYP3A activity was a unique independent predictor of variability of atorvastatin metabolism, explaining the majority of the variance in reduction of atorvastatin (60.0%) and formation of ortho-hydroxy atorvastatin (78.8%) and para-hydroxy atorvastatin (83.9%). hydroxy atorvastatin 193-213 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 27211076-4 2016 CYP3A activity was a unique independent predictor of variability of atorvastatin metabolism, explaining the majority of the variance in reduction of atorvastatin (60.0%) and formation of ortho-hydroxy atorvastatin (78.8%) and para-hydroxy atorvastatin (83.9%). para-hydroxy atorvastatin 226-251 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 26371436-3 2016 On the basis of our investigations of analogs of ritonavir, a potent CYP3A4 inactivator and pharmacoenhancer, we have built a pharmacophore model for a CYP3A4-specific inhibitor. Ritonavir 49-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 27169677-1 2016 BACKGROUND: Tamoxifen, a common anti-estrogen breast cancer medication, is a prodrug that undergoes bioactivation via cytochrome P450 enzymes, CYP2D6 and to a lesser degree, CYP3A4 to form the active metabolite endoxifen. Tamoxifen 12-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 27169677-1 2016 BACKGROUND: Tamoxifen, a common anti-estrogen breast cancer medication, is a prodrug that undergoes bioactivation via cytochrome P450 enzymes, CYP2D6 and to a lesser degree, CYP3A4 to form the active metabolite endoxifen. 4-hydroxy-N-desmethyltamoxifen 211-220 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 27164071-6 2016 The FS extract affected CYP activity with varying potency; its effect on CYP 3A4-catalyzed clozapine oxidation was relatively strong (Ki: 0.11 mg/mL). Clozapine 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-80 27127017-9 2016 The primary end points are: in vivo clearance of CYP3A4, CYP2E1 and CYP1A2 substrates, which will be defined by using well-tested probes; midazolam, chlorzoxazone and caffeine. Midazolam 138-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 26922231-3 2016 Our findings indicated that the major metabolic site switched from the C3" appendage for docetaxel to the taxane ring for 3FDT, and the main metabolizing P450 enzymes switched from CYP3A to CYP3A4 and CYP2E1. Docetaxel 89-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-186 26922231-3 2016 Our findings indicated that the major metabolic site switched from the C3" appendage for docetaxel to the taxane ring for 3FDT, and the main metabolizing P450 enzymes switched from CYP3A to CYP3A4 and CYP2E1. Docetaxel 89-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-196 26922231-3 2016 Our findings indicated that the major metabolic site switched from the C3" appendage for docetaxel to the taxane ring for 3FDT, and the main metabolizing P450 enzymes switched from CYP3A to CYP3A4 and CYP2E1. taxane 106-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-186 26922231-3 2016 Our findings indicated that the major metabolic site switched from the C3" appendage for docetaxel to the taxane ring for 3FDT, and the main metabolizing P450 enzymes switched from CYP3A to CYP3A4 and CYP2E1. taxane 106-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-196 26922231-3 2016 Our findings indicated that the major metabolic site switched from the C3" appendage for docetaxel to the taxane ring for 3FDT, and the main metabolizing P450 enzymes switched from CYP3A to CYP3A4 and CYP2E1. 3fdt 122-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-186 26922231-3 2016 Our findings indicated that the major metabolic site switched from the C3" appendage for docetaxel to the taxane ring for 3FDT, and the main metabolizing P450 enzymes switched from CYP3A to CYP3A4 and CYP2E1. 3fdt 122-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-196 27127017-9 2016 The primary end points are: in vivo clearance of CYP3A4, CYP2E1 and CYP1A2 substrates, which will be defined by using well-tested probes; midazolam, chlorzoxazone and caffeine. Chlorzoxazone 149-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 27127017-9 2016 The primary end points are: in vivo clearance of CYP3A4, CYP2E1 and CYP1A2 substrates, which will be defined by using well-tested probes; midazolam, chlorzoxazone and caffeine. Caffeine 167-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 27127017-12 2016 CONCLUSION: The aim of the CYTONOX trial is to investigate the in vivo activity of CYP3A4, CYP2E1 and CYP1A2 in obese and non-obese children. cytonox 27-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 26888941-3 2016 FA was a weak reversible (IC50= 295 +- 1.0muM) and time-dependent (KI= 216 +- 41muM and kinact= 0.0179 +- 0.001 min(-1)) inhibitor of CYP3A4-catalyzed midazolam-1"-hydroxylase activity in human liver microsomes. Midazolam 151-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 26968005-8 2016 Ivacaftor is a CYP3A substrate; CYP3A inhibitors and inducers should be avoided during its administration. ivacaftor 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-20 26972388-3 2016 As dronedarone is a potent mechanism-based inactivator of CYP3A4 and CYP3A5, a question arose if it exerts a similar inhibitory effect on CYP2J2, a prominent cardiac CYP450 enzyme. Dronedarone 3-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 26950050-5 2016 The impact of phenotyping on the dose selection and pharmacokinetics of CYP3A substrates (docetaxel, irinotecan, tyrosine kinase inhibitors, ciclosporin, tacrolimus) are reviewed. Docetaxel 90-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-77 26950050-5 2016 The impact of phenotyping on the dose selection and pharmacokinetics of CYP3A substrates (docetaxel, irinotecan, tyrosine kinase inhibitors, ciclosporin, tacrolimus) are reviewed. Cyclosporine 141-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-77 27299937-1 2016 Naloxegol, a peripherally acting mu-opioid receptor antagonist for the treatment of opioid-induced constipation, is a substrate for cytochrome P450 (CYP) 3A4/3A5 and the P-glycoprotein (P-gp) transporter. naloxegol 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-161 26968005-8 2016 Ivacaftor is a CYP3A substrate; CYP3A inhibitors and inducers should be avoided during its administration. ivacaftor 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-37 27299937-4 2016 The moderate CYP3A4 inducer efavirenz was predicted to reduce naloxegol exposure by ~50%, whereas weak CYP3A inhibitors were predicted to minimally affect exposure. naloxegol 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 26968005-9 2016 Ivacaftor and its M1 metabolite may inhibit CYP3A and P-gp; therefore, ivacaftor may increase systemic exposure to drugs which are substrates of CYP3A and/or P-gp, increasing the potential for adverse events. ivacaftor 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-49 27299937-4 2016 The moderate CYP3A4 inducer efavirenz was predicted to reduce naloxegol exposure by ~50%, whereas weak CYP3A inhibitors were predicted to minimally affect exposure. naloxegol 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-18 26968005-9 2016 Ivacaftor and its M1 metabolite may inhibit CYP3A and P-gp; therefore, ivacaftor may increase systemic exposure to drugs which are substrates of CYP3A and/or P-gp, increasing the potential for adverse events. ivacaftor 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-150 27299937-5 2016 In summary, the PBPK models reasonably estimated interactions with various CYP3A modulators and can be used to guide dosing in clinical practice when naloxegol is coadministered with such agents. naloxegol 150-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 26968005-9 2016 Ivacaftor and its M1 metabolite may inhibit CYP3A and P-gp; therefore, ivacaftor may increase systemic exposure to drugs which are substrates of CYP3A and/or P-gp, increasing the potential for adverse events. ivacaftor 71-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-49 26968005-9 2016 Ivacaftor and its M1 metabolite may inhibit CYP3A and P-gp; therefore, ivacaftor may increase systemic exposure to drugs which are substrates of CYP3A and/or P-gp, increasing the potential for adverse events. ivacaftor 71-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-150 27225724-0 2016 Effects of Genetic Polymorphism in CYP3A4 and CYP3A5 Genes on Tacrolimus Dose Among Kidney Transplant Recipients. Tacrolimus 62-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 27225724-1 2016 INTRODUCTION: This study aimed to evaluate the effects of single nucleotide polymorphisms CYP3A4*1B and CYP3A5*3 on tacrolimus dose requirement among kidney transplant recipients. Tacrolimus 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 27225724-4 2016 RESULTS: The median tacrolimus dose was significantly lower in the CYP3A4*1/*1 carriers (0.06 mg/kg/d; range, 0.007 mg/kg/d to 0.17 mg/kg/d) as compared to the CYP3A4*1B/*1B carriers (0.1 mg/kg/d; range, 0.03 mg/kg/d to 0.22 mg/kg/d; P = .001). Tacrolimus 20-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 27225724-4 2016 RESULTS: The median tacrolimus dose was significantly lower in the CYP3A4*1/*1 carriers (0.06 mg/kg/d; range, 0.007 mg/kg/d to 0.17 mg/kg/d) as compared to the CYP3A4*1B/*1B carriers (0.1 mg/kg/d; range, 0.03 mg/kg/d to 0.22 mg/kg/d; P = .001). Tacrolimus 20-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 27225724-7 2016 Moreover, we found a correlation between genetic variations in CYP3A4 and CYP3A5 enzymes and tacrolimus blood levels among our kidney transplant recipients. Tacrolimus 93-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 26774838-0 2016 The use of isomeric testosterone dimers to explore allosteric effects in substrate binding to cytochrome P450 CYP3A4. Testosterone 20-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 26774838-3 2016 In order to better understand structural and functional aspects of binding of multiple substrate molecules to CYP3A4 we used resonance Raman and UV-VIS spectroscopy to document the effects of binding of synthetic testosterone dimers of different configurations, cis-TST2 and trans-TST2. Testosterone 213-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 26774838-4 2016 We directly demonstrate that the binding of two steroid molecules, which can assume multiple possible configurations inside the substrate binding pocket of monomeric CYP3A4, can lead to active site structural changes that affect functional properties. Steroids 48-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-172 26970587-0 2016 Hydroxylation of 20-hydroxyvitamin D3 by human CYP3A4. 20-hydroxyvitamin D3 17-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 26970587-4 2016 CYP3A4 is the major drug-metabolising P450 in liver endoplasmic reticulum and can metabolise other active forms of vitamin D, so we examined its ability to metabolise 20(OH)D3. Vitamin D 115-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26970587-5 2016 We found that CYP3A4 metabolises 20(OH)D3 to three major products, 20,24R-dihydroxyvitamin D3 [20,24R(OH)2D3], 20,24S-dihydroxyvitamin D3 [20,24S(OH)2D3] and 20,25-dihydroxyvitamin D3 [20,25(OH)2D3]. ,24r(oh)2d3 97-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 26970587-4 2016 CYP3A4 is the major drug-metabolising P450 in liver endoplasmic reticulum and can metabolise other active forms of vitamin D, so we examined its ability to metabolise 20(OH)D3. (oh)d3 169-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26970587-5 2016 We found that CYP3A4 metabolises 20(OH)D3 to three major products, 20,24R-dihydroxyvitamin D3 [20,24R(OH)2D3], 20,24S-dihydroxyvitamin D3 [20,24S(OH)2D3] and 20,25-dihydroxyvitamin D3 [20,25(OH)2D3]. ,24s-dihydroxyvitamin d3 113-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 26970587-5 2016 We found that CYP3A4 metabolises 20(OH)D3 to three major products, 20,24R-dihydroxyvitamin D3 [20,24R(OH)2D3], 20,24S-dihydroxyvitamin D3 [20,24S(OH)2D3] and 20,25-dihydroxyvitamin D3 [20,25(OH)2D3]. 20-hydroxyvitamin D3 33-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 26970587-5 2016 We found that CYP3A4 metabolises 20(OH)D3 to three major products, 20,24R-dihydroxyvitamin D3 [20,24R(OH)2D3], 20,24S-dihydroxyvitamin D3 [20,24S(OH)2D3] and 20,25-dihydroxyvitamin D3 [20,25(OH)2D3]. 24s(oh)2d3 142-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 26970587-5 2016 We found that CYP3A4 metabolises 20(OH)D3 to three major products, 20,24R-dihydroxyvitamin D3 [20,24R(OH)2D3], 20,24S-dihydroxyvitamin D3 [20,24S(OH)2D3] and 20,25-dihydroxyvitamin D3 [20,25(OH)2D3]. 20,25-dihydroxyvitamin d3 158-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 26970587-5 2016 We found that CYP3A4 metabolises 20(OH)D3 to three major products, 20,24R-dihydroxyvitamin D3 [20,24R(OH)2D3], 20,24S-dihydroxyvitamin D3 [20,24S(OH)2D3] and 20,25-dihydroxyvitamin D3 [20,25(OH)2D3]. 20,24r-dihydroxyvitamin d3 67-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 26970587-5 2016 We found that CYP3A4 metabolises 20(OH)D3 to three major products, 20,24R-dihydroxyvitamin D3 [20,24R(OH)2D3], 20,24S-dihydroxyvitamin D3 [20,24S(OH)2D3] and 20,25-dihydroxyvitamin D3 [20,25(OH)2D3]. oh)2d3 102-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 26970587-6 2016 20,24R(OH)2D3 and 20,24S(OH)2D3, but not 20,25(OH)2D3, were further metabolised to trihydroxyvitamin D3 products by CYP3A4 but with low catalytic efficiency. 20,24r(oh)2d3 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 27142945-6 2016 CYP3A4*1B, CYP3A5*3, CYP3A5*6 and ABCC2 c.1249G>A which have been associated with LPV plasma concentration, showed no significant association. Lopinavir 85-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26970587-6 2016 20,24R(OH)2D3 and 20,24S(OH)2D3, but not 20,25(OH)2D3, were further metabolised to trihydroxyvitamin D3 products by CYP3A4 but with low catalytic efficiency. 20,24s(oh)2d3 18-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 26970587-6 2016 20,24R(OH)2D3 and 20,24S(OH)2D3, but not 20,25(OH)2D3, were further metabolised to trihydroxyvitamin D3 products by CYP3A4 but with low catalytic efficiency. trihydroxyvitamin d3 83-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 26970587-8 2016 Addition of CYP3A family-specific inhibitors, troleandomycin and azamulin, almost completely inhibited production of 20,24R(OH)2D3, 20,24S(OH)2D3 and 20,25(OH)2D3 by human liver microsomes, further supporting that CYP3A4 plays the major role in 20(OH)D3 metabolism by microsomes. Troleandomycin 46-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 214-220 26970587-8 2016 Addition of CYP3A family-specific inhibitors, troleandomycin and azamulin, almost completely inhibited production of 20,24R(OH)2D3, 20,24S(OH)2D3 and 20,25(OH)2D3 by human liver microsomes, further supporting that CYP3A4 plays the major role in 20(OH)D3 metabolism by microsomes. azamulin 65-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 214-220 26272330-1 2016 Piragliatin is a CYP3A substrate; its inactive metabolite M4, formed through cytosolic reductase, is reversibly metabolized back to piragliatin through CYP3A. piragliatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-22 26272330-1 2016 Piragliatin is a CYP3A substrate; its inactive metabolite M4, formed through cytosolic reductase, is reversibly metabolized back to piragliatin through CYP3A. piragliatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-157 26272330-1 2016 Piragliatin is a CYP3A substrate; its inactive metabolite M4, formed through cytosolic reductase, is reversibly metabolized back to piragliatin through CYP3A. piragliatin 132-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-157 26272330-6 2016 In conclusion, a strong CYP3A modifier or concomitant alcohol could lead to a change in exposure to piragliatin with a potential alteration in glucose-lowering effect. piragliatin 100-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 26272330-6 2016 In conclusion, a strong CYP3A modifier or concomitant alcohol could lead to a change in exposure to piragliatin with a potential alteration in glucose-lowering effect. Glucose 143-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 26331791-3 2016 Venlafaxine (VLX) is an antidepressant metabolized mainly by CYP2D6 to O-desmethylvenlafaxine (ODV), CYP3A to N-desmethylvenlafaxine (NDV), and CYP2D6 and CYP3A to N,O-didesmethylvenlafaxine (DDV). Venlafaxine Hydrochloride 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 26331791-3 2016 Venlafaxine (VLX) is an antidepressant metabolized mainly by CYP2D6 to O-desmethylvenlafaxine (ODV), CYP3A to N-desmethylvenlafaxine (NDV), and CYP2D6 and CYP3A to N,O-didesmethylvenlafaxine (DDV). Venlafaxine Hydrochloride 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-160 26331791-3 2016 Venlafaxine (VLX) is an antidepressant metabolized mainly by CYP2D6 to O-desmethylvenlafaxine (ODV), CYP3A to N-desmethylvenlafaxine (NDV), and CYP2D6 and CYP3A to N,O-didesmethylvenlafaxine (DDV). Venlafaxine Hydrochloride 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 26331791-3 2016 Venlafaxine (VLX) is an antidepressant metabolized mainly by CYP2D6 to O-desmethylvenlafaxine (ODV), CYP3A to N-desmethylvenlafaxine (NDV), and CYP2D6 and CYP3A to N,O-didesmethylvenlafaxine (DDV). Venlafaxine Hydrochloride 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-160 26331791-3 2016 Venlafaxine (VLX) is an antidepressant metabolized mainly by CYP2D6 to O-desmethylvenlafaxine (ODV), CYP3A to N-desmethylvenlafaxine (NDV), and CYP2D6 and CYP3A to N,O-didesmethylvenlafaxine (DDV). N-desmethylvenlafaxine 110-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 26967371-0 2016 Role of Enzyme Flexibility in Ligand Access and Egress to Active Site: Bias-Exchange Metadynamics Study of 1,3,7-Trimethyluric Acid in Cytochrome P450 3A4. 1,3,7-trimethyluric acid 107-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-154 27125217-13 2016 Posaconazole interactions with medications metabolized via the CYP3A4 pathway should be considered an additional risk factor for lethal cardiac incidents. posaconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 27128896-3 2016 Aschantin potently inhibited CYP2C8-mediated amodiaquine N-de-ethylation, CYP2C9-mediated diclofenac 4"-hydroxylation, CYP2C19-mediated [S]-mephenytoin 4"-hydroxylation, and CYP3A4-mediated midazolam 1"-hydroxylation, with Ki values of 10.2, 3.7, 5.8, and 12.6 microM, respectively. aschantin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 27143858-2 2016 It was suggested that the substrates of P-glycoprotein or cytochrome P450 3A4 were reduced on a high sodium diet. Sodium 101-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-77 27143858-3 2016 This study aimed to investigate the influence of high sodium diet on the pharmacokinetics and pharmacodynamics of fimasartan, which is a substrate of cytochrome P450 3A4 but not P-glycoprotein. Sodium 54-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-169 27143858-3 2016 This study aimed to investigate the influence of high sodium diet on the pharmacokinetics and pharmacodynamics of fimasartan, which is a substrate of cytochrome P450 3A4 but not P-glycoprotein. fimasartan 114-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-169 26966071-7 2016 Treatment with dexamethasone, phenobarbital, rifampicin, or 1alpha,25-dihydroxyvitamin D3 resulted in 5.8-fold, 13.4-fold, 9.8-fold, or 95.0-fold induction of CYP3A4 expression relative to that in the untreated controls, respectively. Dexamethasone 15-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 26966071-7 2016 Treatment with dexamethasone, phenobarbital, rifampicin, or 1alpha,25-dihydroxyvitamin D3 resulted in 5.8-fold, 13.4-fold, 9.8-fold, or 95.0-fold induction of CYP3A4 expression relative to that in the untreated controls, respectively. Phenobarbital 30-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 26966071-7 2016 Treatment with dexamethasone, phenobarbital, rifampicin, or 1alpha,25-dihydroxyvitamin D3 resulted in 5.8-fold, 13.4-fold, 9.8-fold, or 95.0-fold induction of CYP3A4 expression relative to that in the untreated controls, respectively. Rifampin 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 26966071-7 2016 Treatment with dexamethasone, phenobarbital, rifampicin, or 1alpha,25-dihydroxyvitamin D3 resulted in 5.8-fold, 13.4-fold, 9.8-fold, or 95.0-fold induction of CYP3A4 expression relative to that in the untreated controls, respectively. Calcitriol 60-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 26896706-2 2016 TAM is metabolized to the more active 4-hydroxytamoxifen (4-OH-TAM) and endoxifen by cytochrome P450 (CYP) mainly CYP2D6 and CYP3A4 enzymes. Tamoxifen 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 26896706-2 2016 TAM is metabolized to the more active 4-hydroxytamoxifen (4-OH-TAM) and endoxifen by cytochrome P450 (CYP) mainly CYP2D6 and CYP3A4 enzymes. hydroxytamoxifen 38-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 26896706-2 2016 TAM is metabolized to the more active 4-hydroxytamoxifen (4-OH-TAM) and endoxifen by cytochrome P450 (CYP) mainly CYP2D6 and CYP3A4 enzymes. hydroxytamoxifen 58-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 26896706-2 2016 TAM is metabolized to the more active 4-hydroxytamoxifen (4-OH-TAM) and endoxifen by cytochrome P450 (CYP) mainly CYP2D6 and CYP3A4 enzymes. 4-hydroxy-N-desmethyltamoxifen 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 26967371-6 2016 The approach was applied to mapping of a complex channel network in a complex environment, i.e., CYP3A4 attached to a lipid bilayer mimicking an endoplasmic reticulum membrane. Lipid Bilayers 118-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 27349315-9 2016 In addition, since sorafenib is metabolized by CYP3A4, but not by CYP3A7, an overexpression of CYP3A4 may lead to an increase in the degradation of the drug and then to clinical ineffectiveness. Sorafenib 19-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 26924289-0 2016 Prediction of tacrolimus metabolism and dosage requirements based on CYP3A4 phenotype and CYP3A5(*)3 genotype in Chinese renal transplant recipients. Tacrolimus 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 26924289-3 2016 The endogenous CYP3A4 phenotype was assessed by the ratio of 6beta-hydroxycortisol and 6beta-hydroxycortisone to cortisol and cortisone in urine. 6 beta-hydroxycortisol 61-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 26924289-3 2016 The endogenous CYP3A4 phenotype was assessed by the ratio of 6beta-hydroxycortisol and 6beta-hydroxycortisone to cortisol and cortisone in urine. 6 beta-hydroxycortisone 87-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 26924289-3 2016 The endogenous CYP3A4 phenotype was assessed by the ratio of 6beta-hydroxycortisol and 6beta-hydroxycortisone to cortisol and cortisone in urine. Hydrocortisone 74-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 26924289-3 2016 The endogenous CYP3A4 phenotype was assessed by the ratio of 6beta-hydroxycortisol and 6beta-hydroxycortisone to cortisol and cortisone in urine. Cortisone 100-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 27349315-9 2016 In addition, since sorafenib is metabolized by CYP3A4, but not by CYP3A7, an overexpression of CYP3A4 may lead to an increase in the degradation of the drug and then to clinical ineffectiveness. Sorafenib 19-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 26924289-8 2016 CONCLUSION: This study provides the equations to predict tacrolimus metabolism and dosage requirements based on the endogenous CYP3A4 phenotype, CYP3A5(*)3 genotype and other non-genetic variables. Tacrolimus 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 27349315-10 2016 These results might implicate the necessity of an individualized approach in the treatment of HCC as positivity to CYP3A4 in HCC liver samples might predict a scarce response to sorafenib. Sorafenib 178-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 26749408-2 2016 The effects of rifampin, a strong inducer of CYP3A4 and P-glycoprotein, on the pharmacokinetics of oral and intravenous apixaban were evaluated in an open-label, randomized, sequential crossover study. Rifampin 15-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 26239045-6 2016 These results demonstrate that CYP2C19 genotypes influenced the exposure of tacrolimus when coadministered with voriconazole, although tacrolimus is mainly metabolized by CYP3A. Tacrolimus 135-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-176 26749408-2 2016 The effects of rifampin, a strong inducer of CYP3A4 and P-glycoprotein, on the pharmacokinetics of oral and intravenous apixaban were evaluated in an open-label, randomized, sequential crossover study. apixaban 120-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 26399557-0 2016 Relationships between Endogenous Plasma Biomarkers of Constitutive Cytochrome P450 3A Activity and Single-Time-Point Oral Midazolam Microdose Phenotype in Healthy Subjects. Midazolam 122-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-85 26399557-2 2016 The biomarkers 4beta-hydroxycholesterol (4betaHC) and 6beta-hydroxycortisol (6betaHCL) are sensitive to CYP3A induction and inhibition. cholest-5-ene-3,4-diol 15-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-109 26399557-2 2016 The biomarkers 4beta-hydroxycholesterol (4betaHC) and 6beta-hydroxycortisol (6betaHCL) are sensitive to CYP3A induction and inhibition. cholest-5-ene-3,4-diol 41-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-109 26399557-2 2016 The biomarkers 4beta-hydroxycholesterol (4betaHC) and 6beta-hydroxycortisol (6betaHCL) are sensitive to CYP3A induction and inhibition. 6 beta-hydroxycortisol 54-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-109 26399557-2 2016 The biomarkers 4beta-hydroxycholesterol (4betaHC) and 6beta-hydroxycortisol (6betaHCL) are sensitive to CYP3A induction and inhibition. 6 beta-hydroxycortisol 77-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-109 26399557-4 2016 We investigated whether endogenous plasma biomarkers (4betaHC and 6betaHCL) are associated with basal CYP3A metabolic activity in healthy subjects assessed by a convenient single-time-point oral midazolam (MDZ) phenotyping strategy. cholest-5-ene-3,4-diol 54-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 26399557-4 2016 We investigated whether endogenous plasma biomarkers (4betaHC and 6betaHCL) are associated with basal CYP3A metabolic activity in healthy subjects assessed by a convenient single-time-point oral midazolam (MDZ) phenotyping strategy. 6 beta-hydroxycortisol 66-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 26369775-10 2016 Vonoprazan is metabolized to inactive metabolites mainly by cytochrome P450 (CYP)3A4 and to some extent by CYP2B6, CYP2C19, CYP2D6, and SULT2A1. 1-(5-(2-fluorophenyl)-1-(pyridin-3-ylsulfonyl)-1H-pyrrol-3-yl)-N-methylmethanamine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-84 26713664-7 2016 Moreover, CsA is highly metabolized by cytochrome P450 3A4 (CYP3A4), a polymorphic enzyme leading to variations of Cmax and AUC between 10-20% in patients using CsA. Cyclosporine 10-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-58 26713664-7 2016 Moreover, CsA is highly metabolized by cytochrome P450 3A4 (CYP3A4), a polymorphic enzyme leading to variations of Cmax and AUC between 10-20% in patients using CsA. Cyclosporine 10-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 26713664-7 2016 Moreover, CsA is highly metabolized by cytochrome P450 3A4 (CYP3A4), a polymorphic enzyme leading to variations of Cmax and AUC between 10-20% in patients using CsA. Cyclosporine 161-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-58 26713664-7 2016 Moreover, CsA is highly metabolized by cytochrome P450 3A4 (CYP3A4), a polymorphic enzyme leading to variations of Cmax and AUC between 10-20% in patients using CsA. Cyclosporine 161-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 27196356-1 2016 Cobicistat and ritonavir are structurally distinct compounds that both potently inhibit cytochrome P450 (CYP) 3A, the metabolizing enzyme primarily responsible for the elimination of several antiretroviral medications, and, as such, are pharmacokinetic boosters for antiretroviral agents that require longer dosing intervals. Cobicistat 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-112 27196356-1 2016 Cobicistat and ritonavir are structurally distinct compounds that both potently inhibit cytochrome P450 (CYP) 3A, the metabolizing enzyme primarily responsible for the elimination of several antiretroviral medications, and, as such, are pharmacokinetic boosters for antiretroviral agents that require longer dosing intervals. Ritonavir 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-112 26433738-4 2016 Dose-adjusted tacrolimus concentration was used as a surrogate marker of CYP3A4 activity. Tacrolimus 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 26433738-9 2016 Liver transplant recipients with impaired renal function or a low dose-adjusted tacrolimus concentration suggesting a high CYP3A4 are at risk of low 1,25(OH)2D3 concentrations. Tacrolimus 80-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 26433738-9 2016 Liver transplant recipients with impaired renal function or a low dose-adjusted tacrolimus concentration suggesting a high CYP3A4 are at risk of low 1,25(OH)2D3 concentrations. Calcitriol 149-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 26947771-7 2016 Between 79 and 83% of the overall variation in apparent clearance of tramadol enantiomers was explained by fraction unbound, CYP2D6, and CYP3A in vivo activities and body weight. Tramadol 69-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-142 26947771-9 2016 Individually, CYP2D6 and CYP3A activities were shown to have moderate contribution on clearance of tramadol enantiomers (11-16% and 11-18%, respectively). Tramadol 99-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-30 27518169-12 2016 That concentration of EGCG is equivalent to one-half to one-third of its Ki value for CYP1A2 and CYP3A4 in this study. epigallocatechin gallate 22-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 27019957-2 2016 Data from in vitro hepatocyte studies suggested that NVS123 is mainly metabolized by CYP3A4. nvs123 53-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 26964624-2 2016 Here, we refined the genetic basis underlying the functional effects of a CYP3A haplotype on urinary estrone glucuronide (E1G) levels and tested for an association between CYP3A genotype and outcome in patients with chronic lymphocytic leukemia (CLL), breast, or lung cancers. Estrone 101-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-79 27019957-4 2016 One approach to overcome NVS123 developability issues was to increase plasma exposure by coadministrating it with an inhibitor of CYP3A4 such as ritonavir. Ritonavir 145-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 26693810-0 2016 In Vivo Cytochrome P450 3A Isoenzyme Activity and Pharmacokinetics of Imatinib in Relation to Therapeutic Outcome in Patients With Chronic Myeloid Leukemia. Imatinib Mesylate 70-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-26 26693810-1 2016 BACKGROUND: Cytochrome P450 3A (CYP3A) isoenzyme metabolic activity varies between individuals and is therefore a possible candidate of influence on the therapeutic outcome of the tyrosine kinase inhibitor imatinib in patients with chronic myeloid leukemia (CML). Imatinib Mesylate 206-214 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-30 26693810-1 2016 BACKGROUND: Cytochrome P450 3A (CYP3A) isoenzyme metabolic activity varies between individuals and is therefore a possible candidate of influence on the therapeutic outcome of the tyrosine kinase inhibitor imatinib in patients with chronic myeloid leukemia (CML). Imatinib Mesylate 206-214 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-37 26693810-2 2016 The aim of this study was to investigate the influence of CYP3A metabolic activity on the plasma concentration and outcome of imatinib in patients with CML. Imatinib Mesylate 126-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 26693810-3 2016 METHODS: Forty-three patients with CML were phenotyped for CYP3A activity using quinine as a probe drug and evaluated for clinical response parameters. Quinine 80-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 26693810-8 2016 These results indicate that although imatinib is metabolized by CYP3A enzymes, this activity is not the rate-limiting step in imatinib metabolism and excretion. Imatinib Mesylate 37-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 26939024-5 2016 To confirm that the emission is from the heme, we destroyed the heme by titration with cumene hydroperoxide and measured the changes in emission upon titration with compounds known to bind to the distal face of the heme in two human cytochrome P450 enzymes, known as CYP3A4 and CYP2C9. Heme 41-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 267-273 27006687-7 2016 RESULTS: Sodium tanshinone IIA sulfonate inhibited the activity of CYP3A4 in a dose-dependent manner by the HLMs and CYP3A4 isoform. tanshinone II A sodium sulfonate 9-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 27006687-7 2016 RESULTS: Sodium tanshinone IIA sulfonate inhibited the activity of CYP3A4 in a dose-dependent manner by the HLMs and CYP3A4 isoform. tanshinone II A sodium sulfonate 9-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 27006687-10 2016 CONCLUSION: This in vitro study showed that STS mainly inhibited the activities of CYP3A4. tanshinone II A sodium sulfonate 44-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 26964624-2 2016 Here, we refined the genetic basis underlying the functional effects of a CYP3A haplotype on urinary estrone glucuronide (E1G) levels and tested for an association between CYP3A genotype and outcome in patients with chronic lymphocytic leukemia (CLL), breast, or lung cancers. Glucuronides 109-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-79 26806573-0 2016 Effects of salvianolic acid B and tanshinone IIA on the pharmacokinetics of losartan in rats by regulating the activities and expression of CYP3A4 and CYP2C9. Losartan 76-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 26827781-5 2016 With human liver microsomes, DDPH was a noncompetitive inhibitor of CYP2D6 (Ki = 0.85 +- 0.06 muM) and mixed inhibitor of CYP3A (Ki = 2.15 +- 0.41 muM). 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino)propane 29-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-127 26805467-11 2016 The expression levels of CYP3A4, UGT1A, SULT1A1, P-gp, MRP2, and MRP3 were remarkably increased in the CS-treated cells, whereas the protein levels of SULT1A3 and BCRP were decreased. 7,3'-dihydroxy-4'-methoxyisoflavone 103-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 26385839-5 2016 It performed well in recovering the observed effect of the CYP3A4 inhibitors ketoconazole and cyclosporine, and the CYP3A4 inducer rifampicin, as well as in predicting interactions with S-warfarin and sildenafil. Ketoconazole 77-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 26369773-5 2016 The Michaelis-Menten constant (K m) and the maximum rate of metabolite formation (V max) for cytochrome P450 3A4-mediated darunavir biotransformation and inhibition by ritonavir were determined experimentally, while the contributions of hepatocyte influx and efflux transporters were assessed by sensitivity analysis. Darunavir 122-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-112 26369773-5 2016 The Michaelis-Menten constant (K m) and the maximum rate of metabolite formation (V max) for cytochrome P450 3A4-mediated darunavir biotransformation and inhibition by ritonavir were determined experimentally, while the contributions of hepatocyte influx and efflux transporters were assessed by sensitivity analysis. Ritonavir 168-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-112 26385839-5 2016 It performed well in recovering the observed effect of the CYP3A4 inhibitors ketoconazole and cyclosporine, and the CYP3A4 inducer rifampicin, as well as in predicting interactions with S-warfarin and sildenafil. Cyclosporine 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 26385839-5 2016 It performed well in recovering the observed effect of the CYP3A4 inhibitors ketoconazole and cyclosporine, and the CYP3A4 inducer rifampicin, as well as in predicting interactions with S-warfarin and sildenafil. Rifampin 131-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 26668209-8 2016 The results indicate that, like ketoconazole, the alternative clinical CYP3A4/5 inhibitors ritonavir, clarithromycin, and itraconazole each have unique transporter inhibition profiles. Ritonavir 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 26668209-1 2016 Ketoconazole is a potent CYP3A4/5 inhibitor and, until recently, recommended by the Food and Drug Administration (FDA) and the European Medicines Agency as a strong CYP3A4/5 inhibitor in clinical drug-drug interaction (DDI) studies. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 26360628-3 2016 In this study, inhibition of human recombinant CYP2D6 and CYP3A4 by 27 amine stimulants associated with dietary supplements and their analogs was evaluated by luminescence assays. Amines 71-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 26360628-6 2016 Results of this study illustrate that several amine stimulants associated with dietary supplements inhibit CYP2D6 and CYP3A4 in vitro, and these compounds may participate in adverse drug-dietary supplement interactions in vivo. Amines 46-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 26668209-1 2016 Ketoconazole is a potent CYP3A4/5 inhibitor and, until recently, recommended by the Food and Drug Administration (FDA) and the European Medicines Agency as a strong CYP3A4/5 inhibitor in clinical drug-drug interaction (DDI) studies. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 26668209-8 2016 The results indicate that, like ketoconazole, the alternative clinical CYP3A4/5 inhibitors ritonavir, clarithromycin, and itraconazole each have unique transporter inhibition profiles. Clarithromycin 102-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 26668209-8 2016 The results indicate that, like ketoconazole, the alternative clinical CYP3A4/5 inhibitors ritonavir, clarithromycin, and itraconazole each have unique transporter inhibition profiles. Itraconazole 122-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 27276192-0 2016 Effects of EPHX1 and CYP3A4*22 genetic polymorphisms on carbamazepine metabolism and drug response among Tunisian epileptic patients. Carbamazepine 56-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 26739683-0 2016 Effects of CYP3A4 Inhibitors Ketoconazole and Verapamil and the CYP3A4 Inducer Rifampicin on the Pharmacokinetic Parameters of Fostamatinib: Results from In Vitro and Phase I Clinical Studies. Rifampin 79-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 26739683-0 2016 Effects of CYP3A4 Inhibitors Ketoconazole and Verapamil and the CYP3A4 Inducer Rifampicin on the Pharmacokinetic Parameters of Fostamatinib: Results from In Vitro and Phase I Clinical Studies. fostamatinib 127-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 26739683-0 2016 Effects of CYP3A4 Inhibitors Ketoconazole and Verapamil and the CYP3A4 Inducer Rifampicin on the Pharmacokinetic Parameters of Fostamatinib: Results from In Vitro and Phase I Clinical Studies. fostamatinib 127-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 26739683-2 2016 The active metabolite of fostamatinib, R406, is primarily metabolized by CYP3A4. fostamatinib 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 26739683-10 2016 Microsomal metabolism of R406 was markedly inhibited by CYP3A4 inhibitors and, in the expressed CYP450 studies, the rate of R406 disappearance was greatest with CYP3A4. R406 25-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 26739683-10 2016 Microsomal metabolism of R406 was markedly inhibited by CYP3A4 inhibitors and, in the expressed CYP450 studies, the rate of R406 disappearance was greatest with CYP3A4. R406 25-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 26739683-14 2016 CONCLUSION: The oxidative metabolism of R406 is predominantly catalyzed by CYP3A4. R406 40-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 26739683-15 2016 In clinical studies, exposure to R406 is affected by concomitant administration of CYP3A4 inducers/inhibitors. R406 33-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 26684498-8 2016 Predictions of DDI using deleobuvir alone would have significantly over-predicted the DDI potential for CYP3A4 inhibition (AUC ratio of 6.15). deleobuvir 25-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 27276192-1 2016 The aim of this study was to evaluate the impact of polymorphisms in the EPHX1 (c.416A > G, c.337T > C) and CYP3A4*22 genes involved in carbamazepine (CBZ) metabolism and pharmacoresistance among 118 Tunisian patients with epilepsy under maintenance dose of CBZ. Carbamazepine 142-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 26886336-1 2016 Fluvoxamine-perpetrated drug-drug interactions (DDIs) of victims metabolized by multiple cytochrome P450 isoforms (CYP1A2, CYP2C19, and CYP3A4) were simulated using 2 compartment-based tube modeling, assuming a multiple inhibition-constant (Ki) model, as well as a previously reported single Ki model. Fluvoxamine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 27276192-5 2016 The CYP3A4*22 variant allele is significantly associated with lower CBZ-D:CBZ-E ratio and seems also to be associated with less activity of the cytochrome. cbz-d 68-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 27276192-5 2016 The CYP3A4*22 variant allele is significantly associated with lower CBZ-D:CBZ-E ratio and seems also to be associated with less activity of the cytochrome. cbz-e 74-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 26660633-7 2016 The half inhibitory concentration of tolvaptan on cell growth in HEK293/SULT1C3 cells and HEK293/CYP3A4 & SULT1C3 cells was significantly lower than that in the corresponding HEK293/vector cells or HEK293/CYP3A4 & SULT vector cells. Tolvaptan 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 26689604-8 2016 We illustrated this strategy for two drugs often included in phenotyping cocktails, midazolam (probe for CYP3A) and digoxin (P-glycoprotein), based on the data of a previous study, and were able to find a sparse and flexible design. Midazolam 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-110 26660633-7 2016 The half inhibitory concentration of tolvaptan on cell growth in HEK293/SULT1C3 cells and HEK293/CYP3A4 & SULT1C3 cells was significantly lower than that in the corresponding HEK293/vector cells or HEK293/CYP3A4 & SULT vector cells. Tolvaptan 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 209-215 26981194-6 2016 Metabolism of vitamin E begins with one cycle of CYP4F2/CYP3A4-dependent omega-hydroxylation followed by five cycles of subsequent beta-oxidation, and forms the water-soluble end-product carboxyethylhydroxychroman. Vitamin E 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 26899743-0 2016 Single-Walled Carbon Nanotubes Inhibit the Cytochrome P450 Enzyme, CYP3A4. Carbon 14-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 26903378-8 2016 Thalidomide-treated embryos with the human CYP3A gene cluster showed limb abnormalities, and human CYP3A was expressed in the placenta, suggesting that human CYP3A in the placenta may contribute to the teratogenicity of thalidomide. Thalidomide 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-48 26903378-8 2016 Thalidomide-treated embryos with the human CYP3A gene cluster showed limb abnormalities, and human CYP3A was expressed in the placenta, suggesting that human CYP3A in the placenta may contribute to the teratogenicity of thalidomide. Thalidomide 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-104 26903378-8 2016 Thalidomide-treated embryos with the human CYP3A gene cluster showed limb abnormalities, and human CYP3A was expressed in the placenta, suggesting that human CYP3A in the placenta may contribute to the teratogenicity of thalidomide. Thalidomide 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-104 26903378-8 2016 Thalidomide-treated embryos with the human CYP3A gene cluster showed limb abnormalities, and human CYP3A was expressed in the placenta, suggesting that human CYP3A in the placenta may contribute to the teratogenicity of thalidomide. Thalidomide 220-231 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-48 26814638-10 2016 Differential scanning calorimetry (DSC) of CYP3A4-nanodiscs suggests membrane-induced stabilization compared to that of aggregated CYP3A4 in buffer, and this stabilization is enhanced upon addition of the ligand ketoconazole. Ketoconazole 212-224 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 26814638-10 2016 Differential scanning calorimetry (DSC) of CYP3A4-nanodiscs suggests membrane-induced stabilization compared to that of aggregated CYP3A4 in buffer, and this stabilization is enhanced upon addition of the ligand ketoconazole. Ketoconazole 212-224 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 26814638-11 2016 This ligand-induced stabilization is accompanied by a very large increase in DeltaH for CYP3A4 denaturation in nanodiscs, possibly due to increased CYP3A4-membrane interactions. deltah 77-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 26814638-11 2016 This ligand-induced stabilization is accompanied by a very large increase in DeltaH for CYP3A4 denaturation in nanodiscs, possibly due to increased CYP3A4-membrane interactions. deltah 77-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 26903378-8 2016 Thalidomide-treated embryos with the human CYP3A gene cluster showed limb abnormalities, and human CYP3A was expressed in the placenta, suggesting that human CYP3A in the placenta may contribute to the teratogenicity of thalidomide. Thalidomide 220-231 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-104 26899743-1 2016 We report a detailed computational and experimental study of the interaction of single-walled carbon nanotubes (SWCNTs) with the drug-metabolizing cytochrome P450 enzyme, CYP3A4. Carbon 94-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 26903378-8 2016 Thalidomide-treated embryos with the human CYP3A gene cluster showed limb abnormalities, and human CYP3A was expressed in the placenta, suggesting that human CYP3A in the placenta may contribute to the teratogenicity of thalidomide. Thalidomide 220-231 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-104 26899743-2 2016 Dose-dependent inhibition of CYP3A4-mediated conversion of the model compound, testosterone, to its major metabolite, 6beta-hydroxy testosterone was noted. Testosterone 79-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 26899743-2 2016 Dose-dependent inhibition of CYP3A4-mediated conversion of the model compound, testosterone, to its major metabolite, 6beta-hydroxy testosterone was noted. 6 beta-hydroxytestosterone 118-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 26899743-5 2016 Furthermore, covalent functionalization of SWCNTs with polyethylene glycol (PEG) chains mitigated the inhibition of CYP3A4 enzymatic activity. swcnts 43-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 26899743-5 2016 Furthermore, covalent functionalization of SWCNTs with polyethylene glycol (PEG) chains mitigated the inhibition of CYP3A4 enzymatic activity. Polyethylene Glycols 55-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 26899743-5 2016 Furthermore, covalent functionalization of SWCNTs with polyethylene glycol (PEG) chains mitigated the inhibition of CYP3A4 enzymatic activity. Polyethylene Glycols 76-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 26872388-0 2016 Effect of Ethanol on the Metabolic Characteristics of HIV-1 Integrase Inhibitor Elvitegravir and Elvitegravir/Cobicistat with CYP3A: An Analysis Using a Newly Developed LC-MS/MS Method. Ethanol 10-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-131 26901218-4 2016 However, inflammation can downregulate CYP3A4 and other drug metabolizing enzymes and lead to altered metabolism of drugs and essential vitamins and lipids. essential vitamins 126-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 26814364-1 2016 Tamoxifen, a hormonal therapy drug against estrogen receptor-positive breast cancer, can be metabolized by cytochrome P450 enzymes such as CYP3A4 and CYP3A5, and converted to N-desmethyltamoxifen, which is subsequently, metabolized by CYP2D6 and inverted to form 4-hydroxy-N-desmethyltamoxifen (endoxifen). Tamoxifen 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 26814364-1 2016 Tamoxifen, a hormonal therapy drug against estrogen receptor-positive breast cancer, can be metabolized by cytochrome P450 enzymes such as CYP3A4 and CYP3A5, and converted to N-desmethyltamoxifen, which is subsequently, metabolized by CYP2D6 and inverted to form 4-hydroxy-N-desmethyltamoxifen (endoxifen). N-desmethyltamoxifen 175-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 26814364-1 2016 Tamoxifen, a hormonal therapy drug against estrogen receptor-positive breast cancer, can be metabolized by cytochrome P450 enzymes such as CYP3A4 and CYP3A5, and converted to N-desmethyltamoxifen, which is subsequently, metabolized by CYP2D6 and inverted to form 4-hydroxy-N-desmethyltamoxifen (endoxifen). 4-hydroxy-N-desmethyltamoxifen 263-293 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 26814364-1 2016 Tamoxifen, a hormonal therapy drug against estrogen receptor-positive breast cancer, can be metabolized by cytochrome P450 enzymes such as CYP3A4 and CYP3A5, and converted to N-desmethyltamoxifen, which is subsequently, metabolized by CYP2D6 and inverted to form 4-hydroxy-N-desmethyltamoxifen (endoxifen). 4-hydroxy-N-desmethyltamoxifen 295-304 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 26872388-0 2016 Effect of Ethanol on the Metabolic Characteristics of HIV-1 Integrase Inhibitor Elvitegravir and Elvitegravir/Cobicistat with CYP3A: An Analysis Using a Newly Developed LC-MS/MS Method. elvitegravir 97-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-131 26872388-0 2016 Effect of Ethanol on the Metabolic Characteristics of HIV-1 Integrase Inhibitor Elvitegravir and Elvitegravir/Cobicistat with CYP3A: An Analysis Using a Newly Developed LC-MS/MS Method. Cobicistat 110-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-131 26872388-3 2016 Previously, we have shown that ethanol alters ART-CYP3A4 interactions with protease inhibitors thereby altering their metabolisms. Ethanol 31-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 26872388-5 2016 In this study, we characterized EVG and cobicistat (COBI)-boosted EVG metabolism in human microsomes followed by ethanol-EVG, ethanol-COBI-EVG interaction with CYP3A. ethanol-cobi-evg 126-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-165 26872388-11 2016 Inhibition studies demonstrated that EVG inhibits CYP3A4, and 20 mM ethanol causes a decrease in the IC50 of EVG. elvitegravir 37-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 26872388-12 2016 However, in the presence of COBI we were unable to determine these parameters effectively because COBI, being a strong inhibitor of CYP3A4, blocked the EVG/ethanol-CYP3A4 interactions. Cobicistat 98-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 26872388-12 2016 However, in the presence of COBI we were unable to determine these parameters effectively because COBI, being a strong inhibitor of CYP3A4, blocked the EVG/ethanol-CYP3A4 interactions. Cobicistat 98-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 26872388-12 2016 However, in the presence of COBI we were unable to determine these parameters effectively because COBI, being a strong inhibitor of CYP3A4, blocked the EVG/ethanol-CYP3A4 interactions. elvitegravir 152-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 26872388-12 2016 However, in the presence of COBI we were unable to determine these parameters effectively because COBI, being a strong inhibitor of CYP3A4, blocked the EVG/ethanol-CYP3A4 interactions. elvitegravir 152-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 26872388-12 2016 However, in the presence of COBI we were unable to determine these parameters effectively because COBI, being a strong inhibitor of CYP3A4, blocked the EVG/ethanol-CYP3A4 interactions. Ethanol 156-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 26872388-12 2016 However, in the presence of COBI we were unable to determine these parameters effectively because COBI, being a strong inhibitor of CYP3A4, blocked the EVG/ethanol-CYP3A4 interactions. Ethanol 156-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 26872388-13 2016 Docking studies predicted a shift of EVG or COBI binding to the active site of CYP3A4 in the presence of ethanol. elvitegravir 37-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 26872388-13 2016 Docking studies predicted a shift of EVG or COBI binding to the active site of CYP3A4 in the presence of ethanol. Cobicistat 44-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 26872388-13 2016 Docking studies predicted a shift of EVG or COBI binding to the active site of CYP3A4 in the presence of ethanol. Ethanol 105-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 26872388-14 2016 Taken together, these results suggest that ethanol interacts with microsomal CYP3A and alters EVG-CYP3A4 interaction thereby altering EVG metabolism and inhibition of CYP3A4 by EVG. Ethanol 43-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 26872388-14 2016 Taken together, these results suggest that ethanol interacts with microsomal CYP3A and alters EVG-CYP3A4 interaction thereby altering EVG metabolism and inhibition of CYP3A4 by EVG. Ethanol 43-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 26872388-14 2016 Taken together, these results suggest that ethanol interacts with microsomal CYP3A and alters EVG-CYP3A4 interaction thereby altering EVG metabolism and inhibition of CYP3A4 by EVG. Ethanol 43-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 167-173 26872388-14 2016 Taken together, these results suggest that ethanol interacts with microsomal CYP3A and alters EVG-CYP3A4 interaction thereby altering EVG metabolism and inhibition of CYP3A4 by EVG. elvitegravir 94-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 26872388-14 2016 Taken together, these results suggest that ethanol interacts with microsomal CYP3A and alters EVG-CYP3A4 interaction thereby altering EVG metabolism and inhibition of CYP3A4 by EVG. elvitegravir 94-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 167-173 26872388-14 2016 Taken together, these results suggest that ethanol interacts with microsomal CYP3A and alters EVG-CYP3A4 interaction thereby altering EVG metabolism and inhibition of CYP3A4 by EVG. elvitegravir 134-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 26872388-14 2016 Taken together, these results suggest that ethanol interacts with microsomal CYP3A and alters EVG-CYP3A4 interaction thereby altering EVG metabolism and inhibition of CYP3A4 by EVG. elvitegravir 134-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 26845774-4 2016 The results showed that CK inhibited the enzyme activities of CYP2C9 and CYP3A4 in the HLMs. ginsenoside M1 24-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 26683990-11 2016 A chemical inhibition study with a broad and five specific CYP450 inhibitors revealed that most of the dictamnine metabolites in liver microsomes are mediated by CYP450, with CYP3A4 as the predominant enzyme involved in the formation of M7, the major metabolite. dictamnine 103-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 26845774-8 2016 The results suggested that CK was a substrate and also inhibitors for both CYP2C9 and CYP3A4. ginsenoside M1 27-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 26845774-9 2016 Patients using CK in combination with therapeutic drugs that are substrates of CYP2C9 and CYP3A4 for different reasons should be careful, although the inhibiting potency of CK is much poorer than that of enzyme-specific inhibitors. ginsenoside M1 15-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 26592516-1 2016 AIM: To evaluate the SimCYP simulator ethnicity-specific population model for predicting the pharmacokinetics of midazolam, a typical CYP3A4/5 substrate, in Chinese after oral administration. Midazolam 113-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 26840840-8 2016 Encapsulated C3A cells exhibited greater viability and CYP1A2 and CYP3A4 activity in the DMFBB than in the FBB, although the increases in albumin and urea synthesis were less prominent. dmfbb 89-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 26775663-9 2016 Ginkgolide B increased the expression of CYP3A4 and MDR1 in the cells, which was partially reversed by pretreatment with the selective PXR signaling antagonist sulforaphane, or transfection with PXR siRNA. ginkgolide B 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 26775663-9 2016 Ginkgolide B increased the expression of CYP3A4 and MDR1 in the cells, which was partially reversed by pretreatment with the selective PXR signaling antagonist sulforaphane, or transfection with PXR siRNA. sulforaphane 160-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 26661629-6 2016 We postulate that esomeprazole may have a mild inhibitory effect on CYP3A4, which leads to decreased metabolism of estrogen, thereby increasing serum estrogen levels. Esomeprazole 18-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 26805594-0 2016 Use of 4beta-hydroxycholesterol in animal and human plasma samples as a biomarker for CYP3A induction. cholest-5-ene-3,4-diol 7-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 26805594-1 2016 BACKGROUND: 4beta-hydroxycholesterol (4betaHC) has recently been proposed as a potential endogenous biomarker for CYP3A activity. cholest-5-ene-3,4-diol 12-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 26805594-1 2016 BACKGROUND: 4beta-hydroxycholesterol (4betaHC) has recently been proposed as a potential endogenous biomarker for CYP3A activity. cholest-5-ene-3,4-diol 38-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 26805594-4 2016 CONCLUSION: These assays were applied to multiple studies and demonstrated potential applications of 4betaHC as a CYP3A biomarker across preclinical and clinical settings. cholest-5-ene-3,4-diol 101-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 26574235-0 2016 4beta-hydroxycholesterol correlates with dose but not steady-state concentration of carbamazepine: indication of intestinal CYP3A in biomarker formation? cholest-5-ene-3,4-diol 0-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-129 26574235-1 2016 AIM: 4beta-hydroxycholesterol (4betaOHC) is an endogenous CYP3A(4) biomarker, which is elevated by use of the CYP3A4 inducer carbamazepine. cholest-5-ene-3,4-diol 5-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 26574235-1 2016 AIM: 4beta-hydroxycholesterol (4betaOHC) is an endogenous CYP3A(4) biomarker, which is elevated by use of the CYP3A4 inducer carbamazepine. cholest-5-ene-3,4-diol 5-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 26574235-1 2016 AIM: 4beta-hydroxycholesterol (4betaOHC) is an endogenous CYP3A(4) biomarker, which is elevated by use of the CYP3A4 inducer carbamazepine. 4betaohc 31-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 26574235-1 2016 AIM: 4beta-hydroxycholesterol (4betaOHC) is an endogenous CYP3A(4) biomarker, which is elevated by use of the CYP3A4 inducer carbamazepine. 4betaohc 31-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 26574235-1 2016 AIM: 4beta-hydroxycholesterol (4betaOHC) is an endogenous CYP3A(4) biomarker, which is elevated by use of the CYP3A4 inducer carbamazepine. Carbamazepine 125-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 26574235-1 2016 AIM: 4beta-hydroxycholesterol (4betaOHC) is an endogenous CYP3A(4) biomarker, which is elevated by use of the CYP3A4 inducer carbamazepine. Carbamazepine 125-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 26574235-12 2016 This suggests a stronger inductive effect of carbamazepine on presystemic than systemic CYP3A4 phenotype and might indicate a role of the intestine in 4betaOHC formation. Carbamazepine 45-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 26341813-1 2016 OBJECTIVE: To assess the effect of strong and moderate cytochrome P450 (CYP) 3A4 inhibition on exposure of bitopertin, a glycine reuptake inhibitor primarily metabolized by CYP3A4, and to compare the results with predictions based on physiologically based pharmacokinetic (PBPK) modelling. (4-(3-fluoro-5-trifluoromethylpyridin-2-yl)piperazin-1-yl)(5-methanesulfonyl-2-(2,2,2-trifluoro-1-methylethoxy)phenyl)methanone 107-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-80 26341813-1 2016 OBJECTIVE: To assess the effect of strong and moderate cytochrome P450 (CYP) 3A4 inhibition on exposure of bitopertin, a glycine reuptake inhibitor primarily metabolized by CYP3A4, and to compare the results with predictions based on physiologically based pharmacokinetic (PBPK) modelling. (4-(3-fluoro-5-trifluoromethylpyridin-2-yl)piperazin-1-yl)(5-methanesulfonyl-2-(2,2,2-trifluoro-1-methylethoxy)phenyl)methanone 107-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 26341813-12 2016 CONCLUSION: Strong CYP3A4 inhibitors increase AUC0-inf of bitopertin 7- to 8-fold and hence should not be administered concomitantly with bitopertin. (4-(3-fluoro-5-trifluoromethylpyridin-2-yl)piperazin-1-yl)(5-methanesulfonyl-2-(2,2,2-trifluoro-1-methylethoxy)phenyl)methanone 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 26353895-2 2016 Simeprevir is metabolized by the cytochrome P450 (CYP) system, primarily CYP3A, and is a substrate for several drug transporters, including the organic anion transporting polypeptides (OATPs). Simeprevir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 26259716-5 2016 The interplay between hepatic uptake and CYP3A4 metabolism was verified by simulations with rifampicin, a potent CYP3A4 inducer and OATP1B1/3 inhibitor, and maintenance doses of cyclosporine. Rifampin 92-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 26259716-5 2016 The interplay between hepatic uptake and CYP3A4 metabolism was verified by simulations with rifampicin, a potent CYP3A4 inducer and OATP1B1/3 inhibitor, and maintenance doses of cyclosporine. Rifampin 92-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 26259716-5 2016 The interplay between hepatic uptake and CYP3A4 metabolism was verified by simulations with rifampicin, a potent CYP3A4 inducer and OATP1B1/3 inhibitor, and maintenance doses of cyclosporine. Cyclosporine 178-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 26353895-3 2016 It is susceptible to metabolic drug-drug interactions with drugs that are moderate or strong CYP3A inhibitors (e.g. ritonavir and erythromycin) or CYP3A inducers (e.g. rifampin and efavirenz); coadministration of these drugs may increase or decrease plasma concentrations of simeprevir, respectively, and should be avoided. Ritonavir 116-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 26658225-5 2016 The EC50 of rifampin for CYP3A4 and CYP2C9 was up to 10-fold lower in HepatoPac than the monocultures. Rifampin 12-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 26353895-3 2016 It is susceptible to metabolic drug-drug interactions with drugs that are moderate or strong CYP3A inhibitors (e.g. ritonavir and erythromycin) or CYP3A inducers (e.g. rifampin and efavirenz); coadministration of these drugs may increase or decrease plasma concentrations of simeprevir, respectively, and should be avoided. Erythromycin 130-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 26353895-3 2016 It is susceptible to metabolic drug-drug interactions with drugs that are moderate or strong CYP3A inhibitors (e.g. ritonavir and erythromycin) or CYP3A inducers (e.g. rifampin and efavirenz); coadministration of these drugs may increase or decrease plasma concentrations of simeprevir, respectively, and should be avoided. Simeprevir 275-285 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 26353895-4 2016 Clinical studies have shown that simeprevir is a mild inhibitor of CYP1A2 and intestinal CYP3A but does not inhibit hepatic CYP3A. Simeprevir 33-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-94 26353895-8 2016 Cyclosporine is an inhibitor of OATP1B1/3, BCRP and P-gp, and a mild inhibitor of CYP3A; cyclosporine causes a significant increase in simeprevir plasma concentrations, and coadministration is not recommended. Cyclosporine 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-87 26353895-8 2016 Cyclosporine is an inhibitor of OATP1B1/3, BCRP and P-gp, and a mild inhibitor of CYP3A; cyclosporine causes a significant increase in simeprevir plasma concentrations, and coadministration is not recommended. Cyclosporine 89-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-87 26521259-4 2016 The primary objective of this study was to investigate the effect of CYP3A4*22 and CYP3A5*3 of both donor and recipient on once daily tacrolimus pharmacokinetics. Tacrolimus 134-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 25374256-0 2016 CYP3A4-based drug-drug interaction: CYP3A4 substrates" pharmacokinetic properties and ketoconazole dose regimen effect. Ketoconazole 86-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25374256-1 2016 The aim of the study was to assess the magnitude of the CYP3A4 inhibitory effect of 2 dosing regimens of ketoconazole and the influence of the pharmacokinetic properties of the CYP3A4 substrate on the extent of the substrate exposure increase. Ketoconazole 105-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 25425116-0 2016 In vitro metabolism of bencycloquidium bromide and its inhibitory effects on human P450 isoenzymes: implication of CYP2D6, CYP2C19 and CYP3A4/5. bencycloquidium bromide 23-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 25425116-7 2016 Inhibition studies with selective chemical inhibitors and incubations with human recombinant P450 isoforms demonstrated that the oxidative metabolism of BCQB is mediated by CYP2D6, CYP2C19 and CYP3A4/5, whereas BCQB had no inhibitory effect on any other P450 isoenzyme in humans. bencycloquidium bromide 153-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 193-199 25305360-0 2016 The effect of race on the CYP3A-mediated metabolism of vincristine in pediatric patients with acute lymphoblastic leukemia. Vincristine 55-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-31 26239522-0 2016 Evidence-based choice of ritonavir as index CYP3A inhibitor in drug-drug interaction studies. Ritonavir 25-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-49 26201057-6 2016 Induction of CYP1A2, CYP2B6 and CYP3A4 activities in the tethered spheroids were comparable to, if not higher than that observed in the collagen sandwich cultures. spheroids 66-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 26044116-1 2016 Ketoconazole has been widely used as a strong cytochrome P450 (CYP) 3A (CYP3A) inhibitor in drug-drug interaction (DDI) studies. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-70 26044116-1 2016 Ketoconazole has been widely used as a strong cytochrome P450 (CYP) 3A (CYP3A) inhibitor in drug-drug interaction (DDI) studies. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-77 26813987-2 2016 We report a serious side effect of ibrutinib potentially attributable to interaction with the moderate CYP3A4 inhibitor verapamil. ibrutinib 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 26813987-2 2016 We report a serious side effect of ibrutinib potentially attributable to interaction with the moderate CYP3A4 inhibitor verapamil. Verapamil 120-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 26813987-9 2016 WHAT IS NEW AND CONCLUSION: This is the first description of a serious side effect of ibrutinib likely due to an interaction with the CYP3A4 inhibitor verapamil. ibrutinib 86-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 26813987-9 2016 WHAT IS NEW AND CONCLUSION: This is the first description of a serious side effect of ibrutinib likely due to an interaction with the CYP3A4 inhibitor verapamil. Verapamil 151-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 26813987-10 2016 Prescriptions of ibrutinib must be carefully checked to identify possible interactions with CYP3A4 inhibitors and patients monitored accordingly. ibrutinib 17-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 25305360-1 2016 OBJECTIVE: The purpose of this preliminary study was to compare racial background and CYP3A distribution in pediatric acute lymphoblastic leukemia patients as it relates to vincristine-related neurotoxicity. Vincristine 173-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 26869438-5 2016 Specifically, CYP3A4 activity was increased up to 20-fold as compared to vitamin D treated wild-type Caco-2 cells. Vitamin D 73-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 26869439-6 2016 LPS-activated HKCCs, but not hepatocyte monocultures, treated with trovafloxacin or acetaminophen, compounds associated with immune-mediated hepatotoxicity, showed LPS-dependent decreases in interleukin-6 production with concomitant increases in Cyp3A activity. trovafloxacin 67-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 246-251 26869439-6 2016 LPS-activated HKCCs, but not hepatocyte monocultures, treated with trovafloxacin or acetaminophen, compounds associated with immune-mediated hepatotoxicity, showed LPS-dependent decreases in interleukin-6 production with concomitant increases in Cyp3A activity. Acetaminophen 84-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 246-251 26782648-0 2016 SUMOylation of pregnane X receptor suppresses rifampicin-induced CYP3A4 and P-gp expression and activity in LS174T cells. Rifampin 46-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 26782648-5 2016 Our results revealed that rifampicin-induced PXR transactivation of the CYP3A4 and P-gp promoter was suppressed by SUMOylation of PXR in reporter gene assay. Rifampin 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 26782648-7 2016 Moreover, CYP3A4 enzymatic assay and Rho123 intracellular assay revealed that rifampicin-induced CYP3A4 and P-gp activity was also suppressed by SUMOylated PXR. Rifampin 78-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 26782648-7 2016 Moreover, CYP3A4 enzymatic assay and Rho123 intracellular assay revealed that rifampicin-induced CYP3A4 and P-gp activity was also suppressed by SUMOylated PXR. Rifampin 78-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 26782648-8 2016 Our data collectively indicated for the first time that SUMOylation of PXR exerts suppressive effect on rifampicin-induced expression and activity of CYP3A4 and P-gp, which suggest that alteration in the SUMOylation status of PXR will be expected to affect the CYP3A4 mediated drug metabolism and P-gp mediated drug transport. Rifampin 104-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 26782648-8 2016 Our data collectively indicated for the first time that SUMOylation of PXR exerts suppressive effect on rifampicin-induced expression and activity of CYP3A4 and P-gp, which suggest that alteration in the SUMOylation status of PXR will be expected to affect the CYP3A4 mediated drug metabolism and P-gp mediated drug transport. Rifampin 104-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 261-267 26493547-8 2016 Data submitted to the U.S. Food and Drug Administration demonstrate that dexmedetomidine inhibits CYP 3A4 and may produce adequate liver concentrations that could interfere with tacrolimus metabolism. Dexmedetomidine 73-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-105 26741368-5 2016 We then studied the effect of methamphetamine binding on PIs with CYP3A4. Methamphetamine 30-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 26610396-2 2016 Although the application of ketoconazole, a CYP3A4 inhibitor, led to a decreased cytotoxicity of CYN, no metabolites were detected applying high resolution mass spectrometry. Ketoconazole 28-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 26610396-2 2016 Although the application of ketoconazole, a CYP3A4 inhibitor, led to a decreased cytotoxicity of CYN, no metabolites were detected applying high resolution mass spectrometry. cylindrospermopsin 97-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 26818566-3 2016 Artemether and lumefantrine are metabolised by cytochrome P450 isoenzyme CYP3A4, which lopinavir/ritonavir inhibits, potentially causing clinically important drug-drug interactions. Artemether, Lumefantrine Drug Combination 0-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 26818566-3 2016 Artemether and lumefantrine are metabolised by cytochrome P450 isoenzyme CYP3A4, which lopinavir/ritonavir inhibits, potentially causing clinically important drug-drug interactions. Lopinavir 87-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 26818566-3 2016 Artemether and lumefantrine are metabolised by cytochrome P450 isoenzyme CYP3A4, which lopinavir/ritonavir inhibits, potentially causing clinically important drug-drug interactions. Ritonavir 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 26741368-0 2016 Effect of Methamphetamine on Spectral Binding, Ligand Docking and Metabolism of Anti-HIV Drugs with CYP3A4. Methamphetamine 10-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 26741368-2 2016 This study was undertaken to examine the effect of methamphetamine on the binding and metabolism of PIs with CYP3A4. Methamphetamine 51-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 26741368-9 2016 Our results showed that methamphetamine alters the ritonavir binding to CYP3A4 by decreasing both the deltaAmax (0.0038+-0.0003 vs. 0.0055+-0.0003) and KD (0.043+-0.0001 vs. 0.065+-0.001 nM), while indinavir showed only reduced KD in presence of methamphetamine (0.086+-0.01 vs. 0.174+-0.03 nM). Methamphetamine 24-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 26741368-3 2016 We showed that methamphetamine exhibits a type I spectral change upon binding to CYP3A4 with deltaAmax and KD of 0.016+-0.001 and 204+-18 muM, respectively. Methamphetamine 15-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 26741368-4 2016 Methamphetamine-CYP3A4 docking showed that methamphetamine binds to the heme of CYP3A4 in two modes, both leading to N-demethylation. Methamphetamine 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 26741368-9 2016 Our results showed that methamphetamine alters the ritonavir binding to CYP3A4 by decreasing both the deltaAmax (0.0038+-0.0003 vs. 0.0055+-0.0003) and KD (0.043+-0.0001 vs. 0.065+-0.001 nM), while indinavir showed only reduced KD in presence of methamphetamine (0.086+-0.01 vs. 0.174+-0.03 nM). Ritonavir 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 26741368-4 2016 Methamphetamine-CYP3A4 docking showed that methamphetamine binds to the heme of CYP3A4 in two modes, both leading to N-demethylation. Methamphetamine 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 26741368-4 2016 Methamphetamine-CYP3A4 docking showed that methamphetamine binds to the heme of CYP3A4 in two modes, both leading to N-demethylation. Methamphetamine 43-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 26741368-9 2016 Our results showed that methamphetamine alters the ritonavir binding to CYP3A4 by decreasing both the deltaAmax (0.0038+-0.0003 vs. 0.0055+-0.0003) and KD (0.043+-0.0001 vs. 0.065+-0.001 nM), while indinavir showed only reduced KD in presence of methamphetamine (0.086+-0.01 vs. 0.174+-0.03 nM). deltaamax 102-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 26741368-4 2016 Methamphetamine-CYP3A4 docking showed that methamphetamine binds to the heme of CYP3A4 in two modes, both leading to N-demethylation. Methamphetamine 43-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 26741368-4 2016 Methamphetamine-CYP3A4 docking showed that methamphetamine binds to the heme of CYP3A4 in two modes, both leading to N-demethylation. Heme 72-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 26741368-4 2016 Methamphetamine-CYP3A4 docking showed that methamphetamine binds to the heme of CYP3A4 in two modes, both leading to N-demethylation. Heme 72-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 26741368-4 2016 Methamphetamine-CYP3A4 docking showed that methamphetamine binds to the heme of CYP3A4 in two modes, both leading to N-demethylation. Nitrogen 117-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 26741368-9 2016 Our results showed that methamphetamine alters the ritonavir binding to CYP3A4 by decreasing both the deltaAmax (0.0038+-0.0003 vs. 0.0055+-0.0003) and KD (0.043+-0.0001 vs. 0.065+-0.001 nM), while indinavir showed only reduced KD in presence of methamphetamine (0.086+-0.01 vs. 0.174+-0.03 nM). Indinavir 198-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 26741368-4 2016 Methamphetamine-CYP3A4 docking showed that methamphetamine binds to the heme of CYP3A4 in two modes, both leading to N-demethylation. Nitrogen 117-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 26741368-9 2016 Our results showed that methamphetamine alters the ritonavir binding to CYP3A4 by decreasing both the deltaAmax (0.0038+-0.0003 vs. 0.0055+-0.0003) and KD (0.043+-0.0001 vs. 0.065+-0.001 nM), while indinavir showed only reduced KD in presence of methamphetamine (0.086+-0.01 vs. 0.174+-0.03 nM). Methamphetamine 246-261 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 26741368-10 2016 Furthermore, LC-MS/MS studies in high CYP3A4 human liver microsomes showed a decrease in the formation of hydroxy ritonavir in the presence of methamphetamine. Hydroxy Ritonavir 106-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 26741368-10 2016 Furthermore, LC-MS/MS studies in high CYP3A4 human liver microsomes showed a decrease in the formation of hydroxy ritonavir in the presence of methamphetamine. Methamphetamine 143-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 26741368-11 2016 Finally, CYP3A4 docking with lopinavir and ritonavir in the absence and presence of methamphetamine showed that methamphetamine alters the docking of ritonavir, which is consistent with the results obtained from spectral binding and metabolism studies. Lopinavir 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 26741368-11 2016 Finally, CYP3A4 docking with lopinavir and ritonavir in the absence and presence of methamphetamine showed that methamphetamine alters the docking of ritonavir, which is consistent with the results obtained from spectral binding and metabolism studies. Ritonavir 43-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 26741368-11 2016 Finally, CYP3A4 docking with lopinavir and ritonavir in the absence and presence of methamphetamine showed that methamphetamine alters the docking of ritonavir, which is consistent with the results obtained from spectral binding and metabolism studies. Methamphetamine 112-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 26741368-11 2016 Finally, CYP3A4 docking with lopinavir and ritonavir in the absence and presence of methamphetamine showed that methamphetamine alters the docking of ritonavir, which is consistent with the results obtained from spectral binding and metabolism studies. Ritonavir 150-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 26741368-12 2016 Overall, our results demonstrated differential effects of methamphetamine on the binding and metabolism of PIs with CYP3A4. Methamphetamine 58-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 26618923-7 2016 In experimental colitis models, rifaximin antagonised the effects of tumour necrosis factor-alpha on intestinal epithelial cells by activating pregnane X receptor, which inhibits nuclear factor-kappaB-mediated proinflammatory mediators and induces detoxification genes (e.g. multidrug resistance 1 and cytochrome P450 3A4). Rifaximin 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 302-321 26361765-0 2016 Gomisin A is a Novel Isoform-Specific Probe for the Selective Sensing of Human Cytochrome P450 3A4 in Liver Microsomes and Living Cells. schizandrol B 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-98 26361765-4 2016 In the present study, we introduced gomisin A (GA) with a dibenzocyclooctadiene skeleton as a novel selective probe of CYP3A4. schizandrol B 36-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 26361765-4 2016 In the present study, we introduced gomisin A (GA) with a dibenzocyclooctadiene skeleton as a novel selective probe of CYP3A4. schizandrol B 47-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 26361765-4 2016 In the present study, we introduced gomisin A (GA) with a dibenzocyclooctadiene skeleton as a novel selective probe of CYP3A4. dibenzocyclooctadiene 58-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 26361765-7 2016 GA 8-hydroxylation in both recombinant human CYP3A4 and human liver microsomes followed classic Michaelis-Menten kinetics. schizandrol B 0-2 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 26361765-8 2016 The intrinsic clearance values indicated that CYP3A4 contributed 12.8-fold more than CYP3A5 to GA 8-hydroxylation. schizandrol B 95-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 26361765-9 2016 Molecular docking studies indicated different hydrogen bonds and pi-pi interactions between CYP3A4 and CYP3A5, which might result in the different catalytic activity for GA 8-hydroxylation. Hydrogen 46-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 26361765-9 2016 Molecular docking studies indicated different hydrogen bonds and pi-pi interactions between CYP3A4 and CYP3A5, which might result in the different catalytic activity for GA 8-hydroxylation. schizandrol B 170-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 26361765-10 2016 Furthermore, GA exhibited a stronger inhibitory activity towards CYP3A4 than CYP3A5, which further suggested a preferred selectivity of CYP3A4 for the transformation of GA. schizandrol B 13-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 26361765-10 2016 Furthermore, GA exhibited a stronger inhibitory activity towards CYP3A4 than CYP3A5, which further suggested a preferred selectivity of CYP3A4 for the transformation of GA. schizandrol B 13-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 26361765-10 2016 Furthermore, GA exhibited a stronger inhibitory activity towards CYP3A4 than CYP3A5, which further suggested a preferred selectivity of CYP3A4 for the transformation of GA. schizandrol B 169-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 26361765-10 2016 Furthermore, GA exhibited a stronger inhibitory activity towards CYP3A4 than CYP3A5, which further suggested a preferred selectivity of CYP3A4 for the transformation of GA. schizandrol B 169-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 26779253-4 2015 The drug metabolizing enzyme (DME), CYP2B6, is primarily responsible for EFV metabolism with minor contributions by CYP1A2, CYP2A6, CYP3A4, CYP3A5, and UGT2B7. dme 30-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 26759747-2 2016 Rifampin is a widely used antimicrobial that has major interactions with several medications including warfarin due to its strong P-glycoprotein and liver enzyme inducer activity especially on CYP2C9, CYP3A4, CYP1A2 and CYP2C19. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-207 26759747-2 2016 Rifampin is a widely used antimicrobial that has major interactions with several medications including warfarin due to its strong P-glycoprotein and liver enzyme inducer activity especially on CYP2C9, CYP3A4, CYP1A2 and CYP2C19. Warfarin 103-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-207 26727525-8 2016 In contrast, ART and EtOH treatments decreased CYP3A4 protein expression by 38 +- 17% and 74 +- 15%, respectively, and the combination additively decreased CYP3A4 level by 90 +- 8%. Ethanol 21-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 26727525-8 2016 In contrast, ART and EtOH treatments decreased CYP3A4 protein expression by 38 +- 17% and 74 +- 15%, respectively, and the combination additively decreased CYP3A4 level by 90 +- 8%. Ethanol 21-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 27328703-1 2016 The cytochrome P450 isoform that is primarily involved in the metabolism of the antipsychotic lurasidone is CYP3A4. Lurasidone Hydrochloride 94-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 26361765-11 2016 More importantly, GA has been successfully applied to selectively monitor the modulation of CYP3A4 activities by the inducer rifampin in hepG2 cells, which is consistent with the level change of CYP3A4 mRNA expression. schizandrol B 18-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 26361765-11 2016 More importantly, GA has been successfully applied to selectively monitor the modulation of CYP3A4 activities by the inducer rifampin in hepG2 cells, which is consistent with the level change of CYP3A4 mRNA expression. schizandrol B 18-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 26361765-12 2016 In summary, our results suggested that GA could be used as a novel probe for the selective sensing of CYP3A4 in tissue and cell preparations. schizandrol B 39-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 27328703-3 2016 Atazanavir, an HIV-1 protease inhibitor, has demonstrated to be an inhibitor of CYP3A4 and would be expected to increase the exposure of any drug metabolized by this enzyme. Atazanavir Sulfate 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 26565076-0 2016 Severe Vincristine-induced Neuropathic Pain in a CYP3A5 Nonexpressor With Reduced CYP3A4/5 Activity: Case Study. Vincristine 7-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 27582329-5 2016 The metabolisms to 6beta-hydroxytestosterone by recombinant CYP3A4 were significantly inhibited by VJ-o, VJ-g, and VJ-y in a preincubation time-dependent manner, and CYP3A4 activity in LS180 cells were significantly inhibited by VJ-o and VJ-y. 6 beta-hydroxytestosterone 19-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 27582329-5 2016 The metabolisms to 6beta-hydroxytestosterone by recombinant CYP3A4 were significantly inhibited by VJ-o, VJ-g, and VJ-y in a preincubation time-dependent manner, and CYP3A4 activity in LS180 cells were significantly inhibited by VJ-o and VJ-y. 6 beta-hydroxytestosterone 19-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-172 26352195-6 2016 The prediction of human metabolite levels such as hydroxy nefazodone (OH-NEF), triazoledione form (TD), m-chlorophenylpiperazine and dealkyl metabolites in Cyp3a KO CM was superior to that in Cyp3a KO, PXB or SCID mice. oh-nef 70-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-161 26352195-6 2016 The prediction of human metabolite levels such as hydroxy nefazodone (OH-NEF), triazoledione form (TD), m-chlorophenylpiperazine and dealkyl metabolites in Cyp3a KO CM was superior to that in Cyp3a KO, PXB or SCID mice. 1-(3-chlorophenyl)piperazine 104-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-161 26356245-0 2016 A physiologically based pharmacokinetic modeling approach to predict drug-drug interactions between domperidone and inhibitors of CYP3A4. Domperidone 100-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 26356245-1 2016 Domperidone is a dopamine receptor antagonist and a substrate of CYP3A4, hence there is a potential for CYP3A inhibition-based drug-drug interactions (DDI). Domperidone 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 26356245-1 2016 Domperidone is a dopamine receptor antagonist and a substrate of CYP3A4, hence there is a potential for CYP3A inhibition-based drug-drug interactions (DDI). Domperidone 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 26356245-2 2016 A physiologically based pharmacokinetic model was developed to describe DDIs between domperidone and three different inhibitors of CYP3A4. Domperidone 85-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 27439367-0 2016 Analysis of variants in the HCN4 gene and in three single nucleotide polymorphisms of the CYP3A4 gene for association with ivabradine reduction in heart rate: A preliminary report. Ivabradine 123-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 27439367-4 2016 The aim of the study is to identify variants associated with HR reduction produced by ivabradine in genes involved in the drug metabolism (CYP3A4) or related to the drug target (HCN4). Ivabradine 86-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 27439367-11 2016 However, more research must be undertaken in order to determine the role of variants in HCN4 and CYP3A4 genes in response to ivabradine. Ivabradine 125-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 26317320-10 2016 Simulations indicated concomitant strong CYP3A4 inhibitors or inducers had relevant effects on naloxegol exposure. naloxegol 95-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 26317320-11 2016 CONCLUSIONS: Administration of strong CYP3A4 inhibitors or inducers had a clinically relevant influence on naloxegol pharmacokinetics. naloxegol 107-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 26342857-5 2016 In gene expression level, the CYP360A gene, homologue to CYP3A in mammalian, showed inhibition at low concentration of IBU (0.5mug L(-1)) and induction at high concentration of IBU (50mug L(-1)). Ibuprofen 119-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 26844012-0 2016 Semiphysiologically based pharmacokinetic model for midazolam and CYP3A mediated metabolite 1-OH-midazolam in morbidly obese and weight loss surgery patients. 1-oh-midazolam 92-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 26342857-5 2016 In gene expression level, the CYP360A gene, homologue to CYP3A in mammalian, showed inhibition at low concentration of IBU (0.5mug L(-1)) and induction at high concentration of IBU (50mug L(-1)). Ibuprofen 177-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 26844012-1 2016 This study aimed to describe the pharmacokinetics of midazolam and its cytochrome P450 3A (CYP3A) mediated metabolite 1-OH-midazolam in morbidly obese patients receiving oral and i.v. Midazolam 53-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-96 26844012-1 2016 This study aimed to describe the pharmacokinetics of midazolam and its cytochrome P450 3A (CYP3A) mediated metabolite 1-OH-midazolam in morbidly obese patients receiving oral and i.v. 1-oh-midazolam 118-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-89 26844012-1 2016 This study aimed to describe the pharmacokinetics of midazolam and its cytochrome P450 3A (CYP3A) mediated metabolite 1-OH-midazolam in morbidly obese patients receiving oral and i.v. 1-oh-midazolam 118-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-96 26844012-2 2016 midazolam before (n = 20) and one year after weight loss surgery (n = 18), thereby providing insight into the influence of weight loss surgery on CYP3A activity in the gut wall and liver. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-151 27216792-6 2016 RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan. Losartan 107-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 26651976-1 2016 BACKGROUND: The contribution of the CYP3A5 enzyme to the metabolism of clinically used drugs has been established only for a few CYP3A substrates, such as the immunosuppressant tacrolimus, while for drugs used in the field of psychiatry its role is still vague. Tacrolimus 177-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 26651976-2 2016 METHODS: We herein discuss all published data on the contribution of CYP3A5 and its polymorphisms to the metabolism of antipsychotics and antidepressants that are known to be metabolized by CYP3A enzymes, as well as of carbamazepine, an antiepileptic drug used as mood stabilizer. Carbamazepine 219-232 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 26502771-8 2016 Voriconazole is metabolized by both CYP2C19 and CYP3A4 isoenzymes. Voriconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 26502771-11 2016 Simvastatin inhibits the CYP3A4 isoenzyme. Simvastatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 26512042-6 2016 Phenotyping experiments with human liver microsomes (HLMs) using chemical inhibitors and recombinant human cytochrome P450s demonstrated axitinib was predominately metabolized by CYP3A4/5, with minor contributions from CYP2C19 and CYP1A2. Axitinib 137-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 26512042-7 2016 The apparent substrate concentration at half-maximal velocity (Km) and Vmax values for the formation of axitinib sulfoxide by CYP3A4 or CYP3A5 were 4.0 or 1.9 microM and 9.6 or 1.4 pmol min(-1) pmol(-1), respectively. Axitinib sulfoxide 104-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 26512042-8 2016 Using a CYP3A4-specific inhibitor (Cyp3cide) in liver microsomes expressing CYP3A5, 66% of the axitinib intrinsic clearance was attributable to CYP3A4 and 15% to CYP3A5. Axitinib 95-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 26512042-8 2016 Using a CYP3A4-specific inhibitor (Cyp3cide) in liver microsomes expressing CYP3A5, 66% of the axitinib intrinsic clearance was attributable to CYP3A4 and 15% to CYP3A5. Axitinib 95-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 26512042-11 2016 In summary, CYP3A4 is the major enzyme involved in axitinib clearance with lesser contributions from CYP3A5, CYP2C19, CYP1A2, and UGT1A1. Axitinib 51-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 26123704-10 2016 For CYP3A4, total 1"-hydroxymidazolam concentrations after pretreatment of samples with beta-glucuronidase were needed to obtain adequate reflection of CYP induction by the metabolic ratio. 1-hydroxymethylmidazolam 18-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 26242379-5 2016 Idelalisib is metabolized primarily via aldehyde oxidase (AO) and, to a lesser extent, via cytochrome P450 (CYP) 3A. idelalisib 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-115 26242379-6 2016 Coadministration with the strong CYP3A inhibitor ketoconazole 400 mg once daily resulted in a ~79 % increase in the idelalisib area under the plasma concentration-time curve (AUC). Ketoconazole 49-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 26451002-7 2016 In vitro phenotyping experiments indicated that CYP3A4 was predominantly responsible for metabolizing cobimetinib. cobimetinib 102-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 26452722-10 2016 Rifampin-mediated CYP3A4 induction increased midazolam clearance by 73%, while CYP3A4 inhibition with ritonavir decreased midazolam clearance by 79%. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 26452722-10 2016 Rifampin-mediated CYP3A4 induction increased midazolam clearance by 73%, while CYP3A4 inhibition with ritonavir decreased midazolam clearance by 79%. Midazolam 45-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 26452722-10 2016 Rifampin-mediated CYP3A4 induction increased midazolam clearance by 73%, while CYP3A4 inhibition with ritonavir decreased midazolam clearance by 79%. Ritonavir 102-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 26452722-10 2016 Rifampin-mediated CYP3A4 induction increased midazolam clearance by 73%, while CYP3A4 inhibition with ritonavir decreased midazolam clearance by 79%. Midazolam 122-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 26534988-6 2016 Treatment with pifithrin-mu and transfection with anti-CHIP small-interfering RNA reduced the levels of CYP3A4 mRNA induced by rifampicin, suggesting the contribution of Hsp70 and CHIP to the transactivation of hPXR. pifithrin 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 26534988-6 2016 Treatment with pifithrin-mu and transfection with anti-CHIP small-interfering RNA reduced the levels of CYP3A4 mRNA induced by rifampicin, suggesting the contribution of Hsp70 and CHIP to the transactivation of hPXR. Rifampin 127-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 27117606-4 2016 MX was further reduced or oxidized to M2 (alcohol) and M4 (acid), respectively by enzymes such as aldo-keto reductase 1C1, aldehyde oxidase and possibly CYP3A4. Alcohols 42-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 26693854-4 2016 Furthermore, filgotinib"s interaction potential with CYP3A4 was examined in an open-label study in healthy volunteers, which evaluated the impact of filgotinib co-administration on the CYP3A4-sensitive substrate midazolam. GLPG0634 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 26693854-4 2016 Furthermore, filgotinib"s interaction potential with CYP3A4 was examined in an open-label study in healthy volunteers, which evaluated the impact of filgotinib co-administration on the CYP3A4-sensitive substrate midazolam. GLPG0634 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 26693854-4 2016 Furthermore, filgotinib"s interaction potential with CYP3A4 was examined in an open-label study in healthy volunteers, which evaluated the impact of filgotinib co-administration on the CYP3A4-sensitive substrate midazolam. Midazolam 212-221 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 26693854-7 2016 In the clinic, a lack of relevant pharmacokinetic drug interactions by filgotinib and its active metabolite with substrates of CYP3A4, as well as with organic anion transporters involved in methotrexate elimination were found. GLPG0634 71-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 27165340-0 2016 Formation of A Novel Purine Metabolite through CYP3A4 Bioactivation and Glutathione Conjugation. purine 21-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 27216792-6 2016 RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan. Valsartan 236-245 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 27165340-7 2016 It was demonstrated that the formation of the glutathione conjugate at the C-6 position of the purine ring system was due to the bioactivation of the compound to a di-imine intermediate by CYP3A4, followed by the nucleophilic addition of glutathione. Glutathione 46-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 26693855-0 2016 Inactivation of CYP3A4 by Benzbromarone in Human Liver Microsomes. Benzbromarone 26-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 26693855-6 2016 RESULTS: Benzbromarone metabolism resulted in inhibition of CYP3A4 but not CYP2C9 in a time-dependent manner. Benzbromarone 9-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 27165340-7 2016 It was demonstrated that the formation of the glutathione conjugate at the C-6 position of the purine ring system was due to the bioactivation of the compound to a di-imine intermediate by CYP3A4, followed by the nucleophilic addition of glutathione. purine 95-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 27216792-6 2016 RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan. candesartan 247-258 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 27165340-7 2016 It was demonstrated that the formation of the glutathione conjugate at the C-6 position of the purine ring system was due to the bioactivation of the compound to a di-imine intermediate by CYP3A4, followed by the nucleophilic addition of glutathione. diazene 164-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 26693855-7 2016 Confirmation of pseudo-first order kinetics of inhibition, a requirement for NADPH, and a lack of protection by scavengers suggested that benzbromarone is a mechanism-based CYP3A4 inhibitor. Benzbromarone 138-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 27216792-6 2016 RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan. Irbesartan 260-270 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 27165340-7 2016 It was demonstrated that the formation of the glutathione conjugate at the C-6 position of the purine ring system was due to the bioactivation of the compound to a di-imine intermediate by CYP3A4, followed by the nucleophilic addition of glutathione. Glutathione 238-249 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 27216792-6 2016 RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan. azilsartan 276-286 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 26912097-6 2016 Cyclosporine disposition is less susceptible to these interactions compared with tacrolimus, possibly because cyclosporine is itself a moderately strong CYP3A4- and strong P-gp inhibitor, blunting the effect of additional inhibitors. Cyclosporine 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 26912097-6 2016 Cyclosporine disposition is less susceptible to these interactions compared with tacrolimus, possibly because cyclosporine is itself a moderately strong CYP3A4- and strong P-gp inhibitor, blunting the effect of additional inhibitors. Cyclosporine 110-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 27216792-6 2016 RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan. Telmisartan 368-379 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 26935921-8 2016 Consistent with the previous report, CYP3A4 and CYP2D6 were determined as the major enzymes that contribute to COBI metabolism. Cobicistat 111-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 27280598-2 2016 Several case reports have noted a drug interaction between sodium fusidate and CYP3A4 metabolised statins, leading to statin toxicity. Fusidic Acid 59-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 27216792-6 2016 RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan. eprosartan 381-391 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 27216792-6 2016 RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan. olmesartan 393-403 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 27604990-0 2016 Application of a "Fit for Purpose" PBPK Model to Investigate the CYP3A4 Induction Potential of Enzalutamide. enzalutamide 95-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 30085479-0 2016 EFFECT OF CARBAMAZEPINE ON THE ACTIVITY OF CYP3A4 ISOENZYME IN PATIENTS WITH ALCOHOL ADDICTION. Carbamazepine 10-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 27604990-7 2016 Enzalutamide is a potent CYP3A inducer and a model-based approach to guide dose-selection for enzalutamide combinations that are CYP3A substrates is needed. enzalutamide 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-30 27604990-7 2016 Enzalutamide is a potent CYP3A inducer and a model-based approach to guide dose-selection for enzalutamide combinations that are CYP3A substrates is needed. enzalutamide 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-134 27604990-7 2016 Enzalutamide is a potent CYP3A inducer and a model-based approach to guide dose-selection for enzalutamide combinations that are CYP3A substrates is needed. enzalutamide 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-134 27604990-8 2016 OBJECTIVE: A "fit for purpose" PBPK model of enzalutamide was developed to illustrate the CYP3A4 induction potential, understand the kinetics of de-induction of CYP3A4 following cessation of enzalutamide dosing and guide dose-selection of a co-administered CYP3A substrate. enzalutamide 45-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 27604990-8 2016 OBJECTIVE: A "fit for purpose" PBPK model of enzalutamide was developed to illustrate the CYP3A4 induction potential, understand the kinetics of de-induction of CYP3A4 following cessation of enzalutamide dosing and guide dose-selection of a co-administered CYP3A substrate. enzalutamide 45-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 27604990-8 2016 OBJECTIVE: A "fit for purpose" PBPK model of enzalutamide was developed to illustrate the CYP3A4 induction potential, understand the kinetics of de-induction of CYP3A4 following cessation of enzalutamide dosing and guide dose-selection of a co-administered CYP3A substrate. enzalutamide 45-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 27604990-13 2016 Model application was demonstrated by simulating a drug-drug interaction between enzalutamide and midazolam, a sensitive CYP3A4 substrate. enzalutamide 81-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 27604990-13 2016 Model application was demonstrated by simulating a drug-drug interaction between enzalutamide and midazolam, a sensitive CYP3A4 substrate. Midazolam 98-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 27604990-15 2016 Based on modeling, upon cessation of enzalutamide dosing, it is predicted that at least 8 weeks are needed to re-attain baseline CYP3A4 activity. enzalutamide 37-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 27604990-17 2016 CONCLUSION: A "fit for purpose" PBPK model of enzalutamide was successfully developed using public information that recapitulated it"s observed pharmacokinetics, CYP3A4 induction potential and the potential need for dose-adjustment of co-administered CYP3A substrates. enzalutamide 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 27604990-17 2016 CONCLUSION: A "fit for purpose" PBPK model of enzalutamide was successfully developed using public information that recapitulated it"s observed pharmacokinetics, CYP3A4 induction potential and the potential need for dose-adjustment of co-administered CYP3A substrates. enzalutamide 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-167 30085479-0 2016 EFFECT OF CARBAMAZEPINE ON THE ACTIVITY OF CYP3A4 ISOENZYME IN PATIENTS WITH ALCOHOL ADDICTION. Alcohols 77-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 30085479-1 2016 According to literature data, isoenzyme CYP3A4 of cytochrome P450 is involved in biotransformation of drugs.,At the same time, there is evidence that carbamazepine induces CYP3A4 activity. Carbamazepine 150-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 30085479-1 2016 According to literature data, isoenzyme CYP3A4 of cytochrome P450 is involved in biotransformation of drugs.,At the same time, there is evidence that carbamazepine induces CYP3A4 activity. Carbamazepine 150-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 30085479-2 2016 The purpose of the study was to evaluate the effect of carbamazepine on the CYP3A4 activity in patients with alcohol addiction. Carbamazepine 55-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 30085479-5 2016 The results were used to construct a plot and derive an equation of logarithmic regression reflecting the dependence of CYP3A4 activity on the dose of carbamazepine: y = (5.5 - 9.1) x 10-5 - DeltaDeltax2. Carbamazepine 151-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 30085479-6 2016 These data demonstrate a statistically significant effect of carbamazepine on the activity of CYP3A4 isoenzyme in patients with alcohol addiction treated by haloperidol. Carbamazepine 61-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 30085479-6 2016 These data demonstrate a statistically significant effect of carbamazepine on the activity of CYP3A4 isoenzyme in patients with alcohol addiction treated by haloperidol. Haloperidol 157-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 26120010-2 2016 Lomitapide is extensively metabolized via cytochrome P450 3A (CYP3A) and is a weak CYP3A inhibitor. BMS201038 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-60 27034690-5 2016 Xanthotoxol showed stronger inhibition on CYP3A4 and CYP1A2 compared to other isoenzymes with the IC50 of 7.43 muM for CYP3A4 and 27.82 muM for CYP1A2. xanthotoxol 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 27034690-5 2016 Xanthotoxol showed stronger inhibition on CYP3A4 and CYP1A2 compared to other isoenzymes with the IC50 of 7.43 muM for CYP3A4 and 27.82 muM for CYP1A2. xanthotoxol 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 27034690-8 2016 In addition, the results of molecular docking showed that xanthotoxol was bound to CYP1A2 with hydrophobic and pi-pi bond and CYP3A4 with hydrogen and hydrophobic bond. xanthotoxol 58-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 27034690-8 2016 In addition, the results of molecular docking showed that xanthotoxol was bound to CYP1A2 with hydrophobic and pi-pi bond and CYP3A4 with hydrogen and hydrophobic bond. Hydrogen 138-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 27698677-7 2016 CYP1A2, CYP2C9, CYP2D6, CYP2E1, CYP3A4, and CYP2C19 contributed differently to the metabolism of morusin. morusin 97-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 27698677-8 2016 Compared to other CYP450 isoforms, CYP3A4 played the most significant role in the metabolism of morusin in human liver microsomes. morusin 96-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 25900201-2 2016 Amiodarone (AMD), an antiarrhythmic, presents a risk of liver injury in humans, and its metabolites, formed by cytochrome P450 3A4, are likely more toxic to hepatocytes than AMD is. Amiodarone 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-130 26655108-3 2016 These two enantiomers show differences in metabolism by CYPs: S-warfarin undergoes 7 hydroxylation by CYP2C9 and R-warfarin by CYP3A4 to form 10 hydroxy warfarin. Warfarin 62-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 26655108-3 2016 These two enantiomers show differences in metabolism by CYPs: S-warfarin undergoes 7 hydroxylation by CYP2C9 and R-warfarin by CYP3A4 to form 10 hydroxy warfarin. Warfarin 113-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 26655108-3 2016 These two enantiomers show differences in metabolism by CYPs: S-warfarin undergoes 7 hydroxylation by CYP2C9 and R-warfarin by CYP3A4 to form 10 hydroxy warfarin. hydroxy warfarin 145-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 26655108-12 2016 In addition, we show inhibition of major metabolic pathways of warfarin by sulfaphenazole and ketoconazole which are known specific inhibitors of CYP2C9 and CYP3A4 respectively. Warfarin 63-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 26655108-12 2016 In addition, we show inhibition of major metabolic pathways of warfarin by sulfaphenazole and ketoconazole which are known specific inhibitors of CYP2C9 and CYP3A4 respectively. Sulfaphenazole 75-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 26655108-12 2016 In addition, we show inhibition of major metabolic pathways of warfarin by sulfaphenazole and ketoconazole which are known specific inhibitors of CYP2C9 and CYP3A4 respectively. Ketoconazole 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 26120010-2 2016 Lomitapide is extensively metabolized via cytochrome P450 3A (CYP3A) and is a weak CYP3A inhibitor. BMS201038 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 26120010-2 2016 Lomitapide is extensively metabolized via cytochrome P450 3A (CYP3A) and is a weak CYP3A inhibitor. BMS201038 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 26120010-9 2016 Reductions in lomitapide dose may be required for some patients when administered concomitantly with a weak CYP3A inhibitor. BMS201038 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 26765458-1 2016 Some statins (simvastatin, lovastatin, and atorvastatin) are metabolized by cytochrome P450s 3A4 (CYP3A4). Simvastatin 14-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-96 26765458-1 2016 Some statins (simvastatin, lovastatin, and atorvastatin) are metabolized by cytochrome P450s 3A4 (CYP3A4). Simvastatin 14-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 26765458-1 2016 Some statins (simvastatin, lovastatin, and atorvastatin) are metabolized by cytochrome P450s 3A4 (CYP3A4). Lovastatin 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-96 26765458-1 2016 Some statins (simvastatin, lovastatin, and atorvastatin) are metabolized by cytochrome P450s 3A4 (CYP3A4). Lovastatin 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 26765458-1 2016 Some statins (simvastatin, lovastatin, and atorvastatin) are metabolized by cytochrome P450s 3A4 (CYP3A4). Atorvastatin 43-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-96 26765458-1 2016 Some statins (simvastatin, lovastatin, and atorvastatin) are metabolized by cytochrome P450s 3A4 (CYP3A4). Atorvastatin 43-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 26490246-0 2016 Inactivation of Human Cytochrome P450 3A4 and 3A5 by Dronedarone and N-Desbutyl Dronedarone. Dronedarone 53-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-41 27518624-3 2016 DMSO-treated HuH-7 cells express elevated cytochrome P450 3A4 (CYP3A4) enzyme gene expression and activity compared to untreated HuH-7 cells. Dimethyl Sulfoxide 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-61 27518624-3 2016 DMSO-treated HuH-7 cells express elevated cytochrome P450 3A4 (CYP3A4) enzyme gene expression and activity compared to untreated HuH-7 cells. Dimethyl Sulfoxide 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 27518624-6 2016 This chapter describes a detailed methodology for developing DMSO-treated HuH-7 cells, which are subsequently used for CYP3A4 inhibition and hepatotoxicity studies. Dimethyl Sulfoxide 61-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 26910068-0 2016 In Vitro Approaches to Study Regulation of Hepatic Cytochrome P450 (CYP) 3A Expression by Paclitaxel and Rifampicin. Paclitaxel 90-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-75 26910068-0 2016 In Vitro Approaches to Study Regulation of Hepatic Cytochrome P450 (CYP) 3A Expression by Paclitaxel and Rifampicin. Rifampin 105-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-75 26910068-4 2016 In this investigation, we tested the hypothesis that induction of cytochrome P450 (Cyp)3a11 gene by paclitaxel is downregulated by the inflammatory mediator, lipopolysaccharide (LPS), and that the pro-inflammatory cytokine, tumor necrosis factor (TNF)-alpha, attenuates human CYP3A4 gene induction by rifampicin. Paclitaxel 100-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 276-282 26910068-7 2016 Induction and subsequent downregulation of CYP3A enzyme can impact paclitaxel treatment in cancer patients where inflammatory mediators are activated. Paclitaxel 67-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-48 26910068-10 2016 The cells were then treated with the pro-inflammatory cytokine, TNFalpha, followed by the prototype CYP3A inducer rifampicin. Rifampin 114-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 26910068-11 2016 It is well established that rifampicin activates PXR, leading to CYP3A4 induction. Rifampin 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 26910068-12 2016 We found that induction of CYP3A4-luciferase activity by rifampicin was significantly attenuated by TNFalpha. Rifampin 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 26490246-10 2016 MBI of CYP3A4 and CYP3A5 was further supported by the discovery of glutathione adducts derived from the quinone oxime intermediates of dronedarone and NDBD. Glutathione 67-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 26490246-10 2016 MBI of CYP3A4 and CYP3A5 was further supported by the discovery of glutathione adducts derived from the quinone oxime intermediates of dronedarone and NDBD. 4-nitrosophenol 104-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 26490246-10 2016 MBI of CYP3A4 and CYP3A5 was further supported by the discovery of glutathione adducts derived from the quinone oxime intermediates of dronedarone and NDBD. Dronedarone 135-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 26490246-10 2016 MBI of CYP3A4 and CYP3A5 was further supported by the discovery of glutathione adducts derived from the quinone oxime intermediates of dronedarone and NDBD. N-desbutyldronedarone 151-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 26490246-0 2016 Inactivation of Human Cytochrome P450 3A4 and 3A5 by Dronedarone and N-Desbutyl Dronedarone. N-desbutyldronedarone 69-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-41 26490246-11 2016 In conclusion, dronedarone and NDBD inactivate CYP3A4 and CYP3A5 via unique dual mechanisms of MBI and formation of the metabolite-intermediate complex. Dronedarone 15-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 26490246-4 2016 We demonstrated for the first time that both dronedarone and its main metabolite N-desbutyl dronedarone (NDBD) inactivate CYP3A4 and CYP3A5 in a time-, concentration-, and NADPH-dependent manner. Dronedarone 45-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 26490246-11 2016 In conclusion, dronedarone and NDBD inactivate CYP3A4 and CYP3A5 via unique dual mechanisms of MBI and formation of the metabolite-intermediate complex. N-desbutyldronedarone 31-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 26490246-4 2016 We demonstrated for the first time that both dronedarone and its main metabolite N-desbutyl dronedarone (NDBD) inactivate CYP3A4 and CYP3A5 in a time-, concentration-, and NADPH-dependent manner. N-desbutyldronedarone 81-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 26490246-4 2016 We demonstrated for the first time that both dronedarone and its main metabolite N-desbutyl dronedarone (NDBD) inactivate CYP3A4 and CYP3A5 in a time-, concentration-, and NADPH-dependent manner. N-desbutyldronedarone 105-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 26490246-4 2016 We demonstrated for the first time that both dronedarone and its main metabolite N-desbutyl dronedarone (NDBD) inactivate CYP3A4 and CYP3A5 in a time-, concentration-, and NADPH-dependent manner. NADP 172-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 26490246-5 2016 For the inactivation of CYP3A4, the inactivator concentration at the half-maximum rate of inactivation and inactivation rate constant at an infinite inactivator concentration are 0.87 microM and 0.039 minute(-1), respectively, for dronedarone, and 6.24 microM and 0.099 minute(-1), respectively, for NDBD. Dronedarone 231-242 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 26490246-5 2016 For the inactivation of CYP3A4, the inactivator concentration at the half-maximum rate of inactivation and inactivation rate constant at an infinite inactivator concentration are 0.87 microM and 0.039 minute(-1), respectively, for dronedarone, and 6.24 microM and 0.099 minute(-1), respectively, for NDBD. N-desbutyldronedarone 300-304 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 26490246-7 2016 The partition ratios for the inactivation of CYP3A4 and CYP3A5 by dronedarone are 51.1 and 32.2, and the partition ratios for the inactivation of CYP3A4 and CYP3A5 by NDBD are 35.3 and 36.6. Dronedarone 66-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 26490246-7 2016 The partition ratios for the inactivation of CYP3A4 and CYP3A5 by dronedarone are 51.1 and 32.2, and the partition ratios for the inactivation of CYP3A4 and CYP3A5 by NDBD are 35.3 and 36.6. N-desbutyldronedarone 167-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 26490246-7 2016 The partition ratios for the inactivation of CYP3A4 and CYP3A5 by dronedarone are 51.1 and 32.2, and the partition ratios for the inactivation of CYP3A4 and CYP3A5 by NDBD are 35.3 and 36.6. N-desbutyldronedarone 167-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 26490246-8 2016 Testosterone protected both CYP3A4 and CYP3A5 from inactivation by dronedarone and NDBD. Testosterone 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 26490246-8 2016 Testosterone protected both CYP3A4 and CYP3A5 from inactivation by dronedarone and NDBD. Dronedarone 67-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 26490246-8 2016 Testosterone protected both CYP3A4 and CYP3A5 from inactivation by dronedarone and NDBD. N-desbutyldronedarone 83-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 26366751-4 2016 Vitamin D receptor activation using a vitamin D responsive element-mediated cytochrome P450 3A4 reporter gene assay was investigated in Caco-2 cells transfected with human vitamin D receptor. Vitamin D 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-95 26827958-7 2016 Androgen inhibits vitamin D-mediated induction of CYP24A1, the calcitriol-degrading enzyme, while vitamin D promotes androgen inactivation by inducing phase I monooxygenases (e.g., CYP3A4) and phase II transferases (e.g., SULT2B1b, a DHEA-sulfotransferase). Vitamin D 98-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-187 26942253-11 2016 Cabozantinib carries a risk of multiple pharmacokinetic interactions by interfering with cytochrome P450 isoenzyme CYP3A4 and P-glycoprotein. cabozantinib 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 26153443-12 2016 In vitro studies with human cDNA expressed CYP enzymes and with human liver microsomes (HLM) in the presence of selective chemical inhibitors demonstrated that ASV was primarily catalyzed by CYP3A4 and CYP3A5. asunaprevir 160-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-197 26207435-0 2016 Characterization of midazolam metabolism in locusts: the role of a CYP3A4-like enzyme in the formation of 1"-OH and 4-OH midazolam. Midazolam 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 26207435-0 2016 Characterization of midazolam metabolism in locusts: the role of a CYP3A4-like enzyme in the formation of 1"-OH and 4-OH midazolam. 1"-oh 106-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 26207435-0 2016 Characterization of midazolam metabolism in locusts: the role of a CYP3A4-like enzyme in the formation of 1"-OH and 4-OH midazolam. 4-hydroxymidazolam 116-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 26207435-6 2016 The formation of hydroxylated metabolites could successfully be inhibited by co-administration of ketoconazole, a known CYP3A4/5 inhibitor. Ketoconazole 98-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 26340669-0 2016 Fluoxetine reduces CES1, CES2, and CYP3A4 expression through decreasing PXR and increasing DEC1 in HepG2 cells. Fluoxetine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 26340669-12 2016 Knockdown of DEC1 alone increased the expression of PXR and CYP3A4 and almost abolished the decreases of CES1, CES2, and CYP3A4 induced by FLX. Fluoxetine 139-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 26391142-10 2016 On the other hand, resveratrol showed inhibitory effect on CYP3A4*1, CYP2D6*1, human and rat microsomes, the IC50 of resveratrol was 6.771, 87.87, 45.11 and 35.59 mumol l(-1), respectively. Resveratrol 19-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 26366751-6 2016 Slight but significant increases in the mRNA expression of cytochrome P450 3A4, vitamin D3 24-hydroxylase, multidrug resistance protein 1, and transient receptor potential vanilloid type 6 were observed after 3 days of continual quercetin treatment. Quercetin 229-238 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-78 26366751-8 2016 Moreover, quercetin significantly enhanced cytochrome P450 3A4 reporter activity in Caco-2 cells in a dose-dependent manner, and the expression of exogenous vitamin D receptor further stimulated the vitamin D receptor activity. Quercetin 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-62 26366751-10 2016 Taken together, the data indicates that quercetin upregulates cytochrome P450 3A4 and multidrug resistance protein 1 expression in Caco-2 cells likely via a vitamin D receptor-dependent pathway. Quercetin 40-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-81 26290405-0 2016 Effect of buffer conditions on CYP2C8-mediated paclitaxel 6alpha-hydroxylation and CYP3A4-mediated triazolam alpha- and 4-hydroxylation by human liver microsomes. Triazolam 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 26294260-9 2016 The formation of M1 and M2 in DLM was significantly abrogated in the presence of the specific CYP2D inhibitor, quinidine, and to a lesser extent by the CYP3A inhibitor, ketoconazole, corroborating data from human recombinant isozymes. Ketoconazole 169-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-157 26337900-11 2016 We identified CYP3A4 as the CYP isoform primarily responsible for GM metabolism in human liver microsomes. geissoschizine methylether 66-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 26338061-7 2016 Tamsulosin (TAM) and tolterodine (TOL) inhibited CYP3A4 activity with an enantiospecific pattern. Tamsulosin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 26338061-7 2016 Tamsulosin (TAM) and tolterodine (TOL) inhibited CYP3A4 activity with an enantiospecific pattern. Tamsulosin 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 26338061-7 2016 Tamsulosin (TAM) and tolterodine (TOL) inhibited CYP3A4 activity with an enantiospecific pattern. Tolterodine Tartrate 21-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 26338061-7 2016 Tamsulosin (TAM) and tolterodine (TOL) inhibited CYP3A4 activity with an enantiospecific pattern. Tolterodine Tartrate 34-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 26338061-8 2016 The inhibition of CYP3A4 activity differed for R-TAM (Ki 2.88 +- 0.12 microM) and S-TAM (Ki 14.22 +- 0.53 microM) as well as for S-TOL (Ki 1.71 +- 0.03 microM) and R-TOL (Ki 4.78 +- 0.17 microM). Tamsulosin 47-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 26338061-8 2016 The inhibition of CYP3A4 activity differed for R-TAM (Ki 2.88 +- 0.12 microM) and S-TAM (Ki 14.22 +- 0.53 microM) as well as for S-TOL (Ki 1.71 +- 0.03 microM) and R-TOL (Ki 4.78 +- 0.17 microM). Tamsulosin 82-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 26338061-8 2016 The inhibition of CYP3A4 activity differed for R-TAM (Ki 2.88 +- 0.12 microM) and S-TAM (Ki 14.22 +- 0.53 microM) as well as for S-TOL (Ki 1.71 +- 0.03 microM) and R-TOL (Ki 4.78 +- 0.17 microM). r 47-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 26338061-8 2016 The inhibition of CYP3A4 activity differed for R-TAM (Ki 2.88 +- 0.12 microM) and S-TAM (Ki 14.22 +- 0.53 microM) as well as for S-TOL (Ki 1.71 +- 0.03 microM) and R-TOL (Ki 4.78 +- 0.17 microM). Tolterodine Tartrate 131-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 26456671-4 2015 Hepatoma cells in the gal-alginate scaffold showed higher levels of liver specific products (albumin and urea) and were more responsive to specific inducers (e.g. dexamethasone) and inhibitors (e.g. ketoconazole) of the CYP3A4 system than in conventional monolayer culture. gal-alginate 22-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 26494425-10 2015 Furthermore, cytochrome P450 (CYP) 3A4 was found to be a major enzyme mediating AEPU metabolism. aepu 80-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-38 26712778-3 2015 With midazolam as the probe substrate, GA greatly decreased CYP3A4 activity with IC50 values of 8.195 muM in HLMs and 7.498 muM in the recombinant cDNA-expressed CYP3A4 enzyme system, respectively. Midazolam 5-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 26712778-5 2015 Results from Lineweaver-Burk plots showed that GA could inhibit CYP3A4 activity competitively, with a Ki value of 1.57 muM in HLMs. Glycyrrhetinic Acid 47-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 26712778-10 2015 In conclusion, this study indicates that GA may exert herb-drug interactions by competitively inhibiting CYP3A4. Glycyrrhetinic Acid 41-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 33429678-11 2015 Finally, the conjugation of heparin on GelNB led to suppressed Huh7 cell metabolic activity and improved CYP3A4 activity and urea secretion. Heparin 28-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 26568266-9 2015 For CYP3A4 substrate drugs, the Km value showed the significant relation with Vintra, indicating that the affinity to the enzyme can be a parameter to predict the risk of high intrasubject variability. vintra 78-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 26296069-1 2015 PURPOSE: Repaglinide and pioglitazone are both CYP2C8 and CYP3A4 substrates. repaglinide 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 26409144-4 2015 Multiplex experiments using the highly specific CYP2A6 with its corresponding substrate coumarin as well as the highly promiscuous CYP3A4 with testosterone were conducted. Testosterone 143-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 26256674-1 2015 AIMS: Sirolimus is an mTOR inhibitor metabolized by CYP3A4 and CYP3A5. Sirolimus 6-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 26256674-9 2015 The PBPK model developed based on CL(int) of recombinant CYP3A4, CYP3A5 and CYP2C8 predicted a small CYP3A5*3 effect on simulated sirolimus PK profiles. Sirolimus 130-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 26264702-6 2015 Evacetrapib was a time-dependent inhibitor and inducer of CYP3A. evacetrapib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 26264702-7 2015 The effects of evacetrapib on CYP3A and CYP2C9 were assessed in a phase 1 study using midazolam and tolbutamide as probe substrates, respectively. evacetrapib 15-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-35 26271371-0 2015 Pharmacokinetic interaction between the CYP3A4 inhibitor ketoconazole and the hormone drospirenone in combination with ethinylestradiol or estradiol. Ketoconazole 57-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 26271371-0 2015 Pharmacokinetic interaction between the CYP3A4 inhibitor ketoconazole and the hormone drospirenone in combination with ethinylestradiol or estradiol. drospirenone 86-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 26271371-1 2015 AIMS: The present study was conducted to investigate the influence of the strong CYP3A4 inhibitor ketoconazole (KTZ) on the pharmacokinetics of drospirenone (DRSP) administered in combination with ethinylestradiol (EE) or estradiol (E2). Ketoconazole 98-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 26271371-1 2015 AIMS: The present study was conducted to investigate the influence of the strong CYP3A4 inhibitor ketoconazole (KTZ) on the pharmacokinetics of drospirenone (DRSP) administered in combination with ethinylestradiol (EE) or estradiol (E2). Ketoconazole 112-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 26271371-1 2015 AIMS: The present study was conducted to investigate the influence of the strong CYP3A4 inhibitor ketoconazole (KTZ) on the pharmacokinetics of drospirenone (DRSP) administered in combination with ethinylestradiol (EE) or estradiol (E2). drospirenone 144-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 26271661-2 2015 CYP3A5*3, CYP3A4*1B and CYP3A4*22 alleles of liver grafts may explain about one third of the inter-individual differences in pharmacokinetics of ciclosporin and tacrolimus in recipients. Cyclosporine 145-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 26271661-2 2015 CYP3A5*3, CYP3A4*1B and CYP3A4*22 alleles of liver grafts may explain about one third of the inter-individual differences in pharmacokinetics of ciclosporin and tacrolimus in recipients. Cyclosporine 145-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 26690104-5 2015 CYP3A4/5 played the major role in the hydroxylation of evogliptin to 4(S)-hydroxyevogliptin (M2) and 4(R)-hydroxyevogliptin (M3). 4-(3-amino-4-(2,4,5-trifluorophenyl)butanoyl)-3-(tert-butoxymethyl)piperazin-2-one 55-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26690104-5 2015 CYP3A4/5 played the major role in the hydroxylation of evogliptin to 4(S)-hydroxyevogliptin (M2) and 4(R)-hydroxyevogliptin (M3). 4(s)-hydroxyevogliptin 69-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26690104-5 2015 CYP3A4/5 played the major role in the hydroxylation of evogliptin to 4(S)-hydroxyevogliptin (M2) and 4(R)-hydroxyevogliptin (M3). 4(r)-hydroxyevogliptin 101-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26627649-2 2015 It is demonstrated that using SAXS data it is possible to determine both the shape and localization of the membrane protein cytochrome P450 3A4 (CYP3A4) while it is embedded in the phospholipid bilayer of a nanodisc. Phospholipids 181-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-143 26627649-2 2015 It is demonstrated that using SAXS data it is possible to determine both the shape and localization of the membrane protein cytochrome P450 3A4 (CYP3A4) while it is embedded in the phospholipid bilayer of a nanodisc. Phospholipids 181-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 26271661-2 2015 CYP3A5*3, CYP3A4*1B and CYP3A4*22 alleles of liver grafts may explain about one third of the inter-individual differences in pharmacokinetics of ciclosporin and tacrolimus in recipients. Tacrolimus 161-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 26271661-2 2015 CYP3A5*3, CYP3A4*1B and CYP3A4*22 alleles of liver grafts may explain about one third of the inter-individual differences in pharmacokinetics of ciclosporin and tacrolimus in recipients. Tacrolimus 161-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 26773964-2 2015 The aim of this study was to evaluate the influence of CYP3A5 polymorphism on the increase in CYP3A activity after living kidney transplantation, by measuring the plasma concentration of 4beta-hydroxycholesterol. cholest-5-ene-3,4-diol 187-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 26296069-1 2015 PURPOSE: Repaglinide and pioglitazone are both CYP2C8 and CYP3A4 substrates. Pioglitazone 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 27747723-9 2015 Rivaroxaban, a substrate for cytochrome P450 (CYP) 3A4 and P-glycoprotein (P-gp), is contraindicated in patients concomitantly treated with strong inhibitors of both these systems, e.g. protease inhibitors (PIs) such as ritonavir (based on in vitro data and a pharmacokinetic study in healthy volunteers). Rivaroxaban 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-54 26218204-3 2015 Alogliptin is mainly metabolized by cytochrome P450 (CYP2D6) and CYP3A4. alogliptin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 26177803-9 2015 Asunaprevir has a low potential to perpetrate drug-drug interactions via CYP3A4, P-glycoprotein and OATP, but is a moderate CYP2D6 inhibitor; concomitant drugs that are substrates of CYP2D6 or P-glycoprotein and have a narrow therapeutic index should be used with care. asunaprevir 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 26374173-4 2015 CYP3A4 was the main catalyst of montelukast sulfoxidation and stereoselective 21-hydroxylation, and multiple P450s participated in montelukast 25-hydroxylation. montelukast 32-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26374173-4 2015 CYP3A4 was the main catalyst of montelukast sulfoxidation and stereoselective 21-hydroxylation, and multiple P450s participated in montelukast 25-hydroxylation. montelukast 131-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 27747723-9 2015 Rivaroxaban, a substrate for cytochrome P450 (CYP) 3A4 and P-glycoprotein (P-gp), is contraindicated in patients concomitantly treated with strong inhibitors of both these systems, e.g. protease inhibitors (PIs) such as ritonavir (based on in vitro data and a pharmacokinetic study in healthy volunteers). Ritonavir 220-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-54 26654672-0 2015 CYP3A activity based on plasma 4beta-hydroxycholesterol during the early postpartum period has an effect on the plasma disposition of amlodipine. cholest-5-ene-3,4-diol 31-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 24993184-10 2015 In human liver microsomes, CYP1A2, CYP2C8, CYP2D6 are involved in the metabolism of Imp; CYP3A4 is involved in the metabolism of Ost at all the tested concentrations of Ost, while CYP2C9, CYP2D6 mediate the metabolism at high concentration of Ost. osthol 129-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 26654672-0 2015 CYP3A activity based on plasma 4beta-hydroxycholesterol during the early postpartum period has an effect on the plasma disposition of amlodipine. Amlodipine 134-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 26654672-1 2015 This study aimed to evaluate plasma 4beta-hydroxycholesterol as an endogenous marker of CYP3A4/5 activity in early postpartum women and its impact on the plasma disposition of amlodipine. cholest-5-ene-3,4-diol 36-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 26654672-10 2015 In conclusion, early postpartum women possessed higher CYP3A activity based on plasma 4beta-hydroxycholesterol and had a large pharmacokinetic variability in amlodipine. cholest-5-ene-3,4-diol 86-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 26654672-11 2015 CYP3A activity during the early postpartum period had an effect on the plasma disposition of amlodipine. Amlodipine 93-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 26296860-6 2015 Investigation of inhibitory potency towards 6 CYP isoforms generally revealed low inhibitory potency, but in the case of CYP3A4, a substrate dependent inhibition was noted using testosterone as substrate (IC50: 12.5muM). Testosterone 178-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 26381275-1 2015 PURPOSE: To investigate the potential effects of strong CYP3A inhibitor ketoconazole and strong CYP3A inducer rifampin on the pharmacokinetics of crizotinib in human. Crizotinib 146-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 26381275-1 2015 PURPOSE: To investigate the potential effects of strong CYP3A inhibitor ketoconazole and strong CYP3A inducer rifampin on the pharmacokinetics of crizotinib in human. Crizotinib 146-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-101 26381275-5 2015 RESULTS: Co-administration of a single 150-mg oral dose of crizotinib with the strong CYP3A inhibitor ketoconazole resulted in an area under the plasma-concentration curve extrapolated to infinity (AUC0-inf) 3.2-fold that for crizotinib alone. Crizotinib 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 26381275-5 2015 RESULTS: Co-administration of a single 150-mg oral dose of crizotinib with the strong CYP3A inhibitor ketoconazole resulted in an area under the plasma-concentration curve extrapolated to infinity (AUC0-inf) 3.2-fold that for crizotinib alone. Ketoconazole 102-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 26381275-5 2015 RESULTS: Co-administration of a single 150-mg oral dose of crizotinib with the strong CYP3A inhibitor ketoconazole resulted in an area under the plasma-concentration curve extrapolated to infinity (AUC0-inf) 3.2-fold that for crizotinib alone. Crizotinib 226-236 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 26381275-6 2015 Co-administration of a single 250-mg crizotinib dose with the strong CYP3A inducer rifampin caused an 82 % decrease in crizotinib AUC0-inf. Crizotinib 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 26381275-6 2015 Co-administration of a single 250-mg crizotinib dose with the strong CYP3A inducer rifampin caused an 82 % decrease in crizotinib AUC0-inf. Rifampin 83-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 26381275-6 2015 Co-administration of a single 250-mg crizotinib dose with the strong CYP3A inducer rifampin caused an 82 % decrease in crizotinib AUC0-inf. Crizotinib 119-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 26381275-8 2015 CONCLUSIONS: These findings suggest that CYP3A plays an important role in the metabolism of both crizotinib and PF-06260182, with the extent of this role being greater for PF-06260182. Crizotinib 97-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 26387812-4 2015 METHODS: In this exploratory study, we selected SNPs in genes CYP3A4, NR1I2, POR, IL8, IL13, IL4-R, HIF1A and MET that might possibly be associated with sunitinib treatment outcome. Sunitinib 153-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 24997757-1 2015 Pharmacokinetic (PK) interactions between the cytochrome P450 3A4 (CYP3A4) pathway and transdermally administered ethinyl estradiol (EE) and gestodene (GSD) were investigated. Ethinyl Estradiol 114-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-65 24997757-1 2015 Pharmacokinetic (PK) interactions between the cytochrome P450 3A4 (CYP3A4) pathway and transdermally administered ethinyl estradiol (EE) and gestodene (GSD) were investigated. Ethinyl Estradiol 114-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 24997757-1 2015 Pharmacokinetic (PK) interactions between the cytochrome P450 3A4 (CYP3A4) pathway and transdermally administered ethinyl estradiol (EE) and gestodene (GSD) were investigated. Gestodene 141-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-65 24997757-1 2015 Pharmacokinetic (PK) interactions between the cytochrome P450 3A4 (CYP3A4) pathway and transdermally administered ethinyl estradiol (EE) and gestodene (GSD) were investigated. Gestodene 141-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 24997757-4 2015 In a third study, women received single doses of the CYP3A4 model substrate midazolam, alone and after 3 weeks of concurrent patch application. Midazolam 76-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 24993184-10 2015 In human liver microsomes, CYP1A2, CYP2C8, CYP2D6 are involved in the metabolism of Imp; CYP3A4 is involved in the metabolism of Ost at all the tested concentrations of Ost, while CYP2C9, CYP2D6 mediate the metabolism at high concentration of Ost. osthol 169-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 24993184-10 2015 In human liver microsomes, CYP1A2, CYP2C8, CYP2D6 are involved in the metabolism of Imp; CYP3A4 is involved in the metabolism of Ost at all the tested concentrations of Ost, while CYP2C9, CYP2D6 mediate the metabolism at high concentration of Ost. osthol 169-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 26444948-8 2015 CYP2D6 and CYP3A4 enzyme activities were assessed by comparing plasma log DM/dextrorphan and log DM/methoxymorphinan metabolic ratio (MR) respectively in the presence and absence of khat. Dextrorphan 77-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 26700090-4 2015 CYP2C19*2 loss of function allele was stated and the introduction of haloperidol, a weak CYP3A4 inhibitor, probably explains this interaction. Haloperidol 69-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 26444948-8 2015 CYP2D6 and CYP3A4 enzyme activities were assessed by comparing plasma log DM/dextrorphan and log DM/methoxymorphinan metabolic ratio (MR) respectively in the presence and absence of khat. methoxymorphinan 100-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 26717524-3 2015 A recent pharmacokinetic (PK) study suggested that armodafinil (250 mg/d) reduces key PK parameters of risperidone by about 50%, and key PK parameters of 9-hydroxyrisperidone (paliperidone) by about 20%-30%, probably through induction of CYP3A4. Modafinil 51-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 238-244 26490449-13 2015 PC, DM, DL and PI exhibited the most potent inhibitory activities on CYP3A4-mediated nifedipine oxidation (mean IC50 1.54-6.43 microg/mL). Nifedipine 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 26202517-0 2015 The Pharmacokinetics of the CYP3A Substrate Midazolam in Morbidly Obese Patients Before and One Year After Bariatric Surgery. Midazolam 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 26202517-2 2015 As information about the effects of this procedure on a drug"s pharmacokinetics is limited, we aimed to evaluate the pharmacokinetics of CYP3A probe substrate midazolam after oral and intravenous administration in a cohort of morbidly obese patients that was studied before and 1 year post bariatric surgery. Midazolam 159-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-142 26481538-10 2015 CONCLUSION: The inhibition of CYP1A2, CYP2D6 and CYP3A4 by levomepromazine, demonstrated in vitro in the present study, should also be observed in vivo (especially the CYP2D6 inhibition by levomepromazine), since the calculated K(i) values are below or close to the presumed concentration range for levomepromazine in the liver in vivo. Methotrimeprazine 59-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 26481538-10 2015 CONCLUSION: The inhibition of CYP1A2, CYP2D6 and CYP3A4 by levomepromazine, demonstrated in vitro in the present study, should also be observed in vivo (especially the CYP2D6 inhibition by levomepromazine), since the calculated K(i) values are below or close to the presumed concentration range for levomepromazine in the liver in vivo. Methotrimeprazine 189-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 26481538-10 2015 CONCLUSION: The inhibition of CYP1A2, CYP2D6 and CYP3A4 by levomepromazine, demonstrated in vitro in the present study, should also be observed in vivo (especially the CYP2D6 inhibition by levomepromazine), since the calculated K(i) values are below or close to the presumed concentration range for levomepromazine in the liver in vivo. Methotrimeprazine 189-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 26481538-11 2015 Therefore pharmacokinetic interactions involving levomepromazine and CYP2D6, CYP1A2 or CYP3A4 substrates are likely to occur in patients during co-administration of the above-mentioned substrates/drugs. Methotrimeprazine 49-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 26615671-1 2015 AIM: The present study investigated in Tunisian renal transplant patients, genetic polymorphisms of CYP3A4 -392A>G and CYP3A5 6986A>G and their influence on tacrolimus (Tac) pharmacokinetics during early and late post-transplant (PT) phases and established customized ranges of Tac doses matching the C0 target levels according to CYP3A4 and CYP3A5 genotype combination and the PT phase. Tacrolimus 163-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 26615671-1 2015 AIM: The present study investigated in Tunisian renal transplant patients, genetic polymorphisms of CYP3A4 -392A>G and CYP3A5 6986A>G and their influence on tacrolimus (Tac) pharmacokinetics during early and late post-transplant (PT) phases and established customized ranges of Tac doses matching the C0 target levels according to CYP3A4 and CYP3A5 genotype combination and the PT phase. Tacrolimus 163-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 337-343 26817280-0 2015 A non-invasive CYP3A4 biomarker and body mass index predict cyclosporine dosage requirements in Chinese renal transplant recipients. Cyclosporine 60-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 26817280-1 2015 An endogenous CYP3A4 biomarker for in vivo metabolism of cyclosporine should be useful for optimizing individual dosage. Cyclosporine 57-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 26817280-7 2015 In summary, there is a significant relationship between endogenous CYP3A4 biomarker (assessed by urinary HOM) and in vivo metabolism of cyclosporine in renal transplant recipients. Cyclosporine 136-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 26360837-2 2015 The aim of this study was to evaluate the influence of the genetic polymorphisms of CYP2C9, CYP2D6 and CYP3A4 on the pharmacokinetics (PK) of celecoxib and its two main metabolites, hydroxyl-celecoxib and carboxy-celecoxib, in healthy Chinese subjects, based on a bioequivalence study of celecoxib. Celecoxib 142-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 25853922-0 2015 Influence of CYP2D6 and CYP3A4 Phenotypes, Drug Interactions, and Vitamin D Status on Tamoxifen Biotransformation. Tamoxifen 86-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 25853922-9 2015 Median plasma levels of TAM (161.50 ng mL) and HTF (1.32 ng mL) in CYP2D6 IM/CYP3A4 poor metabolizer patients were higher (P < 0.05) than those from CYP2D6 IM/CYP3A4 extensive metabolizer patients (122.07 ng mL and 0.61 ng mL, respectively). Tamoxifen 24-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 25853922-9 2015 Median plasma levels of TAM (161.50 ng mL) and HTF (1.32 ng mL) in CYP2D6 IM/CYP3A4 poor metabolizer patients were higher (P < 0.05) than those from CYP2D6 IM/CYP3A4 extensive metabolizer patients (122.07 ng mL and 0.61 ng mL, respectively). Tamoxifen 24-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 25853922-9 2015 Median plasma levels of TAM (161.50 ng mL) and HTF (1.32 ng mL) in CYP2D6 IM/CYP3A4 poor metabolizer patients were higher (P < 0.05) than those from CYP2D6 IM/CYP3A4 extensive metabolizer patients (122.07 ng mL and 0.61 ng mL, respectively). N-OCTANOYL-L-HOMOSERINE LACTONE 47-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 25853922-12 2015 CONCLUSIONS: CYP3A4 contributes to the bioactivation of TAM through formation of HTF and becomes increasingly important in case of reduced or absent CYP2D6 activity. Tamoxifen 56-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 26559489-6 2015 In addition, CYP3A4 expression in the hiPS-ELCs was induced by treatment with 1, 25-dihydroxyvitamin D3 or rifampicin, which are known to induce CYP3A4 expression, indicating that the hiPS-ELCs have CYP3A4 induction potency. Calcitriol 78-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 26443405-9 2015 CYP2D6 and CYP3A4 played an important role in the isomerization and glycination of limonoids in HLMs, whereas other CYP isoforms were considerably less active. Limonins 83-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 26819743-1 2015 BACKGROUND: Concomitant use of clarithromycin (CAM) and rifampicin (RFP) for the treatment of pulmonary Mycobacterium avium complex (MAC) disease affects the systemic concentrations of both drugs due to CYP3A4-related interactions. Clarithromycin 31-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 26819743-1 2015 BACKGROUND: Concomitant use of clarithromycin (CAM) and rifampicin (RFP) for the treatment of pulmonary Mycobacterium avium complex (MAC) disease affects the systemic concentrations of both drugs due to CYP3A4-related interactions. Clarithromycin 47-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 26819743-1 2015 BACKGROUND: Concomitant use of clarithromycin (CAM) and rifampicin (RFP) for the treatment of pulmonary Mycobacterium avium complex (MAC) disease affects the systemic concentrations of both drugs due to CYP3A4-related interactions. Rifampin 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 26819743-1 2015 BACKGROUND: Concomitant use of clarithromycin (CAM) and rifampicin (RFP) for the treatment of pulmonary Mycobacterium avium complex (MAC) disease affects the systemic concentrations of both drugs due to CYP3A4-related interactions. Rifampin 68-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 26819743-5 2015 Serum drug concentrations and urinary levels of endogenous cortisol (F) and 6 beta-hydroxycortisol (6betaOHF), the metabolite of F by CYP3A4, were measured, and evaluated 6betaOHF/F ratio as a CYP3A4 activity marker. 6 beta-hydroxycortisol 76-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 26819743-11 2015 The explanation for the low levels of serum CAM in pulmonary MAC disease patients is that RFP-mediated CYP3A4 induction reached a maximum by day 15 and remained high thereafter. Clarithromycin 44-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 26819743-13 2015 CONCLUSIONS: Our study demonstrated that serum CAM concentrations in pulmonary MAC disease patients were continuously low because of RFP-mediated CYP3A4 induction, which may be responsible for the unsatisfactory clinical outcomes. Clarithromycin 47-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 26559489-6 2015 In addition, CYP3A4 expression in the hiPS-ELCs was induced by treatment with 1, 25-dihydroxyvitamin D3 or rifampicin, which are known to induce CYP3A4 expression, indicating that the hiPS-ELCs have CYP3A4 induction potency. Calcitriol 78-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 26559489-6 2015 In addition, CYP3A4 expression in the hiPS-ELCs was induced by treatment with 1, 25-dihydroxyvitamin D3 or rifampicin, which are known to induce CYP3A4 expression, indicating that the hiPS-ELCs have CYP3A4 induction potency. Calcitriol 78-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 26559489-6 2015 In addition, CYP3A4 expression in the hiPS-ELCs was induced by treatment with 1, 25-dihydroxyvitamin D3 or rifampicin, which are known to induce CYP3A4 expression, indicating that the hiPS-ELCs have CYP3A4 induction potency. Rifampin 107-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 26559489-6 2015 In addition, CYP3A4 expression in the hiPS-ELCs was induced by treatment with 1, 25-dihydroxyvitamin D3 or rifampicin, which are known to induce CYP3A4 expression, indicating that the hiPS-ELCs have CYP3A4 induction potency. Rifampin 107-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 26559489-6 2015 In addition, CYP3A4 expression in the hiPS-ELCs was induced by treatment with 1, 25-dihydroxyvitamin D3 or rifampicin, which are known to induce CYP3A4 expression, indicating that the hiPS-ELCs have CYP3A4 induction potency. Rifampin 107-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 26081137-2 2015 AZD2327 and N-deethylated AZD2327 (M1) are substrates of cytochrome P450 3A (CYP3A4) and comprise a complex multiple inhibitory system that causes competitive and time-dependent inhibition of CYP3A4. 4-((3-aminophenyl)(4-(4-fluorobenzyl)piperazin-1-yl)methyl)-N,N-diethylbenzamide 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 26276083-6 2015 Studies showed the involvement of CYP1A2, CYP2B6, CYP2C19, and CYP3A4 in N-dealkylation of all three compounds and additionally CYP2D6 for lefetamine and NEDPA. Nitrogen 73-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 26276083-6 2015 Studies showed the involvement of CYP1A2, CYP2B6, CYP2C19, and CYP3A4 in N-dealkylation of all three compounds and additionally CYP2D6 for lefetamine and NEDPA. lephetamine 139-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 26614990-1 2015 OBJECTIVE: To investigate the propensity of plumbagin to inhibit the three isoforms of human cytochrome P450 (CYP), i.e., CYP1A2, CYP2C19, and CYP3A4 using human liver microsomes in vitro. plumbagin 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 26614990-3 2015 Phenacetin O-deethylation, omeprazole hydroxylation and nifedipine oxidation were used as selective substrates for CYP1A2, CYP2C19 and CYP3A4 activities, respectively. Phenacetin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 26614990-3 2015 Phenacetin O-deethylation, omeprazole hydroxylation and nifedipine oxidation were used as selective substrates for CYP1A2, CYP2C19 and CYP3A4 activities, respectively. Omeprazole 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 26614990-3 2015 Phenacetin O-deethylation, omeprazole hydroxylation and nifedipine oxidation were used as selective substrates for CYP1A2, CYP2C19 and CYP3A4 activities, respectively. Nifedipine 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 26614990-7 2015 The inhibitory activities on CYP1A2-mediated phenacetin O-deethylation and CYP3A4-mediated nifedipine oxidation were moderate. Nifedipine 91-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 26614990-9 2015 The corresponding IC50 values of plumbagin and ketoconazole (selective inhibitor) for CYP3A4 were (2.37 +- 0.10) and (0.18 +- 0.06) muM, respectively. Ketoconazole 47-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 26648692-5 2015 Suvorexant is metabolized by the hepatic CYP3A system and should be avoided in combination with strong CYP3A inhibitors. suvorexant 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 26648692-5 2015 Suvorexant is metabolized by the hepatic CYP3A system and should be avoided in combination with strong CYP3A inhibitors. suvorexant 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 26276083-6 2015 Studies showed the involvement of CYP1A2, CYP2B6, CYP2C19, and CYP3A4 in N-dealkylation of all three compounds and additionally CYP2D6 for lefetamine and NEDPA. N-Ethyl-alpha-phenylphenethylamine hydrochloride 154-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 26341324-0 2015 A food contaminant ochratoxin A suppresses pregnane X receptor (PXR)-mediated CYP3A4 induction in primary cultures of human hepatocytes. ochratoxin A 19-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 26209290-5 2015 O-desmethyltramadol formation was mediated only by CYP2D6, while N-desmethyltramadol was mediated in part by CYP3A4. N-demethyltramadol 65-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 25892190-9 2015 The CYP3A activity was detectable, but below the LLOQ in day 3 animals and increased gradually with age to reach the highest level in adults. lloq 49-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-9 25892190-10 2015 The CYP3cide and ketoconazole inhibition, and testosterone and midazolam reduction of Luciferin-IPA metabolism in minipig liver microsomes substantiate that Luciferin-IPA is metabolized by CYP3A in minipigs. Testosterone 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-194 25892190-10 2015 The CYP3cide and ketoconazole inhibition, and testosterone and midazolam reduction of Luciferin-IPA metabolism in minipig liver microsomes substantiate that Luciferin-IPA is metabolized by CYP3A in minipigs. Midazolam 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-194 25892190-10 2015 The CYP3cide and ketoconazole inhibition, and testosterone and midazolam reduction of Luciferin-IPA metabolism in minipig liver microsomes substantiate that Luciferin-IPA is metabolized by CYP3A in minipigs. luciferin-ipa 157-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-194 25892190-11 2015 A positive correlation was found between CYP3A abundance and biotransformation of Luciferin-IPA (Pearson r = 0.863; p < 0.0001). luciferin-ipa 82-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 26081137-2 2015 AZD2327 and N-deethylated AZD2327 (M1) are substrates of cytochrome P450 3A (CYP3A4) and comprise a complex multiple inhibitory system that causes competitive and time-dependent inhibition of CYP3A4. 4-((3-aminophenyl)(4-(4-fluorobenzyl)piperazin-1-yl)methyl)-N,N-diethylbenzamide 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-198 26081137-2 2015 AZD2327 and N-deethylated AZD2327 (M1) are substrates of cytochrome P450 3A (CYP3A4) and comprise a complex multiple inhibitory system that causes competitive and time-dependent inhibition of CYP3A4. 4-((3-aminophenyl)(4-(4-fluorobenzyl)piperazin-1-yl)methyl)-N,N-diethylbenzamide 26-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 26081137-2 2015 AZD2327 and N-deethylated AZD2327 (M1) are substrates of cytochrome P450 3A (CYP3A4) and comprise a complex multiple inhibitory system that causes competitive and time-dependent inhibition of CYP3A4. 4-((3-aminophenyl)(4-(4-fluorobenzyl)piperazin-1-yl)methyl)-N,N-diethylbenzamide 26-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-198 26081137-3 2015 The aim of the current work was to develop a physiologically based pharmacokinetic (PBPK) model to predict quantitatively the magnitude of CYP3A4 mediated drug-drug interaction with midazolam as the substrate. Midazolam 182-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 26081137-5 2015 The inhibition of CYP3A4 by AZD2327, using midazolam as a probe drug, was reasonably predicted. 4-((3-aminophenyl)(4-(4-fluorobenzyl)piperazin-1-yl)methyl)-N,N-diethylbenzamide 28-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 26081137-5 2015 The inhibition of CYP3A4 by AZD2327, using midazolam as a probe drug, was reasonably predicted. Midazolam 43-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 26044579-1 2015 AIM: In view of the increasing prevalence of obesity in adolescents, the aim of this study was to determine the pharmacokinetics of the CYP3A substrate midazolam and its metabolites in overweight and obese adolescents. Midazolam 152-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-141 26387027-4 2015 Pharmacokinetic parameters were derived from plasma concentrations of risperidone and its active metabolite, 9-hydroxyrisperidone (formed via CYP2D6 and CYP3A4), collected before and over 4 days after risperidone administration, and from steady-state plasma concentrations of armodafinil and its circulating metabolites, R-modafinil acid and modafinil sulfone. Risperidone 118-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 26178713-2 2015 HIV patients with chronic myeloid leukemia or gastrointestinal stromal tumour may need imatinib, a CYP3A4 substrate with known exposure response-relationships. Imatinib Mesylate 87-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 26363009-3 2015 We identified CYP3A4 as the major enzyme involved in the metabolism of vemurafenib in in vitro assays with human liver microsomes. Vemurafenib 71-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 26363009-4 2015 However, mice expressing human CYP3A4 did not process vemurafenib to a greater extent than CYP3A4-null animals, suggesting that other pregnane X receptor (PXR)-regulated pathways may contribute more significantly to vemurafenib metabolism in vivo. Vemurafenib 216-227 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 26387027-10 2015 CONCLUSION: Consistent with CYP3A4 induction, risperidone and 9-hydroxyrisperidone systemic exposure was reduced in the presence of armodafinil. Modafinil 132-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 26265743-3 2015 Results of this screen revealed that the prescribed androgen receptor antagonist flutamide activated the intrinsic midazolam hydroxylase activity of CYP3A in human hepatic microsomes (66%), rat and human hepatocytes (36 and 160%, respectively), and in vivo in male Sprague-Dawley rats (>2-fold, combined area under the curve of primary rat in vivo midazolam metabolites). Flutamide 81-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-154 26301745-0 2015 Transport and uptake of clausenamide enantiomers in CYP3A4-transfected Caco-2 cells: An insight into the efflux-metabolism alliance. clausenamide 24-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 26301745-1 2015 The present study developed a CYP3A4-expressed Caco-2 monolayer model at which effects of the efflux-metabolism alliance on the transport and uptake of clausenamide (CLA) enantiomers as CYP3A4 substrates were investigated. clausenamide 152-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 26301745-1 2015 The present study developed a CYP3A4-expressed Caco-2 monolayer model at which effects of the efflux-metabolism alliance on the transport and uptake of clausenamide (CLA) enantiomers as CYP3A4 substrates were investigated. clausenamide 152-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 186-192 26301745-1 2015 The present study developed a CYP3A4-expressed Caco-2 monolayer model at which effects of the efflux-metabolism alliance on the transport and uptake of clausenamide (CLA) enantiomers as CYP3A4 substrates were investigated. clausenamide 166-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 26301745-1 2015 The present study developed a CYP3A4-expressed Caco-2 monolayer model at which effects of the efflux-metabolism alliance on the transport and uptake of clausenamide (CLA) enantiomers as CYP3A4 substrates were investigated. clausenamide 166-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 186-192 26301745-3 2015 Their bidirectional transports were significantly reduced by 75.6-87.5% after treatment with verapamil (a P-glycoprotein inhibitor) that increased the rate of metabolism by CYP3A4, whereas the CYP3A4 inhibitor ketoconazole treatment markedly enhanced the basolateral to apical flux of (-) and (+)CLA with ERs being 2.934+-1.432 and 1.877+-0.148(x10(-6)cm/s) respectively. Verapamil 93-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 26301745-3 2015 Their bidirectional transports were significantly reduced by 75.6-87.5% after treatment with verapamil (a P-glycoprotein inhibitor) that increased the rate of metabolism by CYP3A4, whereas the CYP3A4 inhibitor ketoconazole treatment markedly enhanced the basolateral to apical flux of (-) and (+)CLA with ERs being 2.934+-1.432 and 1.877+-0.148(x10(-6)cm/s) respectively. Verapamil 93-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 193-199 26301745-3 2015 Their bidirectional transports were significantly reduced by 75.6-87.5% after treatment with verapamil (a P-glycoprotein inhibitor) that increased the rate of metabolism by CYP3A4, whereas the CYP3A4 inhibitor ketoconazole treatment markedly enhanced the basolateral to apical flux of (-) and (+)CLA with ERs being 2.934+-1.432 and 1.877+-0.148(x10(-6)cm/s) respectively. Ketoconazole 210-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 193-199 26301745-4 2015 These changes could be blocked by the duel CYP3A4/P-glycoprotein inhibitor cyclosporine A, consequently, Papp values for CLA enantiomers in both directions were significantly greater than those obtained by using verapamil or ketoconazole, and their ERs were similar to those following (-) or (+)-isomer treatment alone. Cyclosporine 75-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 26301745-4 2015 These changes could be blocked by the duel CYP3A4/P-glycoprotein inhibitor cyclosporine A, consequently, Papp values for CLA enantiomers in both directions were significantly greater than those obtained by using verapamil or ketoconazole, and their ERs were similar to those following (-) or (+)-isomer treatment alone. LY 165163 105-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 26301745-4 2015 These changes could be blocked by the duel CYP3A4/P-glycoprotein inhibitor cyclosporine A, consequently, Papp values for CLA enantiomers in both directions were significantly greater than those obtained by using verapamil or ketoconazole, and their ERs were similar to those following (-) or (+)-isomer treatment alone. Verapamil 212-221 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 26301745-4 2015 These changes could be blocked by the duel CYP3A4/P-glycoprotein inhibitor cyclosporine A, consequently, Papp values for CLA enantiomers in both directions were significantly greater than those obtained by using verapamil or ketoconazole, and their ERs were similar to those following (-) or (+)-isomer treatment alone. Ketoconazole 225-237 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 26301745-7 2015 This effect disappeared in the presence of a CYP3A4 inducer dexamethasone. Dexamethasone 60-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 26301745-8 2015 These results indicated that CYP3A4 could influence P-gp efflux, transport and uptake of CLA enantiomers as CYP3A4 substrates and that a duel inhibition to CYP3A4/ P-glycoprotein could enhance their absorption and bioavailability, which provides new insight into the efflux-metabolism alliance and will benefit the clinical pharmacology of (-)CLA as a candidate drug for treatment of Alzheimer"s disease. clausenamide 89-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 26301745-8 2015 These results indicated that CYP3A4 could influence P-gp efflux, transport and uptake of CLA enantiomers as CYP3A4 substrates and that a duel inhibition to CYP3A4/ P-glycoprotein could enhance their absorption and bioavailability, which provides new insight into the efflux-metabolism alliance and will benefit the clinical pharmacology of (-)CLA as a candidate drug for treatment of Alzheimer"s disease. clausenamide 89-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 26301745-8 2015 These results indicated that CYP3A4 could influence P-gp efflux, transport and uptake of CLA enantiomers as CYP3A4 substrates and that a duel inhibition to CYP3A4/ P-glycoprotein could enhance their absorption and bioavailability, which provides new insight into the efflux-metabolism alliance and will benefit the clinical pharmacology of (-)CLA as a candidate drug for treatment of Alzheimer"s disease. clausenamide 89-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 26104860-3 2015 Enantioselective CE with highly sulfated gamma-cyclodextrin as chiral selector was employed for analyzing in vitro (i) the kinetics of the N-demethylation of ketamine mediated by canine CYP3A12 and (ii) interactions occurring with racemic medetomidine and dexmedetomidine during coincubation with ketamine and canine liver microsomes (CLM), canine CYP3A12, human liver microsomes (HLM), and human CYP3A4. gamma-cyclodextrin 41-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 397-403 26104860-3 2015 Enantioselective CE with highly sulfated gamma-cyclodextrin as chiral selector was employed for analyzing in vitro (i) the kinetics of the N-demethylation of ketamine mediated by canine CYP3A12 and (ii) interactions occurring with racemic medetomidine and dexmedetomidine during coincubation with ketamine and canine liver microsomes (CLM), canine CYP3A12, human liver microsomes (HLM), and human CYP3A4. Nitrogen 139-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 397-403 26104860-3 2015 Enantioselective CE with highly sulfated gamma-cyclodextrin as chiral selector was employed for analyzing in vitro (i) the kinetics of the N-demethylation of ketamine mediated by canine CYP3A12 and (ii) interactions occurring with racemic medetomidine and dexmedetomidine during coincubation with ketamine and canine liver microsomes (CLM), canine CYP3A12, human liver microsomes (HLM), and human CYP3A4. Ketamine 158-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 397-403 26265743-3 2015 Results of this screen revealed that the prescribed androgen receptor antagonist flutamide activated the intrinsic midazolam hydroxylase activity of CYP3A in human hepatic microsomes (66%), rat and human hepatocytes (36 and 160%, respectively), and in vivo in male Sprague-Dawley rats (>2-fold, combined area under the curve of primary rat in vivo midazolam metabolites). Midazolam 115-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-154 26265743-4 2015 In addition, a screen of the pharmacologically active metabolite 2-hydroxy-flutamide revealed that this principle metabolite increased CYP3A metabolism of midazolam in human microsomes (30%) and hepatocytes (110%). hydroxyflutamide 65-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-140 26329790-2 2015 Organic anion transporting polypeptide (OATP) 1B1 activity markedly affects the hepatic uptake of simvastatin acid, whereas both simvastatin and simvastatin acid are sensitive to changes in cytochrome P450 3A4 activity. simvastatin acid 145-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-209 26265743-4 2015 In addition, a screen of the pharmacologically active metabolite 2-hydroxy-flutamide revealed that this principle metabolite increased CYP3A metabolism of midazolam in human microsomes (30%) and hepatocytes (110%). Midazolam 155-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-140 26329790-3 2015 Clopidogrel and its metabolites inhibit OATP1B1 and CYP3A4 in vitro. Clopidogrel 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 26265743-5 2015 Importantly, both flutamide and 2-hydroxy-flutamide demonstrated a pronounced increase in the CYP3A-mediated metabolism of commonly paired medications, nifedipine (antihypertensive) and amiodarone (antiarrhythmic), in multispecies hepatocytes (100% over baseline). Flutamide 18-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-99 26265743-5 2015 Importantly, both flutamide and 2-hydroxy-flutamide demonstrated a pronounced increase in the CYP3A-mediated metabolism of commonly paired medications, nifedipine (antihypertensive) and amiodarone (antiarrhythmic), in multispecies hepatocytes (100% over baseline). hydroxyflutamide 32-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-99 26265743-5 2015 Importantly, both flutamide and 2-hydroxy-flutamide demonstrated a pronounced increase in the CYP3A-mediated metabolism of commonly paired medications, nifedipine (antihypertensive) and amiodarone (antiarrhythmic), in multispecies hepatocytes (100% over baseline). Nifedipine 152-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-99 26354948-9 2015 Rifampin treatment induced systemic CYP3A metabolism of (11)C-verapamil; however, it reduced the ER by 6%. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 26265743-5 2015 Importantly, both flutamide and 2-hydroxy-flutamide demonstrated a pronounced increase in the CYP3A-mediated metabolism of commonly paired medications, nifedipine (antihypertensive) and amiodarone (antiarrhythmic), in multispecies hepatocytes (100% over baseline). Amiodarone 186-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-99 26586934-0 2015 Reductive metabolism of oxymatrine is catalyzed by microsomal CYP3A4. oxymatrine 24-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 26744738-8 2015 Daclatasvir and asunaprevir are substrates for cytochrome P450 3A4 enzymatic pathway; thus, there is a substantial potential for drug interactions. daclatasvir 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-66 26744738-8 2015 Daclatasvir and asunaprevir are substrates for cytochrome P450 3A4 enzymatic pathway; thus, there is a substantial potential for drug interactions. asunaprevir 16-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-66 26421491-0 2015 Effects of CYP3A4/5 and ABCB1 genetic polymorphisms on carbamazepine metabolism and transport in Chinese patients with epilepsy treated with carbamazepine in monotherapy and bitherapy. Carbamazepine 55-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 26296708-1 2015 In this study, IC50 shift and time-dependent inhibition (TDI) experiments were carried out to measure the ability of amiodarone (AMIO), and its circulating human metabolites, to reversibly and irreversibly inhibit CYP1A2, CYP2C9, CYP2D6, and CYP3A4 activities in human liver microsomes. Amiodarone 117-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 242-248 26296708-1 2015 In this study, IC50 shift and time-dependent inhibition (TDI) experiments were carried out to measure the ability of amiodarone (AMIO), and its circulating human metabolites, to reversibly and irreversibly inhibit CYP1A2, CYP2C9, CYP2D6, and CYP3A4 activities in human liver microsomes. Amiodarone 129-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 242-248 26296708-3 2015 Based on these values, the minor metabolite N,N-didesethylamiodarone (DDEA) is predicted to be the major cause of DDIs with xenobiotics primarily metabolized by CYP1A2, CYP2C9, or CYP3A4, while AMIO and its N-monodesethylamiodarone (MDEA) derivative are the most likely cause of interactions involving inhibition of CYP2D6 metabolism. n,n-didesethylamiodarone 44-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 26296708-3 2015 Based on these values, the minor metabolite N,N-didesethylamiodarone (DDEA) is predicted to be the major cause of DDIs with xenobiotics primarily metabolized by CYP1A2, CYP2C9, or CYP3A4, while AMIO and its N-monodesethylamiodarone (MDEA) derivative are the most likely cause of interactions involving inhibition of CYP2D6 metabolism. Di-N-desethylamiodarone 70-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 26296708-3 2015 Based on these values, the minor metabolite N,N-didesethylamiodarone (DDEA) is predicted to be the major cause of DDIs with xenobiotics primarily metabolized by CYP1A2, CYP2C9, or CYP3A4, while AMIO and its N-monodesethylamiodarone (MDEA) derivative are the most likely cause of interactions involving inhibition of CYP2D6 metabolism. Amiodarone 194-198 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 26296708-3 2015 Based on these values, the minor metabolite N,N-didesethylamiodarone (DDEA) is predicted to be the major cause of DDIs with xenobiotics primarily metabolized by CYP1A2, CYP2C9, or CYP3A4, while AMIO and its N-monodesethylamiodarone (MDEA) derivative are the most likely cause of interactions involving inhibition of CYP2D6 metabolism. desethylamiodarone 207-231 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 26296708-3 2015 Based on these values, the minor metabolite N,N-didesethylamiodarone (DDEA) is predicted to be the major cause of DDIs with xenobiotics primarily metabolized by CYP1A2, CYP2C9, or CYP3A4, while AMIO and its N-monodesethylamiodarone (MDEA) derivative are the most likely cause of interactions involving inhibition of CYP2D6 metabolism. desethylamiodarone 233-237 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 26296708-5 2015 The TDI experiments showed DDEA to be a potent inactivator of CYP1A2 (KI = 0.46 muM, kinact = 0.030 minute(-1)), while MDEA was a moderate inactivator of both CYP2D6 (KI = 2.7 muM, kinact = 0.018 minute(-1)) and CYP3A4 (KI = 2.6 muM, kinact = 0.016 minute(-1)). Di-N-desethylamiodarone 27-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 212-218 26296708-5 2015 The TDI experiments showed DDEA to be a potent inactivator of CYP1A2 (KI = 0.46 muM, kinact = 0.030 minute(-1)), while MDEA was a moderate inactivator of both CYP2D6 (KI = 2.7 muM, kinact = 0.018 minute(-1)) and CYP3A4 (KI = 2.6 muM, kinact = 0.016 minute(-1)). desethylamiodarone 119-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 212-218 26296708-7 2015 Additional metabolic studies strongly suggest that CYP3A4 is the primary microsomal enzyme involved in the metabolism of AMIO to both MDEA and DDEA. Amiodarone 121-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 26296708-7 2015 Additional metabolic studies strongly suggest that CYP3A4 is the primary microsomal enzyme involved in the metabolism of AMIO to both MDEA and DDEA. desethylamiodarone 134-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 26296708-7 2015 Additional metabolic studies strongly suggest that CYP3A4 is the primary microsomal enzyme involved in the metabolism of AMIO to both MDEA and DDEA. Di-N-desethylamiodarone 143-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 26586934-4 2015 The current studies demonstrated that OMT could be metabolized to MT rapidly in HLMs and HIMs and CYP3A4 greatly contributed to this transformation. oxymatrine 38-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 27022466-2 2015 In vitro studies have also shown that vitamin D may affect the expression of CYP3A4. Vitamin D 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 27022466-4 2015 The secondary aim was to investigate the association between 25-hydroxy vitamin D in serum and CYP3A activity. 25-hydroxyvitamin D 61-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-100 27022466-6 2015 In addition, the correlation between miR-27b and CYP3A activity, measured by dextromethorphan N-demethylation and 6beta-hydroxylation of testosterone and the gene expression of CYP3A4, VDR and PPAR alpha were assessed in 20 human liver samples. dextromethorphan n 77-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 27022466-6 2015 In addition, the correlation between miR-27b and CYP3A activity, measured by dextromethorphan N-demethylation and 6beta-hydroxylation of testosterone and the gene expression of CYP3A4, VDR and PPAR alpha were assessed in 20 human liver samples. Testosterone 137-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 27022466-7 2015 A significant association between circulatory miR-27b levels and 4beta-hydroxycholesterol ratio was found; P = 0.04, and between hepatic miR-27b levels and CYP3A activity, measured by dextromethorphan N-demethylation in human liver (P = 0.04). dextromethorphan n 184-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-161 27022466-10 2015 In conclusion, this pilot-study supports the hypothesis that miR-27b levels as well as 25-hydroxyvitamin D may affect CYP3A activity in vivo. 25-hydroxyvitamin D 87-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-123 26497728-1 2015 BACKGROUND: Clarithromycin, known as a potent inhibitor of the cytochrome P450 isoenzyme CYP3A, may increase the plasma concentration of statins metabolized by this pathway; therefore, increase the risk of interaction with statins in reference to pharmacokinetic studies. Clarithromycin 12-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-94 26408814-4 2015 The PXR modulatory effects of the synthesized diethylstilbestrol derivatives were further confirmed by the induction of PXR-regulated CYP3A4 expression with compound 1, as well as by the inhibition of the rifaximin-promoted up-regulation of CYP3A4 expression with 2 and its derivative 6. Diethylstilbestrol 46-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 28975914-9 2015 PCZ is an inhibitor of the CYP3A4 enzyme; therefore, monitoring for drug-drug interactions is warranted with other CYP3A4 substrates/inhibitors/inducers. posaconazole 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 28975914-9 2015 PCZ is an inhibitor of the CYP3A4 enzyme; therefore, monitoring for drug-drug interactions is warranted with other CYP3A4 substrates/inhibitors/inducers. posaconazole 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 26408814-4 2015 The PXR modulatory effects of the synthesized diethylstilbestrol derivatives were further confirmed by the induction of PXR-regulated CYP3A4 expression with compound 1, as well as by the inhibition of the rifaximin-promoted up-regulation of CYP3A4 expression with 2 and its derivative 6. Rifaximin 205-214 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 241-247 26232156-9 2015 In the first case, the cause was revealed to be a drug that was added to the patient"s treatment regimen (posaconazole) that inhibits CYP3A4 which is responsible for sirolimus metabolism. posaconazole 106-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 26232156-9 2015 In the first case, the cause was revealed to be a drug that was added to the patient"s treatment regimen (posaconazole) that inhibits CYP3A4 which is responsible for sirolimus metabolism. Sirolimus 166-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 26408814-4 2015 The PXR modulatory effects of the synthesized diethylstilbestrol derivatives were further confirmed by the induction of PXR-regulated CYP3A4 expression with compound 1, as well as by the inhibition of the rifaximin-promoted up-regulation of CYP3A4 expression with 2 and its derivative 6. Diethylstilbestrol 46-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 241-247 26408814-4 2015 The PXR modulatory effects of the synthesized diethylstilbestrol derivatives were further confirmed by the induction of PXR-regulated CYP3A4 expression with compound 1, as well as by the inhibition of the rifaximin-promoted up-regulation of CYP3A4 expression with 2 and its derivative 6. Rifaximin 205-214 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 26395423-4 2015 With the exception of M3 and M8, the formation of all metabolites of lasiocarpine was catalyzed by CYP3A4 in humans. lasiocarpine 69-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 26485399-2 2015 Stilbenes, including resveratrol, belong to a group of dietary health-promoting compounds that also act as inhibitors of CYP3A4. Stilbenes 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 26485399-2 2015 Stilbenes, including resveratrol, belong to a group of dietary health-promoting compounds that also act as inhibitors of CYP3A4. Resveratrol 21-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 26485399-4 2015 To this end, an aldehyde group was attached to resveratrol and the interactions of CYP3A4 with resveratrol, its aldehyde analogue (RA) and a known synthetic inhibitor were studied and compared in two biological models. Resveratrol 95-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 26485399-8 2015 Modeling of the binding site of CYP3A4 revealed a combination of three types of interactions: hydrophobic interactions, electrostatic interactions and hydrogen bonds. Hydrogen 151-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 26300393-0 2015 Genetic variations of hOCT1 gene and CYP3A4/A5 genes and their association with imatinib response in Chronic Myeloid Leukemia. Imatinib Mesylate 80-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 26404412-0 2015 Identification and in silico prediction of metabolites of the model compound, tebufenozide by human CYP3A4 and CYP2C19. tebufenozide 78-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 26404412-1 2015 The metabolites of tebufenozide, a model compound, formed by the yeast-expressed human CYP3A4 and CYP2C19 were identified to clarify the substrate recognition mechanism of the human cytochrome P450 (CYP) isozymes. tebufenozide 19-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 26404412-5 2015 Several alkyl sites of tebufenozide were hydroxylated by CYP3A4 whereas only one site was modified by CYP2C19. tebufenozide 23-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 26282489-6 2015 SAL metabolism is mainly mediated by CYP enzymes; CYP3A4 the major enzyme metabolising SAL. salinomycin 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 26317243-13 2015 CYP3A4 profoundly reduces the oral availability of cabazitaxel. cabazitaxel 51-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26770526-2 2015 The genetic polymorphisms of CYP3A4, CYP3A5 and MDR1 in 216 RT patients were detected by PCR-RFLP, the genetic and clinical factors and blood concentration/dose x body weight (C/D) values of tacrolimus were performed the single factor correlation analysis, and established the dose prediction algorithm of tacrolimus by stepwise multiple regression analysis. Tacrolimus 191-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 26770526-2 2015 The genetic polymorphisms of CYP3A4, CYP3A5 and MDR1 in 216 RT patients were detected by PCR-RFLP, the genetic and clinical factors and blood concentration/dose x body weight (C/D) values of tacrolimus were performed the single factor correlation analysis, and established the dose prediction algorithm of tacrolimus by stepwise multiple regression analysis. Tacrolimus 306-316 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 26282489-6 2015 SAL metabolism is mainly mediated by CYP enzymes; CYP3A4 the major enzyme metabolising SAL. salinomycin 87-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 26282489-9 2015 SAL was found to be a moderate inhibitor of CYP2D6 as well as CYP3A4. salinomycin 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 26348830-0 2015 Augmented Inhibition of CYP3A4 in Human Primary Hepatocytes by Ritonavir Solid Drug Nanoparticles. Ritonavir 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 26282489-10 2015 As CYP3A4 was the major enzyme responsible for metabolism of SAL, in vivo pharmacokinetic study in rats was done to check the effect of concomitant administration of Ketoconazole (KTC) on SAL pharmacokinetics. salinomycin 61-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-9 26282489-10 2015 As CYP3A4 was the major enzyme responsible for metabolism of SAL, in vivo pharmacokinetic study in rats was done to check the effect of concomitant administration of Ketoconazole (KTC) on SAL pharmacokinetics. Ketoconazole 166-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-9 26348830-8 2015 From 68 solid drug nanoparticle formulations tested, 50 (73.5%) for baculosome and 44 (64.7%) for human primary hepatocytes exhibited enhanced CYP3A4 inhibition relative to an aqueous ritonavir solution. baculosome 68-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 26348830-12 2015 These data provide in vitro proof of concept for improved inhibition of CYP3A4 by ritonavir through formation of solid drug nanoparticles. Ritonavir 82-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 26282489-10 2015 As CYP3A4 was the major enzyme responsible for metabolism of SAL, in vivo pharmacokinetic study in rats was done to check the effect of concomitant administration of Ketoconazole (KTC) on SAL pharmacokinetics. Ketoconazole 180-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-9 26282489-11 2015 KTC, being a selective CYP3A4 inhibitor increased the systemic exposure of SAL significantly to 7-fold in AUC0-alpha and 3-fold increase in Cmax of SAL in rats with concomitant KTC administration. Ketoconazole 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 26239802-3 2015 Therefore, the hypothesis to be tested is that meclizine inactivates human CYP3A enzymes. Meclizine 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 26471025-4 2015 This case report describes an incident with QTc prolongation which was probably caused by an interaction induced by a combination of amiodarone, clarithromycin and the CYP3A4-inhibitor fluconazole. Amiodarone 133-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 26471025-4 2015 This case report describes an incident with QTc prolongation which was probably caused by an interaction induced by a combination of amiodarone, clarithromycin and the CYP3A4-inhibitor fluconazole. Fluconazole 185-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 26330331-3 2015 Treatment of NADCs may be complicated by interactions between antiretrovirals and chemotherapy mostly via inhibition or induction of CYP3A4. nadcs 13-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 26330331-4 2015 Erlotinib is used to treat non-small cell lung and pancreatic cancer and is primarily metabolized by CYP3A4 into multiple products including the active metabolite (OSI-420). Erlotinib Hydrochloride 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 26330331-5 2015 Preclinical in vivo assessment was performed to gain a better understanding of CYP3A4-mediated interactions between antiretrovirals and erlotinib. Erlotinib Hydrochloride 136-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 26330331-12 2015 RESULTS: Administration of erlotinib with CYP3A4 inducers (dexamethasone) and inhibitors (ketoconazole and ritonavir) resulted in significant alterations in erlotinib exposure. Erlotinib Hydrochloride 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 26330331-12 2015 RESULTS: Administration of erlotinib with CYP3A4 inducers (dexamethasone) and inhibitors (ketoconazole and ritonavir) resulted in significant alterations in erlotinib exposure. Dexamethasone 59-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 26330331-12 2015 RESULTS: Administration of erlotinib with CYP3A4 inducers (dexamethasone) and inhibitors (ketoconazole and ritonavir) resulted in significant alterations in erlotinib exposure. Ketoconazole 90-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 26330331-12 2015 RESULTS: Administration of erlotinib with CYP3A4 inducers (dexamethasone) and inhibitors (ketoconazole and ritonavir) resulted in significant alterations in erlotinib exposure. Ritonavir 107-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 26330331-12 2015 RESULTS: Administration of erlotinib with CYP3A4 inducers (dexamethasone) and inhibitors (ketoconazole and ritonavir) resulted in significant alterations in erlotinib exposure. Erlotinib Hydrochloride 157-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 26330331-15 2015 CONCLUSION: CYP3A4 inducers and inhibitors altered the exposure of erlotinib. Erlotinib Hydrochloride 67-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 26239802-4 2015 Our findings indicated that meclizine directly inhibited testosterone 6beta-hydroxylation catalyzed by human liver microsomes, recombinant CYP3A4, and recombinant CYP3A5. Meclizine 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 26239802-4 2015 Our findings indicated that meclizine directly inhibited testosterone 6beta-hydroxylation catalyzed by human liver microsomes, recombinant CYP3A4, and recombinant CYP3A5. testosterone 6beta 57-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 26239802-8 2015 Meclizine selectively inactivated CYP3A4, but not CYP3A5. Meclizine 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 26239802-9 2015 In contrast to meclizine, which has a di-substituted piperazine ring, norchlorcyclizine, which is a N-debenzylated meclizine metabolite with a mono-substituted piperazine ring, did not inactivate but directly inhibited hepatic microsomal CYP3A activity. norchlorcyclizine 70-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 238-243 26315684-0 2015 Evaluation of Cytochrome P450 (CYP) 3A4-Based Interactions of Levomilnacipran with Ketoconazole, Carbamazepine or Alprazolam in Healthy Subjects. Levomilnacipran 62-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-39 26377104-0 2015 Evaluation of CYP3A4 inhibition and hepatotoxicity using DMSO-treated human hepatoma HuH-7 cells. Dimethyl Sulfoxide 57-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 26377104-3 2015 HuH-7 cells treated with DMSO for 2 weeks after confluence expressed the highest CYP3A4 gene expression and activity compared to the other two culture conditions. Dimethyl Sulfoxide 25-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 26377104-4 2015 Furthermore, CYP3A4 activity in DMSO-treated HuH-7 cells was compared to that in a human hepatoma cell line (HepG2/C3A) and human bipotent progenitor cell line (HepaRG), which yielded the following ranking: HepaRG > DMSO-treated HuH-7 >> HepG2/C3A cells. Dimethyl Sulfoxide 32-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 26377104-8 2015 DMSO-treated HuH-7 cells yielded minimal CYP3A4 induction compared to that in the HepaRG cells after 48-h treatments. Dimethyl Sulfoxide 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 26377104-10 2015 Overall, DMSO-treated HuH-7 cells are a valuable model for medium- or high-throughput screening of chemicals for CYP3A4 inhibition and hepatotoxicity. Dimethyl Sulfoxide 9-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 26315684-0 2015 Evaluation of Cytochrome P450 (CYP) 3A4-Based Interactions of Levomilnacipran with Ketoconazole, Carbamazepine or Alprazolam in Healthy Subjects. Ketoconazole 83-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-39 26239802-10 2015 In conclusion, meclizine inhibited human CYP3A enzymes by both direct inhibition and mechanism-based inactivation. Meclizine 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 26315684-0 2015 Evaluation of Cytochrome P450 (CYP) 3A4-Based Interactions of Levomilnacipran with Ketoconazole, Carbamazepine or Alprazolam in Healthy Subjects. Carbamazepine 97-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-39 25929560-6 2015 Enzalutamide reduced the AUC of oral S-warfarin, omeprazole, and midazolam by 56, 70, and 86 %, respectively; therefore, enzalutamide is a moderate inducer of CYP2C9 and CYP2C19 and a strong inducer of CYP3A4. enzalutamide 122-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 26315684-0 2015 Evaluation of Cytochrome P450 (CYP) 3A4-Based Interactions of Levomilnacipran with Ketoconazole, Carbamazepine or Alprazolam in Healthy Subjects. Alprazolam 114-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-39 26315684-9 2015 Co-administration with levomilnacipran of drugs metabolised by CYP3A4, such as alprazolam, requires no dose adjustment due to pharmacokinetic considerations. Levomilnacipran 23-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 26315684-9 2015 Co-administration with levomilnacipran of drugs metabolised by CYP3A4, such as alprazolam, requires no dose adjustment due to pharmacokinetic considerations. Alprazolam 79-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 25929560-6 2015 Enzalutamide reduced the AUC of oral S-warfarin, omeprazole, and midazolam by 56, 70, and 86 %, respectively; therefore, enzalutamide is a moderate inducer of CYP2C9 and CYP2C19 and a strong inducer of CYP3A4. enzalutamide 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-209 25929560-8 2015 It is recommended to avoid concomitant use of enzalutamide with narrow therapeutic index drugs metabolized by CYP2C9, CYP2C19, or CYP3A4, as enzalutamide may decrease their exposure. enzalutamide 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 25929560-8 2015 It is recommended to avoid concomitant use of enzalutamide with narrow therapeutic index drugs metabolized by CYP2C9, CYP2C19, or CYP3A4, as enzalutamide may decrease their exposure. enzalutamide 141-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 26220948-6 2015 Kinetic studies using expressed enzymes demonstrated that the contributions of CYP2B6, CYP2C19, and CYP3A4 to the formation of H4 from 2-oxo-clopidogrel were 18.5%, 26.1%, and 53.5%, respectively. 2-oxo-clopidogrel 135-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 26350273-2 2015 Hydrocodone undergoes cytochrome P-450 (CYP)-mediated metabolism involving the CYP3A4 and CYP2D6 isozymes. Hydrocodone 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 26350273-3 2015 CYP3A4 yields norhydrocodone, a major inactive metabolite, whereas CYP2D6 yields hydromorphone, a minor active metabolite. norhydrocodone 14-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26350273-3 2015 CYP3A4 yields norhydrocodone, a major inactive metabolite, whereas CYP2D6 yields hydromorphone, a minor active metabolite. Hydromorphone 81-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26180127-0 2015 Prediction of Drug-Drug Interactions with Crizotinib as the CYP3A Substrate Using a Physiologically Based Pharmacokinetic Model. Crizotinib 42-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 26180127-1 2015 An orally available multiple tyrosine kinase inhibitor, crizotinib (Xalkori), is a CYP3A substrate, moderate time-dependent inhibitor, and weak inducer. Crizotinib 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 26220948-7 2015 The CLint ratios of H3 formation to H4 formation from 2-oxo-clopidogrel by CYP2B6, CYP2C19, and CYP3A4 were 2.2, 1.0, and 1.7, respectively. HS 3 20-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 26180127-8 2015 Overall, we believe that the crizotinib PBPK model developed, refined, and verified in the present study would adequately predict crizotinib oral exposures in other clinical studies, such as DDIs with weak/moderate CYP3A inhibitors/inducers and drug-disease interactions in patients with hepatic or renal impairment. Crizotinib 29-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-220 26220948-7 2015 The CLint ratios of H3 formation to H4 formation from 2-oxo-clopidogrel by CYP2B6, CYP2C19, and CYP3A4 were 2.2, 1.0, and 1.7, respectively. 2-oxo-clopidogrel 54-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 26150050-0 2015 Evaluation of 6beta-Hydroxycortisol and 6beta-Hydroxycortisone as Biomarkers for Cytochrome P450 3A Activity: Insight into Their Predictive Value for Estimating Oral Immunosuppressant Metabolism. 6 beta-hydroxycortisol 14-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-99 25998042-2 2015 Hepatocellular carcinoma (HCC) pathogenesis is associated with overexpression of MET, and physiologic changes in the livers of HCC patients may decrease CYP3A isozyme-mediated metabolism of foretinib. GSK 1363089 190-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-158 26150050-0 2015 Evaluation of 6beta-Hydroxycortisol and 6beta-Hydroxycortisone as Biomarkers for Cytochrome P450 3A Activity: Insight into Their Predictive Value for Estimating Oral Immunosuppressant Metabolism. 6 beta-hydroxycortisone 40-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-99 26150050-1 2015 The combined clearance of endogenous 6beta-hydroxycortisol and 6beta-hydroxycortisone is suggested biomarker for in vivo cytochrome P450 3A (CYP3A) activity. 6 beta-hydroxycortisol 37-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-139 26150050-1 2015 The combined clearance of endogenous 6beta-hydroxycortisol and 6beta-hydroxycortisone is suggested biomarker for in vivo cytochrome P450 3A (CYP3A) activity. 6 beta-hydroxycortisol 37-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-146 26150050-1 2015 The combined clearance of endogenous 6beta-hydroxycortisol and 6beta-hydroxycortisone is suggested biomarker for in vivo cytochrome P450 3A (CYP3A) activity. 6 beta-hydroxycortisone 63-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-139 26150050-1 2015 The combined clearance of endogenous 6beta-hydroxycortisol and 6beta-hydroxycortisone is suggested biomarker for in vivo cytochrome P450 3A (CYP3A) activity. 6 beta-hydroxycortisone 63-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-146 26150050-7 2015 Regarding the biopharmaceutical characteristics, the endogenous CYP3A biomarker explains 74.5% of variability in oral cyclosporine clearance between individuals. Cyclosporine 118-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 26516577-7 2015 In addition, PXR (rifampicin) and CAR-selective (carbamazepine and phenytoin) inducers of CYP3A4 and CYP2B6 induction, respectively, were demonstrated. Rifampin 18-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 26045286-5 2015 Presumably, itraconazole by inhibiting CYP3A4 enzyme caused an increase in plasma methylprednisolone levels. Itraconazole 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 26045286-5 2015 Presumably, itraconazole by inhibiting CYP3A4 enzyme caused an increase in plasma methylprednisolone levels. Methylprednisolone 82-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 26238175-7 2015 In LS180 human colon adenocarcinoma cells, 3-hydroxyflavone, quercetin, and tamarixetin increased CYP3A4, CYP3A5, and ABCB1 mRNA expression, whereas galangin and isorhamnetin increased CYP3A4 and ABCB1 but not CYP3A5 mRNA expression. Quercetin 61-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 26238175-7 2015 In LS180 human colon adenocarcinoma cells, 3-hydroxyflavone, quercetin, and tamarixetin increased CYP3A4, CYP3A5, and ABCB1 mRNA expression, whereas galangin and isorhamnetin increased CYP3A4 and ABCB1 but not CYP3A5 mRNA expression. Quercetin 61-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 26238175-7 2015 In LS180 human colon adenocarcinoma cells, 3-hydroxyflavone, quercetin, and tamarixetin increased CYP3A4, CYP3A5, and ABCB1 mRNA expression, whereas galangin and isorhamnetin increased CYP3A4 and ABCB1 but not CYP3A5 mRNA expression. tamarixetin 76-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 26238175-7 2015 In LS180 human colon adenocarcinoma cells, 3-hydroxyflavone, quercetin, and tamarixetin increased CYP3A4, CYP3A5, and ABCB1 mRNA expression, whereas galangin and isorhamnetin increased CYP3A4 and ABCB1 but not CYP3A5 mRNA expression. tamarixetin 76-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 26456786-9 2015 Using human CYPs, CYP1A2, CYP2C19, CYP2D6, and/or CYP3A4 were found to catalyze N-oxide formation and N-, O-demethylation and/or oxidation. n-oxide 80-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 26456786-9 2015 Using human CYPs, CYP1A2, CYP2C19, CYP2D6, and/or CYP3A4 were found to catalyze N-oxide formation and N-, O-demethylation and/or oxidation. Nitrogen 80-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 26238175-7 2015 In LS180 human colon adenocarcinoma cells, 3-hydroxyflavone, quercetin, and tamarixetin increased CYP3A4, CYP3A5, and ABCB1 mRNA expression, whereas galangin and isorhamnetin increased CYP3A4 and ABCB1 but not CYP3A5 mRNA expression. 3-hydroxyflavone 43-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 26238175-7 2015 In LS180 human colon adenocarcinoma cells, 3-hydroxyflavone, quercetin, and tamarixetin increased CYP3A4, CYP3A5, and ABCB1 mRNA expression, whereas galangin and isorhamnetin increased CYP3A4 and ABCB1 but not CYP3A5 mRNA expression. 3-hydroxyflavone 43-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 26516590-0 2015 Evacetrapib: in vitro and clinical disposition, metabolism, excretion, and assessment of drug interaction potential with strong CYP3A and CYP2C8 inhibitors. evacetrapib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-133 26516590-5 2015 In vitro, CYP3A was responsible for about 90% of evacetrapib"s CYP-associated clearance, while CYP2C8 accounted for about 10%. evacetrapib 49-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 26516590-9 2015 In clinical DDI studies, the ratios of geometric least squares means for evacetrapib with/without the CYP3A inhibitor ketoconazole were 2.37 for area under the curve (AUC)(0- ) and 1.94 for C max. Ketoconazole 118-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 26516590-11 2015 Although in vitro results indicated that both CYP3A and CYP2C8 metabolized evacetrapib, clinical studies confirmed that evacetrapib is primarily metabolized by CYP3A. evacetrapib 75-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-51 26516590-11 2015 Although in vitro results indicated that both CYP3A and CYP2C8 metabolized evacetrapib, clinical studies confirmed that evacetrapib is primarily metabolized by CYP3A. evacetrapib 120-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-165 26516577-7 2015 In addition, PXR (rifampicin) and CAR-selective (carbamazepine and phenytoin) inducers of CYP3A4 and CYP2B6 induction, respectively, were demonstrated. Carbamazepine 49-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 26516590-12 2015 However, given the modest increase in evacetrapib exposure and robust clinical safety profile to date, there is a low likelihood of clinically relevant DDI with concomitant use of strong CYP3A or CYP2C8 inhibitors. evacetrapib 38-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-192 26516577-7 2015 In addition, PXR (rifampicin) and CAR-selective (carbamazepine and phenytoin) inducers of CYP3A4 and CYP2B6 induction, respectively, were demonstrated. Phenytoin 67-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 26467116-12 2015 Among the CYPs, CYP3A4 played an important role in the hydroxylation reaction of tussilagone in vitro. tussilagone 81-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 26608490-1 2015 UNLABELLED: Rivaroxaban, a selective inhibitor of active factor X, is metabolized by cytochrom P450 3A4 (CYP3A4) and is a substrate for transporter protein--P-glycoprotein (P-gp). Rivaroxaban 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-103 26608490-1 2015 UNLABELLED: Rivaroxaban, a selective inhibitor of active factor X, is metabolized by cytochrom P450 3A4 (CYP3A4) and is a substrate for transporter protein--P-glycoprotein (P-gp). Rivaroxaban 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 26608490-2 2015 Amiodarone, an antiarrhytmic agent, is classified as moderate CYP3A4 and P-gp inhibitor. Amiodarone 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 26196221-7 2015 Moreover, parathion and bisphenol A are the activators of PXR and inducers of CYP3A4 mRNA and protein in the primary cultures of human hepatocytes. Parathion 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 26196221-7 2015 Moreover, parathion and bisphenol A are the activators of PXR and inducers of CYP3A4 mRNA and protein in the primary cultures of human hepatocytes. bisphenol A 24-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 25776278-3 2015 In human liver microsomes, SIPI5357 showed the strongest inhibition of CYP2D6, followed by CYP3A4 (testosterone) and CYP2C8. sipi5357 27-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 26366873-0 2015 Optical Isomers of Atorvastatin, Rosuvastatin and Fluvastatin Enantiospecifically Activate Pregnane X Receptor PXR and Induce CYP2A6, CYP2B6 and CYP3A4 in Human Hepatocytes. Atorvastatin 19-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 26404338-7 2015 However, incubation of the cells with 50 and 100 microM TCAS caused a profound decrease in the activities of CYP1A and CYP3A, which was probably due to cytotoxic effects, suggesting that exposure to TCAS might be a health concern. Trichloroacetic Acid 56-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-124 26404338-7 2015 However, incubation of the cells with 50 and 100 microM TCAS caused a profound decrease in the activities of CYP1A and CYP3A, which was probably due to cytotoxic effects, suggesting that exposure to TCAS might be a health concern. Trichloroacetic Acid 199-203 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-124 26366873-0 2015 Optical Isomers of Atorvastatin, Rosuvastatin and Fluvastatin Enantiospecifically Activate Pregnane X Receptor PXR and Induce CYP2A6, CYP2B6 and CYP3A4 in Human Hepatocytes. Rosuvastatin Calcium 33-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 26366873-0 2015 Optical Isomers of Atorvastatin, Rosuvastatin and Fluvastatin Enantiospecifically Activate Pregnane X Receptor PXR and Induce CYP2A6, CYP2B6 and CYP3A4 in Human Hepatocytes. Fluvastatin 50-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 26002511-5 2015 The data reported here demonstrate CYP3A4 to be the major CYP enzyme responsible for the oxidative metabolism of AKB-48, preferentially performing the oxidation on the adamantyl moiety. adamantyl 168-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 26002511-7 2015 Adverse drug-drug interactions (DDIs) could potentially occur in cases with co-intake of strong CYP3A4 inhibitors, e.g., HIV antivirals and azole antifungal agents. Azoles 140-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 25776278-8 2015 However, positive controls (50 microM omeprazole and 25 microM rifampin) caused the anticipated CYP induction, but the highest concentration of SIPI5357 (5 microM; 10 times plasma Cmax ) had a minimal effect on CYP1A2 and CYP3A4 mRNA levels in freshly isolated human hepatocytes, suggesting that SIPI5357 is not an inducer of these enzymes. sipi5357 144-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 222-228 25923589-7 2015 CONCLUSIONS: Ritonavir produces CYP3A inhibition equivalent to or greater than ketoconazole, and is the best index CYP3A inhibitor alternative to ketoconazole. Ritonavir 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 25923589-1 2015 AIMS: The regulatory prohibition of ketoconazole as a CYP3A index inhibitor in drug-drug interaction (DDI) studies has compelled consideration of alternative inhibitors. Ketoconazole 36-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-59 25923589-7 2015 CONCLUSIONS: Ritonavir produces CYP3A inhibition equivalent to or greater than ketoconazole, and is the best index CYP3A inhibitor alternative to ketoconazole. Ritonavir 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-37 26114223-0 2015 Progressive decline in tacrolimus clearance after renal transplantation is partially explained by decreasing CYP3A4 activity and increasing haematocrit. Tacrolimus 23-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 26114223-5 2015 In mixed model analysis, decreasing CYP3A4 activity, measured by apparent oral MDZ clearance (924 +- 443 ml min(-1) at day 7 vs. 730 +- 344 ml min(-1) at month 1; P < 0.001), explained 55.4% of the decline in tacrolimus clearance in the first month. Tacrolimus 212-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 26114223-6 2015 CYP3A4 activity decreased by 18.9 ml min(-1) for every milligram of methylprednisolone dose tapering within the first month; beyond this point it remained stable. Methylprednisolone 68-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26095142-0 2015 The effect of atorvastatin treatment on serum oxysterol concentrations and cytochrome P450 3A4 activity. Atorvastatin 14-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-94 26114223-9 2015 CONCLUSIONS: The maturation of tacrolimus disposition in the first year after renal transplantation observed in CYP3A5*3/*3 homozygous patients can partly be explained by a (steroid tapering-related) decline in CYP3A4 activity and a progressive increase in haematocrit. Tacrolimus 31-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-217 26095142-1 2015 AIMS: Atorvastatin is known to both inhibit and induce the cytochrome P450 3A4 (CYP3A4) enzyme in vitro. Atorvastatin 6-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-78 26114223-9 2015 CONCLUSIONS: The maturation of tacrolimus disposition in the first year after renal transplantation observed in CYP3A5*3/*3 homozygous patients can partly be explained by a (steroid tapering-related) decline in CYP3A4 activity and a progressive increase in haematocrit. Steroids 174-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-217 26095142-1 2015 AIMS: Atorvastatin is known to both inhibit and induce the cytochrome P450 3A4 (CYP3A4) enzyme in vitro. Atorvastatin 6-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 26095142-2 2015 Some clinical studies indicate that atorvastatin inhibits CYP3A4 but there are no well-controlled longer term studies that could evaluate the inducing effect of atorvastatin. Atorvastatin 36-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 26119961-0 2015 4beta-hydroxycholesterol as an endogenous CYP3A marker in cancer patients treated with taxanes. cholest-5-ene-3,4-diol 0-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 26095142-3 2015 We aimed to determine if atorvastatin induces or inhibits CYP3A4 activity as measured by the 4beta-hydroxycholesterol to cholesterol ratio (4betaHC : C). Atorvastatin 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 26095142-10 2015 CONCLUSIONS: The results establish atorvastatin as an inhibitor of CYP3A4 activity. Atorvastatin 35-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 26119961-0 2015 4beta-hydroxycholesterol as an endogenous CYP3A marker in cancer patients treated with taxanes. Taxoids 87-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 26119961-3 2015 In this study, we evaluated the endogenous CYP3A4 marker 4beta-hydroxycholesterol (4beta-OHC) as a potential individual taxane PK predictor. cholest-5-ene-3,4-diol 57-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 26119961-3 2015 In this study, we evaluated the endogenous CYP3A4 marker 4beta-hydroxycholesterol (4beta-OHC) as a potential individual taxane PK predictor. 4beta-ohc 83-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 26119961-3 2015 In this study, we evaluated the endogenous CYP3A4 marker 4beta-hydroxycholesterol (4beta-OHC) as a potential individual taxane PK predictor. taxane 120-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 27137144-1 2015 Ponatinib, an oral tyrosine kinase inhibitor with significant activity in heavily pretreated patients with chronic myeloid leukemia, is a CYP3A4 substrate. ponatinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 26319088-11 2015 Moreover, as cobicistat is metabolized predominantly by CYP3A, plasma concentrations may increase or decrease on coadministration with CYP3A inhibitors or inducers, respectively. Cobicistat 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 26293521-1 2015 BACKGROUND AND OBJECTIVE: The polymorphic enzyme P450 oxidoreductase (POR) transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH) to cytochrome P450 (CYP) 3A enzyme s, which metabolize atorvastatin. NADP 100-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-179 26293521-1 2015 BACKGROUND AND OBJECTIVE: The polymorphic enzyme P450 oxidoreductase (POR) transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH) to cytochrome P450 (CYP) 3A enzyme s, which metabolize atorvastatin. NADP 145-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-179 26293521-1 2015 BACKGROUND AND OBJECTIVE: The polymorphic enzyme P450 oxidoreductase (POR) transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH) to cytochrome P450 (CYP) 3A enzyme s, which metabolize atorvastatin. Atorvastatin 207-219 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-179 27137144-2 2015 This open-label, nonrandomized, fixed-order crossover study evaluated the effect of multiple oral doses of rifampin, a strong CYP3A4 inducer, on the pharmacokinetics of ponatinib (45 mg, single dose). Rifampin 107-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 26319088-11 2015 Moreover, as cobicistat is metabolized predominantly by CYP3A, plasma concentrations may increase or decrease on coadministration with CYP3A inhibitors or inducers, respectively. Cobicistat 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-140 26135009-4 2015 Desloratadine (10 microM) caused no inhibition (<15%) of CYP1A2, CYP2C8, CYP2C9, or CYP2C19 and weak inhibition (32-48%) of CYP2B6, CYP2D6, and CYP3A4/5. desloratadine 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 26070839-4 2015 The results indicated Bama minipigs and human CYP3A enzymes showed similar metabolic kinetics and metabolite profiles using testosterone, midazolam, and nifedipine as substrates. Testosterone 124-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-51 26070839-4 2015 The results indicated Bama minipigs and human CYP3A enzymes showed similar metabolic kinetics and metabolite profiles using testosterone, midazolam, and nifedipine as substrates. Midazolam 138-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-51 26070839-4 2015 The results indicated Bama minipigs and human CYP3A enzymes showed similar metabolic kinetics and metabolite profiles using testosterone, midazolam, and nifedipine as substrates. Nifedipine 153-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-51 26138612-7 2015 4"-Desmethyl-TMP, which is believed to be a reactive TMP metabolite precursor, was formed by several P450s, including CYP3A4, correlated with multiple P450 activities, but was inhibited primarily by ketoconazole (up to 50%), suggesting that CYP3A4 makes a major contribution to TMP 4"-demethylation. 4"-desmethyl-tmp 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 26138612-7 2015 4"-Desmethyl-TMP, which is believed to be a reactive TMP metabolite precursor, was formed by several P450s, including CYP3A4, correlated with multiple P450 activities, but was inhibited primarily by ketoconazole (up to 50%), suggesting that CYP3A4 makes a major contribution to TMP 4"-demethylation. 4"-desmethyl-tmp 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 241-247 26138612-7 2015 4"-Desmethyl-TMP, which is believed to be a reactive TMP metabolite precursor, was formed by several P450s, including CYP3A4, correlated with multiple P450 activities, but was inhibited primarily by ketoconazole (up to 50%), suggesting that CYP3A4 makes a major contribution to TMP 4"-demethylation. Trimethoprim 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 26138612-7 2015 4"-Desmethyl-TMP, which is believed to be a reactive TMP metabolite precursor, was formed by several P450s, including CYP3A4, correlated with multiple P450 activities, but was inhibited primarily by ketoconazole (up to 50%), suggesting that CYP3A4 makes a major contribution to TMP 4"-demethylation. Trimethoprim 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 241-247 26138612-7 2015 4"-Desmethyl-TMP, which is believed to be a reactive TMP metabolite precursor, was formed by several P450s, including CYP3A4, correlated with multiple P450 activities, but was inhibited primarily by ketoconazole (up to 50%), suggesting that CYP3A4 makes a major contribution to TMP 4"-demethylation. Ketoconazole 199-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 26184414-1 2015 PURPOSE: The aim of this study was to investigate the effect of itraconazole (ITCZ), a potent inhibitor of CYP3A4 and P-glycoprotein, on the blood concentration 12 h after tacrolimus administration (C 12h) in relation to CYP3A5 6986A>G and ABCB1 3435C>T genotype status in patients with connective tissue disease (CTD). Itraconazole 64-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 26138612-7 2015 4"-Desmethyl-TMP, which is believed to be a reactive TMP metabolite precursor, was formed by several P450s, including CYP3A4, correlated with multiple P450 activities, but was inhibited primarily by ketoconazole (up to 50%), suggesting that CYP3A4 makes a major contribution to TMP 4"-demethylation. Ketoconazole 199-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 241-247 26138612-7 2015 4"-Desmethyl-TMP, which is believed to be a reactive TMP metabolite precursor, was formed by several P450s, including CYP3A4, correlated with multiple P450 activities, but was inhibited primarily by ketoconazole (up to 50%), suggesting that CYP3A4 makes a major contribution to TMP 4"-demethylation. tmp 4" 278-284 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 26138612-9 2015 Overall, CYP2C9 and CYP3A4 appear to be the most significant contributors to TMP primary metabolism. Trimethoprim 77-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 26184414-7 2015 CONCLUSIONS: In CYP3A5*3/*3 patients, because the metabolic pathway for tacrolimus occurs only through CYP3A4, the combination with ITCZ seems to lead to a higher risk of acute renal dysfunction. Tacrolimus 72-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 26104034-0 2015 Effect of CYP3A4*1G, CYP3A5*3, POR*28, and ABCB1 C3435T on the pharmacokinetics of nifedipine in healthy Chinese volunteers. Nifedipine 83-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 26104034-3 2015 The aim of the present study was to investigate the effect of CYP3A4*1G, CYP3A5*3, ABCB1-C3435T, and POR*28 genetic polymorphisms on nifedipine pharmacokinetics in healthy Chinese volunteers. Nifedipine 133-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 26104034-9 2015 In addition, the POR*28 CT/TT group was found to have longer t1/2 but lower Cmax than the CYP3A4*1G GG group (p = 0.032 and p = 0.002, respectively) as well as the CYP3A4*1G GG and the CYP3A5*3 GG group (p = 0.038 and p = 0.036, respectively) compared with the POR*28 CC group. Carbon Tetrachloride 24-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 26104034-11 2015 CONCLUSION: Both CYP3A5*3 and POR*28 polymorphisms are found to be associated with the difference in disposition of nifedipine; POR*28 is considered to have an impact on CYP3A4 activity. Nifedipine 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 26227094-5 2015 RESULTS: The significant influences of CYP3A5*3, CYP3A4*1G, and POR*28 polymorphisms on tacrolimus dose-adjusted trough concentrations (C0/D) were observed in 83 renal recipients. Tacrolimus 88-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 25854986-0 2015 Pharmacokinetic (PK) drug interaction studies of cabozantinib: Effect of CYP3A inducer rifampin and inhibitor ketoconazole on cabozantinib plasma PK and effect of cabozantinib on CYP2C8 probe substrate rosiglitazone plasma PK. cabozantinib 49-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 25854986-2 2015 In vitro data indicate that (1) cytochrome P450 (CYP) 3A4 is the primary CYP isoenzyme involved in the metabolism of cabozantinib, and (2) CYP2C8 is the CYP isoenzyme most potently inhibited by cabozantinib with potential for in vivo inhibition at clinically relevant plasma exposures. cabozantinib 117-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-57 25854986-2 2015 In vitro data indicate that (1) cytochrome P450 (CYP) 3A4 is the primary CYP isoenzyme involved in the metabolism of cabozantinib, and (2) CYP2C8 is the CYP isoenzyme most potently inhibited by cabozantinib with potential for in vivo inhibition at clinically relevant plasma exposures. cabozantinib 194-206 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-57 25854986-3 2015 Pharmacokinetic (PK) drug-drug interactions (DDIs) were evaluated clinically between cabozantinib and (1) a CYP3A inducer (rifampin) in healthy volunteers, (2) a CYP3A inhibitor (ketoconazole) in healthy volunteers, and (3) a CYP2C8 substrate (rosiglitazone) in patients with solid tumors. cabozantinib 85-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 25880724-1 2015 The objectives of the present study were to evaluate safety and tolerability as well as the effects of multiple doses of lanicemine on the pharmacokinetics of a CYP3A substrate, midazolam. AZD6765 121-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-166 25880724-1 2015 The objectives of the present study were to evaluate safety and tolerability as well as the effects of multiple doses of lanicemine on the pharmacokinetics of a CYP3A substrate, midazolam. Midazolam 178-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-166 25988261-2 2015 To investigate the effect of acute and short-term intake of high-dose quercetin on CYP3A-mediated metabolism, 10 healthy volunteers received 7.5 mg oral midazolam without, with a single dose of 1500 mg quercetin and after 1-week supplementation with 1500 mg quercetin daily. Quercetin 70-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 25988261-6 2015 We conclude that a single dose of quercetin would not provoke any toxic adverse events when coadministered with midazolam, whereas repeated quercetin intake can reduce systemic exposure to the orally given drug by increasing its CYP3A-catalyzed metabolism. Quercetin 140-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 229-234 26322261-1 2015 Ritonavir is a potent inhibitor of the cytochrome P450 enzyme CYP3A4 and is subject to multiple drug-drug interactions. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 26334901-6 2015 When compared with the wild-type genotype, the variant genotypes rs5767743 and rs5767700 correlated with significantly increased PPARalpha and CYP3A4 mRNA expression and lower tacrolimus trough concentration/dose ratios (P < 0.05 for all).Donor PPARalpha gene polymorphisms influence the susceptibility to metabolic disorders following LT and may also be associated with a fasten tacrolimus metabolism because of elevated CYP3A4 expression. Tacrolimus 176-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 26334901-6 2015 When compared with the wild-type genotype, the variant genotypes rs5767743 and rs5767700 correlated with significantly increased PPARalpha and CYP3A4 mRNA expression and lower tacrolimus trough concentration/dose ratios (P < 0.05 for all).Donor PPARalpha gene polymorphisms influence the susceptibility to metabolic disorders following LT and may also be associated with a fasten tacrolimus metabolism because of elevated CYP3A4 expression. Tacrolimus 176-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 425-431 26334901-6 2015 When compared with the wild-type genotype, the variant genotypes rs5767743 and rs5767700 correlated with significantly increased PPARalpha and CYP3A4 mRNA expression and lower tacrolimus trough concentration/dose ratios (P < 0.05 for all).Donor PPARalpha gene polymorphisms influence the susceptibility to metabolic disorders following LT and may also be associated with a fasten tacrolimus metabolism because of elevated CYP3A4 expression. Tacrolimus 383-393 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 26334901-6 2015 When compared with the wild-type genotype, the variant genotypes rs5767743 and rs5767700 correlated with significantly increased PPARalpha and CYP3A4 mRNA expression and lower tacrolimus trough concentration/dose ratios (P < 0.05 for all).Donor PPARalpha gene polymorphisms influence the susceptibility to metabolic disorders following LT and may also be associated with a fasten tacrolimus metabolism because of elevated CYP3A4 expression. Tacrolimus 383-393 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 425-431 25976223-0 2015 CYP3A4*18B and CYP3A5*3 polymorphisms contribute to pharmacokinetic variability of cyclosporine among healthy Chinese subjects. Cyclosporine 83-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25976223-8 2015 The Cmax of cyclosporine in CYP3A4*1/*1 was significantly greater than that in CYP3A4*1/*18B in the male group (P=0.023), but not the female group. Cyclosporine 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 25976223-10 2015 CONCLUSIONS: The results indicate that gender and polymorphism in CYP3A4*18B and CYP3A5*3 significantly affect cyclosporine pharmacokinetics in healthy subjects. Cyclosporine 111-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 25976224-11 2015 (4) The combined administration of Berberine with Clarithromycin had a powerful inhibitive effect on CYP3A activities than use of a single drug alone. Berberine 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 25976224-11 2015 (4) The combined administration of Berberine with Clarithromycin had a powerful inhibitive effect on CYP3A activities than use of a single drug alone. Clarithromycin 50-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 26284404-0 2015 [Detection of cytochrome P450 3A4 gene polymorphism guides for labor analgesia with sufentanil medication]. Sufentanil 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-33 25940823-3 2015 Tamoxifen is bioactivated by cytochrome P450 (CYP) enzymes such as CYP2B6, CYP2C9, CYP2C19, CYP2D6 and CYP3A4/5, resulting in the formation of active metabolites, including 4-hydroxy-tamoxifen and endoxifen. Tamoxifen 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 26284404-7 2015 CONCLUSION: The parturient women carrying CT heterozygotes and TT homozygotes of CYP3A4 rs2242480 required less sufentanil in accouchement sans douleur. Sufentanil 112-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 25940823-3 2015 Tamoxifen is bioactivated by cytochrome P450 (CYP) enzymes such as CYP2B6, CYP2C9, CYP2C19, CYP2D6 and CYP3A4/5, resulting in the formation of active metabolites, including 4-hydroxy-tamoxifen and endoxifen. 4'-hydroxytamoxifen 173-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 25940823-3 2015 Tamoxifen is bioactivated by cytochrome P450 (CYP) enzymes such as CYP2B6, CYP2C9, CYP2C19, CYP2D6 and CYP3A4/5, resulting in the formation of active metabolites, including 4-hydroxy-tamoxifen and endoxifen. 4-hydroxy-N-desmethyltamoxifen 197-206 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 26163112-5 2015 CYP1A2 played a more prominent role than CYP3A4 and CYP2D6 in the 4-O-demethylation of homoegonol to M1. homoegonol 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 26380154-2 2015 The aim of this study was to evaluate 24-hour variation in the pharmacokinetics of the CYP3A substrate midazolam. Midazolam 103-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 26055620-6 2015 The major pathway in humans was hydroxylation of the oxazole moiety of M1 to form M2 and then successive oxidation to the ketone form (M3) mainly by CYP3A4. Oxazoles 53-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 26055620-6 2015 The major pathway in humans was hydroxylation of the oxazole moiety of M1 to form M2 and then successive oxidation to the ketone form (M3) mainly by CYP3A4. Ketones 122-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 26163112-6 2015 CYP3A4 was responsible for the hydroxylation of homoegonol to M2. homoegonol 48-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25935875-12 2015 CONCLUSION: In patients with ACS, ticagrelor pharmacokinetics is influenced by three genetic loci (SLCO1B1, UGT2B7, and CYP3A4). Ticagrelor 34-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 26223917-5 2015 The enzymatic activity of CYP3A4 was measured using erythromycin and testosterone as probe substrates. Erythromycin 52-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 25760671-1 2015 Idelalisib, a potent phosphatidylinositol-3-kinase delta (PI3Kdelta) inhibitor, is metabolized primarily by aldehyde oxidase to form GS-563117 and to a lesser extent by cytochrome P450 (CYP) 3A and uridine 5"-diphospho-glucuronosyltransferase 1A4. idelalisib 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-193 25760671-2 2015 In vitro, idelalisib inhibits P-glycoprotein (P-gp) and organic anion transporting polypeptides 1B1 and 1B3, and GS-563117 is a time-dependent CYP3A inhibitor. idelalisib 10-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 25760671-8 2015 Coadministration with idelalisib increased plasma exposures of midazolam (138% and 437% for maximum observed plasma concentration [Cmax ] and area under the plasma concentration-time curve from time 0 extrapolated to infinity [AUCinf ], respectively), consistent with the in vitro finding of CYP3A inhibition by GS-563117. idelalisib 22-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 292-297 25760671-8 2015 Coadministration with idelalisib increased plasma exposures of midazolam (138% and 437% for maximum observed plasma concentration [Cmax ] and area under the plasma concentration-time curve from time 0 extrapolated to infinity [AUCinf ], respectively), consistent with the in vitro finding of CYP3A inhibition by GS-563117. Midazolam 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 292-297 25760671-9 2015 Rifampin caused a substantial decrease in idelalisib (58% and 75%, Cmax and AUCinf , respectively) and GS-563117 exposures, indicating an enhanced contribution of CYP3A to idelalisib metabolism under a strongly induced state. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-168 25760671-9 2015 Rifampin caused a substantial decrease in idelalisib (58% and 75%, Cmax and AUCinf , respectively) and GS-563117 exposures, indicating an enhanced contribution of CYP3A to idelalisib metabolism under a strongly induced state. idelalisib 172-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-168 26223917-5 2015 The enzymatic activity of CYP3A4 was measured using erythromycin and testosterone as probe substrates. Testosterone 69-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 26622646-0 2015 Effect of CYP2C19 and CYP3A4 gene polymorphisms on the efficacy of bortezomib-based regimens in patients with multiple myeloma. Bortezomib 67-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 26091900-7 2015 CYP cocktail assays showed that myristicin most significantly inhibits CYP1A2 among five CYP enzymes (CYP1A2, CYP2D6, CYP2E1, CYP3A4 and CYP2C19) from human liver microsomes. myristicin 32-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 26171235-0 2015 Effect of CYP3A perpetrators on ibrutinib exposure in healthy participants. ibrutinib 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 26171235-2 2015 Given the prominent role of CYP3A in ibrutinib metabolism, effect of coadministration of CYP3A perpetrators with ibrutinib was evaluated in healthy adults. ibrutinib 113-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-94 26098410-9 2015 Furthermore, the co-exposure of domperidone and CYP 3A4 inhibitors was significantly associated with an increased odds of ventricular arrhythmia, especially considering the lasting effect of CYP 3A4 inhibitors (1 day apart: aOR 1.91, 95%CI [1.33-2.75], 3 days apart: aOR 1.90, 95%CI [1.33-2.71], 7 days apart: aOR 1.80, 95%CI [1.28-2.54]). Domperidone 32-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-198 26350737-7 2015 Cytochrome b5mc was shown to be capable of stimulating the electrocatalytic activity of CYP3A4 in the presence of its substrate testosterone. Testosterone 128-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 26066995-1 2015 We co-crystallized human cytochrome P450 3A4 (CYP3A4) with progesterone (PRG) under two different conditions, but the resulting complexes contained only one PRG molecule bound to the previously identified peripheral site. Progesterone 59-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 26066995-4 2015 We investigated how citrate affects the function of a soluble CYP3A4 monooxygenase system consisting of equimolar amounts of CYP3A4 and cytochrome P450 reductase (CPR). Citric Acid 20-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 26066995-6 2015 CYP3A4-substrate binding, reduction of CPR with NADPH, and interflavin and interprotein electron transfer were identified as citrate-sensitive steps. NADP 48-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26066995-6 2015 CYP3A4-substrate binding, reduction of CPR with NADPH, and interflavin and interprotein electron transfer were identified as citrate-sensitive steps. Citric Acid 125-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26066995-1 2015 We co-crystallized human cytochrome P450 3A4 (CYP3A4) with progesterone (PRG) under two different conditions, but the resulting complexes contained only one PRG molecule bound to the previously identified peripheral site. Progesterone 59-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-44 25600613-6 2015 The relationship of the IC50 values of 11 inhibitors between tacrolimus and typical CYP3A substrates (midazolam and testosterone) was also analysed. Tacrolimus 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-89 25600613-6 2015 The relationship of the IC50 values of 11 inhibitors between tacrolimus and typical CYP3A substrates (midazolam and testosterone) was also analysed. Midazolam 102-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-89 25600613-7 2015 A strong correlation was found between the IC50 values of tacrolimus and typical CYP3A substrates (r(2) >= 0.85). Tacrolimus 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 25600613-14 2015 within an approximately 2-fold range of observed values) the effect of CYP3A inhibitors on the tacrolimus AUCp.o. Tacrolimus 95-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-76 26211584-1 2015 CYP3A4, a "heme" containing isoform, abundantly found in the liver, gastro-intestinal tract, lungs and renal cells, also known as drug metabolising enzyme (DME) may be responsible for the disease progression in cancers such as lung cancer. Heme 11-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26211584-4 2015 We have used Schrodinger suite 2014, to perform molecular docking of human CYP3A4, by Induced Fit Docking using gemcitabine, cisplatin, carboplatin, docetaxel and paclitaxel drugs. gemcitabine 112-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 26211584-4 2015 We have used Schrodinger suite 2014, to perform molecular docking of human CYP3A4, by Induced Fit Docking using gemcitabine, cisplatin, carboplatin, docetaxel and paclitaxel drugs. Cisplatin 125-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 26211584-4 2015 We have used Schrodinger suite 2014, to perform molecular docking of human CYP3A4, by Induced Fit Docking using gemcitabine, cisplatin, carboplatin, docetaxel and paclitaxel drugs. Carboplatin 136-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 26211584-4 2015 We have used Schrodinger suite 2014, to perform molecular docking of human CYP3A4, by Induced Fit Docking using gemcitabine, cisplatin, carboplatin, docetaxel and paclitaxel drugs. Docetaxel 149-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 26211584-4 2015 We have used Schrodinger suite 2014, to perform molecular docking of human CYP3A4, by Induced Fit Docking using gemcitabine, cisplatin, carboplatin, docetaxel and paclitaxel drugs. Paclitaxel 163-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 25554506-3 2015 We focused on common polymorphisms within important gefitinib exposure genes, including cytochromes P450 (CYPs) CYP3A4*1G, CYP3A5 (*3), and CYP2D6 (*5 and *10) and ATP-binding cassette (ABC) ABCG2 (421C>A) and ABCB1 (1236C>T, 2677G>T/A, and 3435C>T). Gefitinib 52-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 26211584-9 2015 Our investigation has identified the residue Arg 105 to be more frequently involved in drug binding to CYP3A4. Arginine 45-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 26211584-10 2015 Our results suggest that gemcitabine or combination of gemcitabine+carboplatin could serve as an excellent therapy against CYP3A4 in NSCLC patients. gemcitabine 25-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 26211584-10 2015 Our results suggest that gemcitabine or combination of gemcitabine+carboplatin could serve as an excellent therapy against CYP3A4 in NSCLC patients. gemcitabine 55-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 26211584-10 2015 Our results suggest that gemcitabine or combination of gemcitabine+carboplatin could serve as an excellent therapy against CYP3A4 in NSCLC patients. Carboplatin 67-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 26068927-2 2015 The effect of rifampin-induced induction of P-gp and CYP3A4/5 on transport and metabolism of edoxaban through the CYP3A4/5 pathway was investigated in a single-dose edoxaban study. Rifampin 14-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 26068927-2 2015 The effect of rifampin-induced induction of P-gp and CYP3A4/5 on transport and metabolism of edoxaban through the CYP3A4/5 pathway was investigated in a single-dose edoxaban study. Rifampin 14-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 25980322-7 2015 Particularly, drugs strongly inhibiting CYP3A4 such as ketoconazole should not be concurrently administered without dose modification, as they may decrease the clearance of docetaxel. Ketoconazole 55-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 25980322-7 2015 Particularly, drugs strongly inhibiting CYP3A4 such as ketoconazole should not be concurrently administered without dose modification, as they may decrease the clearance of docetaxel. Docetaxel 173-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 26068927-2 2015 The effect of rifampin-induced induction of P-gp and CYP3A4/5 on transport and metabolism of edoxaban through the CYP3A4/5 pathway was investigated in a single-dose edoxaban study. edoxaban 93-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 25881619-1 2015 OBJECTIVES: Emerging data suggest that the combination of tacrolimus and the CCR5 antagonist maraviroc, both cytochrome P450-3A4 substrates, may be effective in preventing graft-versus-host disease in patients undergoing allogeneic HSCT. Tacrolimus 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-128 26068927-2 2015 The effect of rifampin-induced induction of P-gp and CYP3A4/5 on transport and metabolism of edoxaban through the CYP3A4/5 pathway was investigated in a single-dose edoxaban study. edoxaban 93-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 25808545-5 2015 We show that vitamin K2 and lithocholic acid, a by-product of intestinal flora, activate pregnane X receptor (PXR) and subsequent CYP3A4 and CYP2C9 expression in hPSC-derived and isolated fetal hepatocytes. Vitamin K 2 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 25808545-5 2015 We show that vitamin K2 and lithocholic acid, a by-product of intestinal flora, activate pregnane X receptor (PXR) and subsequent CYP3A4 and CYP2C9 expression in hPSC-derived and isolated fetal hepatocytes. Lithocholic Acid 28-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 26164721-0 2015 Individual and Combined Associations of Genetic Variants in CYP3A4, CYP3A5, and SLCO1B1 With Simvastatin and Simvastatin Acid Plasma Concentrations. Simvastatin 93-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 26164721-0 2015 Individual and Combined Associations of Genetic Variants in CYP3A4, CYP3A5, and SLCO1B1 With Simvastatin and Simvastatin Acid Plasma Concentrations. simvastatin acid 109-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 26067485-2 2015 PATIENTS & METHODS: We studied genetic correlates of tacrolimus trough concentrations with POR*28, CYP3A4*22 and ABCC2 haplotypes in a large, ethnically diverse kidney transplant cohort (n = 2008). Tacrolimus 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 25907981-7 2015 RESULTS: Data indicated that treatment of LS174T cells with piperine markedly increased both CYP3A4 and PXR mRNA and protein. piperine 60-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 25907981-8 2015 Transient transfection experiments indicated that transcriptional activation of the CYP3A4 gene via piperine was PXR-dependent. piperine 100-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 25907981-11 2015 CONCLUSION: Piperine is a potential agonist of PXR and an inducer of PXR, which may induce CYP3A4 gene expression at the mRNA and protein levels. piperine 12-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 26151793-7 2015 It is postulated that this interaction was mediated by acitretin inhibition of CYP3A4, the primary enzyme responsible for sirolimus metabolism. Sirolimus 122-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 26312962-1 2015 Concurrent administration of oxycodone and phenytoin may cause, through induction of CYP3A4 enzymes, decreased analgesic effects of oxycodone. Oxycodone 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 26312962-1 2015 Concurrent administration of oxycodone and phenytoin may cause, through induction of CYP3A4 enzymes, decreased analgesic effects of oxycodone. Phenytoin 43-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 26312962-1 2015 Concurrent administration of oxycodone and phenytoin may cause, through induction of CYP3A4 enzymes, decreased analgesic effects of oxycodone. Oxycodone 132-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 26160721-2 2015 This study is aimed to analyze the relationship between beta-lactam allergy and 10 single nucleotide polymorphisms (SNPs) in interleukin-10 (IL-10), IL-13, IL-4Ralpha, high-affinity immunoglobulin E-receptor beta chain (FcepsilonRIbeta), interferon gamma receptor 2 (IFNGR2), and CYP3A4, and within the Han Chinese population of Northwest China. beta-Lactams 56-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 280-286 26181194-1 2015 INTRODUCTION: Armodafinil, a moderate inducer of cytochrome P450 (CYP) 3A4, has been studied as adjunctive therapy to maintenance medications for major depressive episodes associated with bipolar I disorder. Modafinil 14-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-74 26181194-2 2015 We evaluated the effect of daily dosing with armodafinil on the pharmacokinetics and safety of the CYP3A4 substrate aripiprazole, an atypical antipsychotic used to treat bipolar I disorder. Modafinil 45-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 25908587-11 2015 In conclusion, tumor CYP3A4 induction by sorafenib is a novel mechanism to account for variability in systemic drug levels; however, declining systemic sorafenib levels may only be a minor resistance mechanism. Sorafenib 41-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 26181194-7 2015 Armodafinil reduced systemic exposure to aripiprazole (Cmax, - 8%; AUC0- , -34%) and dehydro-aripiprazole, which is both formed and eliminated in part via CYP3A4 (Cmax, - 10%; AUC0- , - 32%). Modafinil 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 26181194-7 2015 Armodafinil reduced systemic exposure to aripiprazole (Cmax, - 8%; AUC0- , -34%) and dehydro-aripiprazole, which is both formed and eliminated in part via CYP3A4 (Cmax, - 10%; AUC0- , - 32%). Aripiprazole 41-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 26181194-7 2015 Armodafinil reduced systemic exposure to aripiprazole (Cmax, - 8%; AUC0- , -34%) and dehydro-aripiprazole, which is both formed and eliminated in part via CYP3A4 (Cmax, - 10%; AUC0- , - 32%). dehydroaripiprazole 85-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 26181194-7 2015 Armodafinil reduced systemic exposure to aripiprazole (Cmax, - 8%; AUC0- , -34%) and dehydro-aripiprazole, which is both formed and eliminated in part via CYP3A4 (Cmax, - 10%; AUC0- , - 32%). cmax 163-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 26240881-13 2015 Lomitapide is extensively metabolised by cytochrome P450 isoenzyme CYP3A4 and also inhibits P-glycoprotein, hence a risk of multiple pharmacokinetic interactions. BMS201038 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 26133240-0 2015 A Mechanism-Based Model for the Prediction of the Metabolic Sites of Steroids Mediated by Cytochrome P450 3A4. Steroids 69-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-109 26133240-5 2015 The newly established model was applied to predict the metabolic site(s) of steroids; a class of CYP3A4-preferred substrates. Steroids 76-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 26133240-10 2015 In summary, a mechanism-based prediction model was established for the first time, which could be used to predict the metabolic site(s) of CYP3A4 on steroids with high predictive accuracy. Steroids 149-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 25858508-0 2015 Mechanism-based inhibition of Alantolactone on human cytochrome P450 3A4 in vitro and activity of hepatic cytochrome P450 in mice. alantolactone 30-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-72 25908587-11 2015 In conclusion, tumor CYP3A4 induction by sorafenib is a novel mechanism to account for variability in systemic drug levels; however, declining systemic sorafenib levels may only be a minor resistance mechanism. Sorafenib 152-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 26039043-0 2015 Effects of the CYP3A4*1B Genetic Polymorphism on the Pharmacokinetics of Tacrolimus in Adult Renal Transplant Recipients: A Meta-Analysis. Tacrolimus 73-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 25915157-6 2015 CYP3A4, the liver"s major drug-metabolizing enzyme, was at least partially responsible for BM stroma"s ability to protect multiple myeloma (MM) and leukemia cells from bortezomib and etoposide, respectively, both in vitro and in vivo. Bortezomib 168-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25915157-6 2015 CYP3A4, the liver"s major drug-metabolizing enzyme, was at least partially responsible for BM stroma"s ability to protect multiple myeloma (MM) and leukemia cells from bortezomib and etoposide, respectively, both in vitro and in vivo. Etoposide 183-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25915157-7 2015 Moreover, clarithromycin overcame stromal-mediated MM resistance to dexamethasone, suggesting that CYP3A4 inhibition plays a role in its ability to augment the activity of lenalidomide and dexamethasone as part of the BiRd regimen. Clarithromycin 10-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 25915157-7 2015 Moreover, clarithromycin overcame stromal-mediated MM resistance to dexamethasone, suggesting that CYP3A4 inhibition plays a role in its ability to augment the activity of lenalidomide and dexamethasone as part of the BiRd regimen. Dexamethasone 68-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 25915157-7 2015 Moreover, clarithromycin overcame stromal-mediated MM resistance to dexamethasone, suggesting that CYP3A4 inhibition plays a role in its ability to augment the activity of lenalidomide and dexamethasone as part of the BiRd regimen. Lenalidomide 172-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 25915157-7 2015 Moreover, clarithromycin overcame stromal-mediated MM resistance to dexamethasone, suggesting that CYP3A4 inhibition plays a role in its ability to augment the activity of lenalidomide and dexamethasone as part of the BiRd regimen. Dexamethasone 189-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 28930203-8 2015 Results: Vinpocetine showed a strong inhibition of P-gp (EC50 8 microM) and a moderate inhibition of recombinant CYP3A4 and CYP2D6 (IC50 2.8 and 6.5 microM) with no activity towards CYP2C9, CYP2C19 and CYP1A2 enzymes. vinpocetine 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 26039043-1 2015 BACKGROUND AND OBJECTIVE: The association between the CYP3A4*1B single nucleotide polymorphism (SNP) and tacrolimus pharmacokinetics in different studies is controversial. Tacrolimus 105-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 26039043-2 2015 Therefore, a meta-analysis was employed to evaluate the correlation between the CYP3A4*1B genetic polymorphism and tacrolimus pharmacokinetics at different post-transplantation times in adult renal transplant recipients. Tacrolimus 115-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 26039043-7 2015 In light of the heterogeneity, the analysis was repeated after removing the only study in an Indian population, and CYP3A4*1/*1 European recipients (mostly Caucasian) required a lower weight-adjusted tacrolimus daily dose within the first year post-transplantation. Tacrolimus 200-210 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 26039043-8 2015 The tacrolimus trough concentration/weight-adjusted tacrolimus daily dose ratio (C0/Dose ratio) was significantly higher in CYP3A4*1/*1 recipients than in CYP3A4*1B carriers at 6 months (WMD 52.588; 95% CI 22.387 ~ 82.789) and 12 months (WMD 62.219; 95% CI 14.218 ~ 110.221) post-transplantation. Tacrolimus 4-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 26039043-8 2015 The tacrolimus trough concentration/weight-adjusted tacrolimus daily dose ratio (C0/Dose ratio) was significantly higher in CYP3A4*1/*1 recipients than in CYP3A4*1B carriers at 6 months (WMD 52.588; 95% CI 22.387 ~ 82.789) and 12 months (WMD 62.219; 95% CI 14.218 ~ 110.221) post-transplantation. Tacrolimus 4-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 26039043-8 2015 The tacrolimus trough concentration/weight-adjusted tacrolimus daily dose ratio (C0/Dose ratio) was significantly higher in CYP3A4*1/*1 recipients than in CYP3A4*1B carriers at 6 months (WMD 52.588; 95% CI 22.387 ~ 82.789) and 12 months (WMD 62.219; 95% CI 14.218 ~ 110.221) post-transplantation. Tacrolimus 52-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 26039043-10 2015 CONCLUSION: Based on our meta-analysis, the CYP3A4*1B genetic polymorphism affects tacrolimus dose requirements and tacrolimus trough concentration/weight-adjusted tacrolimus daily dose ratio within the first year post-transplantation in adult renal transplant recipients, especially in European recipients (mostly Caucasian). Tacrolimus 83-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 26039043-10 2015 CONCLUSION: Based on our meta-analysis, the CYP3A4*1B genetic polymorphism affects tacrolimus dose requirements and tacrolimus trough concentration/weight-adjusted tacrolimus daily dose ratio within the first year post-transplantation in adult renal transplant recipients, especially in European recipients (mostly Caucasian). Tacrolimus 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 26039043-10 2015 CONCLUSION: Based on our meta-analysis, the CYP3A4*1B genetic polymorphism affects tacrolimus dose requirements and tacrolimus trough concentration/weight-adjusted tacrolimus daily dose ratio within the first year post-transplantation in adult renal transplant recipients, especially in European recipients (mostly Caucasian). Tacrolimus 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 25770114-9 2015 Simeprevir is also prone to drug interactions because of cytochrome P450(CYP) 3A4, CYP1A2, P-glycoprotein, and OATP1 involvement and is not recommended for use in combination with several HIV antiretrovirals (ARVs). Simeprevir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-81 25424246-6 2015 This demonstrated that the paclitaxel metabolism was mainly catalysed by CYP3A4 in HL60. Paclitaxel 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 25424246-7 2015 There were no significant differences found for the inhibitory effects caused by the four inhibitors of the paclitaxel metabolism in HL54, indicating that both CYP2C8 and CYP3A4 play important roles in paclitaxel metabolism in HL54. Paclitaxel 202-212 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 25424246-5 2015 When using HL60, losartan and the CYP3A4-selective inhibitors, erythromycin and ketoconazole, caused a greater inhibition of the paclitaxel metabolism than quercetin, a CYP2C8-selective inhibitor. Erythromycin 63-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 25424246-8 2015 These findings suggest that 50 mumol/L of losartan inhibits both CYP2C8 and CYP3A4 in HLMs. Losartan 42-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 25424246-5 2015 When using HL60, losartan and the CYP3A4-selective inhibitors, erythromycin and ketoconazole, caused a greater inhibition of the paclitaxel metabolism than quercetin, a CYP2C8-selective inhibitor. Ketoconazole 80-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 25424246-10 2015 The CYP2C8*3 allele carriers are likely susceptible to the interactions of losartan and CYP3A4 inhibitors to paclitaxel metabolism. Paclitaxel 109-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 25424246-5 2015 When using HL60, losartan and the CYP3A4-selective inhibitors, erythromycin and ketoconazole, caused a greater inhibition of the paclitaxel metabolism than quercetin, a CYP2C8-selective inhibitor. Paclitaxel 129-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 25424246-5 2015 When using HL60, losartan and the CYP3A4-selective inhibitors, erythromycin and ketoconazole, caused a greater inhibition of the paclitaxel metabolism than quercetin, a CYP2C8-selective inhibitor. Quercetin 156-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 25443889-8 2015 Quantifying victim DDI potential was also demonstrated using fmCYP3A estimates from ketoconazole clinical DDI studies to predict the magnitude of interaction on co-administration with the CYP3A inducer, rifampicin (1.6-3.3 fold error). Ketoconazole 84-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 26124807-3 2015 The crystal structure of CYP3A4 with the ligand ketoconazole was chosen from protein data bank (http://www.rcsb.org/pdb). Ketoconazole 48-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 25443889-8 2015 Quantifying victim DDI potential was also demonstrated using fmCYP3A estimates from ketoconazole clinical DDI studies to predict the magnitude of interaction on co-administration with the CYP3A inducer, rifampicin (1.6-3.3 fold error). Rifampin 203-213 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 26124807-5 2015 RESULTS: Gomisin G can be well docked into the activity site of CYP3A4, and distance between gomisin G the heme active site was 2.75 A. Heme 107-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 25556837-6 2015 A modest correlation was observed between liver/intestinal CYP3A4 activity and methadone dose at steady state (Spearman rank correlation coefficient [rs ] = 0.21, P = 0.06) but not with highest dose ever used (rs = 0.15, P = 0.18) or dose-normalized R,S-methadone trough concentrations (rs = -0.05, P = 0.64). Methadone 79-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 26124807-6 2015 To evaluate whether the inhibitors of CYP3A4 can affect the metabolism of gomisin G, co-docking of gomisin G and ketoconazole was further performed. Ketoconazole 113-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 26124807-7 2015 The distance between ketoconazole and activity center (2.10 A) is closer than the distance between gomisin G and activity center of CYP3A4, indicating the easy influence of CYP3A4"s strong inhibitor towards the metabolism of gomisin G. CONCLUSION: Gomisin G is a good substrate of CYP3A4, and CYP3A4 inhibitors easily affect the metabolism of Gomisin G. Ketoconazole 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 26124807-7 2015 The distance between ketoconazole and activity center (2.10 A) is closer than the distance between gomisin G and activity center of CYP3A4, indicating the easy influence of CYP3A4"s strong inhibitor towards the metabolism of gomisin G. CONCLUSION: Gomisin G is a good substrate of CYP3A4, and CYP3A4 inhibitors easily affect the metabolism of Gomisin G. Ketoconazole 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 26124807-7 2015 The distance between ketoconazole and activity center (2.10 A) is closer than the distance between gomisin G and activity center of CYP3A4, indicating the easy influence of CYP3A4"s strong inhibitor towards the metabolism of gomisin G. CONCLUSION: Gomisin G is a good substrate of CYP3A4, and CYP3A4 inhibitors easily affect the metabolism of Gomisin G. Ketoconazole 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 25556837-7 2015 Concomitant CYP3A4 inhibitors only affected the relationship between methadone dose and R,S-methadone trough concentration. Methadone 69-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 25556837-7 2015 Concomitant CYP3A4 inhibitors only affected the relationship between methadone dose and R,S-methadone trough concentration. r,s-methadone 88-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 25862215-1 2015 INTRODUCTION: This open-label, randomized, two-period drug interaction study assessed lisdexamfetamine dimesylate (LDX) effects on cytochrome P450 (CYP) enzyme (CYP1A2, CYP2D6, CYP2C19, and CYP3A) activity. Lisdexamfetamine Dimesylate 86-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-195 25382218-6 2015 For CYP3A4, ketamine as probe substrate and highly sulfated gamma-cyclodextrin as chiral selector, improved separation conditions for ketamine and norketamine enantiomers compared to a previously published electrophoretically mediated microanalysis method were elucidated. Ketamine 12-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 25382218-6 2015 For CYP3A4, ketamine as probe substrate and highly sulfated gamma-cyclodextrin as chiral selector, improved separation conditions for ketamine and norketamine enantiomers compared to a previously published electrophoretically mediated microanalysis method were elucidated. gamma-cyclodextrin 60-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 25382218-6 2015 For CYP3A4, ketamine as probe substrate and highly sulfated gamma-cyclodextrin as chiral selector, improved separation conditions for ketamine and norketamine enantiomers compared to a previously published electrophoretically mediated microanalysis method were elucidated. Ketamine 134-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 25382218-6 2015 For CYP3A4, ketamine as probe substrate and highly sulfated gamma-cyclodextrin as chiral selector, improved separation conditions for ketamine and norketamine enantiomers compared to a previously published electrophoretically mediated microanalysis method were elucidated. norketamine 147-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 25382218-7 2015 The new approach was thoroughly validated for the CYP3A4-mediated N-demethylation pathway of ketamine and applied to the determination of its kinetic parameters and the inhibition characteristics in presence of ketoconazole and dexmedetomidine. Nitrogen 66-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 25382218-7 2015 The new approach was thoroughly validated for the CYP3A4-mediated N-demethylation pathway of ketamine and applied to the determination of its kinetic parameters and the inhibition characteristics in presence of ketoconazole and dexmedetomidine. Ketamine 93-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 25382218-7 2015 The new approach was thoroughly validated for the CYP3A4-mediated N-demethylation pathway of ketamine and applied to the determination of its kinetic parameters and the inhibition characteristics in presence of ketoconazole and dexmedetomidine. Ketoconazole 211-223 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 25382218-7 2015 The new approach was thoroughly validated for the CYP3A4-mediated N-demethylation pathway of ketamine and applied to the determination of its kinetic parameters and the inhibition characteristics in presence of ketoconazole and dexmedetomidine. Dexmedetomidine 228-243 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 25802327-5 2015 Then, CYP3A activity was measured by 1"-OH-midazolam formation. 1"-oh-midazolam 37-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-11 25802327-11 2015 This prediction is consistent with the observation of similar increases in T2 and T3 oral clearance of indinavir (a CYP3A cleared drug) versus postpartum. Indinavir 103-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 25882073-3 2015 Therefore, the aim of this clinical study was to clarify the effects of Cremophor EL on the inhibition of CYP3A and P-gp in the human small intestine. cremophor EL 72-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-111 25868557-10 2015 Modeling based on estimated Ki values and plasma concentrations from the literature suggest that the orally administered azoles, particularly ketoconazole and voriconazole, have the greatest potential for inhibiting CYP3A4 pathways, as does voriconazole for the CYP2B6 pathways. Voriconazole 159-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-222 25797167-6 2015 As these agents are substrates of permeability glycoprotein (P-gp) efflux transporter and/or CYP3A4 enzymes, articles focusing on the co-administration of NOACs and drugs affecting these pathways are discussed. noacs 155-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 25797167-9 2015 Prescribers should be vigilant against combination prescription of NOACs with strong inhibitors (such as ketoconazole) or inducers of P-gp and/or CYP3A4 (such as rifampicin). Rifampin 162-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 24756863-5 2015 The predicted binding mode of GNF-351 into CYP3A4 appeared to adopt an orientation with interactions between their flat aromatic rings and Phe 302 and Phe 304. Phenylalanine 139-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 24756863-5 2015 The predicted binding mode of GNF-351 into CYP3A4 appeared to adopt an orientation with interactions between their flat aromatic rings and Phe 302 and Phe 304. Phenylalanine 151-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 25850339-0 2015 Relative contributions of the major human CYP450 to the metabolism of icotinib and its implication in prediction of drug-drug interaction between icotinib and CYP3A4 inhibitors/inducers using physiologically based pharmacokinetic modeling. icotinib 70-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 25850339-7 2015 RESULTS: Final contribution of CYP450 isoforms determined by HLM showed that CYP3A4 provided major contributions to the metabolism of icotinib. icotinib 134-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 25868557-8 2015 Azoles were next screened at the highest achievable concentration for non-CYP3A4 pathways. Azoles 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 25868557-10 2015 Modeling based on estimated Ki values and plasma concentrations from the literature suggest that the orally administered azoles, particularly ketoconazole and voriconazole, have the greatest potential for inhibiting CYP3A4 pathways, as does voriconazole for the CYP2B6 pathways. Voriconazole 241-253 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-222 25868557-10 2015 Modeling based on estimated Ki values and plasma concentrations from the literature suggest that the orally administered azoles, particularly ketoconazole and voriconazole, have the greatest potential for inhibiting CYP3A4 pathways, as does voriconazole for the CYP2B6 pathways. Azoles 121-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-222 25868557-10 2015 Modeling based on estimated Ki values and plasma concentrations from the literature suggest that the orally administered azoles, particularly ketoconazole and voriconazole, have the greatest potential for inhibiting CYP3A4 pathways, as does voriconazole for the CYP2B6 pathways. Ketoconazole 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-222 25651378-1 2015 Fentanyl is primarily metabolized by CYP3A, but has also been suggested to act as a weak inhibitor of CYP3A. Fentanyl 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-42 25868121-3 2015 Quetiapine, an antipsychotic metabolized by only CYP3A4, displayed higher serum levels in CYP3A4*22 carriers. Quetiapine Fumarate 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 25868121-3 2015 Quetiapine, an antipsychotic metabolized by only CYP3A4, displayed higher serum levels in CYP3A4*22 carriers. Quetiapine Fumarate 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 25868121-4 2015 Aripiprazole, haloperidol, pimozide, and risperidone are antipsychotics that are metabolized by CYP3A4 and CYP2D6. Aripiprazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 25651378-1 2015 Fentanyl is primarily metabolized by CYP3A, but has also been suggested to act as a weak inhibitor of CYP3A. Fentanyl 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 25868121-4 2015 Aripiprazole, haloperidol, pimozide, and risperidone are antipsychotics that are metabolized by CYP3A4 and CYP2D6. Haloperidol 14-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 25868121-4 2015 Aripiprazole, haloperidol, pimozide, and risperidone are antipsychotics that are metabolized by CYP3A4 and CYP2D6. Pimozide 27-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 25651378-2 2015 We investigated the influence of CYP3A inhibition by ketoconazole on the pharmacokinetics of intravenously administered fentanyl and the effect of fentanyl on CYP3A activity. Ketoconazole 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 25868121-4 2015 Aripiprazole, haloperidol, pimozide, and risperidone are antipsychotics that are metabolized by CYP3A4 and CYP2D6. Risperidone 41-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 25651378-2 2015 We investigated the influence of CYP3A inhibition by ketoconazole on the pharmacokinetics of intravenously administered fentanyl and the effect of fentanyl on CYP3A activity. Fentanyl 147-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-164 25651378-8 2015 Midazolam was administered as a CYP3A probe drug. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-37 25651378-11 2015 Fentanyl had no influence on midazolam exposure and CYP3A activity whereas ketoconazole decreased CYP3A activity to 13%. Ketoconazole 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 25651378-13 2015 Clinically fentanyl dosage adjustments may become necessary when ketoconazole or other strong CYP3A inhibitors are given simultaneously. Fentanyl 11-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-99 25176283-6 2015 Fentanyl is N-dealkylated by CYP3A4 into the inactive norfentanyl. Fentanyl 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 25176283-6 2015 Fentanyl is N-dealkylated by CYP3A4 into the inactive norfentanyl. norfentanyl 54-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 25162215-10 2015 CONCLUSIONS: This study suggests that the age-dependent changes in sirolimus clearance can be explained by size-related increases in CYP3A metabolic capacity, most likely due to liver and intestinal growth. Sirolimus 67-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-138 25640685-9 2015 Tetrahydropalmatine and Ber demonstrated both reversible and irreversible inhibition of CYP2D6 and CYP3A4. tetrahydropalmatine 0-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 25640685-9 2015 Tetrahydropalmatine and Ber demonstrated both reversible and irreversible inhibition of CYP2D6 and CYP3A4. Berberine 24-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 25640685-10 2015 Tetrahydropalmatine and Ber displayed H-bond and several Pi-bond connections with specific amino acid residues of CYP1A2, CYP2D6 and CYP3A4, giving further knowledge to the identified reversible and irreversible herb-drug interactions. tetrahydropalmatine 0-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 25640685-1 2015 The three purified herbal compounds tetrahydropalmatine (Tet), neferine and berberine (Ber) were explored in vitro for basic inhibition mechanisms towards recombinant human CYP1A2, CYP2D6 and CYP3A4 metabolic activities. Berberine 76-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-198 25640685-2 2015 Phenacetin, dextromethorphan and testosterone, respectively, were used as CYP1A2, CYP2D6 and CYP3A4 substrates, and their metabolites were determined by validated HPLC methodologies. Phenacetin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 25640685-2 2015 Phenacetin, dextromethorphan and testosterone, respectively, were used as CYP1A2, CYP2D6 and CYP3A4 substrates, and their metabolites were determined by validated HPLC methodologies. Testosterone 33-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 25271728-4 2015 Recently, CYP3A4*22 was reported to additionally affect tacrolimus pharmacokinetics (PK). Tacrolimus 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 26288843-4 2015 METHODS: We genotyped CYP2A6, CYP2B6 and CYP3A4, which encode enzymes principally involved in EFV metabolism, from patients enrolled in the multinational SMART, FIRST and ESPRIT studies, for whom outcome data of treatment adherence was available. efavirenz 94-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 25801005-3 2015 Methadone is N-demethylated to 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP) by CYP2B6 and CYP3A4 in vitro, but by CYP2B6 in vivo. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 25801005-3 2015 Methadone is N-demethylated to 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP) by CYP2B6 and CYP3A4 in vitro, but by CYP2B6 in vivo. 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine 31-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 25801005-3 2015 Methadone is N-demethylated to 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP) by CYP2B6 and CYP3A4 in vitro, but by CYP2B6 in vivo. 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine 82-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 25860621-4 2015 Experiments using pan- or isoform-selective CYP inhibitors showed that CYP2B6 and CYP3A4 are responsible for the bioactivation of cyclophosphamide. Cyclophosphamide 130-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 25860621-9 2015 The detoxication of leflunomide by microsomes was attributed to mainly CYP3A4-dependent metabolism. Leflunomide 20-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 25878177-11 2015 Given the extensive metabolism of perampanel, systemic exposure is clearly reduced with concomitant administration of CYP3A4 inducers. perampanel 34-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 25878177-1 2015 OBJECTIVE: Evaluate the impact of concomitant enzyme (CYP3A4)-inducer antiepileptic drugs (EIAEDs) on the efficacy and safety of perampanel in patients from the 3 phase-III clinical trials. perampanel 129-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 26288843-8 2015 FINDINGS: Patients with highest pharmacogenetic risk, as defined by cumulative SNPs in CYP2A6, CYP2B6 and CYP3A4, have an increased risk of discontinuation of EFV containing therapy compared to patients with lower genetic risk scores (adjusted HR 1.9, 95% CI 1.2, 3.1, P = 0.009). efavirenz 159-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 25678418-3 2015 6beta-Hydroxylation of many steroids, including cortisol, cortisone, progesterone and testosterone, was catalyzed primarily by CYP3A4. 6beta 0-5 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 25955319-11 2015 Of the twenty-seven SNPs assessed in the enzyme target and metabolism pathway, five SNPs in two genes, CYP3A4 (rs2242480; rs4646437; rs4986910), and CYP3A5 (rs15524; rs776746) were significantly associated with modifying finasteride concentrations. Finasteride 221-232 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 25678418-3 2015 6beta-Hydroxylation of many steroids, including cortisol, cortisone, progesterone and testosterone, was catalyzed primarily by CYP3A4. Steroids 28-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 25678418-3 2015 6beta-Hydroxylation of many steroids, including cortisol, cortisone, progesterone and testosterone, was catalyzed primarily by CYP3A4. Hydrocortisone 48-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 25725071-8 2015 In conclusion, GW4064 represses CYP3A4 expression in human hepatocytes, potentially through upregulation of SHP expression and subsequent repression of CYP3A4 promoter activity. GW 4064 15-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 25725071-0 2015 GW4064, an agonist of farnesoid X receptor, represses CYP3A4 expression in human hepatocytes by inducing small heterodimer partner expression. GW 4064 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 25678418-3 2015 6beta-Hydroxylation of many steroids, including cortisol, cortisone, progesterone and testosterone, was catalyzed primarily by CYP3A4. Cortisone 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 25725071-8 2015 In conclusion, GW4064 represses CYP3A4 expression in human hepatocytes, potentially through upregulation of SHP expression and subsequent repression of CYP3A4 promoter activity. GW 4064 15-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 25678418-3 2015 6beta-Hydroxylation of many steroids, including cortisol, cortisone, progesterone and testosterone, was catalyzed primarily by CYP3A4. Progesterone 69-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 25725071-4 2015 The effects of 3-(2,6-dichlorophenyl)-4-(3"-carboxy-2-chlorostilben-4-yl)oxymethyl-5-isopropylisoxazole (GW4064), a synthetic agonist of FXR, on the expression and activity of CYP3A4 were examined in primary human hepatocytes by using quantitative real-time polymerase chain reaction and S9 phenotyping. 3-(2,6-dichlorophenyl)-4-(3"-carboxy-2-chlorostilben-4-yl)oxymethyl-5-isopropylisoxazole 15-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 25678418-3 2015 6beta-Hydroxylation of many steroids, including cortisol, cortisone, progesterone and testosterone, was catalyzed primarily by CYP3A4. Testosterone 86-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 25725071-5 2015 In human hepatocytes, treatment of GW4064 (1 muM) for 48 hours resulted in a 75% decrease in CYP3A4 mRNA expression and a 25% decrease in CYP3A4 activity, accompanied by ~3-fold increase in SHP mRNA expression. GW 4064 35-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 25678418-4 2015 CYP1A2 and CYP3A4, respectively, are likely the major hepatic enzymes responsible for 2-/4-hydroxylation and 16alpha-hydroxylation of estradiol and estrone, steroids that can contribute to breast cancer risk. Estradiol 134-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 25725071-5 2015 In human hepatocytes, treatment of GW4064 (1 muM) for 48 hours resulted in a 75% decrease in CYP3A4 mRNA expression and a 25% decrease in CYP3A4 activity, accompanied by ~3-fold increase in SHP mRNA expression. GW 4064 35-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 25678418-4 2015 CYP1A2 and CYP3A4, respectively, are likely the major hepatic enzymes responsible for 2-/4-hydroxylation and 16alpha-hydroxylation of estradiol and estrone, steroids that can contribute to breast cancer risk. Estrone 148-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 25678418-4 2015 CYP1A2 and CYP3A4, respectively, are likely the major hepatic enzymes responsible for 2-/4-hydroxylation and 16alpha-hydroxylation of estradiol and estrone, steroids that can contribute to breast cancer risk. Steroids 157-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 25678418-6 2015 Some metabolic activities of CYP3A4, including dehydroepiandrosterone 7beta-/16alpha-hydroxylation, estrone 2-hydroxylation and testosterone 6beta-hydroxylation, were higher than those for polymorphically expressed CYP3A5. dehydroepiandrosterone 7beta 47-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 25678418-6 2015 Some metabolic activities of CYP3A4, including dehydroepiandrosterone 7beta-/16alpha-hydroxylation, estrone 2-hydroxylation and testosterone 6beta-hydroxylation, were higher than those for polymorphically expressed CYP3A5. Estrone 100-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 25678418-6 2015 Some metabolic activities of CYP3A4, including dehydroepiandrosterone 7beta-/16alpha-hydroxylation, estrone 2-hydroxylation and testosterone 6beta-hydroxylation, were higher than those for polymorphically expressed CYP3A5. testosterone 6beta 128-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 26011143-7 2015 Key factors to consider with riociguat are a patient"s systolic blood pressure, drug interactions mediated by CYP1A1, CYP3A4, and P-glycoprotein, cost, and teratogenicity requiring enrollment in a Risk Evaluation and Mitigation Strategy program. riociguat 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 25501671-0 2015 Effect of brivaracetam on CYP3A activity, measured by oral midazolam. brivaracetam 10-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-31 25501671-2 2015 A phase I, open-label, randomized study was conducted in 42 healthy male participants to assess the effect of brivaracetam on CYP3A activity using midazolam as a probe. brivaracetam 110-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-131 25624269-1 2015 The purpose of the present study was to assess the effect of resveratrol (RSV) pretreatment on CYP3A4 enzyme activity and pharmacokinetics of carbamazepine (CBZ) in healthy human volunteers. Resveratrol 61-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 25624269-1 2015 The purpose of the present study was to assess the effect of resveratrol (RSV) pretreatment on CYP3A4 enzyme activity and pharmacokinetics of carbamazepine (CBZ) in healthy human volunteers. Resveratrol 74-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 26003161-10 2015 RESULTS: A drug interaction between the cytochrome P450 3A4 inhibitor ticagrelor and substrate atorvastatin 80 mg may have precipitated development of rhabdomyolysis in this patient. Atorvastatin 95-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-59 26003161-12 2015 CONCLUSION: Rhabdomyolysis was observed possibly because of a drug interaction between once-daily ticagrelor and atorvastatin 80 mg. Clinicians need to be aware of this possible drug interaction via CYP3A4 and potential complications. Atorvastatin 113-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 199-205 25470032-1 2015 This open label drug-drug interaction (DDI) study investigated the effect of a strong CYP3A inhibitor ketoconazole on the PK and safety profile of GSK239512. Ketoconazole 102-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 25470032-1 2015 This open label drug-drug interaction (DDI) study investigated the effect of a strong CYP3A inhibitor ketoconazole on the PK and safety profile of GSK239512. GSK239512 147-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 25470032-2 2015 To mitigate the tolerability concerns of high GSK239512 exposures resulting from CYP3A inhibition, a 2-cohort adaptive design was used to facilitate a stepwise selection of dose levels and subject numbers. GSK239512 46-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 25385188-1 2015 BACKGROUND & AIMS: The first generation protease inhibitors, boceprevir (BOC) and telaprevir (TVR), are both CYP3A4 inhibitors, which predispose drug-drug interactions (DDIs). Adenosine Monophosphate 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 25385188-1 2015 BACKGROUND & AIMS: The first generation protease inhibitors, boceprevir (BOC) and telaprevir (TVR), are both CYP3A4 inhibitors, which predispose drug-drug interactions (DDIs). N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 25385188-1 2015 BACKGROUND & AIMS: The first generation protease inhibitors, boceprevir (BOC) and telaprevir (TVR), are both CYP3A4 inhibitors, which predispose drug-drug interactions (DDIs). N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 77-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 25385188-1 2015 BACKGROUND & AIMS: The first generation protease inhibitors, boceprevir (BOC) and telaprevir (TVR), are both CYP3A4 inhibitors, which predispose drug-drug interactions (DDIs). telaprevir 86-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 25385188-1 2015 BACKGROUND & AIMS: The first generation protease inhibitors, boceprevir (BOC) and telaprevir (TVR), are both CYP3A4 inhibitors, which predispose drug-drug interactions (DDIs). telaprevir 98-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 25624269-9 2015 Thus, there is a potential pharmacokinetic interaction between RSV and CBZ including other CYP3A4 substrates. Resveratrol 63-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 25624269-8 2015 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to RSV-mediated inhibition of CYP3A4 enzyme. Carbamazepine 84-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 25624269-8 2015 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to RSV-mediated inhibition of CYP3A4 enzyme. Carbamazepine 84-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 25624269-8 2015 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to RSV-mediated inhibition of CYP3A4 enzyme. Resveratrol 111-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 25624269-8 2015 The results suggest that the altered CYP3A4 enzyme activity and pharmacokinetics of CBZ might be attributed to RSV-mediated inhibition of CYP3A4 enzyme. Resveratrol 111-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 25684704-5 2015 Of the crude extracts of C. asiatica screened in vitro, methanolic extract showed potent noncompetitive inhibition of only CYP3A4 enzyme (Ki-64.36 +- 1.82 microg/mL), whereas ethanol solution extract showed potent noncompetitive inhibition of only CYP2D6 enzyme (Ki-36.3 +- 0.44 microg/mL). methanolic 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 25684704-7 2015 Because methanolic extract of C. asiatica showed a relatively high percentage content of quercetin and kaempferol than ethanol solution extract, the inhibitory effect of methanolic extract on CYP3A4 enzyme activity could be attributed to the flavonoids. methanolic 170-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-198 25932626-1 2015 BACKGROUND: The concomitant use of cytochrome P450 3A4 (CYP3A4) metabolized statins (simvastatin, lovastatin, and atorvastatin) with CYP3A4 inhibitors has been shown to increase the rate of adverse events. Simvastatin 85-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-54 25684704-7 2015 Because methanolic extract of C. asiatica showed a relatively high percentage content of quercetin and kaempferol than ethanol solution extract, the inhibitory effect of methanolic extract on CYP3A4 enzyme activity could be attributed to the flavonoids. Flavonoids 242-252 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-198 25684704-5 2015 Of the crude extracts of C. asiatica screened in vitro, methanolic extract showed potent noncompetitive inhibition of only CYP3A4 enzyme (Ki-64.36 +- 1.82 microg/mL), whereas ethanol solution extract showed potent noncompetitive inhibition of only CYP2D6 enzyme (Ki-36.3 +- 0.44 microg/mL). Ethanol 57-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 25684704-6 2015 The flavonoids, quercetin, and kaempferol showed potent (IC50 values less than 100 muM) inhibition of CYP3A4 activity, whereas quercetin alone showed potent inhibition of CYP2D6 activity in HLM. Flavonoids 4-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 25684704-6 2015 The flavonoids, quercetin, and kaempferol showed potent (IC50 values less than 100 muM) inhibition of CYP3A4 activity, whereas quercetin alone showed potent inhibition of CYP2D6 activity in HLM. Quercetin 16-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 25684704-6 2015 The flavonoids, quercetin, and kaempferol showed potent (IC50 values less than 100 muM) inhibition of CYP3A4 activity, whereas quercetin alone showed potent inhibition of CYP2D6 activity in HLM. kaempferol 31-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 25932626-1 2015 BACKGROUND: The concomitant use of cytochrome P450 3A4 (CYP3A4) metabolized statins (simvastatin, lovastatin, and atorvastatin) with CYP3A4 inhibitors has been shown to increase the rate of adverse events. Simvastatin 85-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 25932626-1 2015 BACKGROUND: The concomitant use of cytochrome P450 3A4 (CYP3A4) metabolized statins (simvastatin, lovastatin, and atorvastatin) with CYP3A4 inhibitors has been shown to increase the rate of adverse events. Simvastatin 85-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 25932626-1 2015 BACKGROUND: The concomitant use of cytochrome P450 3A4 (CYP3A4) metabolized statins (simvastatin, lovastatin, and atorvastatin) with CYP3A4 inhibitors has been shown to increase the rate of adverse events. Lovastatin 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-54 25932626-1 2015 BACKGROUND: The concomitant use of cytochrome P450 3A4 (CYP3A4) metabolized statins (simvastatin, lovastatin, and atorvastatin) with CYP3A4 inhibitors has been shown to increase the rate of adverse events. Lovastatin 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 25932626-1 2015 BACKGROUND: The concomitant use of cytochrome P450 3A4 (CYP3A4) metabolized statins (simvastatin, lovastatin, and atorvastatin) with CYP3A4 inhibitors has been shown to increase the rate of adverse events. Lovastatin 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 25644970-8 2015 There was a non-significant trend of lower cyclosporine dose requirement in CYP3A4*22 carriers. Cyclosporine 43-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 25932626-1 2015 BACKGROUND: The concomitant use of cytochrome P450 3A4 (CYP3A4) metabolized statins (simvastatin, lovastatin, and atorvastatin) with CYP3A4 inhibitors has been shown to increase the rate of adverse events. Atorvastatin 114-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-54 25932626-1 2015 BACKGROUND: The concomitant use of cytochrome P450 3A4 (CYP3A4) metabolized statins (simvastatin, lovastatin, and atorvastatin) with CYP3A4 inhibitors has been shown to increase the rate of adverse events. Atorvastatin 114-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 25932626-1 2015 BACKGROUND: The concomitant use of cytochrome P450 3A4 (CYP3A4) metabolized statins (simvastatin, lovastatin, and atorvastatin) with CYP3A4 inhibitors has been shown to increase the rate of adverse events. Atorvastatin 114-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 25470432-8 2015 In both cells, the expressions of CYP2C8, CYP2C9, CYP3A4 and constitutive androstane receptor (CAR) were decreased by MTZ treatment. Metronidazole 118-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 26767297-2 2015 METHODS: The CES1, cytochrome P450 3A4, CYP450 2C19, CYP450 1A2 and CYP450 2B6 which involved in Clopidogrel metabolism were selected at first, the chemical ligand database were created then, and finally the interaction effects between the ligand database and Clopidogrel metabolism target were explored. Clopidogrel 97-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-38 26767297-2 2015 METHODS: The CES1, cytochrome P450 3A4, CYP450 2C19, CYP450 1A2 and CYP450 2B6 which involved in Clopidogrel metabolism were selected at first, the chemical ligand database were created then, and finally the interaction effects between the ligand database and Clopidogrel metabolism target were explored. Clopidogrel 260-271 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-38 26767297-6 2015 CONCLUSION: It is suggested that Fufang Danshen Dripping Pill has inhibitory effects on Clopidogrel metabolism enzymes target such as CES1, Cytochrome P450 3A4, CYP450 2C19, CYP450 1A2 and CYP450 2B6. Clopidogrel 88-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-159 25919277-3 2015 In the current study, we constructed both normal and cooperative binding models of human CYP3A4 with antifungal drug ketoconazoles (KLN). Ketoconazole 117-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 25919277-3 2015 In the current study, we constructed both normal and cooperative binding models of human CYP3A4 with antifungal drug ketoconazoles (KLN). kln 132-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 25651456-0 2015 In silico prediction of the site of oxidation by cytochrome P450 3A4 that leads to the formation of the toxic metabolites of pyrrolizidine alkaloids. Pyrrolizidine Alkaloids 125-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-68 25651456-1 2015 In humans, the metabolic bioactivation of pyrrolizidine alkaloids (PAs) is mediated mainly by cytochrome P450 3A4 (CYP3A4) via the hydroxylation of their necine bases at C3 or C8 of heliotridine- and retronecine-type PAs or at the N atom of the methyl substituent of otonecine-type PAs. Pyrrolizidine Alkaloids 42-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-113 25651456-1 2015 In humans, the metabolic bioactivation of pyrrolizidine alkaloids (PAs) is mediated mainly by cytochrome P450 3A4 (CYP3A4) via the hydroxylation of their necine bases at C3 or C8 of heliotridine- and retronecine-type PAs or at the N atom of the methyl substituent of otonecine-type PAs. Pyrrolizidine Alkaloids 42-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 25651456-1 2015 In humans, the metabolic bioactivation of pyrrolizidine alkaloids (PAs) is mediated mainly by cytochrome P450 3A4 (CYP3A4) via the hydroxylation of their necine bases at C3 or C8 of heliotridine- and retronecine-type PAs or at the N atom of the methyl substituent of otonecine-type PAs. necine 154-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-113 25651456-1 2015 In humans, the metabolic bioactivation of pyrrolizidine alkaloids (PAs) is mediated mainly by cytochrome P450 3A4 (CYP3A4) via the hydroxylation of their necine bases at C3 or C8 of heliotridine- and retronecine-type PAs or at the N atom of the methyl substituent of otonecine-type PAs. necine 154-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 25651456-1 2015 In humans, the metabolic bioactivation of pyrrolizidine alkaloids (PAs) is mediated mainly by cytochrome P450 3A4 (CYP3A4) via the hydroxylation of their necine bases at C3 or C8 of heliotridine- and retronecine-type PAs or at the N atom of the methyl substituent of otonecine-type PAs. retronecine 182-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-113 25651456-1 2015 In humans, the metabolic bioactivation of pyrrolizidine alkaloids (PAs) is mediated mainly by cytochrome P450 3A4 (CYP3A4) via the hydroxylation of their necine bases at C3 or C8 of heliotridine- and retronecine-type PAs or at the N atom of the methyl substituent of otonecine-type PAs. retronecine 182-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 25651456-1 2015 In humans, the metabolic bioactivation of pyrrolizidine alkaloids (PAs) is mediated mainly by cytochrome P450 3A4 (CYP3A4) via the hydroxylation of their necine bases at C3 or C8 of heliotridine- and retronecine-type PAs or at the N atom of the methyl substituent of otonecine-type PAs. retronecine 200-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-113 25651456-1 2015 In humans, the metabolic bioactivation of pyrrolizidine alkaloids (PAs) is mediated mainly by cytochrome P450 3A4 (CYP3A4) via the hydroxylation of their necine bases at C3 or C8 of heliotridine- and retronecine-type PAs or at the N atom of the methyl substituent of otonecine-type PAs. retronecine 200-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 25651456-1 2015 In humans, the metabolic bioactivation of pyrrolizidine alkaloids (PAs) is mediated mainly by cytochrome P450 3A4 (CYP3A4) via the hydroxylation of their necine bases at C3 or C8 of heliotridine- and retronecine-type PAs or at the N atom of the methyl substituent of otonecine-type PAs. Nitrogen 231-232 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-113 25651456-1 2015 In humans, the metabolic bioactivation of pyrrolizidine alkaloids (PAs) is mediated mainly by cytochrome P450 3A4 (CYP3A4) via the hydroxylation of their necine bases at C3 or C8 of heliotridine- and retronecine-type PAs or at the N atom of the methyl substituent of otonecine-type PAs. Nitrogen 231-232 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 25651456-1 2015 In humans, the metabolic bioactivation of pyrrolizidine alkaloids (PAs) is mediated mainly by cytochrome P450 3A4 (CYP3A4) via the hydroxylation of their necine bases at C3 or C8 of heliotridine- and retronecine-type PAs or at the N atom of the methyl substituent of otonecine-type PAs. otonecine 267-276 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-113 25651456-1 2015 In humans, the metabolic bioactivation of pyrrolizidine alkaloids (PAs) is mediated mainly by cytochrome P450 3A4 (CYP3A4) via the hydroxylation of their necine bases at C3 or C8 of heliotridine- and retronecine-type PAs or at the N atom of the methyl substituent of otonecine-type PAs. otonecine 267-276 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 25651456-5 2015 Similarly, according to the predicted binding orientation in the active site of the crystal structure of human CYP3A4 (PDB code: 4I4G ), the alkaloids were positioned in such a way that the C3 atom of lasiocarpine and retrorsine and the C26 of senkirkin were closest to the catalytic heme Fe. Alkaloids 141-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 25651456-5 2015 Similarly, according to the predicted binding orientation in the active site of the crystal structure of human CYP3A4 (PDB code: 4I4G ), the alkaloids were positioned in such a way that the C3 atom of lasiocarpine and retrorsine and the C26 of senkirkin were closest to the catalytic heme Fe. lasiocarpine 201-213 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 25651456-5 2015 Similarly, according to the predicted binding orientation in the active site of the crystal structure of human CYP3A4 (PDB code: 4I4G ), the alkaloids were positioned in such a way that the C3 atom of lasiocarpine and retrorsine and the C26 of senkirkin were closest to the catalytic heme Fe. retrorsine 218-228 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 25651456-5 2015 Similarly, according to the predicted binding orientation in the active site of the crystal structure of human CYP3A4 (PDB code: 4I4G ), the alkaloids were positioned in such a way that the C3 atom of lasiocarpine and retrorsine and the C26 of senkirkin were closest to the catalytic heme Fe. Heme 284-288 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 25651456-5 2015 Similarly, according to the predicted binding orientation in the active site of the crystal structure of human CYP3A4 (PDB code: 4I4G ), the alkaloids were positioned in such a way that the C3 atom of lasiocarpine and retrorsine and the C26 of senkirkin were closest to the catalytic heme Fe. Iron 289-291 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 25453994-10 2015 CONCLUSIONS: Our data suggest that selection of dialysis modality is a major determinant of exposure to the CYP3A4 probe midazolam. Midazolam 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 25835492-1 2015 PURPOSE: To investigate the effect of vitamin D3 on hepatic Cytochrome P450 enzyme (CYP) 3A4 in patients with abnormal glucose regulation using the endogenous marker 4beta-hydroxycholesterol (4beta-OHC):cholesterol ratio. Cholecalciferol 38-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-92 25835492-1 2015 PURPOSE: To investigate the effect of vitamin D3 on hepatic Cytochrome P450 enzyme (CYP) 3A4 in patients with abnormal glucose regulation using the endogenous marker 4beta-hydroxycholesterol (4beta-OHC):cholesterol ratio. Glucose 119-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-92 25623616-9 2015 Compared to conventional in vitro BDI methodologies of assessment, the introduction of human plasma into the in vitro study model changed the observed inhibitory effect of silybin A, silybin B and hydrastine and berberine on CYP2C9 and CYP3A4/5, respectively, results which more closely mirrored those generated in clinical study. Silybin 172-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 236-242 25451157-7 2015 GSK5182 N-demethylation and hydroxylation is mainly mediated by CYP3A4, whereas FMO1 and FMO3 contribute to the formation of GSK5182 N-oxide from GSK5182. GSK5182 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 25291152-8 2015 Thus, well-controlled GDM did not change the activity of CYP2D6 and CYP3A involved in metoprolol metabolism. Metoprolol 86-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 25410880-5 2015 First, these stable cells were tested by treatment with 1alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3), all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) that induce CYP3A4 and P-gp in the intestines. 1alpha,25-dihydroxyvitamin d3 (1,25(oh)2d3 56-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 25410880-8 2015 The mixed cells showed a significant increase in the CYP3A4 and ABCB1 reporter activities following treatment with 1,25(OH)2 D3, ATRA, and 9-cis RA. Calcitriol 115-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 25410880-8 2015 The mixed cells showed a significant increase in the CYP3A4 and ABCB1 reporter activities following treatment with 1,25(OH)2 D3, ATRA, and 9-cis RA. Tretinoin 129-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 25410880-8 2015 The mixed cells showed a significant increase in the CYP3A4 and ABCB1 reporter activities following treatment with 1,25(OH)2 D3, ATRA, and 9-cis RA. Isotretinoin 141-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 25609219-6 2015 Finally, a further validation, on the basis of drug-drug-interaction prediction, was performed by comparing observed values of clopidogrel and clopi-H4 with or without dronedarone (moderate CYP3A4 inhibitor) coadministration using a previously developed and validated physiologically based PBPK dronedarone model. Dronedarone 168-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-196 25449654-11 2015 Substitution of strong inhibitors or strong inducers of CYP3A or CYP2C8 is recommended during treatment with dabrafenib. dabrafenib 109-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 25650381-8 2015 CYP3A4 mRNA expression level was increased by these compounds and induced by the addition of 1alpha,25-dihydroxyvitamin D3. Calcitriol 93-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25650381-9 2015 CYP3A4/5 activity was also induced by 1alpha,25-dihydroxyvitamin D3 in cells differentiated in the presence of the compounds. Calcitriol 38-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25894154-1 2015 OBJECTIVES: Tacrolimus is the cornerstone for immunosuppression in renal transplant and is metabolized by the cytochrome P 450 3A (CYP3A) subfamily of enzymes in the liver and small intestine. Tacrolimus 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-129 25894154-1 2015 OBJECTIVES: Tacrolimus is the cornerstone for immunosuppression in renal transplant and is metabolized by the cytochrome P 450 3A (CYP3A) subfamily of enzymes in the liver and small intestine. Tacrolimus 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-136 25535219-4 2015 Rifampicin and rifapentine, two anti-TB drugs now being optimized to shorten TB treatment duration, are potent inducers of CYP3A4. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 25535219-4 2015 Rifampicin and rifapentine, two anti-TB drugs now being optimized to shorten TB treatment duration, are potent inducers of CYP3A4. rifapentine 15-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 25535219-4 2015 Rifampicin and rifapentine, two anti-TB drugs now being optimized to shorten TB treatment duration, are potent inducers of CYP3A4. Terbium 37-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 25535219-4 2015 Rifampicin and rifapentine, two anti-TB drugs now being optimized to shorten TB treatment duration, are potent inducers of CYP3A4. Terbium 77-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 25418605-0 2015 Inhibitory effect of single and repeated doses of nilotinib on the pharmacokinetics of CYP3A substrate midazolam. nilotinib 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 25248340-8 2015 We found that doxapram was metabolized by CYP3A4/5. Doxapram 14-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 25515945-0 2015 Effects of CYP3A4 polymorphisms on the plasma concentration of voriconazole. Voriconazole 63-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 25515945-2 2015 The impact of activity of the genes encoding CYP3A4, CYP3A5, and CYP2C9 on the pharmacokinetics of voriconazole cannot be ignored because, second to CYP2C19, they are the most important enzymes involved in voriconazole metabolism. Voriconazole 99-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 25515945-2 2015 The impact of activity of the genes encoding CYP3A4, CYP3A5, and CYP2C9 on the pharmacokinetics of voriconazole cannot be ignored because, second to CYP2C19, they are the most important enzymes involved in voriconazole metabolism. Voriconazole 206-218 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 25515945-3 2015 The influence of genetic polymorphisms in CYP3A4, CYP3A5, and CYP2C9 on the plasma concentrations of voriconazole was evaluated in the present study. Voriconazole 101-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 25515945-4 2015 The study cohort comprised 158 patients with IFIs in whom 22 single-nucleotide polymorphisms (SNPs) in CYP3A4, CYP3A5, and CYP2C9 were genotyped using the Sequenom MassARRAY RS1000 system, and voriconazole plasma concentrations were measured by high-performance liquid chromatography (HPLC). Voriconazole 193-205 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 25515945-7 2015 This study has identified a new SNP related to the metabolism of voriconazole, potentially providing novel insight into the influence of CYP3A4 on the pharmacokinetics of this antifungal agent. Voriconazole 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 25418605-0 2015 Inhibitory effect of single and repeated doses of nilotinib on the pharmacokinetics of CYP3A substrate midazolam. Midazolam 103-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 25418605-1 2015 Effects of single and repeated doses of nilotinib on the pharmacokinetics of midazolam, a cytochrome P450 3A (CYP3A) substrate, were assessed in 2 separate studies. Midazolam 77-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-108 25418605-1 2015 Effects of single and repeated doses of nilotinib on the pharmacokinetics of midazolam, a cytochrome P450 3A (CYP3A) substrate, were assessed in 2 separate studies. Midazolam 77-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-115 25418605-6 2015 These results indicate that single-dose and repeated-dose administration of nilotinib results in weak and moderate inhibition of CYP3A, respectively. nilotinib 76-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-134 25418605-7 2015 Therefore, appropriate monitoring and dose adjustment may be needed for drugs that are mainly metabolized by CYP3A, and have narrow therapeutic index, when coadministered with nilotinib. nilotinib 176-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-114 25512016-5 2015 WHAT IS NEW AND CONCLUSION: Cyclosporine is a moderate inhibitor of the cytochrome P450 CYP3A4 isoenzyme, which is known to increase the serum level of atorvastatin. Cyclosporine 28-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 25449227-2 2015 In vitro studies indicated that faldaprevir inhibited CYP2B6, CYP2C9, and CYP3A, and was a weak-to-moderate inactivator of CYP3A4. faldaprevir 32-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-79 25512016-5 2015 WHAT IS NEW AND CONCLUSION: Cyclosporine is a moderate inhibitor of the cytochrome P450 CYP3A4 isoenzyme, which is known to increase the serum level of atorvastatin. Atorvastatin 152-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 25449227-2 2015 In vitro studies indicated that faldaprevir inhibited CYP2B6, CYP2C9, and CYP3A, and was a weak-to-moderate inactivator of CYP3A4. faldaprevir 32-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 25449227-4 2015 Faldaprevir 120 mg once daily in HCV-infected patients demonstrated weak inhibition of hepatic and intestinal CYP3A (oral midazolam: 1.52-fold increase in AUC(0- )), and had no relevant effects on CYP2C9 or CYP1A2. faldaprevir 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-115 24905729-11 2015 In vitro, rifampicin PXR-dependently upregulated biotransformation phase 1 (CYP3A4), phase 2 (UGT1A1) and phase 3 (MRP2) enzymes/carriers as well as the basolateral bile salt exporter OSTbeta. Rifampin 10-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 24905729-14 2015 PXR-dependent induction of CYP3A4, UGT1A1, MRP2 and OSTbeta could contribute to the anticholestatic effect of rifampicin in PHSF. Rifampin 110-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 25599164-2 2015 Although sirolimus is being used increasingly for the prevention of GVHD, it is a substrate of CYP3A4, which is inhibited by voriconazole, and concurrent administration can lead to significantly increased exposure to sirolimus. Sirolimus 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 25449227-6 2015 These studies suggest that faldaprevir shows a dose-dependent inhibition of CYP3A and CYP2C9, and does not induce CYP isoforms. faldaprevir 27-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 25757445-1 2015 STUDY OBJECTIVES: To evaluate the effect of Roux-en-Y gastric bypass surgery (RYGB) on the pharmacokinetics of midazolam (a CYP3A4 substrate) and digoxin (a P-glycoprotein substrate). Midazolam 111-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 25761690-0 2015 Taurine modulates catalytic activity of cytochrome P450 3A4. Taurine 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-59 25761690-1 2015 The influence of the biologically active compound taurine on the stability and catalytic properties of the hemoprotein cytochrome P450 3A4 has been investigated. Taurine 50-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-138 25761690-3 2015 Taurine at concentrations in the range 10-70 microM stimulated the electrochemical reduction of cytochrome P450 3A4, and the reduction was the highest (115 +- 3%) in the presence of 50 microM taurine. Taurine 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-115 25761690-3 2015 Taurine at concentrations in the range 10-70 microM stimulated the electrochemical reduction of cytochrome P450 3A4, and the reduction was the highest (115 +- 3%) in the presence of 50 microM taurine. Taurine 192-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-115 25761690-5 2015 Taurine protected cytochrome P450 3A4 due to stabilizing it during electrolysis at controlled voltage in the presence of erythromycin as a substrate. Taurine 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-37 25434721-7 2015 However, overexpression of CYP3A5 attenuated the inducibility of CYP3A4 in response to dexamethasone. Dexamethasone 87-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 25434721-9 2015 Furthermore, a pharmacokinetic assay using quinidine and amlodipine showed that CYP3A4 enzyme activity per mg of microsomal protein was also decreased in the group overexpressing CYP3A5 compared with the dexamethasone-induced control group. Quinidine 43-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 25434721-9 2015 Furthermore, a pharmacokinetic assay using quinidine and amlodipine showed that CYP3A4 enzyme activity per mg of microsomal protein was also decreased in the group overexpressing CYP3A5 compared with the dexamethasone-induced control group. Amlodipine 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 25657337-6 2015 In vitro triazolam 4-hydroxylation (probe reaction for CYP3A4) was reduced by >50% in hepatic microsomes from CYP3A4-HBN mice compared with controls. Triazolam 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 25657337-6 2015 In vitro triazolam 4-hydroxylation (probe reaction for CYP3A4) was reduced by >50% in hepatic microsomes from CYP3A4-HBN mice compared with controls. Triazolam 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 25657337-8 2015 This effect was confirmed by the concentration-dependent restoration of CYP3A4-mediated triazolam turnover and CYP2D6-mediated bufuralol and debrisoquine turnover on addition of Escherichia coli membranes containing recombinant Cyb5. Triazolam 88-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 25657337-9 2015 In vivo, the peak plasma concentration and area under the concentration time curve from 0 to 8 hours (AUC0-8 h) of triazolam were increased 4- and 5.7-fold, respectively, in CYP3A4-HBN mice. Triazolam 115-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 25287072-0 2015 The CYP3A4*22 C>T single nucleotide polymorphism is associated with reduced midazolam and tacrolimus clearance in stable renal allograft recipients. Midazolam 79-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 25287072-0 2015 The CYP3A4*22 C>T single nucleotide polymorphism is associated with reduced midazolam and tacrolimus clearance in stable renal allograft recipients. Tacrolimus 93-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 25287072-1 2015 Tacrolimus, a dual substrate of CYP3A4 and CYP3A5 has a narrow therapeutic index and is characterized by high between-subject variability in oral bioavailability. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 25287072-2 2015 This study investigated the effects of the recently described CYP3A4*22 intron 6 C>T single nucleotide polymorphism on in vivo CYP3A4 activity as measured by midazolam (MDZ) clearance and tacrolimus pharmacokinetics in two cohorts of renal allograft recipients, taking into account the CYP3A5*1/*3 genotype and other determinants of drug disposition. Midazolam 172-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 25287072-3 2015 In CYP3A5 non-expressers, the presence of one CYP3A4*22T-allele was associated with a 31.7-33.6% reduction in MDZ apparent oral clearance, reflecting reduced in vivo CYP3A4 activity. Midazolam 110-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 25287072-3 2015 In CYP3A5 non-expressers, the presence of one CYP3A4*22T-allele was associated with a 31.7-33.6% reduction in MDZ apparent oral clearance, reflecting reduced in vivo CYP3A4 activity. Midazolam 110-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-172 25387130-2 2015 The purpose of this study was to clarify species differences in the heteroactivation of CYP3A substrates by efavirenz, which is known from clinical studies to activate midazolam 1"-hydroxylation, and to assess the feasibility of an animal model. Midazolam 168-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-93 25387130-4 2015 In monkey and human liver microsomes, efavirenz activated CYP3A-mediated midazolam 1"-hydroxylation, but had no effect in rat liver microsomes. Midazolam 73-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 25654496-0 2015 Effect of cholesterol on the structure of membrane-attached cytochrome P450 3A4. Cholesterol 10-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-79 25654496-3 2015 We analyzed the behavior of CYP3A4 immersed in a 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC) membrane with various amounts of cholesterol. 1,2-oleoylphosphatidylcholine 49-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 25654496-3 2015 We analyzed the behavior of CYP3A4 immersed in a 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC) membrane with various amounts of cholesterol. 1,2-oleoylphosphatidylcholine 91-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 25654496-3 2015 We analyzed the behavior of CYP3A4 immersed in a 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC) membrane with various amounts of cholesterol. Cholesterol 130-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 25654496-4 2015 The presence of cholesterol caused ordering and thickening of the membrane and led to greater immersion and inclination of CYP3A4 toward the membrane. Cholesterol 16-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 25654496-5 2015 Cholesterol also lowered the flexibility of and tended to concentrate around membrane-immersed parts of CYP3A4. Cholesterol 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 25654496-6 2015 Further, the pattern of the CYP3A4 active-site access channels was altered in the presence of cholesterol. Cholesterol 94-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 25654496-7 2015 In summary, cholesterol in the membrane affected the positioning and structural features of CYP3A4, which in turn may have implications for the activity of this enzyme in various membranes and membrane parts with different cholesterol content. Cholesterol 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 25654496-7 2015 In summary, cholesterol in the membrane affected the positioning and structural features of CYP3A4, which in turn may have implications for the activity of this enzyme in various membranes and membrane parts with different cholesterol content. Cholesterol 223-234 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 25815288-3 2015 The first experiment validated the effects of ergot alkaloids [0, 20, and 40 muM of ergotamine (ET), dihydroergotamine (DHET), and ergonovine (EN)] on human CYP3A4 using the P450-Glo assay (Promega V9800). Ergot Alkaloids 46-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 25815288-3 2015 The first experiment validated the effects of ergot alkaloids [0, 20, and 40 muM of ergotamine (ET), dihydroergotamine (DHET), and ergonovine (EN)] on human CYP3A4 using the P450-Glo assay (Promega V9800). Ergotamine 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 25815288-3 2015 The first experiment validated the effects of ergot alkaloids [0, 20, and 40 muM of ergotamine (ET), dihydroergotamine (DHET), and ergonovine (EN)] on human CYP3A4 using the P450-Glo assay (Promega V9800). Dihydroergotamine 101-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 25815288-3 2015 The first experiment validated the effects of ergot alkaloids [0, 20, and 40 muM of ergotamine (ET), dihydroergotamine (DHET), and ergonovine (EN)] on human CYP3A4 using the P450-Glo assay (Promega V9800). Ergonovine 131-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 25588704-0 2015 Kidney transplant recipients carrying the CYP3A4*22 allelic variant have reduced tacrolimus clearance and often reach supratherapeutic tacrolimus concentrations. Tacrolimus 81-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 25588704-0 2015 Kidney transplant recipients carrying the CYP3A4*22 allelic variant have reduced tacrolimus clearance and often reach supratherapeutic tacrolimus concentrations. Tacrolimus 135-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 25761690-5 2015 Taurine protected cytochrome P450 3A4 due to stabilizing it during electrolysis at controlled voltage in the presence of erythromycin as a substrate. Erythromycin 121-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-37 25599164-2 2015 Although sirolimus is being used increasingly for the prevention of GVHD, it is a substrate of CYP3A4, which is inhibited by voriconazole, and concurrent administration can lead to significantly increased exposure to sirolimus. Voriconazole 125-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 25599164-2 2015 Although sirolimus is being used increasingly for the prevention of GVHD, it is a substrate of CYP3A4, which is inhibited by voriconazole, and concurrent administration can lead to significantly increased exposure to sirolimus. Sirolimus 217-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 25618289-2 2015 The principal active metabolite - endoxifen - is generated through hepatic metabolism of tamoxifen, with key roles for cytochrome P450 (CYP) CYP2D6 and CYP3A. 4-hydroxy-N-desmethyltamoxifen 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-157 27128217-4 2015 The purpose of these studies was to evaluate the effect of ketoconazole, a potent inhibitor of CYP3A4, and rifampin, a potent inducer of CYP3A4, on the pharmacokinetics of tivozanib. Ketoconazole 59-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 25618289-2 2015 The principal active metabolite - endoxifen - is generated through hepatic metabolism of tamoxifen, with key roles for cytochrome P450 (CYP) CYP2D6 and CYP3A. Tamoxifen 89-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-157 25618289-6 2015 Genetic variants of other CYP enzymes, including CYP3A4 and CYP2C9/19, as well as co-medication interfering with the metabolic activity of CYP2D6 and CYP3A4 have been shown to affect endoxifen concentrations and may also contribute to the variability in response to tamoxifen. 4-hydroxy-N-desmethyltamoxifen 183-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 25618289-6 2015 Genetic variants of other CYP enzymes, including CYP3A4 and CYP2C9/19, as well as co-medication interfering with the metabolic activity of CYP2D6 and CYP3A4 have been shown to affect endoxifen concentrations and may also contribute to the variability in response to tamoxifen. 4-hydroxy-N-desmethyltamoxifen 183-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 25618289-6 2015 Genetic variants of other CYP enzymes, including CYP3A4 and CYP2C9/19, as well as co-medication interfering with the metabolic activity of CYP2D6 and CYP3A4 have been shown to affect endoxifen concentrations and may also contribute to the variability in response to tamoxifen. Tamoxifen 266-275 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 25618289-6 2015 Genetic variants of other CYP enzymes, including CYP3A4 and CYP2C9/19, as well as co-medication interfering with the metabolic activity of CYP2D6 and CYP3A4 have been shown to affect endoxifen concentrations and may also contribute to the variability in response to tamoxifen. Tamoxifen 266-275 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 26097795-2 2015 In vitro evidence indicates that lenvatinib metabolism may be modulated by ketoconazole, an inhibitor of CYP3A4 and p-glycoprotein. lenvatinib 33-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 26097795-2 2015 In vitro evidence indicates that lenvatinib metabolism may be modulated by ketoconazole, an inhibitor of CYP3A4 and p-glycoprotein. Ketoconazole 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 27128217-4 2015 The purpose of these studies was to evaluate the effect of ketoconazole, a potent inhibitor of CYP3A4, and rifampin, a potent inducer of CYP3A4, on the pharmacokinetics of tivozanib. Rifampin 107-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 27128217-4 2015 The purpose of these studies was to evaluate the effect of ketoconazole, a potent inhibitor of CYP3A4, and rifampin, a potent inducer of CYP3A4, on the pharmacokinetics of tivozanib. tivozanib 172-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 27128217-8 2015 However, coadministration of tivozanib with rifampin caused a significant decrease in the area under the curve from 0 to infinity and half-life and an increase in clearance of tivozanib, which suggest increased clearance via the enhanced CYP3A4-mediated metabolism of tivozanib. tivozanib 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 238-244 24445680-5 2015 Western blot data indicated that matrine at 140 mg/L at 72 h induced protein expression of CYP2A6, CYP2B6 and CYP3A4. matrine 33-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 27128217-8 2015 However, coadministration of tivozanib with rifampin caused a significant decrease in the area under the curve from 0 to infinity and half-life and an increase in clearance of tivozanib, which suggest increased clearance via the enhanced CYP3A4-mediated metabolism of tivozanib. Rifampin 44-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 238-244 25274942-3 2015 We analyzed the association of CYP3A4*22 allele with response to atorvastatin and simvastatin. Atorvastatin 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 25504504-9 2015 In summary, CYP3A4 dominantly mediated 5beta-hydroxylation and was found to be a major metabolic pathway of RB in the human liver, whereas its major metabolite (5-HRB) displayed better druglikeness than its parent compound RB. 5beta 39-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 25274942-3 2015 We analyzed the association of CYP3A4*22 allele with response to atorvastatin and simvastatin. Simvastatin 82-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 25274942-7 2015 RESULTS: In the entire cohort population, 41 individuals carried CYP3A4*22 allele (18 in atorvastatin and 23 in simvastatin treatment). Atorvastatin 89-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 25274942-7 2015 RESULTS: In the entire cohort population, 41 individuals carried CYP3A4*22 allele (18 in atorvastatin and 23 in simvastatin treatment). Simvastatin 112-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 25803093-1 2015 BACKGROUND: Bosutinib is an orally bioavailable dual Src/Abl tyrosine kinase inhibitor and a CYP3A4 enzyme substrate. bosutinib 12-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 25504504-9 2015 In summary, CYP3A4 dominantly mediated 5beta-hydroxylation and was found to be a major metabolic pathway of RB in the human liver, whereas its major metabolite (5-HRB) displayed better druglikeness than its parent compound RB. bufogenin 108-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 25803093-2 2015 This study assessed the safety, tolerability, and pharmacokinetics of bosutinib when coadministered with the CYP3A4 inducer rifampin in 24 healthy men. Rifampin 124-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 25858605-4 2015 Dolutegravir is metabolized by UGT1A1 and, to a lesser extent, by CYP3A4, without being an inducer or inhibitor of the usual metabolic systems. dolutegravir 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 25656284-0 2015 Sertraline-induced potentiation of the CYP3A4-dependent neurotoxicity of carbamazepine: an in vitro study. Carbamazepine 73-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 25560051-3 2015 Tramadol is metabolized to M1 mainly by cytochrome P450 (CYP)2D6 enzyme and to other metabolites by CYP3A4 and CYP2B6. Tramadol 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 25656284-13 2015 SIGNIFICANCE: These results demonstrate an unexpected neurotoxic interaction between CBZ and SRT, apparently related to increased CYP3A4-mediated production of reactive CBZ metabolites. Carbamazepine 85-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 25656284-0 2015 Sertraline-induced potentiation of the CYP3A4-dependent neurotoxicity of carbamazepine: an in vitro study. Sertraline 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 25656284-13 2015 SIGNIFICANCE: These results demonstrate an unexpected neurotoxic interaction between CBZ and SRT, apparently related to increased CYP3A4-mediated production of reactive CBZ metabolites. Carbamazepine 169-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 25837459-6 2015 We speculate a significant interference on adverse events (mainly atrial fibrillation and consequently acute coronary syndromes) and on the outcome of unfavorable interactions between ivabradine and diltiazem, verapamil and strong inhibitors of CYP3A4 (4.6% of the total population). Ivabradine 184-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 245-251 24390778-1 2015 Omeprazole (OMP) is effective in the treatment of gastric hyperacidity and is metabolized by CYP2C19 and CYP3A4. Omeprazole 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 24390778-1 2015 Omeprazole (OMP) is effective in the treatment of gastric hyperacidity and is metabolized by CYP2C19 and CYP3A4. Omeprazole 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 24390778-8 2015 The activities of CYP2C19 and CYP3A4 were determined as AUC(OH-OMP)/AUC(OMP) and AUC(OMP-SUL)/AUC(OMP), respectively. oh-omp 60-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 24464299-3 2015 Inhibitory activity on CYP3A4 was measured with and without the addition of NIPRISAN( ), by testing different concentrations of the product at 37 C in reactive mixtures with ketoconazole (2.5 muM) as the positive control. Ketoconazole 175-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 25322914-0 2015 Time-dependent inhibition of CYP3A4 by gallic acid in human liver microsomes and recombinant systems. Gallic Acid 39-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 25407158-2 2015 The urinary ratio of 6-beta hydroxycortisol to cortisol (6betaHF : F) is a marker of CYP3A4 induction. 6 beta-hydroxycortisol 21-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 25407158-2 2015 The urinary ratio of 6-beta hydroxycortisol to cortisol (6betaHF : F) is a marker of CYP3A4 induction. Hydrocortisone 35-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 25407158-12 2015 The trend towards an inverse relationship between the change in the 6betaHF : F ratio and the change in the LPV AUC antepartum vs. postpartum suggests that CYP3A induction may be one mechanism behind altered LPV exposure during pregnancy. Lopinavir 108-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-161 25457200-11 2015 HLCs secreted albumin and metabolized testosterone (CYP3A) and dextrorphan (CYP2D6) like fetal hepatocytes. Testosterone 38-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-57 25322914-8 2015 Those results indicate that CYP3A4 inactivation by gallic acid was independent on NADPH and was mainly mediated its oxidative products. Gallic Acid 51-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 26038696-3 2015 To identify the enzymes involved in this metabolism, we examined NADPH-dependent metabolism by recombinant P450 isoforms belonging to the CYP1, 2, and 3 families, and revealed that CYP3A4 had the activity. NADP 65-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-187 26038696-4 2015 However, the CYP3A4 -specific inhibitor, ketoconazole, decreased the activity in human liver microsomes by only 36%, suggesting that other enzymes could be involved in ED-71 metabolism. Ketoconazole 41-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 25322914-2 2015 Inhibitory characteristics of gallic acid on CYP3A4 were still unclear. Gallic Acid 30-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 25322914-8 2015 Those results indicate that CYP3A4 inactivation by gallic acid was independent on NADPH and was mainly mediated its oxidative products. NADP 82-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 25322914-3 2015 The objective of this work is hence to investigate inhibitory characteristics of gallic acid on CYP3A4 using testosterone as the probe substrate in human liver microsomes (HLMs) and recombinant CYP3A4 (rCYP3A4) systems. Gallic Acid 81-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 25322914-9 2015 4.In conclusion, we showed that gallic acid weakly and time-dependently inactivated CYP3A4 via its oxidative products. Gallic Acid 32-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 25322914-3 2015 The objective of this work is hence to investigate inhibitory characteristics of gallic acid on CYP3A4 using testosterone as the probe substrate in human liver microsomes (HLMs) and recombinant CYP3A4 (rCYP3A4) systems. Gallic Acid 81-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 25322914-3 2015 The objective of this work is hence to investigate inhibitory characteristics of gallic acid on CYP3A4 using testosterone as the probe substrate in human liver microsomes (HLMs) and recombinant CYP3A4 (rCYP3A4) systems. Testosterone 109-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 25322914-4 2015 2.Gallic acid caused concentration-dependent loss of CYP3A4 activity with IC50 values of 615.2 muM and 669.5 muM in HLM and rCYP3A4 systems, respectively. Gallic Acid 2-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 25733917-4 2015 As a substrate of CYP 3A4, dolutegravir is affected by rifampin, efavirenz, tipranavir/ritonavir, fosamprenavir/ritonavir, and dose increase is required. dolutegravir 27-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-25 25733917-4 2015 As a substrate of CYP 3A4, dolutegravir is affected by rifampin, efavirenz, tipranavir/ritonavir, fosamprenavir/ritonavir, and dose increase is required. Rifampin 55-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-25 25733917-4 2015 As a substrate of CYP 3A4, dolutegravir is affected by rifampin, efavirenz, tipranavir/ritonavir, fosamprenavir/ritonavir, and dose increase is required. efavirenz 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-25 25733917-4 2015 As a substrate of CYP 3A4, dolutegravir is affected by rifampin, efavirenz, tipranavir/ritonavir, fosamprenavir/ritonavir, and dose increase is required. Ritonavir 87-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-25 25733917-4 2015 As a substrate of CYP 3A4, dolutegravir is affected by rifampin, efavirenz, tipranavir/ritonavir, fosamprenavir/ritonavir, and dose increase is required. fosamprenavir 98-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-25 25733917-4 2015 As a substrate of CYP 3A4, dolutegravir is affected by rifampin, efavirenz, tipranavir/ritonavir, fosamprenavir/ritonavir, and dose increase is required. Ritonavir 112-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-25 25451919-4 2015 Intriguingly, CYP3A4 Ser(P)/Thr(P) and ubiquitinated Lys residues reside within the cytosol-accessible surface loop and/or conformationally assembled acidic Asp/Glu clusters, leading us to propose that such post-translational Ser/Thr protein phosphorylation primes CYP3A4 for ubiquitination. Serine 21-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 25534598-1 2015 BACKGROUND: The cytochrome P450 3A4 (CYP3A4) inhibitor clarithromycin may also inhibit liver-specific organic anion-transporting polypeptides (OATP1B1 and OATP1B3). Clarithromycin 55-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-35 25534598-1 2015 BACKGROUND: The cytochrome P450 3A4 (CYP3A4) inhibitor clarithromycin may also inhibit liver-specific organic anion-transporting polypeptides (OATP1B1 and OATP1B3). Clarithromycin 55-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 25534598-9 2015 INTERPRETATION: Among older adults taking a statin not metabolized by CYP3A4, co-prescription of clarithromycin versus azithromycin was associated with a modest but statistically significant increase in the 30-day absolute risk of adverse outcomes. Clarithromycin 97-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 25534598-9 2015 INTERPRETATION: Among older adults taking a statin not metabolized by CYP3A4, co-prescription of clarithromycin versus azithromycin was associated with a modest but statistically significant increase in the 30-day absolute risk of adverse outcomes. Azithromycin 119-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 25451919-4 2015 Intriguingly, CYP3A4 Ser(P)/Thr(P) and ubiquitinated Lys residues reside within the cytosol-accessible surface loop and/or conformationally assembled acidic Asp/Glu clusters, leading us to propose that such post-translational Ser/Thr protein phosphorylation primes CYP3A4 for ubiquitination. Serine 21-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 265-271 25533469-9 2015 Here we report the results of intermolecular cross-linking of CYP3A4 oligomers with thiol-reactive bifunctional reagents as well as the luminescence resonance energy transfer measurements of interprobe distances in the oligomers of labeled CYP3A4 single-cysteine mutants. Sulfhydryl Compounds 84-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 25451919-4 2015 Intriguingly, CYP3A4 Ser(P)/Thr(P) and ubiquitinated Lys residues reside within the cytosol-accessible surface loop and/or conformationally assembled acidic Asp/Glu clusters, leading us to propose that such post-translational Ser/Thr protein phosphorylation primes CYP3A4 for ubiquitination. Threonine 28-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 25533469-9 2015 Here we report the results of intermolecular cross-linking of CYP3A4 oligomers with thiol-reactive bifunctional reagents as well as the luminescence resonance energy transfer measurements of interprobe distances in the oligomers of labeled CYP3A4 single-cysteine mutants. Cysteine 254-262 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 240-246 25451919-4 2015 Intriguingly, CYP3A4 Ser(P)/Thr(P) and ubiquitinated Lys residues reside within the cytosol-accessible surface loop and/or conformationally assembled acidic Asp/Glu clusters, leading us to propose that such post-translational Ser/Thr protein phosphorylation primes CYP3A4 for ubiquitination. Threonine 28-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 265-271 25451919-4 2015 Intriguingly, CYP3A4 Ser(P)/Thr(P) and ubiquitinated Lys residues reside within the cytosol-accessible surface loop and/or conformationally assembled acidic Asp/Glu clusters, leading us to propose that such post-translational Ser/Thr protein phosphorylation primes CYP3A4 for ubiquitination. Lysine 53-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 265-271 25451919-4 2015 Intriguingly, CYP3A4 Ser(P)/Thr(P) and ubiquitinated Lys residues reside within the cytosol-accessible surface loop and/or conformationally assembled acidic Asp/Glu clusters, leading us to propose that such post-translational Ser/Thr protein phosphorylation primes CYP3A4 for ubiquitination. Aspartic Acid 157-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 25451919-4 2015 Intriguingly, CYP3A4 Ser(P)/Thr(P) and ubiquitinated Lys residues reside within the cytosol-accessible surface loop and/or conformationally assembled acidic Asp/Glu clusters, leading us to propose that such post-translational Ser/Thr protein phosphorylation primes CYP3A4 for ubiquitination. Aspartic Acid 157-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 265-271 25451919-4 2015 Intriguingly, CYP3A4 Ser(P)/Thr(P) and ubiquitinated Lys residues reside within the cytosol-accessible surface loop and/or conformationally assembled acidic Asp/Glu clusters, leading us to propose that such post-translational Ser/Thr protein phosphorylation primes CYP3A4 for ubiquitination. Glutamic Acid 161-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 25451919-4 2015 Intriguingly, CYP3A4 Ser(P)/Thr(P) and ubiquitinated Lys residues reside within the cytosol-accessible surface loop and/or conformationally assembled acidic Asp/Glu clusters, leading us to propose that such post-translational Ser/Thr protein phosphorylation primes CYP3A4 for ubiquitination. Glutamic Acid 161-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 265-271 25451919-4 2015 Intriguingly, CYP3A4 Ser(P)/Thr(P) and ubiquitinated Lys residues reside within the cytosol-accessible surface loop and/or conformationally assembled acidic Asp/Glu clusters, leading us to propose that such post-translational Ser/Thr protein phosphorylation primes CYP3A4 for ubiquitination. Serine 226-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 25451919-4 2015 Intriguingly, CYP3A4 Ser(P)/Thr(P) and ubiquitinated Lys residues reside within the cytosol-accessible surface loop and/or conformationally assembled acidic Asp/Glu clusters, leading us to propose that such post-translational Ser/Thr protein phosphorylation primes CYP3A4 for ubiquitination. Threonine 230-233 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 25451919-6 2015 Our findings reveal that such CYP3A4 Asp/Glu/Ser(P)/Thr(P) surface clusters are indeed important for its intermolecular electrostatic interactions with each of these E2-E3 subcomponents. Aspartic Acid 37-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 25451919-6 2015 Our findings reveal that such CYP3A4 Asp/Glu/Ser(P)/Thr(P) surface clusters are indeed important for its intermolecular electrostatic interactions with each of these E2-E3 subcomponents. Glutamic Acid 41-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 25451919-6 2015 Our findings reveal that such CYP3A4 Asp/Glu/Ser(P)/Thr(P) surface clusters are indeed important for its intermolecular electrostatic interactions with each of these E2-E3 subcomponents. Serine 45-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 25451919-6 2015 Our findings reveal that such CYP3A4 Asp/Glu/Ser(P)/Thr(P) surface clusters are indeed important for its intermolecular electrostatic interactions with each of these E2-E3 subcomponents. Threonine 52-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 25451919-7 2015 By imparting additional negative charge to these Asp/Glu clusters, such Ser/Thr phosphorylation would generate P450 phosphodegrons for molecular recognition by the E2-E3 complexes, thereby controlling the timing of CYP3A4 ubiquitination and endoplasmic reticulum-associated degradation. Aspartic Acid 49-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-221 25451919-7 2015 By imparting additional negative charge to these Asp/Glu clusters, such Ser/Thr phosphorylation would generate P450 phosphodegrons for molecular recognition by the E2-E3 complexes, thereby controlling the timing of CYP3A4 ubiquitination and endoplasmic reticulum-associated degradation. Glutamic Acid 53-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-221 25451919-7 2015 By imparting additional negative charge to these Asp/Glu clusters, such Ser/Thr phosphorylation would generate P450 phosphodegrons for molecular recognition by the E2-E3 complexes, thereby controlling the timing of CYP3A4 ubiquitination and endoplasmic reticulum-associated degradation. Serine 72-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-221 25451919-7 2015 By imparting additional negative charge to these Asp/Glu clusters, such Ser/Thr phosphorylation would generate P450 phosphodegrons for molecular recognition by the E2-E3 complexes, thereby controlling the timing of CYP3A4 ubiquitination and endoplasmic reticulum-associated degradation. Threonine 76-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-221 25648948-0 2015 Serum alanine transaminase total bilirubin concentrations predict CYP3A activity as measured by midazolam and 1"-hydroxylation. Bilirubin 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 25619394-5 2015 The metabolism of testosterone (TEST, 10 mumol/L) and dextromethorphan (DEM, 1 mumol/L), the two typical substrates for CYP3A4 and CYP2D6, in the cells was examined in the presence of different agents. Testosterone 18-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 25619394-5 2015 The metabolism of testosterone (TEST, 10 mumol/L) and dextromethorphan (DEM, 1 mumol/L), the two typical substrates for CYP3A4 and CYP2D6, in the cells was examined in the presence of different agents. Dextromethorphan 54-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 25619394-5 2015 The metabolism of testosterone (TEST, 10 mumol/L) and dextromethorphan (DEM, 1 mumol/L), the two typical substrates for CYP3A4 and CYP2D6, in the cells was examined in the presence of different agents. Dextromethorphan 72-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 25619394-7 2015 The metabolism of TEST and DEM in HepG2 cells was dose-dependently inhibited by the specific CYP3A4 inhibitor ketoconazole and CYP2D6 inhibitor quinidine. Ketoconazole 110-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 25648948-0 2015 Serum alanine transaminase total bilirubin concentrations predict CYP3A activity as measured by midazolam and 1"-hydroxylation. Midazolam 96-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 25648948-10 2015 Multiple linear regression analysis showed a statistically significant linear relationship between the activity of CYP3A and alanine transaminase (ALT, R2=0.682, P=0.000), and total bilirubin (TB, R2=0.519, P=0.002). Bilirubin 193-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 25648948-13 2015 The decrease in the activity of CYP3A was determined by the increase in the serum concentration of ALT and TB and not by patient"s age or body weight. Bilirubin 107-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-37 25542144-0 2015 Diindolylmethane, a naturally occurring compound, induces CYP3A4 and MDR1 gene expression by activating human PXR. 3,3'-diindolylmethane 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 25648948-14 2015 ALT and TB therefore might have predictive value for the activity of CYP3A. Bilirubin 8-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 25542144-3 2015 Here, we studied whether 3,3"-diindolylmethane (DIM), a natural health supplement, could induce hPXR-mediated regulation of CYP3A4 and MDR1 in human hepatocytes and intestinal cells. 3,3'-diindolylmethane 25-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 25429094-3 2015 Clarithromycin is an inhibitor of CYP3A4, whereas azithromycin is not. Clarithromycin 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 25542144-3 2015 Here, we studied whether 3,3"-diindolylmethane (DIM), a natural health supplement, could induce hPXR-mediated regulation of CYP3A4 and MDR1 in human hepatocytes and intestinal cells. 3,3'-diindolylmethane 48-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 25542144-8 2015 The inductive effects of DIM on CYP3A4 and MDR1 expression caution the use of DIM in conjunction with other medications metabolized and transported via CYP3A4 and MDR1, respectively. 3,3'-diindolylmethane 25-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 25542144-8 2015 The inductive effects of DIM on CYP3A4 and MDR1 expression caution the use of DIM in conjunction with other medications metabolized and transported via CYP3A4 and MDR1, respectively. 3,3'-diindolylmethane 25-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 25542144-8 2015 The inductive effects of DIM on CYP3A4 and MDR1 expression caution the use of DIM in conjunction with other medications metabolized and transported via CYP3A4 and MDR1, respectively. 3,3'-diindolylmethane 78-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 25542144-8 2015 The inductive effects of DIM on CYP3A4 and MDR1 expression caution the use of DIM in conjunction with other medications metabolized and transported via CYP3A4 and MDR1, respectively. 3,3'-diindolylmethane 78-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 25451053-5 2015 In a 3-day monotherapy study with HCV genotype 1-infected patients, ABT-450 was coadministered with ritonavir, a cytochrome P450 3A4 inhibitor shown previously to markedly increase peak, trough, and overall drug exposures of ABT-450. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 68-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-132 25451053-5 2015 In a 3-day monotherapy study with HCV genotype 1-infected patients, ABT-450 was coadministered with ritonavir, a cytochrome P450 3A4 inhibitor shown previously to markedly increase peak, trough, and overall drug exposures of ABT-450. Ritonavir 100-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-132 25661339-2 2015 It was reported that telaprevir is a substrate of P-glycoprotein (ABCB1) and cytochrome P450 3A4. telaprevir 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-96 25512422-11 2015 Strong inducers of the cytochrome P450 isoenzyme CYP3A4 should be avoided when considering the use of bedaquiline. bedaquiline 102-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 26225230-5 2015 Simulated clearance estimates with a sirolimus physiologically based pharmacokinetic model that included CYP3A4/5/7 and CYP2C8 maturation profiles were in close agreement with observed in vivo clearance values. Sirolimus 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 25438721-3 2015 Armodafinil and the mood stabilizer carbamazepine are both inducers of and substrates for cytochrome P450 (CYP3A4). Modafinil 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 25438721-3 2015 Armodafinil and the mood stabilizer carbamazepine are both inducers of and substrates for cytochrome P450 (CYP3A4). Carbamazepine 36-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 25438721-15 2015 IMPLICATIONS: Systemic exposure to both carbamazepine and armodafinil was reduced after pretreatment with the other drug; systemic exposure to the metabolites of each drug, which are formed via CYP3A4, was increased. Modafinil 58-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 25052959-3 2015 HS-23 slightly inhibited CYP2A6, CYP2B6, CYP2C9, CYP2C19, and CYP3A4 enzyme activities in human liver microsomes with IC50 values of 80.6, 160.7, 169.5, 85.4, and 76.6 mug/mL, respectively. hs-23 0-5 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 25670523-2 2015 A ruxolitinib physiologically based pharmacokinetic model was constructed using all baseline PK data in healthy subjects, and verified by retrospective predictions of observed drug-drug interactions with rifampin (a potent CYP3A4 inducer), ketoconazole (a potent CYP3A4 reversible inhibitor) and erythromycin (a moderate time-dependent inhibitor of CYP3A4). ruxolitinib 2-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 223-229 25670523-2 2015 A ruxolitinib physiologically based pharmacokinetic model was constructed using all baseline PK data in healthy subjects, and verified by retrospective predictions of observed drug-drug interactions with rifampin (a potent CYP3A4 inducer), ketoconazole (a potent CYP3A4 reversible inhibitor) and erythromycin (a moderate time-dependent inhibitor of CYP3A4). ruxolitinib 2-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 263-269 25670523-2 2015 A ruxolitinib physiologically based pharmacokinetic model was constructed using all baseline PK data in healthy subjects, and verified by retrospective predictions of observed drug-drug interactions with rifampin (a potent CYP3A4 inducer), ketoconazole (a potent CYP3A4 reversible inhibitor) and erythromycin (a moderate time-dependent inhibitor of CYP3A4). ruxolitinib 2-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 263-269 25670523-3 2015 The model prospectively predicts that 100-200 mg daily dose of fluconazole, a dual inhibitor of CYP3A4 and 2C9, would increase ruxolitinib plasma concentration area under the curve by ~two-fold, and that as a perpetrator, ruxolitinib is highly unlikely to have any discernible effect on digoxin, a sensitive P-glycoprotein substrate. Fluconazole 63-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-110 25670523-3 2015 The model prospectively predicts that 100-200 mg daily dose of fluconazole, a dual inhibitor of CYP3A4 and 2C9, would increase ruxolitinib plasma concentration area under the curve by ~two-fold, and that as a perpetrator, ruxolitinib is highly unlikely to have any discernible effect on digoxin, a sensitive P-glycoprotein substrate. ruxolitinib 127-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-110 25670523-3 2015 The model prospectively predicts that 100-200 mg daily dose of fluconazole, a dual inhibitor of CYP3A4 and 2C9, would increase ruxolitinib plasma concentration area under the curve by ~two-fold, and that as a perpetrator, ruxolitinib is highly unlikely to have any discernible effect on digoxin, a sensitive P-glycoprotein substrate. Digoxin 287-294 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-110 25324279-7 2015 The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered. Simvastatin 47-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 25324279-7 2015 The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered. Amiodarone 106-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 25324279-7 2015 The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered. MDEA 115-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 25480923-7 2015 Enzyme activities of CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, and CYP3A4 were reduced upon 48-72 hours exposure to IL-6 in PHH and HepaRG. 4,5,6,7-tetrachlorophthalide 123-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 25480923-7 2015 Enzyme activities of CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, and CYP3A4 were reduced upon 48-72 hours exposure to IL-6 in PHH and HepaRG. heparg 131-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 25324279-7 2015 The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered. Amiodarone 207-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 25324279-7 2015 The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered. MDEA 268-272 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 25639891-5 2015 Lapatinib exhibits both covalent binding to the apoprotein and formation of a metabolite-intermediate complex in an enzyme-selective manner (CYP3A4 versus CYP3A5), each with different reactive metabolites. Lapatinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 25324279-7 2015 The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered. Warfarin 308-316 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 25324279-7 2015 The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered. Amiodarone 207-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 25760537-4 2015 Formation of alpha-hydroxytriazolam catalyzed by CYP3A was decreased by IL-1beta and IL-6. alpha-hydroxytriazolam 13-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 25324279-7 2015 The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered. MDEA 268-272 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 25417855-1 2015 WHAT IS KNOWN AND OBJECTIVE: Azole antifungals, prescribed prophylactically to avoid severe infections in immunosuppressed organ transplant recipients, can interact with drug substrates of CYP3A4. Azoles 29-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 25159194-4 2015 Oxidative metabolism of pomalidomide was predominately mediated by CYP1A2 and CYP3A4, and pomalidomide was shown to be a P-gp substrate. pomalidomide 24-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 25417855-6 2015 WHAT IS NEW AND CONCLUSION: Orally administered voriconazole inhibits intestinal and hepatic cytochrome P450-3A4 activity and thereby reduces everolimus metabolism. Voriconazole 48-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-112 25159194-5 2015 In healthy males, co-administration of oral (4 mg) pomalidomide with ketoconazole (CYP3A/P-gp inhibitor) or carbamazepine (CYP3A/P-gp inducer) did not result in clinically relevant changes in pomalidomide exposure. Ketoconazole 69-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 25159194-9 2015 Pomalidomide dose should be reduced by 50% if co-administered with strong CYP1A2 inhibitors and strong CYP3A/P-gp inhibitors. pomalidomide 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 25535031-5 2015 In contrast, desmethyl bosentan induced mRNA expression of cytochrome P450 3A4 (CYP3A4, about 6-fold at 50 muM), ABCB1 (P-gp, about 4.5-fold at 50 muM), and ABCG2 (breast cancer resistance protein, about 2-fold at 50 muM), whereas CYP2C19, ABCB11, and ABCC2 (multidrug resistance-associated protein 2) were not induced in LS180 cells. Desmethyl Bosentan 13-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-78 24898833-2 2015 Data are scarce for this subgroup of patients; however, data for the interaction of antiepileptic drugs with the pituitary axis have shown that chronic use of many antiepileptic drugs, such as carbamazepine, oxcarbazepine, and topiramate, enhances hepatic cytochrome P450 3A4 (CYP3A4) activity, and can decrease serum concentrations of sex hormones. Carbamazepine 193-206 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 256-275 24898833-2 2015 Data are scarce for this subgroup of patients; however, data for the interaction of antiepileptic drugs with the pituitary axis have shown that chronic use of many antiepileptic drugs, such as carbamazepine, oxcarbazepine, and topiramate, enhances hepatic cytochrome P450 3A4 (CYP3A4) activity, and can decrease serum concentrations of sex hormones. Carbamazepine 193-206 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 277-283 24898833-2 2015 Data are scarce for this subgroup of patients; however, data for the interaction of antiepileptic drugs with the pituitary axis have shown that chronic use of many antiepileptic drugs, such as carbamazepine, oxcarbazepine, and topiramate, enhances hepatic cytochrome P450 3A4 (CYP3A4) activity, and can decrease serum concentrations of sex hormones. Oxcarbazepine 208-221 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 256-275 24898833-2 2015 Data are scarce for this subgroup of patients; however, data for the interaction of antiepileptic drugs with the pituitary axis have shown that chronic use of many antiepileptic drugs, such as carbamazepine, oxcarbazepine, and topiramate, enhances hepatic cytochrome P450 3A4 (CYP3A4) activity, and can decrease serum concentrations of sex hormones. Oxcarbazepine 208-221 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 277-283 24898833-2 2015 Data are scarce for this subgroup of patients; however, data for the interaction of antiepileptic drugs with the pituitary axis have shown that chronic use of many antiepileptic drugs, such as carbamazepine, oxcarbazepine, and topiramate, enhances hepatic cytochrome P450 3A4 (CYP3A4) activity, and can decrease serum concentrations of sex hormones. Topiramate 227-237 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 256-275 24898833-2 2015 Data are scarce for this subgroup of patients; however, data for the interaction of antiepileptic drugs with the pituitary axis have shown that chronic use of many antiepileptic drugs, such as carbamazepine, oxcarbazepine, and topiramate, enhances hepatic cytochrome P450 3A4 (CYP3A4) activity, and can decrease serum concentrations of sex hormones. Topiramate 227-237 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 277-283 25727956-5 2015 Next, concentration dependent inhibition of liver microsomal CYP3A4 down to 42% (at rocuronium concentration 189 muM) was found. Rocuronium 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 25727956-6 2015 This effect has been confirmed with two CYP3A4 substrates, testosterone (formation of 6beta-hydroxytestosterone) and diazepam (temazepam formation). Testosterone 59-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 25727956-6 2015 This effect has been confirmed with two CYP3A4 substrates, testosterone (formation of 6beta-hydroxytestosterone) and diazepam (temazepam formation). 6 beta-hydroxytestosterone 86-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 25727956-6 2015 This effect has been confirmed with two CYP3A4 substrates, testosterone (formation of 6beta-hydroxytestosterone) and diazepam (temazepam formation). Temazepam 127-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 25727956-11 2015 The results open a possibility that interactions of rocuronium with drugs metabolized by CYP3A4 (and possibly also CYP2C19) may be observed. Rocuronium 52-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 25535031-5 2015 In contrast, desmethyl bosentan induced mRNA expression of cytochrome P450 3A4 (CYP3A4, about 6-fold at 50 muM), ABCB1 (P-gp, about 4.5-fold at 50 muM), and ABCG2 (breast cancer resistance protein, about 2-fold at 50 muM), whereas CYP2C19, ABCB11, and ABCC2 (multidrug resistance-associated protein 2) were not induced in LS180 cells. Desmethyl Bosentan 13-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 25145883-4 2015 HR strongly inhibited CYP1A2 and moderately inhibited CYP2C19, CYP2D6, and CYP3A4 (testosterone) but not CYP2A6, CYP2B6, CYP2C8, CYP2C9, and CYP3A4 (midazolam). Testosterone 83-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 25004135-3 2015 METHODS: Midazolam plasma concentrations during CYP3A baseline (n = 93), inhibition (n = 40), and induction/activation (n = 33) were obtained from 7 studies in healthy adults. Midazolam 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 25004135-11 2015 CONCLUSIONS: During CYP3A induction/activation, but not baseline or inhibition, midazolam partial AUC0-1, AUC0-2, and AUC0-4 reliably estimated systemic CL and consequently hepatic CYP3A activity in healthy adults. Midazolam 80-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-186 25545162-0 2015 Concurrent cooperativity and substrate inhibition in the epoxidation of carbamazepine by cytochrome P450 3A4 active site mutants inspired by molecular dynamics simulations. Carbamazepine 72-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-108 25183402-11 2015 Structure-activity relationship analysis showed that CYP2B6 and CYP3A4 inducers are bulky lipophilic molecules with a higher number of heavy atoms and a lower number of hydrogen bond donors. Hydrogen 169-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 25545162-1 2015 Cytochrome P450 3A4 (CYP3A4) is the major human P450 responsible for the metabolism of carbamazepine (CBZ). Carbamazepine 87-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 25545162-1 2015 Cytochrome P450 3A4 (CYP3A4) is the major human P450 responsible for the metabolism of carbamazepine (CBZ). Carbamazepine 87-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 25545162-1 2015 Cytochrome P450 3A4 (CYP3A4) is the major human P450 responsible for the metabolism of carbamazepine (CBZ). Carbamazepine 102-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 25545162-1 2015 Cytochrome P450 3A4 (CYP3A4) is the major human P450 responsible for the metabolism of carbamazepine (CBZ). Carbamazepine 102-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 25545162-2 2015 To explore the mechanisms of interactions of CYP3A4 with this anticonvulsive drug, we carried out multiple molecular dynamics (MD) simulations, starting with the complex of CYP3A4 manually docked with CBZ. Carbamazepine 201-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 25444842-5 2015 A review of the current literature on relative bioavailability (Frel) between CR and IR formulations of CYP3A substrates was conducted. Chromium 78-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-109 25545162-3 2015 On the basis of these simulations, we engineered CYP3A4 mutants I369F, I369L, A370V, and A370L, in which the productive binding orientation was expected to be stabilized, thus leading to increased turnover of CBZ to the 10,11-epoxide product. Carbamazepine 209-212 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 25444842-7 2015 From the literature review, only three CYP3A4 substrates showed higher Frel when formulated as CR. Chromium 95-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 25545162-3 2015 On the basis of these simulations, we engineered CYP3A4 mutants I369F, I369L, A370V, and A370L, in which the productive binding orientation was expected to be stabilized, thus leading to increased turnover of CBZ to the 10,11-epoxide product. 10,11-epoxide 220-233 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 25545162-5 2015 Evaluation of the kinetics profiles of CBZ epoxidation demonstrate that CYP3A4-containing bacterial membranes (bactosomes) as well as purified CYP3A4 (wild-type and mutants I369L/F) exhibit substrate inhibition in reconstituted systems. Carbamazepine 39-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 25545162-7 2015 MD simulations with two to four CBZ molecules provide evidence that the substrate-binding pocket of CYP3A4 can accommodate more than one molecule of CBZ. Carbamazepine 32-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 25545162-7 2015 MD simulations with two to four CBZ molecules provide evidence that the substrate-binding pocket of CYP3A4 can accommodate more than one molecule of CBZ. Carbamazepine 149-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 25545162-8 2015 Analysis of the kinetics profiles of CBZ metabolism with a model that combines the formalism of the Hill equation with an allowance for substrate inhibition demonstrates that the mechanism of interactions of CBZ with CYP3A4 involves multiple substrate-binding events (most likely three). Carbamazepine 37-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-223 25545162-8 2015 Analysis of the kinetics profiles of CBZ metabolism with a model that combines the formalism of the Hill equation with an allowance for substrate inhibition demonstrates that the mechanism of interactions of CBZ with CYP3A4 involves multiple substrate-binding events (most likely three). Carbamazepine 208-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-223 25489883-3 2015 It has been shown that cytochrome P450 (CYP) 3A4 has a major role in SRF biotransformation to the pharmacologically active N-oxide (SRF-Nox) and two other metabolites. n-oxide 123-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-48 25462116-7 2015 CYP2C9 and CYP3A4, which metabolize DF to p-benzoquinone imines, were tested to investigate the applicability of human P450s. 1,4-benzoquinoneimine 42-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 25489883-3 2015 It has been shown that cytochrome P450 (CYP) 3A4 has a major role in SRF biotransformation to the pharmacologically active N-oxide (SRF-Nox) and two other metabolites. srf-nox 132-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-48 25398452-0 2015 Whole-exome sequencing reveals defective CYP3A4 variants predictive of paclitaxel dose-limiting neuropathy. Paclitaxel 71-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 25398452-9 2015 Relative to CYP3A4 wild-type patients, those carrying CYP3A4 defective variants had more severe neuropathy (2- and 1.3-fold higher risk of neuropathy for loss-of-function and missense variants, respectively, P = 0.045) and higher probability of neuropathy-induced paclitaxel treatment modifications (7- and 3-fold higher risk for loss-of-function and missense variants, respectively, P = 5.9 x 10(-5)). Paclitaxel 264-274 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 25398452-11 2015 CYP3A4 defective variants may provide a basis for paclitaxel treatment individualization. Paclitaxel 50-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25499431-3 2015 These studies show that donepezil is a weak inhibitor of CYP3A4 (IC50=54.68+-1.00muM) whereas the reference agent ketoconazole exhibited potent inhibition (CYP3A4 IC50=0.20+-0.01muM). Donepezil 24-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 25499431-3 2015 These studies show that donepezil is a weak inhibitor of CYP3A4 (IC50=54.68+-1.00muM) whereas the reference agent ketoconazole exhibited potent inhibition (CYP3A4 IC50=0.20+-0.01muM). Donepezil 24-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 25499431-0 2015 Investigating the binding interactions of the anti-Alzheimer"s drug donepezil with CYP3A4 and P-glycoprotein. Donepezil 68-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 25499431-3 2015 These studies show that donepezil is a weak inhibitor of CYP3A4 (IC50=54.68+-1.00muM) whereas the reference agent ketoconazole exhibited potent inhibition (CYP3A4 IC50=0.20+-0.01muM). Ketoconazole 114-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 25499431-5 2015 At higher concentrations, donepezil exhibited significant inhibition of CYP3A4 (69%, 84% and 87% inhibition at 100, 250 and 500muM, respectively). Donepezil 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 25499431-1 2015 The anti-Alzheimer"s agent donepezil is known to bind to the hepatic enzyme CYP3A4, but its relationship with the efflux transporter P-glycoprotein (P-gp) is not as well elucidated. Donepezil 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 25499431-8 2015 The molecular docking studies show that the 5,6-dimethoxyindan-1-one moiety of donepezil was oriented closer to the heme center in CYP3A4 whereas in the P-gp binding site, the protonated benzylpiperidine pharmacophore of donepezil played a major role in its binding ability. 5,6-dimethoxyindan-1-one 44-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 25499431-2 2015 We conducted in vitro inhibition studies of donepezil using human recombinant CYP3A4 and P-gp. Donepezil 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 25499431-8 2015 The molecular docking studies show that the 5,6-dimethoxyindan-1-one moiety of donepezil was oriented closer to the heme center in CYP3A4 whereas in the P-gp binding site, the protonated benzylpiperidine pharmacophore of donepezil played a major role in its binding ability. Donepezil 79-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 25499431-8 2015 The molecular docking studies show that the 5,6-dimethoxyindan-1-one moiety of donepezil was oriented closer to the heme center in CYP3A4 whereas in the P-gp binding site, the protonated benzylpiperidine pharmacophore of donepezil played a major role in its binding ability. Heme 116-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 25499431-9 2015 Energy parameters indicate that donepezil complex with both CYP3A4 and P-gp was less stable (CDOCKER energies=-15.05 and -4.91kcal/mol, respectively) compared to the ketoconazole-CYP3A4 and P-gp complex (CDOCKER energies=-41.89 and -20.03kcal/mol, respectively). Donepezil 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 25499431-9 2015 Energy parameters indicate that donepezil complex with both CYP3A4 and P-gp was less stable (CDOCKER energies=-15.05 and -4.91kcal/mol, respectively) compared to the ketoconazole-CYP3A4 and P-gp complex (CDOCKER energies=-41.89 and -20.03kcal/mol, respectively). Donepezil 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 25499431-9 2015 Energy parameters indicate that donepezil complex with both CYP3A4 and P-gp was less stable (CDOCKER energies=-15.05 and -4.91kcal/mol, respectively) compared to the ketoconazole-CYP3A4 and P-gp complex (CDOCKER energies=-41.89 and -20.03kcal/mol, respectively). Ketoconazole 166-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 25636872-7 2015 Moreover, the presence of hydroxyl group at C-2 position of triterpenic acid in MA compared with oleanolic acid could magnify its competitive inhibition on human CYP3A4 activity. triterpenic acid 60-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 25636872-7 2015 Moreover, the presence of hydroxyl group at C-2 position of triterpenic acid in MA compared with oleanolic acid could magnify its competitive inhibition on human CYP3A4 activity. Oleanolic Acid 97-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 26736983-1 2015 The mechanism of drug-drug interaction between saquinavir, a protease inhibitor used effectively for HIV/AIDS treatment, and itraconazole, an azole antifungal agent, is hypothesized to involve competitive inhibition at CYP3A4 enzyme, an important drug metabolizing enzyme in humans. Saquinavir 47-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 26736983-1 2015 The mechanism of drug-drug interaction between saquinavir, a protease inhibitor used effectively for HIV/AIDS treatment, and itraconazole, an azole antifungal agent, is hypothesized to involve competitive inhibition at CYP3A4 enzyme, an important drug metabolizing enzyme in humans. Itraconazole 125-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 25634447-1 2015 The chemotherapeutic agent vincristine, used for treatment of acute lymphoblastic leukemia is metabolized preferentially by polymorphic cytochrome P450 3A5 (CYP3A5) with higher clearance rate than cytochrome P450 3A4 (CYP3A4). Vincristine 27-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-216 26736983-1 2015 The mechanism of drug-drug interaction between saquinavir, a protease inhibitor used effectively for HIV/AIDS treatment, and itraconazole, an azole antifungal agent, is hypothesized to involve competitive inhibition at CYP3A4 enzyme, an important drug metabolizing enzyme in humans. Azoles 132-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 25634447-1 2015 The chemotherapeutic agent vincristine, used for treatment of acute lymphoblastic leukemia is metabolized preferentially by polymorphic cytochrome P450 3A5 (CYP3A5) with higher clearance rate than cytochrome P450 3A4 (CYP3A4). Vincristine 27-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 218-224 25634447-3 2015 We modeled the structure of CYP3A5 and its interaction with vincristine, compared with CYP3A4-vincristine complex using molecular docking and simulation studies. Vincristine 94-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 25634447-6 2015 This leads to higher binding affinity of vincristine towards CYP3A5 compared to CYP3A4 and explains the preferential metabolism of vincristine by CYP3A5. Vincristine 41-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 25634447-6 2015 This leads to higher binding affinity of vincristine towards CYP3A5 compared to CYP3A4 and explains the preferential metabolism of vincristine by CYP3A5. Vincristine 131-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 26002734-7 2015 In the second example, lithocholic acid (3alpha-hydroxy-5beta-cholan-24-oic acid), an endogenous bile acid, served as a substrate for human CYP3A4 and yielded five different metabolites via aliphatic hydroxylation and dehydrogenation reactions. Lithocholic Acid 23-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 26002734-7 2015 In the second example, lithocholic acid (3alpha-hydroxy-5beta-cholan-24-oic acid), an endogenous bile acid, served as a substrate for human CYP3A4 and yielded five different metabolites via aliphatic hydroxylation and dehydrogenation reactions. Bile Acids and Salts 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 26736983-2 2015 The resulting interaction between these CYP3A4 substrates can be utilized clinically as a pharmacokinetic booster for prolonging saquinavir dosing regimen and/or decreasing saquinavir dose requirement in HIV/AIDS patients. Saquinavir 129-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 26736983-2 2015 The resulting interaction between these CYP3A4 substrates can be utilized clinically as a pharmacokinetic booster for prolonging saquinavir dosing regimen and/or decreasing saquinavir dose requirement in HIV/AIDS patients. Saquinavir 173-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 26736984-1 2015 BACKGROUND: Concomitant use of simvastatin, a HMG-CoA reductase inhibitor, with a potent CYP3A4 inhibitor, itraconazole, can result in a serious drug-drug interaction induced severe adverse event, rhabdomyolysis. Simvastatin 31-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 26736984-1 2015 BACKGROUND: Concomitant use of simvastatin, a HMG-CoA reductase inhibitor, with a potent CYP3A4 inhibitor, itraconazole, can result in a serious drug-drug interaction induced severe adverse event, rhabdomyolysis. Itraconazole 107-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 25845867-3 2015 A two-way pharmacokinetic interaction was hypothesized for KAE609 and PPQ, as both drugs are CYP3A4 substrates and inhibitors. NITD 609 59-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 25470746-5 2015 In addition, the effect of doravirine (120 mg for 14 days) on single-dose pharmacokinetics of the CYP3A substrate midazolam was evaluated (10 subjects). Midazolam 114-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 25385099-2 2015 Faldaprevir is known to inhibit P-glycoprotein, CYP3A4, and UDP-glucuronosyltransferase 1A1. faldaprevir 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 25845867-3 2015 A two-way pharmacokinetic interaction was hypothesized for KAE609 and PPQ, as both drugs are CYP3A4 substrates and inhibitors. piperaquine 70-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 25845873-3 2015 From the interaction between atazanavir and DTG via CYP3A4 and UGT1A1 and placental efflux transporter inhibition and considering the infant"s probable enzymatic immaturity, the DTG elimination half-life was estimated to be 4-fold longer in neonates than in adults. Atazanavir Sulfate 29-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 25845873-3 2015 From the interaction between atazanavir and DTG via CYP3A4 and UGT1A1 and placental efflux transporter inhibition and considering the infant"s probable enzymatic immaturity, the DTG elimination half-life was estimated to be 4-fold longer in neonates than in adults. dolutegravir 44-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 25744459-1 2015 The aim of this study was to characterize the kinetics of metabolite formation of the phosphodiesterase type-5 (PDE5) inhibitors sildenafil and tadalafil by CYP3A4, CYP3A5, and CYP3A7 isoforms. Sildenafil Citrate 129-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 25069801-6 2015 AITC-mediated reduction in the transcriptional activity of PXR and CAR correlated well with the suppression of CYP3A4 and CYP2B6 expression in HepG2 cells, which reflected the reduced catalytic activities of both of these genes following AITC treatment in differentiated HepaRG cells. allyl isothiocyanate 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 25744459-1 2015 The aim of this study was to characterize the kinetics of metabolite formation of the phosphodiesterase type-5 (PDE5) inhibitors sildenafil and tadalafil by CYP3A4, CYP3A5, and CYP3A7 isoforms. Tadalafil 144-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 25747989-4 2015 Some in vitro studies have suggested that simvastatin could attenuate clopidogrel activation via inhibiting CYP3A activity. Simvastatin 42-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 25747989-4 2015 Some in vitro studies have suggested that simvastatin could attenuate clopidogrel activation via inhibiting CYP3A activity. Clopidogrel 70-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 25744459-2 2015 The formations of N-desmethyl sildenafil and desmethylene tadalafil were examined using CYP3A supersomes co-expressing human P450 oxidoreductase and cytochrome b5. Sildenafil Citrate 18-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-93 25744459-3 2015 Both sildenafil N-demethylation and tadalafil demethylenation were catalyzed by CYP3A4, CYP3A5, and to a lesser extent by CYP3A7. Sildenafil Citrate 5-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 25747989-11 2015 In summary, the inhibitory effect of simvastatin on the hydrolysis of clopidogrel and its principal metabolites may have offset the influence of simvastatin-mediated inhibition of CYP3A, and permitted the unaltered formation of the clopidogrel active metabolite. Simvastatin 37-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-185 25744459-3 2015 Both sildenafil N-demethylation and tadalafil demethylenation were catalyzed by CYP3A4, CYP3A5, and to a lesser extent by CYP3A7. Tadalafil 36-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 25747989-11 2015 In summary, the inhibitory effect of simvastatin on the hydrolysis of clopidogrel and its principal metabolites may have offset the influence of simvastatin-mediated inhibition of CYP3A, and permitted the unaltered formation of the clopidogrel active metabolite. Clopidogrel 70-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-185 25744459-7 2015 The intrinsic clearance (CLint) values of reactions 1 and 2 for sildenafil N-demethylation were 0.733 and 0.033 microL/min/pmol P450 for CYP3A4, 0.788 and 0.019 microL/min/pmol P450 for CYP3A5, and 0.079 and 0.004 microL/min/pmol P450 for CYP3A7, respectively. Sildenafil Citrate 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 25747989-11 2015 In summary, the inhibitory effect of simvastatin on the hydrolysis of clopidogrel and its principal metabolites may have offset the influence of simvastatin-mediated inhibition of CYP3A, and permitted the unaltered formation of the clopidogrel active metabolite. Simvastatin 145-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-185 25744459-8 2015 The CLint values of reactions 1 and 2 for tadalafil demethylenation were 0.187 and 0.014 microL/min/pmol P450 for CYP3A4, 0.050 and <0.001 microL/min/pmol P450 for CYP3A5, and 0.004 and <0.001 microL/min/pmol P450 for CYP3A7, respectively. Tadalafil 42-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 25883814-5 2015 We describe a particularly severe case of rhabdomyolysis after the introduction of ciprofloxacin, a weak CYP3A4 inhibitor, in a patient who previously tolerated the simvastatin-amlodipine combination. Ciprofloxacin 83-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 26094899-9 2015 These results suggest that clofazimine and prothionamide are likely to cause clinically relevant DDIs when co-administered with products metabolized by CYP3A4 and CYP2B6, respectively. Clofazimine 27-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 26094899-9 2015 These results suggest that clofazimine and prothionamide are likely to cause clinically relevant DDIs when co-administered with products metabolized by CYP3A4 and CYP2B6, respectively. Prothionamide 43-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 26094899-10 2015 Isoniazid and rifapentine may cause DDIs with drugs metabolized by CYP3A4. Isoniazid 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 26094899-10 2015 Isoniazid and rifapentine may cause DDIs with drugs metabolized by CYP3A4. rifapentine 14-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 25883814-5 2015 We describe a particularly severe case of rhabdomyolysis after the introduction of ciprofloxacin, a weak CYP3A4 inhibitor, in a patient who previously tolerated the simvastatin-amlodipine combination. simvastatin-amlodipine 165-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 27128004-10 2015 Hence, strong CYP3A4 inducers should be avoided or used with careful evaluation of clinical efficacy when administered with abiraterone acetate. Abiraterone Acetate 124-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 25391550-1 2015 Cytochrome P450 (CYP) 3A4 has been considered to be the most important enzyme system for metabolism of lopinavir/ritonavir (LPV/r), a widely used HIV protease inhibitor (PI) recommended during pregnancy. Lopinavir 103-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-25 25391550-1 2015 Cytochrome P450 (CYP) 3A4 has been considered to be the most important enzyme system for metabolism of lopinavir/ritonavir (LPV/r), a widely used HIV protease inhibitor (PI) recommended during pregnancy. Ritonavir 113-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-25 25408262-11 2015 An additional analysis was performed to characterize the association between the cytochrome P450 (CYP) 1A1, CYP1A2 and CYP3A4 genotypes and the erlotinib pharmacokinetic parameters. Erlotinib Hydrochloride 144-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 27128001-0 2015 The effects of CYP3A4 induction and inhibition on the pharmacokinetics of alisporivir in humans. alisporivir 74-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 26423040-2 2015 So as to avoid mechanism-based inactivation (MBI) of CYP3A4, 1,3-benzodioxol ring of the lead compound was modified. 1,3-benzodioxol 61-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 25968921-1 2015 Tacrolimus is a calcineurin inhibitor primarily metabolized by CYP3A4 and secondarily by CYP3A5. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 27128001-1 2015 In vitro data suggest that alisporivir is a substrate and inhibitor of CYP3A4 and P-gp. alisporivir 27-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 27128001-2 2015 Hence, the potential for drug-drug interactions when alisporivir is co-administered with CYP3A4 and/or P-gp inhibitors such as ketoconazole, azithromycin and CYP3A4 inducers such as rifampin were evaluated in three separate clinical studies. alisporivir 53-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 27128001-2 2015 Hence, the potential for drug-drug interactions when alisporivir is co-administered with CYP3A4 and/or P-gp inhibitors such as ketoconazole, azithromycin and CYP3A4 inducers such as rifampin were evaluated in three separate clinical studies. alisporivir 53-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 27128001-2 2015 Hence, the potential for drug-drug interactions when alisporivir is co-administered with CYP3A4 and/or P-gp inhibitors such as ketoconazole, azithromycin and CYP3A4 inducers such as rifampin were evaluated in three separate clinical studies. Rifampin 182-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 27128001-3 2015 Co-administration with ketoconazole (a strong CYP3A4 inhibitor) increased the Cmax , AUC and terminal elimination half-life of alisporivir by approximately two-, eight- ,and threefold, respectively. Ketoconazole 23-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 27128001-3 2015 Co-administration with ketoconazole (a strong CYP3A4 inhibitor) increased the Cmax , AUC and terminal elimination half-life of alisporivir by approximately two-, eight- ,and threefold, respectively. alisporivir 127-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 27128001-5 2015 Rifampin (a CYP3A4 inducer) caused an approximate 90% reduction in alisporivir Cmax and AUC and a fourfold reduction in alisporivir terminal elimination half-life. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 27128001-5 2015 Rifampin (a CYP3A4 inducer) caused an approximate 90% reduction in alisporivir Cmax and AUC and a fourfold reduction in alisporivir terminal elimination half-life. alisporivir 67-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 27128001-5 2015 Rifampin (a CYP3A4 inducer) caused an approximate 90% reduction in alisporivir Cmax and AUC and a fourfold reduction in alisporivir terminal elimination half-life. alisporivir 120-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 27128001-6 2015 Alisporivir as an inhibitor of CYP3A4 caused a 39% increase in azithromycin exposure. alisporivir 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 27128001-6 2015 Alisporivir as an inhibitor of CYP3A4 caused a 39% increase in azithromycin exposure. Azithromycin 63-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 27128001-7 2015 The results from these studies establish alisporivir as a sensitive CYP3A4 substrate in vivo. alisporivir 41-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 27128001-8 2015 Consequently, co-administered potent CYP3A4 inhibitors and inducers are likely to cause clinically significant changes in the exposure to alisporivir. alisporivir 138-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 25968921-8 2015 Increase of tacrolimus trough concentrations is due to the inhibition of CYP3A4. Tacrolimus 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 25600201-7 2015 The results showed significant time-dependent inhibition of tested samples on CYP3A4 with crude methanol (39KC), fractions 45A, 45B and 45D given IC50 fold decrease of 3.29, 2.26, 1.91 and 1.49, respective. Methanol 96-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 25600204-6 2015 Newly designed 96-well hanging-drop plates were capable of maintaining human CYP3A-dependent midazolam hydroxylation activities for up to 4 days using only 10% of the recommended initial 7.2x10(4) cells per well. Midazolam 93-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 25975016-2 2015 Ibrutinib (Imbruvica) is metabolized in the liver mainly by the isoenzyme CYP3A4 and to a minor extent by CYP2D6. ibrutinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 25975016-2 2015 Ibrutinib (Imbruvica) is metabolized in the liver mainly by the isoenzyme CYP3A4 and to a minor extent by CYP2D6. ibrutinib 11-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 25600201-11 2015 At least one phytoconstituent in the crude methanol extract of Kalanchoe crenata is a reversible and time-dependent inhibitor of CYP3A4. Methanol 43-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 25600204-2 2015 To evaluate time-dependent cytochrome P450 induction precisely, induction of CYP1A2, CYP2B6, and CYP3A4 mRNA was confirmed (>2-fold) by the treatment with omeprazole, phenobarbital, and rifampicin, respectively, for 24 or 48 h on day 3 from the start of culture. Omeprazole 158-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 25600204-2 2015 To evaluate time-dependent cytochrome P450 induction precisely, induction of CYP1A2, CYP2B6, and CYP3A4 mRNA was confirmed (>2-fold) by the treatment with omeprazole, phenobarbital, and rifampicin, respectively, for 24 or 48 h on day 3 from the start of culture. Phenobarbital 170-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 25495693-7 2015 Perampanel is extensively metabolized (>90%) in the liver, primarily by cytochrome P450 (CYP) 3A4, to various pharmacologically inactive metabolites. perampanel 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-100 26635974-4 2015 In search of finding the protein responsible for the accumulation of vorozole in the liver, fluorometric high-throughput screening assays were used to test the inhibitory capability of vorozole and letrozole on a series of liver cytochrome P450s (CYP1A1, CYP1A2, CYP2A6, and CYP3A4). vorozole 69-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 275-281 26635974-5 2015 It was determined that vorozole is a potent inhibitor of CYP1A1 (IC50 = 0.469 muM) and a moderate inhibitor of CYP2A6 and CYP3A4 (IC50 = 24.4 and 98.1 muM, resp.). vorozole 23-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 26635974-6 2015 Letrozole is only a moderate inhibitor of CYP1A1 and CYP2A6 (IC50 = 69.8 and 106 muM) and a very weak inhibitor of CYP3A4 (<10% inhibition at 1 mM). Letrozole 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 26635974-7 2015 Since CYP3A4 makes up the majority of the CYP content found in the human liver, and vorozole inhibits it moderately well but letrozole does not, CYP3A4 is a good candidate for the protein that [(11)C]-vorozole is binding to in the liver. vorozole 201-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 26635974-7 2015 Since CYP3A4 makes up the majority of the CYP content found in the human liver, and vorozole inhibits it moderately well but letrozole does not, CYP3A4 is a good candidate for the protein that [(11)C]-vorozole is binding to in the liver. vorozole 201-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 26089940-0 2015 Comparison of Paeoniflorin and Albiflorin on Human CYP3A4 and CYP2D6. peoniflorin 14-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 26089940-0 2015 Comparison of Paeoniflorin and Albiflorin on Human CYP3A4 and CYP2D6. albiflorin 31-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 26089940-3 2015 In order to explore the efficacy and safety of peony, effects of paeoniflorin and albiflorin (the principal components of peony) on cytochrome P450 (CYP) 3A4 and CYP2D6 were analyzed in human hepatoma HepG2 cells and evaluated from the level of recombinant CYP enzymes in vitro. albiflorin 82-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-157 26089940-4 2015 The findings indicated that albiflorin possessed stronger regulation on the mRNA expression of CYP3A4 and CYP2D6 than paeoniflorin. albiflorin 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 26089940-5 2015 For the protein level of CYP3A4, albiflorin showed significant induction or inhibition with the concentration increasing from 10(-7) M to 10(-5) M, but no remarkable variation was observed in paeoniflorin-treated group. albiflorin 33-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 26089940-6 2015 Enzyme activity assay implied that both paeoniflorin and albiflorin could regulate CYP3A4 and CYP2D6 with varying degrees. peoniflorin 40-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 26089940-6 2015 Enzyme activity assay implied that both paeoniflorin and albiflorin could regulate CYP3A4 and CYP2D6 with varying degrees. albiflorin 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 26626238-6 2015 Inhibitory effect on CYP3A4 activity by typical inhibitors (ketoconazole, hyperforin) and natural medicines (Cat"s Claw, Devil"s Claw, Feverfew, Peppermint Oil, Red Clover, and Siberian Eleuthero) were evaluated. Ketoconazole 60-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 26639694-6 2015 It is further metabolized by CYP3A4 to a tetrahydropyridine and then conjugated by glucuronidation and sulphation. Pyrrolidines 41-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 26639694-7 2015 Reduced haloperidol is back-oxidized to haloperidol by CYP3A4 and CYP2D6. Haloperidol 8-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 26639694-7 2015 Reduced haloperidol is back-oxidized to haloperidol by CYP3A4 and CYP2D6. Haloperidol 40-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 26639694-8 2015 Haloperidol is N-dealkylated by CYP3A4 and CYP2D6 to 4-chlorophenyl-4-hydroxypiperidine and p-fluorobenzoyl propionic acid. Haloperidol 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 26639694-8 2015 Haloperidol is N-dealkylated by CYP3A4 and CYP2D6 to 4-chlorophenyl-4-hydroxypiperidine and p-fluorobenzoyl propionic acid. 4-CHLOROPHENYL-4-HYDROXYPIPERIDINE 53-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 25877445-0 2015 Reversible, time-dependent inhibition of CYP3A-mediated metabolism of midazolam and tacrolimus by telaprevir in human liver microsomes. Midazolam 70-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 25877445-0 2015 Reversible, time-dependent inhibition of CYP3A-mediated metabolism of midazolam and tacrolimus by telaprevir in human liver microsomes. Tacrolimus 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 25327846-0 2015 Introduction of a nitrogen-containing side chain appended on C-10 of cethromycin leads to reduced CYP3A4 inhibition (WO2014049356A1). Nitrogen 18-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 25327846-0 2015 Introduction of a nitrogen-containing side chain appended on C-10 of cethromycin leads to reduced CYP3A4 inhibition (WO2014049356A1). cethromycin 69-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 25327846-4 2015 However, the 3"-dimethylamino group is readily metabolized to a nitroso group, which would inhibit CYP3A4, a very important metabolic enzyme responsible for nearly half of all marketed drugs. Dimethyl amidogen 16-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 26639694-8 2015 Haloperidol is N-dealkylated by CYP3A4 and CYP2D6 to 4-chlorophenyl-4-hydroxypiperidine and p-fluorobenzoyl propionic acid. p-fluorobenzoyl propionic acid 92-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 26639694-9 2015 The correlation between CYP2D6 and CYP3A4 activity and the rate of biotransformation of haloperidol was demonstrated in a number of studies on patients with schizophrenia [1, 2, 5]. Haloperidol 88-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 26639694-11 2015 OBJECTIVE: To estimate the correlation between CYP3A4 isoenzyme activity and the efficacy and safety of haloperidol in patients with alcohol abuse during the exacerbation of the addiction. Haloperidol 104-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 26639694-14 2015 Determination of CYP3A4 activity was performed using high performance liquid chromatography with mass spectrometry (HPLC/ MS) by determination of endogenous substrate of this isoenzyme and its metabolite in urine - the ratio: cortisol/6-beta-hydroxycortisol. Hydrocortisone 226-234 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 26639694-14 2015 Determination of CYP3A4 activity was performed using high performance liquid chromatography with mass spectrometry (HPLC/ MS) by determination of endogenous substrate of this isoenzyme and its metabolite in urine - the ratio: cortisol/6-beta-hydroxycortisol. 6 beta-hydroxycortisol 235-257 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 26639694-28 2015 CONCLUSIONS: The results demonstrate the correlation between CYP3A4 activities and the efficacy and safety of haloperidol in alcohol abusers during the exacerbation of the addiction. Haloperidol 110-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 26639694-28 2015 CONCLUSIONS: The results demonstrate the correlation between CYP3A4 activities and the efficacy and safety of haloperidol in alcohol abusers during the exacerbation of the addiction. Alcohols 125-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 26639694-29 2015 The inverse correlation indicates that the higher the activity of CYP3A4 is, the lower the efficacy of haloperidol is. Haloperidol 103-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 26639694-30 2015 Also it can be assumed that the presence of strong correlation between the activity of CYP3A4 and the efficacy of haloperidol in group of patients, who received higher doses of haloperidol, may indicate that CYP3A4 is involved in haloperidol metabolism when it is used at higher doses. Haloperidol 114-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 26639694-30 2015 Also it can be assumed that the presence of strong correlation between the activity of CYP3A4 and the efficacy of haloperidol in group of patients, who received higher doses of haloperidol, may indicate that CYP3A4 is involved in haloperidol metabolism when it is used at higher doses. Haloperidol 114-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 208-214 26639694-30 2015 Also it can be assumed that the presence of strong correlation between the activity of CYP3A4 and the efficacy of haloperidol in group of patients, who received higher doses of haloperidol, may indicate that CYP3A4 is involved in haloperidol metabolism when it is used at higher doses. Haloperidol 177-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 26639694-30 2015 Also it can be assumed that the presence of strong correlation between the activity of CYP3A4 and the efficacy of haloperidol in group of patients, who received higher doses of haloperidol, may indicate that CYP3A4 is involved in haloperidol metabolism when it is used at higher doses. Haloperidol 177-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 208-214 26639694-30 2015 Also it can be assumed that the presence of strong correlation between the activity of CYP3A4 and the efficacy of haloperidol in group of patients, who received higher doses of haloperidol, may indicate that CYP3A4 is involved in haloperidol metabolism when it is used at higher doses. Haloperidol 177-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 26639694-30 2015 Also it can be assumed that the presence of strong correlation between the activity of CYP3A4 and the efficacy of haloperidol in group of patients, who received higher doses of haloperidol, may indicate that CYP3A4 is involved in haloperidol metabolism when it is used at higher doses. Haloperidol 177-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 208-214 26639694-31 2015 LIMITATIONS OF THE STUDY: It should be noted that in this research the activity of CYP3A4 was determined using high performance liquid chromatography with mass spectrometry (HPLC/MS) by determination the ratio of cortisol/6-beta-hydroxycortisol for the fist time. Hydrocortisone 213-221 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 26639694-31 2015 LIMITATIONS OF THE STUDY: It should be noted that in this research the activity of CYP3A4 was determined using high performance liquid chromatography with mass spectrometry (HPLC/MS) by determination the ratio of cortisol/6-beta-hydroxycortisol for the fist time. 6 beta-hydroxycortisol 222-244 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 25693997-3 2015 As boceprevir is a potent inhibitor of CYP3A4, potential pharmacokinetic interactions may occur when it is coadministered with sildenafil. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 3-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 25693997-3 2015 As boceprevir is a potent inhibitor of CYP3A4, potential pharmacokinetic interactions may occur when it is coadministered with sildenafil. Sildenafil Citrate 127-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 25103957-2 2015 A series of in vitro experiments conducted early in the development of ivacaftor indicated ivacaftor and metabolites may have the potential to inhibit cytochrome P450 (CYP) 2C8, CYP2C9, CYP3A, and CYP2D6, as well as P-glycoprotein (P-gp). ivacaftor 71-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 186-191 25103957-2 2015 A series of in vitro experiments conducted early in the development of ivacaftor indicated ivacaftor and metabolites may have the potential to inhibit cytochrome P450 (CYP) 2C8, CYP2C9, CYP3A, and CYP2D6, as well as P-glycoprotein (P-gp). ivacaftor 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 186-191 25103957-5 2015 The results indicate ivacaftor is a weak inhibitor of CYP3A and P-gp, but has no effect on CYP2C8 or CYP2D6. ivacaftor 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-59 25103957-7 2015 Based on these results, caution and appropriate monitoring are recommended when concomitant substrates of CYP2C9, CYP3A and/or P-gp are used during treatment with ivacaftor, particularly drugs with a narrow therapeutic index, such as warfarin. ivacaftor 163-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 25103957-7 2015 Based on these results, caution and appropriate monitoring are recommended when concomitant substrates of CYP2C9, CYP3A and/or P-gp are used during treatment with ivacaftor, particularly drugs with a narrow therapeutic index, such as warfarin. Warfarin 234-242 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 26158282-2 2015 Telaprevir is a P-glycoprotein substrate and it is metabolized by CYP3A4/5. telaprevir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 26517132-0 2015 First Analysis of the Association Between CYP3A4/5, ABCB1 Genetic Polymorphisms and Oxcarbazepine Metabolism and Transport in Chinese Epileptic Patients with Oxcarbazepine Monotherapy and Bitherapy. Oxcarbazepine 84-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 26517132-0 2015 First Analysis of the Association Between CYP3A4/5, ABCB1 Genetic Polymorphisms and Oxcarbazepine Metabolism and Transport in Chinese Epileptic Patients with Oxcarbazepine Monotherapy and Bitherapy. Oxcarbazepine 158-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 26517132-3 2015 This study aims to examine the genetic effects of CYP3A4, CYP3A5, and ABCB1 on OXC metabolism and transport in Chinese epileptic patients using OXC as monotherapy and bitherapy with lamotrigine (LTG), levetiracetam (LEV), or valproic acid (VPA). Oxcarbazepine 79-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 25877445-0 2015 Reversible, time-dependent inhibition of CYP3A-mediated metabolism of midazolam and tacrolimus by telaprevir in human liver microsomes. telaprevir 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 25877445-1 2015 PURPOSE: Telaprevir inhibits CYP3A resulting in drug-drug interactions (DDI) of unprecedented magnitude. telaprevir 9-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 25877445-3 2015 METHODS: We performed a static mechanistic DDI prediction to evaluate whether previously reported competitive inhibition of CYP3A by telaprevir and its diastereomeric metabolite - VRT-127394 is sufficient to explain the remarkable reduction in oral clearance observed with oral midazolam and tacrolimus. telaprevir 133-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-129 25877445-3 2015 METHODS: We performed a static mechanistic DDI prediction to evaluate whether previously reported competitive inhibition of CYP3A by telaprevir and its diastereomeric metabolite - VRT-127394 is sufficient to explain the remarkable reduction in oral clearance observed with oral midazolam and tacrolimus. Midazolam 278-287 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-129 25877445-3 2015 METHODS: We performed a static mechanistic DDI prediction to evaluate whether previously reported competitive inhibition of CYP3A by telaprevir and its diastereomeric metabolite - VRT-127394 is sufficient to explain the remarkable reduction in oral clearance observed with oral midazolam and tacrolimus. Tacrolimus 292-302 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-129 26626238-6 2015 Inhibitory effect on CYP3A4 activity by typical inhibitors (ketoconazole, hyperforin) and natural medicines (Cat"s Claw, Devil"s Claw, Feverfew, Peppermint Oil, Red Clover, and Siberian Eleuthero) were evaluated. hyperforin 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 26626238-7 2015 The inhibitors had nearly equal IC50 values in fAd-CYP3A4 cells, Ad-CYP3A4 cells and recombinant CYP3A4 microsomes. Flavin-Adenine Dinucleotide 47-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 26626238-8 2015 Cat"s Claw, Peppermint Oil and Siberian Eleuthero inhibited CYP3A4 activity more potently than 0.1 muM ketoconazole in fAd-CYP3A4 cells. Ketoconazole 103-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 26180597-0 2015 Interactions between CYP3A4 and Dietary Polyphenols. Polyphenols 40-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 25240575-0 2015 Impact of CYP3A4 and MDR1 gene (G2677T) polymorphisms on dose requirement of the cyclosporine in renal transplant Egyptian recipients. Cyclosporine 81-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 25240575-6 2015 Interindividual heterogeneity in expression of ABCB1 and CYP3A4 has been suspected to be one of the factors resulting in cyclosporine (CsA) pharmacokinetic variation. Cyclosporine 121-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 25240575-6 2015 Interindividual heterogeneity in expression of ABCB1 and CYP3A4 has been suspected to be one of the factors resulting in cyclosporine (CsA) pharmacokinetic variation. Cyclosporine 135-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 25240575-7 2015 This study aimed to investigate the impact of inter-individual CYP3A4 rs4646437C>T and MDR1 G2677T/A polymorphisms on cyclosporine dose requirements among a sample of renal transplant Egyptian recipients. Cyclosporine 121-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 25240575-8 2015 Fifty adult Egyptian patients on CsA were genotyped for CYP3A4 rs4646437C>T and MDR1 G2677T/A and correlated with CsA dose requirement and dose-adjusted CsA (C0) blood levels at 3, 6, and 9 months post transplantation. Cyclosporine 117-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 25240575-8 2015 Fifty adult Egyptian patients on CsA were genotyped for CYP3A4 rs4646437C>T and MDR1 G2677T/A and correlated with CsA dose requirement and dose-adjusted CsA (C0) blood levels at 3, 6, and 9 months post transplantation. Cyclosporine 117-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 25240575-9 2015 CYP3A4 rs4646437C>T influenced significantly cyclosporine kinetics, the T carriers requiring higher cyclosporine dose. Cyclosporine 48-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25240575-9 2015 CYP3A4 rs4646437C>T influenced significantly cyclosporine kinetics, the T carriers requiring higher cyclosporine dose. Cyclosporine 103-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25240575-11 2015 Genotyping of both CYP3A4 and MDR1 SNPs may be helpful in providing pre-transplant pharmacogenetic information to individualize CsA dosing. Cyclosporine 128-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 26180597-7 2015 This review focuses on interactions between dietary polyphenols and CYP3A4 as they relate to structural considerations, food-drug interactions, and potential negative consequences of interactions between CYP3A4 and polyphenols. Polyphenols 215-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 26180597-5 2015 Recent studies have pointed to the role of gut microbiota in the metabolic fate of polyphenolics in human, suggesting their involvement in the complex interactions between dietary polyphenols and CYP3A4. polyphenolics 83-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 196-202 26180597-7 2015 This review focuses on interactions between dietary polyphenols and CYP3A4 as they relate to structural considerations, food-drug interactions, and potential negative consequences of interactions between CYP3A4 and polyphenols. Polyphenols 52-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 204-210 26088794-0 2015 CYP3A4 * 1G Genetic Polymorphism Influences Metabolism of Fentanyl in Human Liver Microsomes in Chinese Patients. Fentanyl 58-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26088794-1 2015 PURPOSE: This study aimed to investigate whether CYP3A4*1G genetic polymorphism influences the metabolism of fentanyl in human liver microsomes in Chinese patients. Fentanyl 109-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 26088794-12 2015 There was positive correlation between CYP3A4 mRNA and metabolic rate of fentanyl (p < 0.01). Fentanyl 73-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 25916520-0 2015 Relationship between mRNA expression levels of CYP3A4, CYP3A5 and SXR in peripheral mononuclear blood cells and aging in young kidney transplant recipients under tacrolimus treatment. Tacrolimus 162-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 26088794-13 2015 CONCLUSIONS: CYP3A4*1G genetic polymorphism decreases the metabolism of fentanyl. Fentanyl 72-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 25893704-0 2015 CYP3A4*22 is related to increased plasma levels of 4-hydroxytamoxifen and partially compensates for reduced CYP2D6 activation of tamoxifen. hydroxytamoxifen 51-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26088794-14 2015 There is a positive correlation between CYP3A4 mRNA level and metabolism of fentanyl. Fentanyl 76-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 25893704-0 2015 CYP3A4*22 is related to increased plasma levels of 4-hydroxytamoxifen and partially compensates for reduced CYP2D6 activation of tamoxifen. Tamoxifen 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 26228923-4 2015 CYP3A4*1G, MDR1 1236-2677-3435 diplotype and NR1I2 -25385C > T explained 21.4% of variability of tacrolimus C0D7/D in CYP3A5 nonexpressers. Tacrolimus 100-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25893704-1 2015 AIM: To evaluate the impact of CYP3A4*22 in the formation of endoxifen (EDF) and hydroxytamoxifen (HTF), under different CYP2D6 genotypic backgrounds. 4-hydroxy-N-desmethyltamoxifen 61-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 25893704-1 2015 AIM: To evaluate the impact of CYP3A4*22 in the formation of endoxifen (EDF) and hydroxytamoxifen (HTF), under different CYP2D6 genotypic backgrounds. 4-hydroxy-N-desmethyltamoxifen 72-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 25893704-1 2015 AIM: To evaluate the impact of CYP3A4*22 in the formation of endoxifen (EDF) and hydroxytamoxifen (HTF), under different CYP2D6 genotypic backgrounds. hydroxytamoxifen 81-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 25893704-1 2015 AIM: To evaluate the impact of CYP3A4*22 in the formation of endoxifen (EDF) and hydroxytamoxifen (HTF), under different CYP2D6 genotypic backgrounds. hydroxytamoxifen 99-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 25893704-5 2015 HTF and TAM levels were respectively 47 and 53% higher in CYP3A4*22 carriers compared with *1/*1 patients in the whole group. hydroxytamoxifen 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 25893704-5 2015 HTF and TAM levels were respectively 47 and 53% higher in CYP3A4*22 carriers compared with *1/*1 patients in the whole group. Tamoxifen 8-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 26228923-6 2015 Genotyping of CYP3A4/MDR1/NR1I2 polymorphisms may be helpful for better guiding tacrolimus dosing in CYP3A5 nonexpressers. Tacrolimus 80-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 26827407-9 2015 DISCUSSION: The metabolism of warfarin involves several cytochrome P450 isoenzymes, including CYP1A2, CYP2C9, CYP2C19, and CYP3A4. Warfarin 30-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 26827407-10 2015 Mirtazapine is metabolized primarily by CYP2D6 and CYP3A4, with lesser contributions by CYP1A2. Mirtazapine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 25811791-5 2015 The results showed that celastrol inhibited the five types of human cytochrome P450 isoforms, with the IC50 values of 2.65 muM (CYP3A4), 5.99 muM (CYP2C19), 6.27 muM (CYP2D6), 7.66 muM (CYP1A2) and 9.38 muM (CYP2E1), respectively. celastrol 24-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 25811791-7 2015 Celastrol was also a mixed-type inhibitor of CYP3A4, with Ki and Kis values of 2.02 and 5.49 muM, respectively. celastrol 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 26053557-11 2015 A cocktail assay showed that CYP1A2, CYP2C9, CYP2C19, CYP2E1 and CYP3A4 can be inhibited by rutaecarpine in human liver microsomes. rutecarpine 92-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 25948306-3 2015 (1) Some factors relating to CYP2D6, CYP3A, ATP-binding cassette sub-family B member 1 (ABCB1), and opioid receptor mu 1 (OPRM1) involve oxycodone pharmacokinetics and sensitivity in humans. Oxycodone 137-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-42 25948306-8 2015 The activities of CYP3A, ABCB1, and OPRM1 contribute to the interindividual variations in clinical responses to fentanyl in cancer patients. Fentanyl 112-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-23 26053559-7 2015 CYP3A was assigned as the main isoform involved in both 5beta-hydroxylation and 3-oxidation in all studied liver microsomes. 5beta 56-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 26053559-10 2015 In summary, CYP3A mediated 5beta-hydroxylation and 3-oxidation were two major metabolic pathways of BF in hepatic microsomes from human and five studied animals, but kinetic analysis demonstrated that the intrinsic clearances of these two metabolic pathways were much different among various species. 5beta 27-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 26053559-10 2015 In summary, CYP3A mediated 5beta-hydroxylation and 3-oxidation were two major metabolic pathways of BF in hepatic microsomes from human and five studied animals, but kinetic analysis demonstrated that the intrinsic clearances of these two metabolic pathways were much different among various species. bufalin 100-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 25552904-5 2015 Netupitant, is a new NK-1 receptor antagonist with a high binding affinity, a long half-life of 90 hours, is metabolized by CYP3A4, and is an inhibitor of CYP3A4. netupitant 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 25518025-0 2014 Prediction of Metabolic Interactions With Oxycodone via CYP2D6 and CYP3A Inhibition Using a Physiologically Based Pharmacokinetic Model. Oxycodone 42-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-72 25552904-5 2015 Netupitant, is a new NK-1 receptor antagonist with a high binding affinity, a long half-life of 90 hours, is metabolized by CYP3A4, and is an inhibitor of CYP3A4. netupitant 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 25450675-4 2014 In this study, we determined the kinetic parameters for glyburide depletion by CYP3A isoenzymes; characterized glyburide metabolism by human fetal liver tissues collected during the first or early second trimester of pregnancy; and identified the major enzyme responsible for glyburide metabolism in human fetal livers. Glyburide 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-84 25521244-9 2014 Dovitinib weakly inhibited CYP2C19, CYP3A4, P-gp and OATPs. 4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 25450675-5 2014 CYP3A4 had the highest metabolic capacity towards glyburide, followed by CYP3A7 and CYP3A5 (Clint,u=37.1, 13.0, and 8.7ml/min/nmol P450, respectively). Glyburide 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25398138-0 2014 Cooperative binding of aflatoxin B1 by cytochrome P450 3A4: a computational study. Aflatoxin B1 23-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-58 25398138-1 2014 Aflatoxin B1 (AFB1)-the most potent natural carcinogen known to men-is metabolized by cytochrome P450 3A4 (CYP3A4), either to the genotoxic AFB1 exo-8,9-epoxide or to the detoxified 3alpha-hydroxy AFB1. Aflatoxin B1 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-105 25398138-1 2014 Aflatoxin B1 (AFB1)-the most potent natural carcinogen known to men-is metabolized by cytochrome P450 3A4 (CYP3A4), either to the genotoxic AFB1 exo-8,9-epoxide or to the detoxified 3alpha-hydroxy AFB1. Aflatoxin B1 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 25372302-6 2014 The major GSH conjugate was identified as 4"-OH-5"-glutathionyl-MFA and was formed at the highest activity by CYP1A2 and to a lesser extent by CYP2C9 and CYP3A4. Glutathione 10-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 25398138-1 2014 Aflatoxin B1 (AFB1)-the most potent natural carcinogen known to men-is metabolized by cytochrome P450 3A4 (CYP3A4), either to the genotoxic AFB1 exo-8,9-epoxide or to the detoxified 3alpha-hydroxy AFB1. Aflatoxin B1 14-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-105 25398138-1 2014 Aflatoxin B1 (AFB1)-the most potent natural carcinogen known to men-is metabolized by cytochrome P450 3A4 (CYP3A4), either to the genotoxic AFB1 exo-8,9-epoxide or to the detoxified 3alpha-hydroxy AFB1. Aflatoxin B1 14-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 25372302-6 2014 The major GSH conjugate was identified as 4"-OH-5"-glutathionyl-MFA and was formed at the highest activity by CYP1A2 and to a lesser extent by CYP2C9 and CYP3A4. 4"-oh-5"-glutathionyl-mfa 42-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 25398138-1 2014 Aflatoxin B1 (AFB1)-the most potent natural carcinogen known to men-is metabolized by cytochrome P450 3A4 (CYP3A4), either to the genotoxic AFB1 exo-8,9-epoxide or to the detoxified 3alpha-hydroxy AFB1. Aflatoxin B1 140-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-105 25372302-7 2014 Two minor GSH conjugates resulted from secondary oxidation of 5-hydroxy-MFA and were formed at the highest activity by CYP1A2 and to a lesser extent by CYP3A4. Glutathione 10-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 25372302-7 2014 Two minor GSH conjugates resulted from secondary oxidation of 5-hydroxy-MFA and were formed at the highest activity by CYP1A2 and to a lesser extent by CYP3A4. 5-hydroxy-mfa 62-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 25398138-1 2014 Aflatoxin B1 (AFB1)-the most potent natural carcinogen known to men-is metabolized by cytochrome P450 3A4 (CYP3A4), either to the genotoxic AFB1 exo-8,9-epoxide or to the detoxified 3alpha-hydroxy AFB1. Aflatoxin B1 140-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 25398138-1 2014 Aflatoxin B1 (AFB1)-the most potent natural carcinogen known to men-is metabolized by cytochrome P450 3A4 (CYP3A4), either to the genotoxic AFB1 exo-8,9-epoxide or to the detoxified 3alpha-hydroxy AFB1. exo-8,9-epoxide 145-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-105 25398138-1 2014 Aflatoxin B1 (AFB1)-the most potent natural carcinogen known to men-is metabolized by cytochrome P450 3A4 (CYP3A4), either to the genotoxic AFB1 exo-8,9-epoxide or to the detoxified 3alpha-hydroxy AFB1. exo-8,9-epoxide 145-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 25398138-1 2014 Aflatoxin B1 (AFB1)-the most potent natural carcinogen known to men-is metabolized by cytochrome P450 3A4 (CYP3A4), either to the genotoxic AFB1 exo-8,9-epoxide or to the detoxified 3alpha-hydroxy AFB1. 3alpha-hydroxy afb1 182-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-105 25398138-1 2014 Aflatoxin B1 (AFB1)-the most potent natural carcinogen known to men-is metabolized by cytochrome P450 3A4 (CYP3A4), either to the genotoxic AFB1 exo-8,9-epoxide or to the detoxified 3alpha-hydroxy AFB1. 3alpha-hydroxy afb1 182-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 25456428-8 2014 When incubated with hydrolyzed ginkgolides at 10mug/mL, the relative activity and relative mRNA expression level of CYP3A4 remarkably increased to 4.59+-3.67 and 17.2+-9.16-fold of the corresponding vehicle control values, respectively. Ginkgolides 31-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 25548518-10 2014 A molecular docking study showed that XKB bound to the active site of human cytochrome P450 3A4 and rat Cyp3a2 homology model via the formation of hydrogen bonds. Hydrogen 147-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-95 25451576-0 2014 Demethylation of neferine in human liver microsomes and formation of quinone methide metabolites mediated by CYP3A4 accentuates its cytotoxicity. quinone 69-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 25451576-4 2014 Approaches using chemical inhibitors and recombinant human enzymes to characterize the involved enzymes and kinetic studies indicated that the demethylation of neferine by cytochrome P450 (CYP) 2D6 and CYP3A4 fitted a biphasic kinetic profile. neferine 160-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 202-208 25451576-6 2014 Based on its structure containing para-methylene phenol and results from a product ion scan, GSH tends to conjugate with C9" after undergoing oxidative metabolism to form the binding site predominated by CYP3A4. Glutathione 93-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 204-210 25451576-9 2014 Metabolic activation mediated by CYP3A4 and GSH depletion significantly enhanced neferine-induced cytotoxicity. neferine 81-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 25224009-7 2014 Furthermore, VT-1161 weakly inhibited human CYP2C9, CYP2C19, and CYP3A4, suggesting a low drug-drug interaction potential. VT-1161 13-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 25520598-0 2014 Size and surface modification of amorphous silica particles determine their effects on the activity of human CYP3A4 in vitro. Silicon Dioxide 43-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 25520598-3 2014 Here, we examined the effects of amorphous silica particles with various sizes and surface modifications on cytochrome P450 3A4 (CYP3A4) activity by means of two different in vitro assays. Silicon Dioxide 43-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-127 25520598-3 2014 Here, we examined the effects of amorphous silica particles with various sizes and surface modifications on cytochrome P450 3A4 (CYP3A4) activity by means of two different in vitro assays. Silicon Dioxide 43-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 25520598-4 2014 Silica nanoparticles with diameters of 30 and 70 nm (nSP30 and nSP70, respectively) tended to inhibit CYP3A4 activity in human liver microsomes (HLMs), but the inhibitory activity of both types of nanoparticles was decreased by carboxyl modification. Silicon Dioxide 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 25520598-5 2014 In contrast, amine-modified nSP70 activated CYP3A4 activity. Amines 13-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 25520598-7 2014 Taken together, these results suggest that the size and surface characteristics of the silica particles determined their effects on CYP3A4 activity and that it may be possible to develop silica particles that do not have undesirable effects on metabolic enzymes by altering their size and surface characteristics. Silicon Dioxide 87-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 25280976-2 2014 Calcium channel blockers (CCBs) are considered to be the best treatment for CsA-induced hypertension, but they may alter the exposure and the effect of CsA by inhibiting the CYP3A4 pathway of CsA metabolism or P-gp. Cyclosporine 152-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 25280976-2 2014 Calcium channel blockers (CCBs) are considered to be the best treatment for CsA-induced hypertension, but they may alter the exposure and the effect of CsA by inhibiting the CYP3A4 pathway of CsA metabolism or P-gp. Cyclosporine 152-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 25916520-5 2015 PATIENTS & METHODS: The correlation between the levels of mRNA specific for key enzymes SXR, CYP3A and ABCB1 involved in the metabolism of tacrolimus was evaluated in PBMCs obtained from a selected population of 29 young kidney transplant recipients. Tacrolimus 143-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-102 25916520-8 2015 tacrolimus-normalized daily dose was strongly correlated with patient"s age and multivariable regression indicates the CYP3A4-specific mRNA as the sole independent variable influencing tacrolimus concentration-to-dose ratio. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 25916520-8 2015 tacrolimus-normalized daily dose was strongly correlated with patient"s age and multivariable regression indicates the CYP3A4-specific mRNA as the sole independent variable influencing tacrolimus concentration-to-dose ratio. Tacrolimus 185-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 24691829-1 2014 Carbamazepine (CBZ), an antiepileptic with narrow therapeutic window, is a substrate of CYP 3A4 which metabolizes CBZ to carbamazepine-10,11-epoxide (CBZE). Carbamazepine 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-95 24691829-1 2014 Carbamazepine (CBZ), an antiepileptic with narrow therapeutic window, is a substrate of CYP 3A4 which metabolizes CBZ to carbamazepine-10,11-epoxide (CBZE). Carbamazepine 15-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-95 24691829-1 2014 Carbamazepine (CBZ), an antiepileptic with narrow therapeutic window, is a substrate of CYP 3A4 which metabolizes CBZ to carbamazepine-10,11-epoxide (CBZE). Carbamazepine 114-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-95 24691829-1 2014 Carbamazepine (CBZ), an antiepileptic with narrow therapeutic window, is a substrate of CYP 3A4 which metabolizes CBZ to carbamazepine-10,11-epoxide (CBZE). carbamazepine epoxide 121-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-95 24691829-1 2014 Carbamazepine (CBZ), an antiepileptic with narrow therapeutic window, is a substrate of CYP 3A4 which metabolizes CBZ to carbamazepine-10,11-epoxide (CBZE). carbamazepine epoxide 150-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-95 24819614-4 2014 We found that U0126, a prototype dual MEK1/2 inhibitor, is a potent inducer of CYP3A4, CYP3A5 and CYP3A7 mRNA expression (>100-fold) in HepG2 cells and CYP3A4 mRNA expression in primary human hepatocytes. U 0126 14-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 24819614-4 2014 We found that U0126, a prototype dual MEK1/2 inhibitor, is a potent inducer of CYP3A4, CYP3A5 and CYP3A7 mRNA expression (>100-fold) in HepG2 cells and CYP3A4 mRNA expression in primary human hepatocytes. U 0126 14-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 24819614-6 2014 In gene reporter assays, U0126 activates a CYP3A4 promoter luciferase reporter construct containing PXR response elements (PXREs), but not a construct containing mutated PXREs. U 0126 25-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 25307552-1 2014 PURPOSE: Cabazitaxel is primarily metabolized by CYP3A. cabazitaxel 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 25139487-3 2014 In this study, the systemic availability of topical erythromycin, hence the influence on the activity of CYP3A, is evaluated in comparison to orally administered erythromycin. Erythromycin 52-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-110 25139487-5 2014 A microdose of midazolam (3 mug orally) was used to determine the effect on CYP3A activity. Midazolam 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 25139487-9 2014 The relationship between erythromycin exposure and CYP3A activity (Hill equation) revealed a 50% reduction of CYP3A activity by an erythromycin AUC of 2106 h ng ml(-1). Erythromycin 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 25139487-9 2014 The relationship between erythromycin exposure and CYP3A activity (Hill equation) revealed a 50% reduction of CYP3A activity by an erythromycin AUC of 2106 h ng ml(-1). Erythromycin 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-115 25139487-9 2014 The relationship between erythromycin exposure and CYP3A activity (Hill equation) revealed a 50% reduction of CYP3A activity by an erythromycin AUC of 2106 h ng ml(-1). Erythromycin 131-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 25139487-9 2014 The relationship between erythromycin exposure and CYP3A activity (Hill equation) revealed a 50% reduction of CYP3A activity by an erythromycin AUC of 2106 h ng ml(-1). Erythromycin 131-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-115 24729431-0 2014 In vitro ketamine CYP3A-mediated metabolism study using mammalian liver S9 fractions, cDNA expressed enzymes and liquid chromatography tandem mass spectrometry. Ketamine 9-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-23 24729431-2 2014 The objectives of this study were to develop a novel HPLC-MS/selected reaction monitoring (SRM) method capable of quantifying ketamine and norketamine using an isotopic dilution strategy in biological matrices and study the formation of norketamine, the principal metabolite of ketamine with and without the presence of midazolam, a well-known CYP3A substrate. norketamine 237-248 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 344-349 25453801-0 2014 Cycloartane-type triterpenes from Euphorbia fischeriana stimulate human CYP3A4 promoter activity. cycloartane-type 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 25453801-0 2014 Cycloartane-type triterpenes from Euphorbia fischeriana stimulate human CYP3A4 promoter activity. Triterpenes 17-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 25307552-13 2014 Co-administration of cabazitaxel with strong CYP3A inhibitors or inducers should be avoided. cabazitaxel 21-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-50 25307552-12 2014 CONCLUSIONS: Cabazitaxel pharmacokinetics are modified by drugs strongly affecting CYP3A. cabazitaxel 13-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 24964176-1 2014 Two previously conducted rivaroxaban studies showed that, separately, renal impairment (RI) and concomitant administration of erythromycin (P-glycoprotein and moderate cytochrome P450 3A4 [CYP3A4] inhibitor) can result in increases in rivaroxaban exposure. Rivaroxaban 25-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-187 25273356-0 2014 Mechanism-based inactivation of human cytochrome P450 3A4 by two piperazine-containing compounds. Piperazine 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-57 25273356-4 2014 Inhibition of CYP3A4 by SCH 66712 and EMTPP was determined to be concentration, time, and NADPH dependent. NADP 90-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 25273356-6 2014 SCH 66712 displays type I binding to CYP3A4 with a spectral binding constant (Ks) of 42.9 +- 2.9 microM. Potassium 78-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 25316200-7 2014 Although partial inhibition of human hepatic and intestinal microsomal CYP2C8, CYP2B6, CYP3A4, CYP2D6 and CYP2C19 by GTE catechins was observed in vitro, a clinical study of drug bioavailability attributed a small risk of increased plasma drug levels only for substrates metabolized by CYP3A4, lacking clinical relevance. Catechin 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 25096076-0 2014 Pharmacokinetic and pharmacogenomic modelling of the CYP3A activity marker 4beta-hydroxycholesterol during efavirenz treatment and efavirenz/rifampicin co-treatment. cholest-5-ene-3,4-diol 75-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 25096076-0 2014 Pharmacokinetic and pharmacogenomic modelling of the CYP3A activity marker 4beta-hydroxycholesterol during efavirenz treatment and efavirenz/rifampicin co-treatment. efavirenz 107-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 25096076-1 2014 OBJECTIVES: To assess the effect of the major efavirenz metabolizing enzyme (CYP2B6) genotype and the effects of rifampicin co-treatment on induction of CYP3A by efavirenz. Rifampin 113-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-158 25096076-7 2014 Efavirenz treatment in arm 1 resulted in 1.74 (relative standard error = 15%), 3.3 (relative standard error = 33.1%) and 4.0 (relative standard error = 37.1%) average fold induction of CYP3A for extensive (CYP2B6*1/*1), intermediate (CYP2B6*1/*6) and slow (CYP2B6*6/*6) efavirenz metabolizers, respectively. efavirenz 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-190 25096076-10 2014 CONCLUSIONS: Our results indicate that efavirenz induction of CYP3A is influenced by CYP2B6 genetic polymorphisms and that efavirenz/rifampicin co-treatment results in higher induction than efavirenz alone. efavirenz 39-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 25216238-7 2014 We are not aware of published reports of significant ketoconazole-associated liver injury in volunteer study participants when ketoconazole has been used as a CYP3A inhibitor in the context of clinical research on drug metabolism. Ketoconazole 127-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-164 24964176-1 2014 Two previously conducted rivaroxaban studies showed that, separately, renal impairment (RI) and concomitant administration of erythromycin (P-glycoprotein and moderate cytochrome P450 3A4 [CYP3A4] inhibitor) can result in increases in rivaroxaban exposure. Rivaroxaban 25-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 25216238-8 2014 Possible alternatives to ketoconazole as prototype CYP3A inhibitors include ritonavir and potentially itraconazole, but not clarithromycin. Ritonavir 76-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 25216238-8 2014 Possible alternatives to ketoconazole as prototype CYP3A inhibitors include ritonavir and potentially itraconazole, but not clarithromycin. Itraconazole 102-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 24964176-1 2014 Two previously conducted rivaroxaban studies showed that, separately, renal impairment (RI) and concomitant administration of erythromycin (P-glycoprotein and moderate cytochrome P450 3A4 [CYP3A4] inhibitor) can result in increases in rivaroxaban exposure. Erythromycin 126-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 25047139-1 2014 WHAT IS KNOWN AND OBJECTIVE: Navitoclax, a first-in-class small molecule Bcl-2 family inhibitor, is metabolized in vitro by the hepatic microsomal cytochrome P450 (CYP) enzymes CYP3A4. navitoclax 29-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 25047139-12 2014 WHAT IS NEW AND CONCLUSION: Co-administration navitoclax with rifampin moderately decreased navitoclax AUC, which could be partly due to the induction effect of rifampin on CYP3A4. Rifampin 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 25047139-12 2014 WHAT IS NEW AND CONCLUSION: Co-administration navitoclax with rifampin moderately decreased navitoclax AUC, which could be partly due to the induction effect of rifampin on CYP3A4. Rifampin 161-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 25253884-8 2014 Second, the mechanism-based inhibition kinetics for DHB were recovered using human intestinal microsomes and the index CYP3A4 reaction, loperamide N-desmethylation (KI [concentration needed to achieve one-half kinact], 5.0 +- 0.9 microM; kinact [maximum inactivation rate constant], 0.38 +- 0.02 minute(-1)). 6',7'-dihydroxybergamottin 52-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 25253884-12 2014 Results suggest that DHB could be used to predict the CYP3A4-mediated effect of GFJ. 6',7'-dihydroxybergamottin 21-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 25322286-6 2014 Multivariate analyses identified the CYP3A5*1/POR*28/CYP3A4*22 genotype combination as the single strongest determinant of tacrolimus dose requirements throughout the first year, explaining between 24-40% of its variability, whereas recipient age, hematocrit, and delayed graft function were additional nongenetic determinants of tacrolimus dose. Tacrolimus 123-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 25274602-2 2014 Given the potent inhibition of CYP3A4 by ritonavir, subtherapeutic doses of ritonavir are used to increase plasma concentrations of other HIV drugs oxidized by CYP3A4, thereby extending their clinical efficacy. Ritonavir 41-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 25274602-2 2014 Given the potent inhibition of CYP3A4 by ritonavir, subtherapeutic doses of ritonavir are used to increase plasma concentrations of other HIV drugs oxidized by CYP3A4, thereby extending their clinical efficacy. Ritonavir 76-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 25274602-2 2014 Given the potent inhibition of CYP3A4 by ritonavir, subtherapeutic doses of ritonavir are used to increase plasma concentrations of other HIV drugs oxidized by CYP3A4, thereby extending their clinical efficacy. Ritonavir 76-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 25274602-3 2014 However, the mechanism of inhibition of CYP3A4 by ritonavir remains unclear. Ritonavir 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 25274602-5 2014 The results presented here demonstrate that inhibition of CYP3A4 by ritonavir occurs by CYP3A4-mediated activation and subsequent formation of a covalent bond to the apoprotein. Ritonavir 68-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 25274602-5 2014 The results presented here demonstrate that inhibition of CYP3A4 by ritonavir occurs by CYP3A4-mediated activation and subsequent formation of a covalent bond to the apoprotein. Ritonavir 68-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 25274602-6 2014 Incubations of [(3)H]ritonavir with reconstituted CYP3A4 and human liver microsomes resulted in a covalent binding stoichiometry equal to 0.93 +- 0.04 moles of ritonavir bound per mole of inactivated CYP3A4. [(3)h]ritonavir 15-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 25274602-6 2014 Incubations of [(3)H]ritonavir with reconstituted CYP3A4 and human liver microsomes resulted in a covalent binding stoichiometry equal to 0.93 +- 0.04 moles of ritonavir bound per mole of inactivated CYP3A4. [(3)h]ritonavir 15-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 25274602-6 2014 Incubations of [(3)H]ritonavir with reconstituted CYP3A4 and human liver microsomes resulted in a covalent binding stoichiometry equal to 0.93 +- 0.04 moles of ritonavir bound per mole of inactivated CYP3A4. Ritonavir 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 25274602-6 2014 Incubations of [(3)H]ritonavir with reconstituted CYP3A4 and human liver microsomes resulted in a covalent binding stoichiometry equal to 0.93 +- 0.04 moles of ritonavir bound per mole of inactivated CYP3A4. Ritonavir 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 25274602-7 2014 The metabolism of [(3)H]ritonavir by CYP3A4 leads to the formation of a covalent adduct specifically to CYP3A4, confirmed by radiometric liquid chromatography-trace and whole-protein mass spectrometry. [(3)h]ritonavir 18-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 25274602-7 2014 The metabolism of [(3)H]ritonavir by CYP3A4 leads to the formation of a covalent adduct specifically to CYP3A4, confirmed by radiometric liquid chromatography-trace and whole-protein mass spectrometry. [(3)h]ritonavir 18-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 25274602-8 2014 Tryptic digestion of the CYP3A4-[(3)H]ritonavir incubations exhibited an adducted peptide (255-RM K: ESRLEDTQKHR-268) associated with a radiochromatic peak and a mass consistent with ritonavir plus 16 Da, in agreement with the whole-protein mass spectrometry. Ritonavir 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 25274602-8 2014 Tryptic digestion of the CYP3A4-[(3)H]ritonavir incubations exhibited an adducted peptide (255-RM K: ESRLEDTQKHR-268) associated with a radiochromatic peak and a mass consistent with ritonavir plus 16 Da, in agreement with the whole-protein mass spectrometry. Ritonavir 183-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 25274602-10 2014 In conclusion, ritonavir exhibited potent time-dependent inactivation of CYP3A, with the mechanism of inactivation occurring though a covalent bond to Lys257 of the CYP3A4 apoprotein. Ritonavir 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 25203739-5 2014 Variabilities in the genes encoding the drug target (aromatase) or its metabolizing enzymes (CYP3A and UGT1A) contribute toward the interindividual variability in anastrozole"s pharmacokinetics and/or pharmacodynamics. Anastrozole 163-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 25203739-6 2014 This paper reviews the role of genetic polymorphisms of CYP19A1, CYP3A4, and UGT1A4 in the responses of female hormone receptor-positive postmenopausal breast cancer patients to anastrozole. Anastrozole 178-189 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 25322286-7 2014 CONCLUSION: Combining the CYP3A5*1, POR*28 and CYP3A4*22 genotypes allows partial differentiation of early tacrolimus dose requirements and the time to reach therapeutic target concentrations after transplantation, but without obvious clinical implications. Tacrolimus 107-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 25521355-3 2014 The polymorphic enzyme POR transfers electrons from NADPH to CYP450 enzymes including CYP3A, which metabolize atorvastatin. Atorvastatin 110-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 25196644-6 2014 Caffeic acid was a potent competitive inhibitor of CYP2D6 (Ki = 1.10 muM) and a weak inhibitor of CYP2C19 and CYP3A4 (IC50 > 100 muM). caffeic acid 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 25521355-3 2014 The polymorphic enzyme POR transfers electrons from NADPH to CYP450 enzymes including CYP3A, which metabolize atorvastatin. NADP 52-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 25196644-7 2014 Quercetin was a potent competitive inhibitor of CYP 2C19 and CYP3A4 (Ki = 1.74 and 4.12 muM, respectively) and a moderate competitive inhibitor of CYP2D6 (Ki = 18.72 muM). Quercetin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 25629144-14 2014 DM1 is metabolised by cytochrome P450 isoenzymes CYP3A4 and CYP3A5 and is also a P-glycoprotein substrate, creating a potential risk of multiple pharmacokinetic interactions. cantuzumab mertansine 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 25561870-0 2014 Modulation of CYP2D6 and CYP3A4 metabolic activities by Ferula asafetida resin. ferula asafetida resin 56-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 24739665-1 2014 BACKGROUND: Previous reports have suggested that imatinib may increase cyclosporine exposure by CYP3A4 inhibition. Imatinib Mesylate 49-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 24739665-1 2014 BACKGROUND: Previous reports have suggested that imatinib may increase cyclosporine exposure by CYP3A4 inhibition. Cyclosporine 71-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 24739665-6 2014 In addition, a validated model-based approach was used to derive quantitative predictions of CYP3A4-mediated drug interactions with imatinib as a victim or precipitant drug. Imatinib Mesylate 132-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24739665-8 2014 The modeling approach predicted weak-to-moderate effect of major CYP3A4 inhibitors on imatinib exposure. Imatinib Mesylate 86-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 24739665-9 2014 However, the inhibitory potency of imatinib was found to be similar to that of verapamil, suggesting significant influence of imatinib on the pharmacokinetics of drugs highly metabolized by CYP3A4. Imatinib Mesylate 35-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-196 24739665-9 2014 However, the inhibitory potency of imatinib was found to be similar to that of verapamil, suggesting significant influence of imatinib on the pharmacokinetics of drugs highly metabolized by CYP3A4. Imatinib Mesylate 126-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-196 24739668-1 2014 BACKGROUND: Both aripiprazole and haloperidol have been used in the treatment of schizophrenia, and are metabolized by the cytochrome P450 (CYP) 2D6 and CYP3A4. Aripiprazole 17-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 24739668-1 2014 BACKGROUND: Both aripiprazole and haloperidol have been used in the treatment of schizophrenia, and are metabolized by the cytochrome P450 (CYP) 2D6 and CYP3A4. Haloperidol 34-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 24739669-3 2014 We thus assessed the role of genetic variation in CYP3A4, CYP3A5, POR, NR1I2, and ABCB1 acting jointly in immunosuppressive drug pathways in tacrolimus (TAC) and ciclosporin (CSA) dose requirement in HTx recipients. Tacrolimus 141-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 24739669-3 2014 We thus assessed the role of genetic variation in CYP3A4, CYP3A5, POR, NR1I2, and ABCB1 acting jointly in immunosuppressive drug pathways in tacrolimus (TAC) and ciclosporin (CSA) dose requirement in HTx recipients. Cyclosporine 162-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 25364403-0 2014 Effects of co-treatment with sulforaphane and autophagy modulators on uridine 5"-diphospho-glucuronosyltransferase 1A isoforms and cytochrome P450 3A4 expression in Caco-2 human colon cancer cells. sulforaphane 29-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-150 25561870-1 2014 Present study investigated the potential effects of Ferula asafetida resin on metabolic activities of human drug metabolizing enzymes: CYP2D6 and CYP3A4. ferula asafetida resin 52-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 25561870-2 2014 Dextromethorphan (DEX) was used as a marker to assess metabolic activities of these enzymes, based on its CYP2D6 and CYP3A4 mediated metabolism to dextrorphan (DOR) and 3-methoxymorphinan (3-MM), respectively. Dextromethorphan 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 25561870-2 2014 Dextromethorphan (DEX) was used as a marker to assess metabolic activities of these enzymes, based on its CYP2D6 and CYP3A4 mediated metabolism to dextrorphan (DOR) and 3-methoxymorphinan (3-MM), respectively. Dextromethorphan 18-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 25561870-2 2014 Dextromethorphan (DEX) was used as a marker to assess metabolic activities of these enzymes, based on its CYP2D6 and CYP3A4 mediated metabolism to dextrorphan (DOR) and 3-methoxymorphinan (3-MM), respectively. Dextrorphan 147-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 25561870-2 2014 Dextromethorphan (DEX) was used as a marker to assess metabolic activities of these enzymes, based on its CYP2D6 and CYP3A4 mediated metabolism to dextrorphan (DOR) and 3-methoxymorphinan (3-MM), respectively. Dextrorphan 160-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 25561870-9 2014 Therefore, using Ferula asafetida with CYP3A4 drug substrates should be cautioned especially those with narrow therapeutic index such as cyclosporine, tacrolimus and carbamazepine. Cyclosporine 137-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 25561870-9 2014 Therefore, using Ferula asafetida with CYP3A4 drug substrates should be cautioned especially those with narrow therapeutic index such as cyclosporine, tacrolimus and carbamazepine. Tacrolimus 151-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 25561870-9 2014 Therefore, using Ferula asafetida with CYP3A4 drug substrates should be cautioned especially those with narrow therapeutic index such as cyclosporine, tacrolimus and carbamazepine. Carbamazepine 166-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 25361167-3 2014 The activities of CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 were attenuated by EEP-B55 in a concentration-dependent manner, and artepillin C, kaempferide, dihydrokaempferide, isosakuranetin, and kaempferol were estimated to have potential for CYP inhibition. isosakuranetin 177-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 25589927-3 2015 Detailed DMPK studies involving cyanide and GSH as trapping agents during microsomal incubations, in addition to deuterium-labeled compounds as mechanistic probes uncovered the molecular basis for the observed CYP3A4 TDI in the series. dmpk 9-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 210-216 25589927-3 2015 Detailed DMPK studies involving cyanide and GSH as trapping agents during microsomal incubations, in addition to deuterium-labeled compounds as mechanistic probes uncovered the molecular basis for the observed CYP3A4 TDI in the series. Cyanides 32-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 210-216 25589927-3 2015 Detailed DMPK studies involving cyanide and GSH as trapping agents during microsomal incubations, in addition to deuterium-labeled compounds as mechanistic probes uncovered the molecular basis for the observed CYP3A4 TDI in the series. Glutathione 44-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 210-216 25589927-3 2015 Detailed DMPK studies involving cyanide and GSH as trapping agents during microsomal incubations, in addition to deuterium-labeled compounds as mechanistic probes uncovered the molecular basis for the observed CYP3A4 TDI in the series. Deuterium 113-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 210-216 25361167-3 2014 The activities of CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 were attenuated by EEP-B55 in a concentration-dependent manner, and artepillin C, kaempferide, dihydrokaempferide, isosakuranetin, and kaempferol were estimated to have potential for CYP inhibition. eep-b55 81-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 25361167-3 2014 The activities of CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 were attenuated by EEP-B55 in a concentration-dependent manner, and artepillin C, kaempferide, dihydrokaempferide, isosakuranetin, and kaempferol were estimated to have potential for CYP inhibition. kaempferol 197-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 25397516-1 2014 INTRODUCTION: COBI, a PK enhancer with no ARV activity is a more selective cytochrome P450 (CYP)3A inhibitor than ritonavir (RTV), does not induce CYP isozymes, and thus has less potential for drug-drug interactions. cobi 14-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 25361167-3 2014 The activities of CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 were attenuated by EEP-B55 in a concentration-dependent manner, and artepillin C, kaempferide, dihydrokaempferide, isosakuranetin, and kaempferol were estimated to have potential for CYP inhibition. Dihydrokaempferide 157-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 25181459-4 2014 Our data showed that metolazone activated hPXR-mediated expression of CYP3A4 and MDR1 in human hepatocytes and intestine cells and increased CYP3A4 promoter activity in various cell lines. Metolazone 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 25181459-4 2014 Our data showed that metolazone activated hPXR-mediated expression of CYP3A4 and MDR1 in human hepatocytes and intestine cells and increased CYP3A4 promoter activity in various cell lines. Metolazone 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 25394094-0 2014 Potential implications of CYP3A4, CYP3A5 and MDR-1 genetic variants on the efficacy of Lopinavir/Ritonavir (LPV/r) monotherapy in HIV-1 patients. Lopinavir 87-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 25274605-5 2014 The goals of our study were to test the assumption of substrate independence of the potency of inhibitors in vivo and to estimate the CR and IR for an extended list of substrates and inhibitors of CYP3A4. Chromium 134-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 24737309-0 2014 Normal CYP3A activity during arsenic trioxide therapy. Arsenic Trioxide 29-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-12 24837659-0 2014 Validation of 4beta-hydroxycholesterol and evaluation of other endogenous biomarkers for the assessment of CYP3A activity in healthy subjects. cholest-5-ene-3,4-diol 14-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-112 24837659-12 2014 CONCLUSIONS: Changes in plasma 4betaHC can be utilized as a surrogate for MDZ PK after multiple doses of potent CYP3A inducers. cholest-5-ene-3,4-diol 31-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-117 24837659-13 2014 There is a more limited dynamic range for 4betaHC for assessment of potential CYP3A inhibitors. cholest-5-ene-3,4-diol 42-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 25236915-0 2014 Influence of CYP3A4 induction/inhibition on the pharmacokinetics of vilazodone in healthy subjects. Vilazodone Hydrochloride 68-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 24890801-2 2014 We have elucidated the influence of CYP3A4 overexpression on the cellular response induced by antitumor acridine derivatives, C-1305 and C-1748, in two hepatocellular carcinoma (HepG2) cell lines, Hep3A4 stably transfected with CYP3A4 isoenzyme, and HepC34 expressing empty vector. Acridines 104-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 24890801-6 2014 In turn, the sub-G1 fraction was dominated in CYP3A4-overexpressing cells following C-1305 exposure. C 1305 84-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 24890801-9 2014 Conversely, cellular response was modulated following C-1305 treatment in CYP3A4-overexpressing cells, although metabolism of this drug was unaltered. C 1305 54-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 28346678-0 2014 CORRIGENDUM: Identification and Characterization of a Defective CYP3A4 Genotype in a Kidney Transplant Patient With Severely Diminished Tacrolimus Clearance. Tacrolimus 136-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 25236915-2 2014 Vilazodone seems to be metabolized primarily by the cytochrome P-450 (CYP) 3A4 isozyme and non-CYP-mediated pathways; concomitant use of drugs that affect CYP3A4 activity could potentially alter systemic exposure to vilazodone. Vilazodone Hydrochloride 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-78 24962564-9 2014 However, the effect of CYP3A4 induction by rifampicin on apremilast clearance is much more pronounced than that of CYP3A4 inhibition by ketoconazole. Rifampin 43-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 25236915-2 2014 Vilazodone seems to be metabolized primarily by the cytochrome P-450 (CYP) 3A4 isozyme and non-CYP-mediated pathways; concomitant use of drugs that affect CYP3A4 activity could potentially alter systemic exposure to vilazodone. Vilazodone Hydrochloride 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 24962564-9 2014 However, the effect of CYP3A4 induction by rifampicin on apremilast clearance is much more pronounced than that of CYP3A4 inhibition by ketoconazole. Ketoconazole 136-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 25236915-2 2014 Vilazodone seems to be metabolized primarily by the cytochrome P-450 (CYP) 3A4 isozyme and non-CYP-mediated pathways; concomitant use of drugs that affect CYP3A4 activity could potentially alter systemic exposure to vilazodone. Vilazodone Hydrochloride 216-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 25236915-16 2014 IMPLICATIONS: These results suggest that up to a 50% decrease of vilazodone dosage should be considered when it is given in combination with strong CYP3A4 inhibitors; conversely, increasing the vilazodone dosage up to a maximum of 80 mg/d should be considered when it is given in combination with strong CYP3A4 inducers. Vilazodone Hydrochloride 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 25008118-2 2014 In vitro data from human liver microsomes suggest that alisporivir is a substrate and a time-dependent inhibitor (TDI) of CYP3A4. alisporivir 55-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 25161167-5 2014 Moreover, recombinant tRNA/miR-27b agents were biologically active in reducing the mRNA and protein expression levels of cytochrome P450 3A4 (CYP3A4), which consequently led to lower midazolam 1"-hydroxylase activity. Midazolam 183-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-140 25161167-5 2014 Moreover, recombinant tRNA/miR-27b agents were biologically active in reducing the mRNA and protein expression levels of cytochrome P450 3A4 (CYP3A4), which consequently led to lower midazolam 1"-hydroxylase activity. Midazolam 183-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 24846165-1 2014 Nilotinib is used to treat chronic myeloid leukemia (CML), and is metabolized by CYP3A. nilotinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 24846165-3 2014 Treatments of HIV patients with CML are with HAART drugs, ritonavir and efavirenz, may cause complex drug interactions through CYP3A inhibition or induction. Ritonavir 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 24846165-3 2014 Treatments of HIV patients with CML are with HAART drugs, ritonavir and efavirenz, may cause complex drug interactions through CYP3A inhibition or induction. efavirenz 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 24944083-8 2014 CYP2C9 inhibitors strongly inhibited S(-)-NAF metabolism, and CYP2C8, CYP2C19 and CYP3A4/5 inhibitors moderately inhibited S(-)-NAF metabolism. naftopidil 123-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 24590863-6 2014 The standardized EJE was incubated with pooled human liver microsomes to assess the CYP2C9-, CYP2D6-, and CYP3A4-mediated metabolism of diclofenac, dextromethorphan, and testosterone, respectively. Diclofenac 136-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 25589928-5 2015 The series also harbored the CYP3A4 TDI liability driven by the presence of both a morpholine and an indole moiety. morpholine 83-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 25589928-5 2015 The series also harbored the CYP3A4 TDI liability driven by the presence of both a morpholine and an indole moiety. indole 101-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 25106415-0 2014 Clinical CYP3A inhibitor alternatives to ketoconazole, clarithromycin and itraconazole, are not transported into the liver by hepatic organic anion transporting polypeptides and organic cation transporter 1. Ketoconazole 41-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-14 25106415-0 2014 Clinical CYP3A inhibitor alternatives to ketoconazole, clarithromycin and itraconazole, are not transported into the liver by hepatic organic anion transporting polypeptides and organic cation transporter 1. Clarithromycin 55-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-14 25106415-0 2014 Clinical CYP3A inhibitor alternatives to ketoconazole, clarithromycin and itraconazole, are not transported into the liver by hepatic organic anion transporting polypeptides and organic cation transporter 1. Itraconazole 74-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-14 25106415-1 2014 Ketoconazole is no longer available for clinical determination of worst-case victim drug-drug interaction (DDI) potential for cytochrome P450 3A (CYP3A)-substrate drugs; clarithromycin and itraconazole are the proposed replacements. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-144 25106415-1 2014 Ketoconazole is no longer available for clinical determination of worst-case victim drug-drug interaction (DDI) potential for cytochrome P450 3A (CYP3A)-substrate drugs; clarithromycin and itraconazole are the proposed replacements. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-151 25106415-1 2014 Ketoconazole is no longer available for clinical determination of worst-case victim drug-drug interaction (DDI) potential for cytochrome P450 3A (CYP3A)-substrate drugs; clarithromycin and itraconazole are the proposed replacements. Clarithromycin 170-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-151 25106415-1 2014 Ketoconazole is no longer available for clinical determination of worst-case victim drug-drug interaction (DDI) potential for cytochrome P450 3A (CYP3A)-substrate drugs; clarithromycin and itraconazole are the proposed replacements. Itraconazole 189-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-151 25359648-7 2014 However, patients taking anticoagulants or cytochrome P450 3A4 substrates (such as clarithromycin, erythromycin, ketoconazole, itraconazole, midazolam and triazolam) in addition to specific vitamin or mineral supplements (vitamins D, E, K, calcium, fluoride, iron, magnesium, selenium or zinc) may face additional challenges. Clarithromycin 83-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-62 25359648-7 2014 However, patients taking anticoagulants or cytochrome P450 3A4 substrates (such as clarithromycin, erythromycin, ketoconazole, itraconazole, midazolam and triazolam) in addition to specific vitamin or mineral supplements (vitamins D, E, K, calcium, fluoride, iron, magnesium, selenium or zinc) may face additional challenges. Erythromycin 99-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-62 25359648-7 2014 However, patients taking anticoagulants or cytochrome P450 3A4 substrates (such as clarithromycin, erythromycin, ketoconazole, itraconazole, midazolam and triazolam) in addition to specific vitamin or mineral supplements (vitamins D, E, K, calcium, fluoride, iron, magnesium, selenium or zinc) may face additional challenges. Ketoconazole 113-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-62 25359648-7 2014 However, patients taking anticoagulants or cytochrome P450 3A4 substrates (such as clarithromycin, erythromycin, ketoconazole, itraconazole, midazolam and triazolam) in addition to specific vitamin or mineral supplements (vitamins D, E, K, calcium, fluoride, iron, magnesium, selenium or zinc) may face additional challenges. Itraconazole 127-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-62 25359648-7 2014 However, patients taking anticoagulants or cytochrome P450 3A4 substrates (such as clarithromycin, erythromycin, ketoconazole, itraconazole, midazolam and triazolam) in addition to specific vitamin or mineral supplements (vitamins D, E, K, calcium, fluoride, iron, magnesium, selenium or zinc) may face additional challenges. Midazolam 141-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-62 25359648-7 2014 However, patients taking anticoagulants or cytochrome P450 3A4 substrates (such as clarithromycin, erythromycin, ketoconazole, itraconazole, midazolam and triazolam) in addition to specific vitamin or mineral supplements (vitamins D, E, K, calcium, fluoride, iron, magnesium, selenium or zinc) may face additional challenges. Triazolam 155-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-62 25272989-4 2014 The reaction phenotype study showed that CYP3A4, CYP2C9, and CYP1A2 were the major cytochrome P450 isozymes in the metabolism of CSA. 3-hydroxy-4-prenyl-5-methoxystilbene-2-carboxylic acid 129-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 25272989-8 2014 CSA reversibly inhibited CYP3A4 and CYP2C9 activities in human liver microsomes with IC50 values of 28.3 and 31.3 muM, respectively, but exhibited no inhibition activities to CYP1A2, CYP2A6, CYP2C19, CYP2D6, and CYP2E1. 3-hydroxy-4-prenyl-5-methoxystilbene-2-carboxylic acid 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 25343516-0 2014 Dual effects of ketoconazole cis-enantiomers on CYP3A4 in human hepatocytes and HepG2 Cells. Ketoconazole 16-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 25343516-1 2014 Antifungal drug ketoconazole causes severe drug-drug interactions by influencing gene expression and catalytic activity of major drug-metabolizing enzyme cytochrome P450 CYP3A4. Ketoconazole 16-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 25343516-4 2014 In the current paper, we have examined the effects of ketoconazole cis-enantiomers on the expression of CYP3A4 in human hepatocytes and HepG2 cells and on catalytic activity of CYP3A4 in human liver microsomes. Ketoconazole 54-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 25343516-5 2014 We show that both ketoconazole enantiomers induce CYP3A4 mRNA and protein in human hepatocytes and HepG2 cells. Ketoconazole 18-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 25343516-7 2014 Catalytic activity of CYP3A4/5 towards two prototypic substrates of CYP3A enzymes, testosterone and midazolam, was determined in presence of both (+)-ketoconazole and (-)-ketoconazole in human liver microsomes. Testosterone 83-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 25343516-7 2014 Catalytic activity of CYP3A4/5 towards two prototypic substrates of CYP3A enzymes, testosterone and midazolam, was determined in presence of both (+)-ketoconazole and (-)-ketoconazole in human liver microsomes. Testosterone 83-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-27 25343516-7 2014 Catalytic activity of CYP3A4/5 towards two prototypic substrates of CYP3A enzymes, testosterone and midazolam, was determined in presence of both (+)-ketoconazole and (-)-ketoconazole in human liver microsomes. Midazolam 100-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 25343516-7 2014 Catalytic activity of CYP3A4/5 towards two prototypic substrates of CYP3A enzymes, testosterone and midazolam, was determined in presence of both (+)-ketoconazole and (-)-ketoconazole in human liver microsomes. Midazolam 100-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-27 25343516-7 2014 Catalytic activity of CYP3A4/5 towards two prototypic substrates of CYP3A enzymes, testosterone and midazolam, was determined in presence of both (+)-ketoconazole and (-)-ketoconazole in human liver microsomes. Ketoconazole 146-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 25343516-7 2014 Catalytic activity of CYP3A4/5 towards two prototypic substrates of CYP3A enzymes, testosterone and midazolam, was determined in presence of both (+)-ketoconazole and (-)-ketoconazole in human liver microsomes. Ketoconazole 146-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-27 25343516-7 2014 Catalytic activity of CYP3A4/5 towards two prototypic substrates of CYP3A enzymes, testosterone and midazolam, was determined in presence of both (+)-ketoconazole and (-)-ketoconazole in human liver microsomes. Ketoconazole 167-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 25343516-7 2014 Catalytic activity of CYP3A4/5 towards two prototypic substrates of CYP3A enzymes, testosterone and midazolam, was determined in presence of both (+)-ketoconazole and (-)-ketoconazole in human liver microsomes. Ketoconazole 167-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-27 25343516-8 2014 Overall, both ketoconazole cis-enantiomers induced CYP3A4 in human cells and inhibited CYP3A4 in human liver microsomes. Ketoconazole 14-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 25343516-8 2014 Overall, both ketoconazole cis-enantiomers induced CYP3A4 in human cells and inhibited CYP3A4 in human liver microsomes. Ketoconazole 14-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 25008118-6 2014 The model predicted an alisporivir AUC increase by 9.4-fold and a decrease by 86% when alisporivir was co-administrated with ketoconazole (CYP3A4 inhibitor) or rifampin (CYP3A4 inducer), respectively. Rifampin 160-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 25008118-3 2014 The aim of the current work was to develop a novel physiologically based pharmacokinetic (PBPK) model to quantitatively assess the magnitude of CYP3A4 mediated drug-drug interactions with alisporivir as the substrate or victim drug. alisporivir 188-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 25008118-6 2014 The model predicted an alisporivir AUC increase by 9.4-fold and a decrease by 86% when alisporivir was co-administrated with ketoconazole (CYP3A4 inhibitor) or rifampin (CYP3A4 inducer), respectively. alisporivir 23-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 25008118-6 2014 The model predicted an alisporivir AUC increase by 9.4-fold and a decrease by 86% when alisporivir was co-administrated with ketoconazole (CYP3A4 inhibitor) or rifampin (CYP3A4 inducer), respectively. alisporivir 23-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 25008118-6 2014 The model predicted an alisporivir AUC increase by 9.4-fold and a decrease by 86% when alisporivir was co-administrated with ketoconazole (CYP3A4 inhibitor) or rifampin (CYP3A4 inducer), respectively. alisporivir 87-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 25008118-6 2014 The model predicted an alisporivir AUC increase by 9.4-fold and a decrease by 86% when alisporivir was co-administrated with ketoconazole (CYP3A4 inhibitor) or rifampin (CYP3A4 inducer), respectively. alisporivir 87-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 25008118-6 2014 The model predicted an alisporivir AUC increase by 9.4-fold and a decrease by 86% when alisporivir was co-administrated with ketoconazole (CYP3A4 inhibitor) or rifampin (CYP3A4 inducer), respectively. Ketoconazole 125-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 25125033-2 2014 This particular characteristic makes it advantageous when combined with drugs metabolized by CYP3A4, such as cyclosporine. Cyclosporine 109-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24655660-1 2014 In vitro studies have shown that vitamin D may induce several cytochrome P450 (CYP) enzymes in general and CYP3A4 in particular. Vitamin D 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 24971633-1 2014 Cerivastatin and repaglinide are substrates of cytochrome P450 (CYP)2C8, CYP3A4, and organic anion-transporting polypeptide (OATP)1B1. cerivastatin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 24655660-2 2014 The primary aim of this study was to investigate the relationship between plasma levels of 25-hydroxyvitamin D3 and suggested in vivo markers of CYP3A activity in healthy volunteers from Sweden and Korea. Calcifediol 91-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-150 24655660-4 2014 In addition, we studied the modulating effects of three vitamin D receptor promoter polymorphisms on the association between 25-hydroxyvitamin D3 and CYP3A enzyme activity in Swedish subjects. Calcifediol 125-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 24655660-5 2014 The plasma levels of 25-hydroxyvitamin D3 were not significantly associated with CYP3A phenotypes in any of the three studies, but after accounting for the vitamin D receptor polymorphism rs4516035, there was a significant positive association between 25-hydroxyvitamin D3 and CYP3A activity (p = 0.004). Calcifediol 252-272 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 277-282 24655660-8 2014 In conclusion, our results suggest that the overall influence on the CYP3A activity by 25-hydroxyvitamin D3 is of marginal importance. Calcifediol 87-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 25164142-6 2014 Both agents inhibit CYP3A4, with cobicistat being a more specific CYP inhibitor than ritonavir. Cobicistat 33-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 25164142-6 2014 Both agents inhibit CYP3A4, with cobicistat being a more specific CYP inhibitor than ritonavir. Ritonavir 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 25047407-2 2014 This open-label, single-centre, 2-period study evaluated the effect of armodafinil, a moderate inducer of cytochrome-P450 (CYP) isoenzyme CYP3A4, on the pharmacokinetics and safety of ziprasidone, an atypical antipsychotic used to treat bipolar I disorder and metabolized in part by CYP3A4. Modafinil 71-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 25047407-2 2014 This open-label, single-centre, 2-period study evaluated the effect of armodafinil, a moderate inducer of cytochrome-P450 (CYP) isoenzyme CYP3A4, on the pharmacokinetics and safety of ziprasidone, an atypical antipsychotic used to treat bipolar I disorder and metabolized in part by CYP3A4. Modafinil 71-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 283-289 25125128-1 2014 BACKGROUND: Tacrolimus is a CYP3A4 inhibitor and can alter colchicine metabolism. Tacrolimus 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 25125128-1 2014 BACKGROUND: Tacrolimus is a CYP3A4 inhibitor and can alter colchicine metabolism. Colchicine 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 24971633-1 2014 Cerivastatin and repaglinide are substrates of cytochrome P450 (CYP)2C8, CYP3A4, and organic anion-transporting polypeptide (OATP)1B1. repaglinide 17-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 25141974-2 2014 As CYP3A activity may influence both clearance and oral bioavailability in a distinct manner, in this study the pharmacokinetics of the CYP3A substrate midazolam were evaluated after semi-simultaneous oral and intravenous administration in morbidly obese patients, and compared with healthy volunteers. Midazolam 152-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-8 25141974-2 2014 As CYP3A activity may influence both clearance and oral bioavailability in a distinct manner, in this study the pharmacokinetics of the CYP3A substrate midazolam were evaluated after semi-simultaneous oral and intravenous administration in morbidly obese patients, and compared with healthy volunteers. Midazolam 152-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-141 25008344-2 2014 Furanocoumarins in grapefruit juice are cornerstone examples of diet-derived xenobiotics that perpetrate interactions with drugs via mechanism-based inhibition of intestinal CYP3A4. Furocoumarins 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 24907142-2 2014 After discontinuation, nevirapine has an inductive effect on cytochrome P450 3A4, which persists for a few weeks and which, after switching to rilpivirine, may reduce rilpivirine exposures and have a negative clinical impact. Nevirapine 23-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-80 25074870-7 2014 The protein phosphatase (PP) inhibitor okadaic acid (100 nM) and transfection with anti-PP1 siRNA but not anti-PP2A siRNA led to reduced expression of CYP3A4 mRNA. Okadaic Acid 39-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 25074871-3 2014 By using astemizole as a probe substrate for CYP4F12 and CYP3A4, it was observed that although CYP4F12 favored astemizole O-demethylation as the primary route of metabolism, CYP3A4 was capable of metabolizing astemizole at multiple sites on the molecule. Astemizole 9-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 25074871-3 2014 By using astemizole as a probe substrate for CYP4F12 and CYP3A4, it was observed that although CYP4F12 favored astemizole O-demethylation as the primary route of metabolism, CYP3A4 was capable of metabolizing astemizole at multiple sites on the molecule. Astemizole 9-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 25074871-3 2014 By using astemizole as a probe substrate for CYP4F12 and CYP3A4, it was observed that although CYP4F12 favored astemizole O-demethylation as the primary route of metabolism, CYP3A4 was capable of metabolizing astemizole at multiple sites on the molecule. Astemizole 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 25074871-3 2014 By using astemizole as a probe substrate for CYP4F12 and CYP3A4, it was observed that although CYP4F12 favored astemizole O-demethylation as the primary route of metabolism, CYP3A4 was capable of metabolizing astemizole at multiple sites on the molecule. Astemizole 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 25074871-3 2014 By using astemizole as a probe substrate for CYP4F12 and CYP3A4, it was observed that although CYP4F12 favored astemizole O-demethylation as the primary route of metabolism, CYP3A4 was capable of metabolizing astemizole at multiple sites on the molecule. Astemizole 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 25074871-3 2014 By using astemizole as a probe substrate for CYP4F12 and CYP3A4, it was observed that although CYP4F12 favored astemizole O-demethylation as the primary route of metabolism, CYP3A4 was capable of metabolizing astemizole at multiple sites on the molecule. Astemizole 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 25074871-5 2014 Conversely, although an isotope effect of 3.8 was observed for the formation of the O-desmethyl metabolite when deuterated astemizole was metabolized by CYP3A4, there was no decrease in the clearance of astemizole. deuterated astemizole 112-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 25074871-5 2014 Conversely, although an isotope effect of 3.8 was observed for the formation of the O-desmethyl metabolite when deuterated astemizole was metabolized by CYP3A4, there was no decrease in the clearance of astemizole. Astemizole 123-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 25074871-7 2014 As predicted, multiple favorable binding orientations were available for astemizole docked into the active site of CYP3A4, but only a single binding orientation with the site of O-demethylation oriented toward the heme was identified for CYP4F12. Astemizole 73-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 25217544-2 2014 CYP3A4 is one of the primary CYP450 isoforms responsible for the metabolism of methadone to EDDP in humans. Methadone 79-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24907142-2 2014 After discontinuation, nevirapine has an inductive effect on cytochrome P450 3A4, which persists for a few weeks and which, after switching to rilpivirine, may reduce rilpivirine exposures and have a negative clinical impact. Rilpivirine 143-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-80 25217544-2 2014 CYP3A4 is one of the primary CYP450 isoforms responsible for the metabolism of methadone to EDDP in humans. 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine 92-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25217544-3 2014 The purpose of this study was to evaluate the role of CYP3A4 genetic polymorphisms in accidental methadone fatalities. Methadone 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 25217544-9 2014 Our findings indicate that there may be two or more SNPs on the CYP3A4 gene that cause or contribute to the methadone poor metabolizer phenotype. Methadone 108-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 24907142-2 2014 After discontinuation, nevirapine has an inductive effect on cytochrome P450 3A4, which persists for a few weeks and which, after switching to rilpivirine, may reduce rilpivirine exposures and have a negative clinical impact. Rilpivirine 167-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-80 24269662-10 2014 In summary, our results suggest that abiraterone inhibits the CYP3A4-mediated inactivation of active vitamin D3 in human liver and intestine, potentially providing additional anti-cancer benefits to prostate cancer patients. abiraterone 37-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 24782075-0 2014 Population pharmacokinetic analysis of circadian rhythms in hepatic CYP3A activity using midazolam. Midazolam 89-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 24269662-0 2014 Abiraterone inhibits 1alpha,25-dihydroxyvitamin D3 metabolism by CYP3A4 in human liver and intestine in vitro. abiraterone 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 24269662-10 2014 In summary, our results suggest that abiraterone inhibits the CYP3A4-mediated inactivation of active vitamin D3 in human liver and intestine, potentially providing additional anti-cancer benefits to prostate cancer patients. Cholecalciferol 101-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 24269662-0 2014 Abiraterone inhibits 1alpha,25-dihydroxyvitamin D3 metabolism by CYP3A4 in human liver and intestine in vitro. Calcitriol 21-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 25193858-3 2014 Tasquinimod is metabolized via cytochrome P4503A4, but ketoconazole at a dose which completely inhibits CYP3A metabolism does not affect tasquinimod"s ability to inhibit endothelial "sprouting" in vitro or anti-cancer efficacy against human prostate cancer xenografts in vivo. Ketoconazole 55-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-109 24269662-4 2014 The purpose of this study was to assess the potential of abiraterone to block hepatic and intestinal inactivation of biologically active vitamin D3in vitro and to evaluate if abiraterone can alter CYP3A4 marker substrate activities. abiraterone 175-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 24269662-8 2014 The mechanism of CYP3A4-mediated inhibition of 1alpha,25(OH)2D3 by abiraterone was competitive (apparent Ki 2.8-4.3muM). Calcitriol 47-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 24269662-8 2014 The mechanism of CYP3A4-mediated inhibition of 1alpha,25(OH)2D3 by abiraterone was competitive (apparent Ki 2.8-4.3muM). abiraterone 67-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 25051018-0 2014 CYP3A4*22 and CYP3A5*3 are associated with increased levels of plasma simvastatin concentrations in the cholesterol and pharmacogenetics study cohort. Simvastatin 70-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25051018-0 2014 CYP3A4*22 and CYP3A5*3 are associated with increased levels of plasma simvastatin concentrations in the cholesterol and pharmacogenetics study cohort. Cholesterol 104-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25051018-1 2014 OBJECTIVE: Simvastatin is primarily metabolized by CYP3A4. Simvastatin 11-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 25051018-3 2014 We aim to determine whether CYP3A4*22 and CYP3A5*3 alleles are associated with increased plasma concentrations of simvastatin lactone (SV) and simvastatin acid (SVA). Simvastatin 114-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 25051018-3 2014 We aim to determine whether CYP3A4*22 and CYP3A5*3 alleles are associated with increased plasma concentrations of simvastatin lactone (SV) and simvastatin acid (SVA). simvastatin acid 143-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 25051018-4 2014 This is the first report evaluating associations between in-vivo simvastatin concentrations and CYP3A4*22, alone or in a combined CYP3A4/5 genotype-defined classification. Simvastatin 65-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 25051018-7 2014 Associations between simvastatin concentrations and CYP3A4*22 and CYP3A5*3 alleles were tested separately and in a combined CYP3A4/5 genotype-defined classification system. Simvastatin 21-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 25051018-13 2014 CONCLUSION: Genetic variation in CYP3A4 was associated with plasma simvastatin concentrations in self-reported Whites. Simvastatin 67-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 25051018-14 2014 Genetic variations in CYP3A4 and CYP3A5 were associated with plasma simvastatin concentrations in self-reported African-Americans. Simvastatin 68-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 25061110-9 2014 Because CYP3A4/5/7 represent up to 40% of total cytochrome P450 in the liver, these data indicate that these enzymes are the major source of H2O2 in human liver microsomes. Hydrogen Peroxide 141-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 24779639-2 2014 In this article, the modulatory effects of extracts from vinegar-baked Radix Bupleuri (VBRB) and saikosaponins on the activity of CYP1A2, CYP2C9 and CYP3A4 were investigated in vitro. saikosaponin D 97-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 25061110-6 2014 Significantly greater activity was detected in preparations containing individual cytochrome P450s coexpressed with CPR (from 6.0 nmol H2O2/min/nmol P450 to 0.2 nmol/min/nmol P450); CYP1A1 was the most active, followed by CYP2D6, CYP3A4, CYP2E1, CYP4A11, CYP1A2, and CYP2C subfamily enzymes. Hydrogen Peroxide 135-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-236 25105339-0 2014 Identification of amino acid and glutathione N-conjugates of toosendanin: bioactivation of the furan ring mediated by CYP3A4. glutathione n 33-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 24479199-4 2010 Mibefradil (Posicor), a potent inhibitor of CYP3A4, was withdrawn from the market after numerous reports of serious drug-drug interactions. Mibefradil 12-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 24479199-5 2010 Terfenadine (Seldane) and Cisapride (Propulsid) were withdrawn after patients taking the recommended dose along with CYP3A4 inhibitors such as ketoconazole developed heart arrhythmia leading to heart attack or death. Ketoconazole 143-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 25044307-11 2014 Ketoconazole (a CYP3A4 inhibitor) and alkaline pH strongly inhibited the hydroxylation of PSA, but moderately suppressed its sulfoxidation in liver microsomes. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 25408661-4 2014 Ifosfamide is also converted by CYP3A4 to inactive but neurotoxic metabolites. Ifosfamide 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 25408661-7 2014 Since ifosfamide and aprepitant are both substrates of CYP3A4, a pharmacokinetic interaction could result in secondary effects such as the potentialization of neurological side effects. Ifosfamide 6-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 24479199-0 2010 ML368 Identification of Imidazopyridines as Selective Inhibitors of the Cytochrome P450 Enzyme CYP3A4 Here we report the first highly selective CYP3A4 inhibitor optimized from an initial lead with 30-fold selectivity over CYP3A5 to yield a series of compounds with greater than 1000-fold selectivity. ML368 0-5 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-100 24479199-0 2010 ML368 Identification of Imidazopyridines as Selective Inhibitors of the Cytochrome P450 Enzyme CYP3A4 Here we report the first highly selective CYP3A4 inhibitor optimized from an initial lead with 30-fold selectivity over CYP3A5 to yield a series of compounds with greater than 1000-fold selectivity. ML368 0-5 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 24479199-0 2010 ML368 Identification of Imidazopyridines as Selective Inhibitors of the Cytochrome P450 Enzyme CYP3A4 Here we report the first highly selective CYP3A4 inhibitor optimized from an initial lead with 30-fold selectivity over CYP3A5 to yield a series of compounds with greater than 1000-fold selectivity. imidazopyridine 24-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-100 24479199-0 2010 ML368 Identification of Imidazopyridines as Selective Inhibitors of the Cytochrome P450 Enzyme CYP3A4 Here we report the first highly selective CYP3A4 inhibitor optimized from an initial lead with 30-fold selectivity over CYP3A5 to yield a series of compounds with greater than 1000-fold selectivity. imidazopyridine 24-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 24479199-4 2010 Mibefradil (Posicor), a potent inhibitor of CYP3A4, was withdrawn from the market after numerous reports of serious drug-drug interactions. Mibefradil 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 25105339-0 2014 Identification of amino acid and glutathione N-conjugates of toosendanin: bioactivation of the furan ring mediated by CYP3A4. furan 95-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 24697814-0 2014 Population pharmacokinetic modelling to assess the impact of CYP2D6 and CYP3A metabolic phenotypes on the pharmacokinetics of tamoxifen and endoxifen. Tamoxifen 126-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-77 24886881-2 2014 In the present study, the effects of artemisinin on pregnane X receptor (PXR)-mediated CYP3A expression and its therapeutic role in inflammatory bowel disease were investigated. artemisinin 37-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 24886881-3 2014 LS174T cells exposed to artemisinin at various concentrations and for different periods of time were examined with respect to the specific induction of CYP3A4 and PXR mRNA expression. artemisinin 24-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 24886881-4 2014 Transient transfection experiments showed transcriptional activation of the CYP3A4 gene through artemisinin to be PXR-dependent. artemisinin 96-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 24886881-5 2014 An electrophoretic-mobility shift assay (EMSA) showed that artemisinin activates the DNA-binding capacity of the PXR for the CYP3A4 element. artemisinin 59-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 24886881-6 2014 These results indicate that the induction of CYP3A4 by artemisinin is mediated through the activation of PXR. artemisinin 55-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 24886881-9 2014 Artemisinin was found to prevent or reduce the severity of colonic inflammation by inducing CYP3A expression by activation of PXR. artemisinin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-97 24973543-3 2014 This investigation revealed that CYP2J2, along with CYP3A4/5 and CYP2D6, efficiently metabolizes ritonavir, and to a CYP2J2-specific (minor) metabolite. Ritonavir 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 24973543-8 2014 A modest (2-6%) contribution of CYP2J2 to ritonavir clearance is predicted which increases to more than 20% in subjects carrying CYP2D6 poor metabolizer polymorphisms and CYP3A4 irreversible inhibition. Ritonavir 42-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 24957823-3 2014 Cytochrome P450 (CYP) 3A, which can be induced or inhibited by ARV and antituberculosis drugs, is a minor (~20%) metabolic pathway for PA-824. Protactinium 135-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-24 25027283-5 2014 In human liver, CYP3A4 plays an important role in biotransforming AFB1 to the toxic product AFB1-8,9-epoxide. aflatoxin B1-2,3-oxide 92-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 24797229-5 2014 These models can predict well the effects of CYP3A4 inhibition and induction on the PK of quetiapine, the PK profile of quetiapine IR in children and adults, and the PK profile of quetiapine XR in adults. Quetiapine Fumarate 90-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 24797229-5 2014 These models can predict well the effects of CYP3A4 inhibition and induction on the PK of quetiapine, the PK profile of quetiapine IR in children and adults, and the PK profile of quetiapine XR in adults. Quetiapine Fumarate 120-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 24797229-5 2014 These models can predict well the effects of CYP3A4 inhibition and induction on the PK of quetiapine, the PK profile of quetiapine IR in children and adults, and the PK profile of quetiapine XR in adults. Quetiapine Fumarate 120-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 24697814-0 2014 Population pharmacokinetic modelling to assess the impact of CYP2D6 and CYP3A metabolic phenotypes on the pharmacokinetics of tamoxifen and endoxifen. 4-hydroxy-N-desmethyltamoxifen 140-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-77 24697814-2 2014 The major metabolic enzymes involved in endoxifen formation are CYP2D6 and CYP3A. 4-hydroxy-N-desmethyltamoxifen 40-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 24981100-6 2014 CONCLUSIONS: Compared to females, males have lower levels of cytochrome P450 3A4 (CYP3A4), for which erythromycin is both a substrate and inhibitor. Erythromycin 101-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-80 24697814-8 2014 In the final model for tamoxifen, the dextromethorphan derived metabolic phenotypes for CYP2D6 as well as CYP3A significantly (P < 0.0001) explained 54% of the observed variability in endoxifen formation (inter-individual variability reduced from 55% to 25%). Tamoxifen 23-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-111 24981100-6 2014 CONCLUSIONS: Compared to females, males have lower levels of cytochrome P450 3A4 (CYP3A4), for which erythromycin is both a substrate and inhibitor. Erythromycin 101-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 24981100-7 2014 Use of CYP3A4-inhibiting drugs such as erythromycin in men may thus result in even lower levels of CYP3A4 and, consequently, higher levels of CYP3A4-metabolized substances. Erythromycin 39-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 25053387-5 2014 METHODS: Inhibition constant (K(i)) of aprepitant for CYP3A-mediated docetaxel hydroxylation was estimated with human liver microsomes. Docetaxel 69-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-59 24697814-8 2014 In the final model for tamoxifen, the dextromethorphan derived metabolic phenotypes for CYP2D6 as well as CYP3A significantly (P < 0.0001) explained 54% of the observed variability in endoxifen formation (inter-individual variability reduced from 55% to 25%). 4-hydroxy-N-desmethyltamoxifen 187-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-111 24981100-7 2014 Use of CYP3A4-inhibiting drugs such as erythromycin in men may thus result in even lower levels of CYP3A4 and, consequently, higher levels of CYP3A4-metabolized substances. Erythromycin 39-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 24981100-7 2014 Use of CYP3A4-inhibiting drugs such as erythromycin in men may thus result in even lower levels of CYP3A4 and, consequently, higher levels of CYP3A4-metabolized substances. Erythromycin 39-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 24697814-9 2014 CONCLUSIONS: We have shown that not only CYP2D6, but also CYP3A enzyme activity influences the tamoxifen to endoxifen conversion in breast cancer patients. Tamoxifen 95-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 24697814-9 2014 CONCLUSIONS: We have shown that not only CYP2D6, but also CYP3A enzyme activity influences the tamoxifen to endoxifen conversion in breast cancer patients. 4-hydroxy-N-desmethyltamoxifen 108-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 24697814-10 2014 Our developed model may be used to assess separately the impact of CYP2D6 and CYP3A mediated drug-drug interactions with tamoxifen without the necessity of administering this anti-oestrogenic drug and to support Bayesian guided therapeutic drug monitoring of tamoxifen in routine clinical practice. Tamoxifen 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 25022720-9 2014 Multiple-dose rifampicin (simultaneous P-gp and CYP3A4 induction) decreased lenvatinib AUC0- (total: 18 %; free: 9 %). Rifampin 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 25022720-9 2014 Multiple-dose rifampicin (simultaneous P-gp and CYP3A4 induction) decreased lenvatinib AUC0- (total: 18 %; free: 9 %). lenvatinib 76-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 25022720-11 2014 CONCLUSION: Lenvatinib exposure was increased by P-gp inhibition; however, based on free concentrations, simultaneous P-gp and CYP3A4 induction results met the prespecified bioequivalence 90 % confidence interval. lenvatinib 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 25008345-3 2014 It is primarily metabolized by human CYP2C19 and CYP3A4 to 5"-OH OMP and a sulfone product, respectively. 5"-oh omp 59-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 25117183-13 2014 Vandetanib with CYP3A4 substrates or omeprazole/ranitidine is unlikely to result in clinically relevant drug-drug interactions. vandetanib 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 24924386-5 2014 Our results demonstrated a strong and predictive relationship between the extent of midazolam AUC change in humans and the various parameters calculated from both CYP3A4 mRNA and enzyme activity. Midazolam 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 27129005-6 2014 The modest increases in AUC and Cmax following co-administration of GSK2336805 plus ritonavir suggest that GSK2336805 when given concomitantly with a single CYP3A/Pgp inhibiting drug will not likely require dose adjustment. Ritonavir 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-162 25008345-3 2014 It is primarily metabolized by human CYP2C19 and CYP3A4 to 5"-OH OMP and a sulfone product, respectively. Sulfones 75-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 25028073-6 2014 CONCLUSION: Felodipine may be a weak in vivo inhibitor of CYP3A and CYP2D6 but is unlikely to act as a significant perpetrator of PK-DDIs. Felodipine 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 24954688-4 2014 Kinetics studies were conducted to evaluate the K i values and mechanism(s) of the inhibition of CYP2E1, CYP3A4, UGT1A1 and UGT1A9 by p-cresol. 4-cresol 134-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 24954688-6 2014 p-Cresol was the most potent individual inhibitor, producing >50% inhibition of CYP2E1, CYP3A4, UGT1A1, UGT1A9 and UGT2B7 at a concentration of 100 muM. 4-cresol 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 25019201-7 2014 Edivoxetine is readily absorbed with metabolism proceeding through the CYP hepatic enzyme pathway, with CYP2D6 and CYP3A4 playing the most prominent roles. alpha-((5-fluoro-2-methoxyphenyl)methyl)-alpha-(tetrahydro-2H-pyran-4-yl)-2-morpholinemethanol 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 24954688-9 2014 K i values for p-cresol inhibition of human liver microsomal CYP2E1, CYP3A4 and UGT1A1 ranged from 43 to 89 muM. 4-cresol 15-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 24950369-0 2014 CYP3A4*22 (c.522-191 C>T; rs35599367) is associated with lopinavir pharmacokinetics in HIV-positive adults. Lopinavir 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25189890-6 2014 Cytochrome P-450 (CYP)3A4 activity was measured by beta-hydroxylation of testosterone using human recombinant CYP3A4. Testosterone 73-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-25 25074401-11 2014 Herbal products and various drugs may increase rivaroxaban levels by inhibiting P-glycoprotein and cytochrome P450 3A4 activity. Rivaroxaban 47-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-118 24357138-11 2014 In conclusion, 11beta-HSD1 and CYP3A4 are principally responsible for the metabolism of TAK-802 in humans and 11beta-HSD1 may be responsible for the observed species difference. 8-(3-(1-((3-fluorophenyl)methyl)-4-piperidinyl)-1-oxopropyl)-1,2,5,6-tetrahydro-4H-pyrrolo(3,2,1-ij)quinolin-4-one 88-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 24836897-2 2014 Hydrocodone is metabolized by cytochrome P450 (CYP) 2D6 into hydromorphone and by CYP3A4 into norhydrocodone. Hydrocodone 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 24836897-2 2014 Hydrocodone is metabolized by cytochrome P450 (CYP) 2D6 into hydromorphone and by CYP3A4 into norhydrocodone. norhydrocodone 94-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 24836897-10 2014 Concurrent use of a CYP2D6 and/or CYP3A4 inhibitor altered hydromorphone and norhydrocodone mole fractions, compared with the control group. Hydromorphone 59-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 24836897-10 2014 Concurrent use of a CYP2D6 and/or CYP3A4 inhibitor altered hydromorphone and norhydrocodone mole fractions, compared with the control group. norhydrocodone 77-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 24860154-2 2014 It is metabolized primarily by the cytochrome P450 isoenzyme 3A4 (CYP3A4) to a less-active N-monodesmethyl metabolite. Nitrogen 91-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-64 24860154-2 2014 It is metabolized primarily by the cytochrome P450 isoenzyme 3A4 (CYP3A4) to a less-active N-monodesmethyl metabolite. Nitrogen 91-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 24950369-2 2014 We investigated the association of CYP3A4*22 with the pharmacokinetics of lopinavir through a population pharmacokinetic approach. Lopinavir 74-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 24950369-7 2014 We observed a 2.3-fold higher lopinavir trough concentration (Ctrough) in individuals with CYP3A4*22/*22, a 1.8-fold higher Ctrough with SLCO1B1 521CC and a 9.7-fold higher Ctrough in individuals homozygous for both single nucleotide polymorphisms, compared with noncarriers. Lopinavir 30-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 24950369-8 2014 A simulated dose-reduction scenario showed that 200/100 mg lopinavir/ritonavir was adequate to achieve therapeutic concentration in individuals with CYP3A4*22/*22 alone or in combination with SLCO1B1 521CC. Lopinavir 59-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 24950369-8 2014 A simulated dose-reduction scenario showed that 200/100 mg lopinavir/ritonavir was adequate to achieve therapeutic concentration in individuals with CYP3A4*22/*22 alone or in combination with SLCO1B1 521CC. Ritonavir 69-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 24666335-11 2014 In vitro phenotyping indicated that CYP3A4 was predominantly responsible for the metabolic clearance of LY2603618. LY2603618 104-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 24928723-0 2014 Use of endogenous cortisol 6beta-hydroxylation clearance for phenotyping in vivo CYP3A activity in women after sequential administration of an oral contraceptive (OC) containing ethinylestradiol and levonorgestrel as weak CYP3A inhibitors. cortisol 6beta 18-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 25141173-0 2014 Omeprazole and lansoprazole enantiomers induce CYP3A4 in human hepatocytes and cell lines via glucocorticoid receptor and pregnane X receptor axis. Omeprazole 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 24910189-4 2014 As measured by liquid chromatography-electrospray ionization tandem mass spectrometry, ethambutol exhibited strong inhibitory potential against CYP1A2 and CYP2E1, moderate against CYP2C19 and CYP2D6 and weak against CYP2A6, CYP2C9 and CYP3A4, based on the IC50 values. Ethambutol 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 235-241 25141173-0 2014 Omeprazole and lansoprazole enantiomers induce CYP3A4 in human hepatocytes and cell lines via glucocorticoid receptor and pregnane X receptor axis. Lansoprazole 15-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 25141173-3 2014 In the current paper, we examined the effects of lansoprazole and omeprazole enantiomers on the expression of key drug-metabolizing enzyme CYP3A4 in human hepatocytes and human cancer cell lines. Lansoprazole 49-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 25141173-3 2014 In the current paper, we examined the effects of lansoprazole and omeprazole enantiomers on the expression of key drug-metabolizing enzyme CYP3A4 in human hepatocytes and human cancer cell lines. Omeprazole 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 25141173-4 2014 Lansoprazole enantiomers, but not omeprazole, were equipotent inducers of CYP3A4 mRNA in HepG2 cells. Lansoprazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 25141173-5 2014 All forms (S-, R-, rac-) of lansoprazole and omeprazole induced CYP3A4 mRNA and protein in human hepatocytes. Lansoprazole 28-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 25141173-5 2014 All forms (S-, R-, rac-) of lansoprazole and omeprazole induced CYP3A4 mRNA and protein in human hepatocytes. Omeprazole 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 25141173-6 2014 The quantitative profiles of CYP3A4 induction by individual forms of lansoprazole and omeprazole exerted enantiospecific patterns. Lansoprazole 69-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 25141173-6 2014 The quantitative profiles of CYP3A4 induction by individual forms of lansoprazole and omeprazole exerted enantiospecific patterns. Omeprazole 86-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 25141173-12 2014 Overall, we demonstrate here that omeprazole and lansoprazole enantiomers induce CYP3A4 in HepG2 cells and human hepatocytes. Omeprazole 34-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 25141173-12 2014 Overall, we demonstrate here that omeprazole and lansoprazole enantiomers induce CYP3A4 in HepG2 cells and human hepatocytes. Lansoprazole 49-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 25120580-1 2014 BACKGROUND: Voriconazole is metabolized by cytochrome P450 (CYP) 2C19 and CYP 3A4. Voriconazole 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-81 25121773-2 2014 The predominant metabolic pathway of oxycodone is CYP3A4-mediated N-demethylation to noroxycodone, while a minor proportion undergoes 3-O-demethylation to oxymorphone by CYP2D6. Oxycodone 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 25121773-2 2014 The predominant metabolic pathway of oxycodone is CYP3A4-mediated N-demethylation to noroxycodone, while a minor proportion undergoes 3-O-demethylation to oxymorphone by CYP2D6. Nitrogen 66-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 25121773-2 2014 The predominant metabolic pathway of oxycodone is CYP3A4-mediated N-demethylation to noroxycodone, while a minor proportion undergoes 3-O-demethylation to oxymorphone by CYP2D6. noroxycodone 85-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 25121773-3 2014 The aim of this study was to investigate the effects of the mild CYP3A4 inhibitor aprepitant on the pharmacokinetics of orally administered controlled-release (CR) oxycodone. (cr) oxycodone 159-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 24910408-6 2014 In addition, in the CCl4 induced HepG2 cells injury model and the CYP3A activity level correlated well with ROS level in several ingredients of SLE treated groups, especially in gamma-schisandrin group. ros 108-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 24910408-6 2014 In addition, in the CCl4 induced HepG2 cells injury model and the CYP3A activity level correlated well with ROS level in several ingredients of SLE treated groups, especially in gamma-schisandrin group. schizandrin 184-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 25120580-7 2014 CYP3A4 inhibition by atazanavir combined with uninhibited CYP2C19 activity resulted in subtherapeutic voriconazole C0. Atazanavir Sulfate 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25120580-7 2014 CYP3A4 inhibition by atazanavir combined with uninhibited CYP2C19 activity resulted in subtherapeutic voriconazole C0. voriconazole c0 102-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24637575-0 2014 Effect of erlotinib on CYP3A activity, evaluated in vitro and by dual probes in patients with cancer. Erlotinib Hydrochloride 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-28 24637575-9 2014 Although erlotinib may be a weak mechanism-based irreversible inhibitor of CYP3A4 in vitro, in vivo, erlotinib did not inhibit CYP3A-mediated metabolism, as determined by the erythromycin breath test and the MDZ pharmacokinetics. Erlotinib Hydrochloride 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 24829290-6 2014 In the inhibition study with selective CYP3A4 inhibitors and incubation in recombinant cDNA-expressed P450 enzymes, all the metabolites of KRO-105714 were formed by CYP3A4 in HLMs. UNII-66G2URF5HG 139-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 24504163-0 2014 CYP3A4 activity reduces the cytotoxic effects of okadaic acid in HepaRG cells. Okadaic Acid 49-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24504163-5 2014 Therefore, a metabolic competent HepaRG cell line was exposed to OA with and without addition of the CYP3A4 inhibitor ketoconazole. Ketoconazole 118-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 24829290-6 2014 In the inhibition study with selective CYP3A4 inhibitors and incubation in recombinant cDNA-expressed P450 enzymes, all the metabolites of KRO-105714 were formed by CYP3A4 in HLMs. UNII-66G2URF5HG 139-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 24829290-8 2014 These results showed that the unusual C-demethylated metabolite M4 was generated from monohydroxyl metabolite M2 via a CYP3A4-mediated enzymatic reaction in HLMs. monohydroxyl 86-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 24832206-0 2014 Interactions of endosulfan and methoxychlor involving CYP3A4 and CYP2B6 in human HepaRG cells. Endosulfan 16-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 24839948-0 2014 Comparison of two endogenous biomarkers of CYP3A4 activity in a drug-drug interaction study between midostaurin and rifampicin. midostaurin 100-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 24832206-0 2014 Interactions of endosulfan and methoxychlor involving CYP3A4 and CYP2B6 in human HepaRG cells. Methoxychlor 31-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 24839948-0 2014 Comparison of two endogenous biomarkers of CYP3A4 activity in a drug-drug interaction study between midostaurin and rifampicin. Rifampin 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 24832206-3 2014 In the present work, we searched for interactions between endosulfan and methoxychlor, two organochlorine pesticides whose major routes of metabolism involve CAR- and PXR-regulated CYP3A4 and CYP2B6, and whose mechanisms of action in humans remain poorly understood. Endosulfan 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-187 24839948-1 2014 PURPOSE: Midostaurin, a multitargeted tyrosine kinase inhibitor, is primarily metabolized by CYP3A4. midostaurin 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24832206-3 2014 In the present work, we searched for interactions between endosulfan and methoxychlor, two organochlorine pesticides whose major routes of metabolism involve CAR- and PXR-regulated CYP3A4 and CYP2B6, and whose mechanisms of action in humans remain poorly understood. Methoxychlor 73-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-187 24839948-11 2014 CONCLUSIONS: Both 6betaCR and 4betaHC levels showed a good dynamic response range upon strong CYP3A4 induction with rifampicin. 6betacr 18-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 24839948-11 2014 CONCLUSIONS: Both 6betaCR and 4betaHC levels showed a good dynamic response range upon strong CYP3A4 induction with rifampicin. cholest-5-ene-3,4-diol 30-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 24832206-3 2014 In the present work, we searched for interactions between endosulfan and methoxychlor, two organochlorine pesticides whose major routes of metabolism involve CAR- and PXR-regulated CYP3A4 and CYP2B6, and whose mechanisms of action in humans remain poorly understood. Hydrocarbons, Chlorinated 91-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-187 24839948-11 2014 CONCLUSIONS: Both 6betaCR and 4betaHC levels showed a good dynamic response range upon strong CYP3A4 induction with rifampicin. Rifampin 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 24832206-7 2014 Endosulfan exerted a direct reversible inhibition of CYP3A4 activity that was confirmed in human liver microsomes. Endosulfan 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 24839948-12 2014 Because of lower inter- and intrasubject variability, 4betaHC appeared more reliable and better predictive of CYP3A4 activity compared with 6betaCR. cholest-5-ene-3,4-diol 54-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 24689515-2 2014 The aims of this analysis were to develop population pharmacokinetic (PPK) models of AZD7325 and midazolam and to assess the induction effect of AZD7325 on CYP3A4 with midazolam as a substrate. 4-amino-8-(2-fluoro-6-methoxy-phenyl)-N-propylcinnoline-3-carboxamide 145-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 24861996-0 2014 Association of ABCB1, CYP3A4, EPHX1, FAS, SCN1A, MICA, and BAG6 polymorphisms with the risk of carbamazepine-induced Stevens-Johnson syndrome/toxic epidermal necrolysis in Chinese Han patients with epilepsy. Carbamazepine 95-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 24889073-5 2014 The predominant role of CYP3A4 was further supported by a dramatic inhibition of metabolite formation in the presence of the CYP3A4 substrates troleandomycin and ketoconazole. Troleandomycin 143-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 24889073-5 2014 The predominant role of CYP3A4 was further supported by a dramatic inhibition of metabolite formation in the presence of the CYP3A4 substrates troleandomycin and ketoconazole. Troleandomycin 143-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 24889073-5 2014 The predominant role of CYP3A4 was further supported by a dramatic inhibition of metabolite formation in the presence of the CYP3A4 substrates troleandomycin and ketoconazole. Ketoconazole 162-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 24889073-5 2014 The predominant role of CYP3A4 was further supported by a dramatic inhibition of metabolite formation in the presence of the CYP3A4 substrates troleandomycin and ketoconazole. Ketoconazole 162-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 24619889-6 2014 Hepatic impairment, CYP2D6 poor metabolizer, and CYP3A inhibitor were estimated to reduce CL/F by about 60%, 40%, and 50%, respectively. Fluorine 93-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 24619889-7 2014 CYP3A inducer resulted in about fourfold increase in CL/F. Fluorine 56-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 24689515-11 2014 WHAT IS NEW AND CONCLUSION: The PPK models developed adequately described the clinical observation of AZD7325-mediated CYP3A4 enzyme induction with midazolam as a probe. 4-amino-8-(2-fluoro-6-methoxy-phenyl)-N-propylcinnoline-3-carboxamide 102-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 24689515-11 2014 WHAT IS NEW AND CONCLUSION: The PPK models developed adequately described the clinical observation of AZD7325-mediated CYP3A4 enzyme induction with midazolam as a probe. Midazolam 148-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 24657506-3 2014 Therefore, we assessed in vitro the potency of riociguat to inhibit important drug metabolising enzymes (cytochrome P450 (CYP) 3A4, CYP2C19, and CYP2D6) and drug transporters (P-glycoprotein (P-gp/ABCB1), breast cancer resistance protein (BCRP/ABCG2), and organic anion transporting polypeptides (OATP) 1B1 and 1B3). riociguat 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-130 24816159-8 2014 The results indicated that CYP2C19 and CYP3A4 might play major roles in the metabolism of m-nisoldipine in human liver microsomes. m-Nisoldipine 90-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 25417952-7 2014 Two studies showed some genetic polymorphism (Cyp 3a4 gene and FAAH Pro129Thr) among heroin and amphetamine users respectively that may contribute to drug dependence. Heroin 85-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-53 25417952-7 2014 Two studies showed some genetic polymorphism (Cyp 3a4 gene and FAAH Pro129Thr) among heroin and amphetamine users respectively that may contribute to drug dependence. Amphetamine 96-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-53 25303298-2 2014 The recently discovered CYP3A4*22 allele (defined as rs35599367) has been shown to affect statin-induced LDL cholesterol lowering. Cholesterol 109-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 24841887-3 2014 The obtained results indicate that CYP3A4 is the main isoform responsible for levomepromazine 5-sulfoxidation (72%) and N-demethylation (78%) at a therapeutic concentration of the drug (10muM). levomepromazine 5-sulfoxidation 78-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 24920405-7 2014 Importantly, the expression level of CYP3A4 showed high correlation (r = 0.943, p < 0.0001) with the functional activity, which was measured using bufalin-a highly selective chemical probe we have developed. bufalin-a 150-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 24799337-0 2014 Involvement of organic cation transporter 1 and CYP3A4 in retrorsine-induced toxicity. retrorsine 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 24799337-8 2014 Compared to mock cells, MDCK-CYP3A4 cells showed a decrease in viability after being treated with RTS. retrorsine 98-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 24841887-6 2014 Moreover, at a higher, toxicological concentration of the neuroleptic (100muM), the relative contribution of CYP1A2 to levomepromazine metabolism visibly increases (from 20% to 28% for 5-sufoxidation, and from 8% to 32% for N-demethylation), while the role of CYP3A4 significantly decreases (from 72% to 59% for 5-sulfoxidation, and from 78% to 47% for N-demethylation). Methotrimeprazine 119-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 260-266 24841887-7 2014 The obtained results indicate that the catalysis of levomepromazine 5-sulfoxidation and N-demethylation in humans shows a strict CYP3A4 preference, especially at a therapeutic drug concentration. levomepromazine 5-sulfoxidation 52-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 24841887-7 2014 The obtained results indicate that the catalysis of levomepromazine 5-sulfoxidation and N-demethylation in humans shows a strict CYP3A4 preference, especially at a therapeutic drug concentration. Nitrogen 88-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 25221991-6 2014 Moreover, rilpivirine is a substrate and weak inducer of the CYP3A4, but there are no significant pharmacokinetic interactions with new anti-hepatitis C compounds such as telaprevir, simeprevir, daclatasvir, ledipasvir, and sofosbuvir, an important issue for a drug with low risk of hepatoxicity. Rilpivirine 10-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 24798279-3 2014 Since ritonavir-boosted regimens are associated with long-term adverse events, cobicistat, a CYP3A4 inhibitor without antiviral activity, has been developed. Cobicistat 79-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24986243-2 2014 In particular, CYP3A4 and CYP3A5 (interacting with more than 60% of licensed drugs) exhibit the most individual variations of gene expression, mostly caused by single nucleotide polymorphisms (SNPs) within the regulatory region of the CYP3A4 and CYP3A5 genes which might affect the level of enzyme production.In this study, we sought to improve the performance of sensitive screening for CYP3A polymorphism detection in twenty HIV-1 infected patients undergoing lopinavir/ritonavir (LPV/r) monotherapy. Lopinavir 462-471 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 24986243-2 2014 In particular, CYP3A4 and CYP3A5 (interacting with more than 60% of licensed drugs) exhibit the most individual variations of gene expression, mostly caused by single nucleotide polymorphisms (SNPs) within the regulatory region of the CYP3A4 and CYP3A5 genes which might affect the level of enzyme production.In this study, we sought to improve the performance of sensitive screening for CYP3A polymorphism detection in twenty HIV-1 infected patients undergoing lopinavir/ritonavir (LPV/r) monotherapy. Lopinavir 462-471 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 235-241 24986243-2 2014 In particular, CYP3A4 and CYP3A5 (interacting with more than 60% of licensed drugs) exhibit the most individual variations of gene expression, mostly caused by single nucleotide polymorphisms (SNPs) within the regulatory region of the CYP3A4 and CYP3A5 genes which might affect the level of enzyme production.In this study, we sought to improve the performance of sensitive screening for CYP3A polymorphism detection in twenty HIV-1 infected patients undergoing lopinavir/ritonavir (LPV/r) monotherapy. Lopinavir 462-471 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-20 24986243-2 2014 In particular, CYP3A4 and CYP3A5 (interacting with more than 60% of licensed drugs) exhibit the most individual variations of gene expression, mostly caused by single nucleotide polymorphisms (SNPs) within the regulatory region of the CYP3A4 and CYP3A5 genes which might affect the level of enzyme production.In this study, we sought to improve the performance of sensitive screening for CYP3A polymorphism detection in twenty HIV-1 infected patients undergoing lopinavir/ritonavir (LPV/r) monotherapy. Ritonavir 472-481 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 24986243-2 2014 In particular, CYP3A4 and CYP3A5 (interacting with more than 60% of licensed drugs) exhibit the most individual variations of gene expression, mostly caused by single nucleotide polymorphisms (SNPs) within the regulatory region of the CYP3A4 and CYP3A5 genes which might affect the level of enzyme production.In this study, we sought to improve the performance of sensitive screening for CYP3A polymorphism detection in twenty HIV-1 infected patients undergoing lopinavir/ritonavir (LPV/r) monotherapy. Ritonavir 472-481 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 235-241 24986243-2 2014 In particular, CYP3A4 and CYP3A5 (interacting with more than 60% of licensed drugs) exhibit the most individual variations of gene expression, mostly caused by single nucleotide polymorphisms (SNPs) within the regulatory region of the CYP3A4 and CYP3A5 genes which might affect the level of enzyme production.In this study, we sought to improve the performance of sensitive screening for CYP3A polymorphism detection in twenty HIV-1 infected patients undergoing lopinavir/ritonavir (LPV/r) monotherapy. Ritonavir 472-481 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-20 24927617-9 2014 The interaction is due to inhibition of CYP3A4-mediated simvastatin clearance. Simvastatin 56-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 24433464-0 2014 Population pharmacokinetic approach to evaluate the effect of CYP2D6, CYP3A, ABCB1, POR and NR1I2 genotypes on donepezil clearance. Donepezil 111-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-75 24825301-0 2014 Solving time-dependent CYP3A4 inhibition for a series of indole-phenylacetic acid dual antagonists of the PGD(2) receptors CRTH2 and DP. indole-phenylacetic acid 57-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 24825301-3 2014 We discovered early in the optimization of these indole-phenylacetic acid compounds that they demonstrated CYP3A4 time-dependent inhibition (TDI). indole 49-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 24825301-3 2014 We discovered early in the optimization of these indole-phenylacetic acid compounds that they demonstrated CYP3A4 time-dependent inhibition (TDI). phenylacetic acid 56-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 24671884-5 2014 The new models were validated by showing improved predictions of the systemic clearances of ropivacaine (major CYP1A2 substrate; minor CYP3A4 substrate) and alfentanil (major CYP3A4 substrate) compared with those using a previous ontogeny function based on in vitro data (alfentanil: mean squared prediction error 3.0 vs. 6.8; ropivacaine: mean squared prediction error 2.3 vs.14.2). Ropivacaine 92-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 24566734-5 2014 From univariate analysis, we found that the SNPs in CYP3A4, CYP3A5, and ABCB1 were associated with the clearance of both sunitinib and SU12662. Sunitinib 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 24768782-1 2014 BACKGROUND: Cyclophosphamide (CP), an alkylating chemotherapeutic drug, is catalyzed by the Phase I cytochrome P450 (CYPs) isozymes - CYP3A4, CYP3A5, CYP2B6, CYP2C8, CYP2C9 and CYP2C19. Cyclophosphamide 12-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 24671884-5 2014 The new models were validated by showing improved predictions of the systemic clearances of ropivacaine (major CYP1A2 substrate; minor CYP3A4 substrate) and alfentanil (major CYP3A4 substrate) compared with those using a previous ontogeny function based on in vitro data (alfentanil: mean squared prediction error 3.0 vs. 6.8; ropivacaine: mean squared prediction error 2.3 vs.14.2). Alfentanil 157-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 24566734-5 2014 From univariate analysis, we found that the SNPs in CYP3A4, CYP3A5, and ABCB1 were associated with the clearance of both sunitinib and SU12662. SU 12662 135-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 25047497-2 2014 Individuals concomitantly taking lobeglitazone and a CYP3A4 inhibitor may experience some adverse effects secondary to increased systemic exposure to lobeglitazone. lobeglitazone 150-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 24778366-8 2014 Our results indicated that NC is a substrate of hOCT1, hOCT3, and CYP3A4; that OCT1 and OCT3 mediate the uptake of NC in hepatocytes and subsequently cause hepatotoxicity; and that NC-induced toxicity could be attenuated by CYP3A4-mediated metabolism. nitidine 27-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 24713129-3 2014 Amodiaquine N-deethylation and midazolam 1"-hydroxylation were used as marker reactions for CYP2C8 and CYP3A activity, respectively. Amodiaquine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 24713129-9 2014 However, lestaurtinib and saracatinib were identified as mechanism-based inhibitors of CYP3A. lestaurtinib 9-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 24713129-9 2014 However, lestaurtinib and saracatinib were identified as mechanism-based inhibitors of CYP3A. saracatinib 26-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 24778366-8 2014 Our results indicated that NC is a substrate of hOCT1, hOCT3, and CYP3A4; that OCT1 and OCT3 mediate the uptake of NC in hepatocytes and subsequently cause hepatotoxicity; and that NC-induced toxicity could be attenuated by CYP3A4-mediated metabolism. nitidine 27-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 224-230 24713129-11 2014 Inhibition of CYP2C8 by bosutinib was predicted to have no clinical relevance, whereas therapeutic lestaurtinib and saracatinib concentrations were predicted to increase the plasma exposure to CYP3A-dependent substrates by >=2.7-fold. lestaurtinib 99-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 193-198 24713129-11 2014 Inhibition of CYP2C8 by bosutinib was predicted to have no clinical relevance, whereas therapeutic lestaurtinib and saracatinib concentrations were predicted to increase the plasma exposure to CYP3A-dependent substrates by >=2.7-fold. saracatinib 116-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 193-198 24778367-7 2014 The formation of human metabolites in locusts was inhibited by ketoconazole, a mammalian CYP3A4 inhibitor, suggesting that the enzyme responsible for the human metabolite formation in locusts is functionally similar to human CYP3A4. Ketoconazole 63-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 24778367-7 2014 The formation of human metabolites in locusts was inhibited by ketoconazole, a mammalian CYP3A4 inhibitor, suggesting that the enzyme responsible for the human metabolite formation in locusts is functionally similar to human CYP3A4. Ketoconazole 63-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 225-231 24695353-0 2014 Reduction of nevirapine-driven HIV mutations by carbamazepine is modulated by CYP3A activity. Carbamazepine 48-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 24687371-3 2014 The present study uses a well-known environmental contaminant, PCB-30 (2,4,6-trichlorobiphenyl), as a prototype endocrine disrupting chemical and integrates predictive (computational) and experimental methods to determine its metabolic transformation by cytochrome P450 3A4 (CYP3A4) and cytochrome P450 2D6 (CYP2D6) into estrogenic byproducts. 2,4,6-trichlorobiphenyl 71-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 254-273 24687371-3 2014 The present study uses a well-known environmental contaminant, PCB-30 (2,4,6-trichlorobiphenyl), as a prototype endocrine disrupting chemical and integrates predictive (computational) and experimental methods to determine its metabolic transformation by cytochrome P450 3A4 (CYP3A4) and cytochrome P450 2D6 (CYP2D6) into estrogenic byproducts. 2,4,6-trichlorobiphenyl 71-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 275-281 24769006-5 2014 Furthermore, alpha-viniferin strongly inhibited CYP2C19-mediated omeprazole 5-hydroxylation and CYP3A4-catalyzed midazolam 1-hydroxylation with IC50 values of 0.93 and 1.2 muM, respectively. alpha-viniferin 13-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 24769006-5 2014 Furthermore, alpha-viniferin strongly inhibited CYP2C19-mediated omeprazole 5-hydroxylation and CYP3A4-catalyzed midazolam 1-hydroxylation with IC50 values of 0.93 and 1.2 muM, respectively. Midazolam 113-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 24748562-7 2014 At 30 muM dabrafenib showed increases in CYP2B6 and CYP3A4 mRNA expression indicative of induction. dabrafenib 10-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 24748562-9 2014 This risk-assessment approach indicated that dabrafenib is unlikely to perpetrate any in vivo DDIs by inhibition mechanisms, but is a likely inducer of CYP3A4 and a victim of CYP3A4 and CYP2C8 inhibitors. dabrafenib 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 24748562-9 2014 This risk-assessment approach indicated that dabrafenib is unlikely to perpetrate any in vivo DDIs by inhibition mechanisms, but is a likely inducer of CYP3A4 and a victim of CYP3A4 and CYP2C8 inhibitors. dabrafenib 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 24695353-6 2014 In contrast, the reduction in HIV-1 mutations by single-dose carbamazepine reached statistical significance at P = 0.04 with an OR of 0.1 (95% CI 0.01-0.90) upon consideration of CYP3A activity, defined as the ratio of 4beta-hydroxycholesterol to cholesterol, and it was more likely in women with higher CYP3A activity. Carbamazepine 61-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-184 24695353-6 2014 In contrast, the reduction in HIV-1 mutations by single-dose carbamazepine reached statistical significance at P = 0.04 with an OR of 0.1 (95% CI 0.01-0.90) upon consideration of CYP3A activity, defined as the ratio of 4beta-hydroxycholesterol to cholesterol, and it was more likely in women with higher CYP3A activity. Carbamazepine 61-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 304-309 24695353-7 2014 These findings were in agreement with CYP3A induction in carbamazepine-treated patients. Carbamazepine 57-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 24695353-8 2014 Likewise, carbamazepine induced CYP3A4, but not CYP2B6, in vitro when combined with nevirapine. Carbamazepine 10-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 24757038-2 2014 Voriconazole, a second-generation triazole antifungal agent, is both a substrate and potent inhibitor of CYP isoenzymes, specifically CYP2C19, CYP2C9, and CYP3A4; thus, the potential for drug-drug interactions with voriconazole is high. Voriconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 25041770-1 2014 Clarithromycin is the most documented cytochrome P450 3A4 (CYP3A4) inhibitor to cause an adverse interaction with simvastatin. Clarithromycin 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-57 25041770-1 2014 Clarithromycin is the most documented cytochrome P450 3A4 (CYP3A4) inhibitor to cause an adverse interaction with simvastatin. Clarithromycin 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 25041770-1 2014 Clarithromycin is the most documented cytochrome P450 3A4 (CYP3A4) inhibitor to cause an adverse interaction with simvastatin. Simvastatin 114-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-57 25041770-1 2014 Clarithromycin is the most documented cytochrome P450 3A4 (CYP3A4) inhibitor to cause an adverse interaction with simvastatin. Simvastatin 114-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 24750851-0 2014 Evaluation of the effects of single-nucleotide polymorphisms in CYP3A4 and CYP4F2 on stable phenprocoumon and acenocoumarol maintenance doses: comment. single-nucleotide 29-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 24750851-0 2014 Evaluation of the effects of single-nucleotide polymorphisms in CYP3A4 and CYP4F2 on stable phenprocoumon and acenocoumarol maintenance doses: comment. Phenprocoumon 92-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 24750851-0 2014 Evaluation of the effects of single-nucleotide polymorphisms in CYP3A4 and CYP4F2 on stable phenprocoumon and acenocoumarol maintenance doses: comment. Acenocoumarol 110-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 24844604-5 2014 Low imatinib levels were predicted in young male patients and those receiving P-gp/CYP3A4 inducers. Imatinib Mesylate 4-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 24611975-3 2014 The activity of CYP3A can be assessed by the urinary ratio of 6beta-hydroxycortisol to cortisol. 6 beta-hydroxycortisol 62-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-21 24611975-3 2014 The activity of CYP3A can be assessed by the urinary ratio of 6beta-hydroxycortisol to cortisol. Hydrocortisone 75-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-21 24815739-0 2014 Evaluation of the effects of single-nucleotide polymorphisms in CYP3A4 and CYP4F2 on stable phenprocoumon and acenocoumarol maintenance doses: reply. single-nucleotide 29-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 24815739-0 2014 Evaluation of the effects of single-nucleotide polymorphisms in CYP3A4 and CYP4F2 on stable phenprocoumon and acenocoumarol maintenance doses: reply. Phenprocoumon 92-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 24757038-2 2014 Voriconazole, a second-generation triazole antifungal agent, is both a substrate and potent inhibitor of CYP isoenzymes, specifically CYP2C19, CYP2C9, and CYP3A4; thus, the potential for drug-drug interactions with voriconazole is high. Triazoles 34-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 25073399-0 2014 Induction of human CYP3A4 by huperzine A, ligustrazine and oridonin through pregnane X receptor-mediated pathways. huperzine A 29-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 24757038-2 2014 Voriconazole, a second-generation triazole antifungal agent, is both a substrate and potent inhibitor of CYP isoenzymes, specifically CYP2C19, CYP2C9, and CYP3A4; thus, the potential for drug-drug interactions with voriconazole is high. Voriconazole 215-227 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 25073399-0 2014 Induction of human CYP3A4 by huperzine A, ligustrazine and oridonin through pregnane X receptor-mediated pathways. tetramethylpyrazine 42-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 24964282-0 2014 Evaluation of 4beta-Hydroxycholesterol as a Clinical Biomarker of CYP3A4 Drug Interactions Using a Bayesian Mechanism-Based Pharmacometric Model. cholest-5-ene-3,4-diol 14-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 25073399-0 2014 Induction of human CYP3A4 by huperzine A, ligustrazine and oridonin through pregnane X receptor-mediated pathways. oridonin 59-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 25073399-4 2014 Huperzine A, ligustrazine and oridonin were identified to be the inducers of CYP3A4. huperzine A 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 25073399-4 2014 Huperzine A, ligustrazine and oridonin were identified to be the inducers of CYP3A4. tetramethylpyrazine 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 25073399-4 2014 Huperzine A, ligustrazine and oridonin were identified to be the inducers of CYP3A4. oridonin 30-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 25073399-6 2014 Besides, huperzine A, ligustrazine and oridonin significantly up-regulated enzymatic activities of CYP3A4. huperzine A 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 25073399-6 2014 Besides, huperzine A, ligustrazine and oridonin significantly up-regulated enzymatic activities of CYP3A4. tetramethylpyrazine 22-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 25073399-6 2014 Besides, huperzine A, ligustrazine and oridonin significantly up-regulated enzymatic activities of CYP3A4. oridonin 39-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 25073399-9 2014 These results indicate that huperzine A, ligustrazine and oridonin induced CYP3A4 expression and activation via PXR dependent pathways, and might contribute to drug-drug interactions. huperzine A 28-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 25073399-9 2014 These results indicate that huperzine A, ligustrazine and oridonin induced CYP3A4 expression and activation via PXR dependent pathways, and might contribute to drug-drug interactions. tetramethylpyrazine 41-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 25073399-9 2014 These results indicate that huperzine A, ligustrazine and oridonin induced CYP3A4 expression and activation via PXR dependent pathways, and might contribute to drug-drug interactions. oridonin 58-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 24964282-1 2014 A Bayesian mechanism-based pharmacokinetic/pharmacodynamic model of cytochrome P450 3A4 (CYP3A4) activity was developed based on a clinical study of the effects of ketoconazole and rifampin on midazolam exposure and plasma 4beta-hydroxycholesterol (4betaHC) concentrations. cholest-5-ene-3,4-diol 223-247 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 24964282-1 2014 A Bayesian mechanism-based pharmacokinetic/pharmacodynamic model of cytochrome P450 3A4 (CYP3A4) activity was developed based on a clinical study of the effects of ketoconazole and rifampin on midazolam exposure and plasma 4beta-hydroxycholesterol (4betaHC) concentrations. cholest-5-ene-3,4-diol 249-256 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-87 24964282-1 2014 A Bayesian mechanism-based pharmacokinetic/pharmacodynamic model of cytochrome P450 3A4 (CYP3A4) activity was developed based on a clinical study of the effects of ketoconazole and rifampin on midazolam exposure and plasma 4beta-hydroxycholesterol (4betaHC) concentrations. cholest-5-ene-3,4-diol 249-256 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 24405273-7 2014 Rose bengal directly inhibited CYP3A4/5 and UGT1A6 in HLM under yellow light with inhibitor concentration that causes 50% inhibition (IC50) values of 0.072 and 0.035 muM, respectively; whereas much less inhibition was observed in the dark with the IC50 values increasing 43- and 120-fold, respectively. Rose Bengal 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 24964282-2 2014 Simulations from the model demonstrated that the dynamic range of 4betaHC as a biomarker of CYP3A4 induction or inhibition was narrower than that of midazolam; an inhibitor that increases midazolam area under the curve by 20-fold may only result in a 20% decrease in 4betaHC after 14 days of dosing. cholest-5-ene-3,4-diol 66-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 24964282-1 2014 A Bayesian mechanism-based pharmacokinetic/pharmacodynamic model of cytochrome P450 3A4 (CYP3A4) activity was developed based on a clinical study of the effects of ketoconazole and rifampin on midazolam exposure and plasma 4beta-hydroxycholesterol (4betaHC) concentrations. Ketoconazole 164-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-87 24964282-2 2014 Simulations from the model demonstrated that the dynamic range of 4betaHC as a biomarker of CYP3A4 induction or inhibition was narrower than that of midazolam; an inhibitor that increases midazolam area under the curve by 20-fold may only result in a 20% decrease in 4betaHC after 14 days of dosing. Midazolam 188-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 24964282-3 2014 Likewise, an inducer that elevates CYP3A4 activity by 1.2-fold would reduce the area under the curve of midazolam by 50% but would only increase 4betaHC levels by 20% after 14 days of dosing. Midazolam 104-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 24964282-3 2014 Likewise, an inducer that elevates CYP3A4 activity by 1.2-fold would reduce the area under the curve of midazolam by 50% but would only increase 4betaHC levels by 20% after 14 days of dosing. cholest-5-ene-3,4-diol 145-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 24964282-5 2014 Only a strong CYP3A4 inhibitor (e.g., ketoconazole) could be detected with similar sample sizes. Ketoconazole 38-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 24964282-1 2014 A Bayesian mechanism-based pharmacokinetic/pharmacodynamic model of cytochrome P450 3A4 (CYP3A4) activity was developed based on a clinical study of the effects of ketoconazole and rifampin on midazolam exposure and plasma 4beta-hydroxycholesterol (4betaHC) concentrations. Ketoconazole 164-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 24964282-1 2014 A Bayesian mechanism-based pharmacokinetic/pharmacodynamic model of cytochrome P450 3A4 (CYP3A4) activity was developed based on a clinical study of the effects of ketoconazole and rifampin on midazolam exposure and plasma 4beta-hydroxycholesterol (4betaHC) concentrations. Rifampin 181-189 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-87 24964282-1 2014 A Bayesian mechanism-based pharmacokinetic/pharmacodynamic model of cytochrome P450 3A4 (CYP3A4) activity was developed based on a clinical study of the effects of ketoconazole and rifampin on midazolam exposure and plasma 4beta-hydroxycholesterol (4betaHC) concentrations. Rifampin 181-189 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 24964282-1 2014 A Bayesian mechanism-based pharmacokinetic/pharmacodynamic model of cytochrome P450 3A4 (CYP3A4) activity was developed based on a clinical study of the effects of ketoconazole and rifampin on midazolam exposure and plasma 4beta-hydroxycholesterol (4betaHC) concentrations. Midazolam 193-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-87 24964282-1 2014 A Bayesian mechanism-based pharmacokinetic/pharmacodynamic model of cytochrome P450 3A4 (CYP3A4) activity was developed based on a clinical study of the effects of ketoconazole and rifampin on midazolam exposure and plasma 4beta-hydroxycholesterol (4betaHC) concentrations. Midazolam 193-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 24964282-1 2014 A Bayesian mechanism-based pharmacokinetic/pharmacodynamic model of cytochrome P450 3A4 (CYP3A4) activity was developed based on a clinical study of the effects of ketoconazole and rifampin on midazolam exposure and plasma 4beta-hydroxycholesterol (4betaHC) concentrations. cholest-5-ene-3,4-diol 223-247 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-87 24865757-8 2014 Lomitapide is contraindicated in patients with moderate-to-severe liver disease, patients with sustained abnormal liver function tests, patients taking strong or moderate CYP3A4 inhibitors, and pregnant patients. BMS201038 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 24836403-13 2014 Only CYP3A4 and CYP3A5 activated otonecine-type PAs, while all 10 CYPs studied showed the ability to activate retronecine-type PAs. Pyrrolizidine Alkaloids 48-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 5-11 24836403-13 2014 Only CYP3A4 and CYP3A5 activated otonecine-type PAs, while all 10 CYPs studied showed the ability to activate retronecine-type PAs. Pyrrolizidine Alkaloids 127-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 5-11 24865757-5 2014 Lomitapide undergoes hepatic metabolism via cytochrome P-450 (CYP) isoenzyme 3A4 and interacts with CYP3A4 substrates including atorvastatin and simvastatin; dose adjustment is recommended when lomitapide is used concurrently with these agents. BMS201038 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 24060671-6 2014 Herein the Advanced Dissolution, Absorption and Metabolism (ADAM) model is applied to the prediction of formulation-specific FE for BCS/BDDCS Class II drug and CYP3A4 substrate nifedipine using as far as possible only in vitro data. Nifedipine 177-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 24924803-1 2014 Levels of enzymes that determine testosterone catabolism such as CYP3A4 have been associated with prostate cancer (PCa) risk. Testosterone 33-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 24865757-5 2014 Lomitapide undergoes hepatic metabolism via cytochrome P-450 (CYP) isoenzyme 3A4 and interacts with CYP3A4 substrates including atorvastatin and simvastatin; dose adjustment is recommended when lomitapide is used concurrently with these agents. Atorvastatin 128-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 24865757-5 2014 Lomitapide undergoes hepatic metabolism via cytochrome P-450 (CYP) isoenzyme 3A4 and interacts with CYP3A4 substrates including atorvastatin and simvastatin; dose adjustment is recommended when lomitapide is used concurrently with these agents. Simvastatin 145-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 24663015-7 2014 Intriguingly, clofazimine (CFZ) exhibited weak inductive effects on CYP3A4 at >0.25 muM in HepaRG cells, while an inhibitory effect was observed at 1.69 muM in the in vitro screening, suggesting that CFZ autoinduces CYP3A4 in the human liver. Clofazimine 14-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 24889062-3 2014 The effect of QHS-PQ on the activity of the CYP2B6 and CYP3A4 was also investigated. qhs-pq 14-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 24889062-10 2014 The enzyme activity of CYP2B6 and CYP3A4 increased 2.1-fold and 3.2-fold, respectively, after two-day oral doses of QHS-PQ. qhs-pq 116-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 24889062-13 2014 The enzyme activity of CYP2B6 and CYP3A4 was induced after the two-day oral doses of QHS-PQ. qhs-pq 85-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 24663015-7 2014 Intriguingly, clofazimine (CFZ) exhibited weak inductive effects on CYP3A4 at >0.25 muM in HepaRG cells, while an inhibitory effect was observed at 1.69 muM in the in vitro screening, suggesting that CFZ autoinduces CYP3A4 in the human liver. Clofazimine 14-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 24663015-7 2014 Intriguingly, clofazimine (CFZ) exhibited weak inductive effects on CYP3A4 at >0.25 muM in HepaRG cells, while an inhibitory effect was observed at 1.69 muM in the in vitro screening, suggesting that CFZ autoinduces CYP3A4 in the human liver. Clofazimine 27-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 24663015-7 2014 Intriguingly, clofazimine (CFZ) exhibited weak inductive effects on CYP3A4 at >0.25 muM in HepaRG cells, while an inhibitory effect was observed at 1.69 muM in the in vitro screening, suggesting that CFZ autoinduces CYP3A4 in the human liver. Clofazimine 27-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 24330024-2 2014 Pharmacokinetic drug interactions between voclosporin and a CYP3A inhibitor, inducer and substrate and a P-glycoprotein inhibitor and substrate were evaluated. voclosporin 42-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 24861746-1 2014 4beta-Hydroxycholesterol (4beta-HC) has been proposed as a new endogenous biomarker for cytochrome P450 3A4/5 activity. cholest-5-ene-3,4-diol 0-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-107 24861746-1 2014 4beta-Hydroxycholesterol (4beta-HC) has been proposed as a new endogenous biomarker for cytochrome P450 3A4/5 activity. cholest-5-ene-3,4-diol 26-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-107 24530864-0 2014 Physiologically based pharmacokinetic modeling of CYP3A4 induction by rifampicin in human: influence of time between substrate and inducer administration. Rifampin 70-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 24530864-2 2014 Rifampicin (RIF) is a potent inducer of CYP3A4 and also acts as a competitive inhibitor which can partially mask the induction. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 24530864-2 2014 Rifampicin (RIF) is a potent inducer of CYP3A4 and also acts as a competitive inhibitor which can partially mask the induction. Rifampin 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 24330024-6 2014 CONCLUSIONS: Administration of voclosporin concomitantly with strong inhibitors and inducers of CYP3A resulted in increased and decreased exposures, respectively, and should be considered contraindicated. voclosporin 31-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-101 24569517-0 2014 Fluoxetine- and norfluoxetine-mediated complex drug-drug interactions: in vitro to in vivo correlation of effects on CYP2D6, CYP2C19, and CYP3A4. Fluoxetine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 24744093-0 2014 Tamoxifen-associated hot flash severity is inversely correlated with endoxifen concentration and CYP3A4*22. Tamoxifen 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 24744093-2 2014 Tamoxifen undergoes hepatic bioactivation by CYP2D6 and CYP3A4 to form the active metabolite endoxifen. Tamoxifen 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 24744093-2 2014 Tamoxifen undergoes hepatic bioactivation by CYP2D6 and CYP3A4 to form the active metabolite endoxifen. 4-hydroxy-N-desmethyltamoxifen 93-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 24744093-9 2014 However, CYP3A4*22 carriers were less likely to have hot flashes with an odds ratio of 8.87 (p < 0.01) even when compared to a cohort with similar endoxifen levels. 4-hydroxy-N-desmethyltamoxifen 150-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 24744093-11 2014 Importantly, this is the first study to show CYP3A4*22 genotype as an independent predictor of hot flash severity during tamoxifen therapy. Tamoxifen 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 24569517-1 2014 Fluoxetine and its circulating metabolite norfluoxetine comprise a complex multiple-inhibitor system that causes reversible or time-dependent inhibition of the cytochrome P450 (CYP) family members CYP2D6, CYP3A4, and CYP2C19 in vitro. Fluoxetine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 205-211 24569517-1 2014 Fluoxetine and its circulating metabolite norfluoxetine comprise a complex multiple-inhibitor system that causes reversible or time-dependent inhibition of the cytochrome P450 (CYP) family members CYP2D6, CYP3A4, and CYP2C19 in vitro. norfluoxetine 42-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 205-211 24569517-0 2014 Fluoxetine- and norfluoxetine-mediated complex drug-drug interactions: in vitro to in vivo correlation of effects on CYP2D6, CYP2C19, and CYP3A4. norfluoxetine 16-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 24785428-2 2014 Perampanel is metabolized primarily via CYP3A4, yet it has a relatively long half-life of 105h; it is, therefore, recommended that perampanel be given once daily (preferably at bedtime). perampanel 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 24705672-6 2014 NigC induced the expression of endogenous CYP3A4 mRNA and protein in both cultured hepatoma cells and primary hepatocytes. nigc 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 24732405-3 2014 Moreover, mitotane induces CYP3A4 expression, thus accelerating the metabolic clearance of a variety of drugs including steroids. Mitotane 10-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 24732405-3 2014 Moreover, mitotane induces CYP3A4 expression, thus accelerating the metabolic clearance of a variety of drugs including steroids. Steroids 120-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 24696463-0 2014 Metabolic activation of the indoloquinazoline alkaloids evodiamine and rutaecarpine by human liver microsomes: dehydrogenation and inactivation of cytochrome P450 3A4. indoloquinazoline alkaloids 28-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-166 24696463-0 2014 Metabolic activation of the indoloquinazoline alkaloids evodiamine and rutaecarpine by human liver microsomes: dehydrogenation and inactivation of cytochrome P450 3A4. evodiamine 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-166 24696463-0 2014 Metabolic activation of the indoloquinazoline alkaloids evodiamine and rutaecarpine by human liver microsomes: dehydrogenation and inactivation of cytochrome P450 3A4. rutecarpine 71-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-166 24696463-8 2014 Formation of the evodiamine and rutaecarpine GSH conjugates was primarily catalyzed by heterologously expressed recombinant CYP3A4 and, to a lesser extent, CYP1A2 and CYP2D6, respectively. evodiamine 17-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 24696463-8 2014 Formation of the evodiamine and rutaecarpine GSH conjugates was primarily catalyzed by heterologously expressed recombinant CYP3A4 and, to a lesser extent, CYP1A2 and CYP2D6, respectively. rutecarpine 32-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 24696463-8 2014 Formation of the evodiamine and rutaecarpine GSH conjugates was primarily catalyzed by heterologously expressed recombinant CYP3A4 and, to a lesser extent, CYP1A2 and CYP2D6, respectively. Glutathione 45-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 24696463-9 2014 It was found that the 3-methyleneindolenine or another reactive intermediate was a mechanism-based inactivator of CYP3A4, with inactivation parameters KI = 29 microM and kinact = 0.029 minute(-1), respectively. 3-methyleneindolenine 22-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 24696463-10 2014 In summary, these findings are of significance in understanding the bioactivation mechanisms of indoloquinazoline alkaloids, and dehydrogenation of evodiamine and rutaecarpine may cause toxicities through formation of electrophilic intermediates and lead to drug-drug interactions mainly via CYP3A4 inactivation. indoloquinazoline alkaloids 96-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 292-298 24696463-10 2014 In summary, these findings are of significance in understanding the bioactivation mechanisms of indoloquinazoline alkaloids, and dehydrogenation of evodiamine and rutaecarpine may cause toxicities through formation of electrophilic intermediates and lead to drug-drug interactions mainly via CYP3A4 inactivation. evodiamine 148-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 292-298 24746233-4 2014 They have a low potential for drug interactions, with the exception of saxagliptin that is largely metabolized by cytochrome CYP3A4/A5. saxagliptin 71-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 24696463-10 2014 In summary, these findings are of significance in understanding the bioactivation mechanisms of indoloquinazoline alkaloids, and dehydrogenation of evodiamine and rutaecarpine may cause toxicities through formation of electrophilic intermediates and lead to drug-drug interactions mainly via CYP3A4 inactivation. rutecarpine 163-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 292-298 24658827-1 2014 PURPOSE: Tacrolimus (Tac) and cyclosporine (CsA) are mainly metabolized by CYP3A4 and CYP3A5. Tacrolimus 9-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 24658827-1 2014 PURPOSE: Tacrolimus (Tac) and cyclosporine (CsA) are mainly metabolized by CYP3A4 and CYP3A5. Cyclosporine 30-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 24658827-1 2014 PURPOSE: Tacrolimus (Tac) and cyclosporine (CsA) are mainly metabolized by CYP3A4 and CYP3A5. Cyclosporine 44-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 24658827-10 2014 CsA C2/D was 53 % higher among CYP3A4*22 carriers (P=0.03). Cyclosporine 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 24658827-12 2014 Furthermore, initial CsA dosing may be improved by pre-transplant CYP3A4*22 determination. Cyclosporine 21-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 24691060-0 2014 Association of CYP3A4*18B and CYP3A5*3 polymorphism with cyclosporine-related liver injury in Chinese renal transplant recipients. Cyclosporine 57-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 24691060-1 2014 OBJECTIVE: The purpose of this study was to investigate the associations between CYP3A4*18B and CYP3A5*3 polymorphism and cyclosporine-related liver injuries in Chinese renal transplant recipients. Cyclosporine 122-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 24691060-4 2014 At 1 month after transplantation, the trough concentration of cyclosporine (C0) in the group with CYP3A4*1/*1(GG alleles) was significantly higher than in the group with CYP3A4*18B/*1 8B(AA alleles) (p < 0.05). Cyclosporine 62-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 24691060-4 2014 At 1 month after transplantation, the trough concentration of cyclosporine (C0) in the group with CYP3A4*1/*1(GG alleles) was significantly higher than in the group with CYP3A4*18B/*1 8B(AA alleles) (p < 0.05). Cyclosporine 62-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 24691060-4 2014 At 1 month after transplantation, the trough concentration of cyclosporine (C0) in the group with CYP3A4*1/*1(GG alleles) was significantly higher than in the group with CYP3A4*18B/*1 8B(AA alleles) (p < 0.05). c0 76-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 24691060-10 2014 CONCLUSIONS: These results suggested that the wild type of CYP3A4*18B is a risk factor for the development of cyclosporine- related liver injuries in Chinese renal transplant recipients. Cyclosporine 110-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 24392691-0 2014 The effect of complementary and alternative medicines on CYP3A4-mediated metabolism of three different substrates: 7-benzyloxy-4-trifluoromethyl-coumarin, midazolam and docetaxel. 7-benzyloxy-4-trifluoromethylcoumarin 115-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 24417304-1 2014 WHAT IS KNOWN AND OBJECTIVE: Sunitinib, a CYP3A4 substrate, is standard of care treatment in metastatic renal cell carcinoma (mRCC) and is administered orally as a single dose of 50 mg, in a 4 weeks on/2 weeks off regimen. Sunitinib 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 24417304-16 2014 Due to adverse drug reactions and comorbidity, patients under sunitinib, a CYP3A4 substrate, took an average of 6 8 comedications provoking an important risk of major-to-moderate drug-drug interactions. Sunitinib 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 24392691-0 2014 The effect of complementary and alternative medicines on CYP3A4-mediated metabolism of three different substrates: 7-benzyloxy-4-trifluoromethyl-coumarin, midazolam and docetaxel. Midazolam 155-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 24392691-0 2014 The effect of complementary and alternative medicines on CYP3A4-mediated metabolism of three different substrates: 7-benzyloxy-4-trifluoromethyl-coumarin, midazolam and docetaxel. Docetaxel 169-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 24392691-6 2014 The oncolytic CYP3A4 substrate docetaxel was used to establish the predictive value of the model substrates for pharmacokinetic interactions between CAM and anticancer drugs in vitro, and to more closely predict these interactions in vivo. Docetaxel 31-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 24392691-7 2014 METHODS: The inhibition of CYP3A4-mediated metabolism of 7-benzyloxy-4-trifluoromethyl-coumarin (BFC) by CAM was assessed in Supersomes, using the fluorometric CYP3A4 inhibition assay. 7-benzyloxy-4-trifluoromethylcoumarin 57-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 24392691-7 2014 METHODS: The inhibition of CYP3A4-mediated metabolism of 7-benzyloxy-4-trifluoromethyl-coumarin (BFC) by CAM was assessed in Supersomes, using the fluorometric CYP3A4 inhibition assay. 7-benzyloxy-4-trifluoromethylcoumarin 57-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 24392691-7 2014 METHODS: The inhibition of CYP3A4-mediated metabolism of 7-benzyloxy-4-trifluoromethyl-coumarin (BFC) by CAM was assessed in Supersomes, using the fluorometric CYP3A4 inhibition assay. 7-benzyloxy-4-trifluoromethylcoumarin 97-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 24392691-7 2014 METHODS: The inhibition of CYP3A4-mediated metabolism of 7-benzyloxy-4-trifluoromethyl-coumarin (BFC) by CAM was assessed in Supersomes, using the fluorometric CYP3A4 inhibition assay. 7-benzyloxy-4-trifluoromethylcoumarin 97-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 24392691-8 2014 In human liver microsomes (HLM) the inhibition of CYP3A4-mediated metabolism of midazolam and docetaxel was determined, using liquid-chromatography coupled to tandem mass spectrometry (LC-MS/MS). Midazolam 80-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 24392691-8 2014 In human liver microsomes (HLM) the inhibition of CYP3A4-mediated metabolism of midazolam and docetaxel was determined, using liquid-chromatography coupled to tandem mass spectrometry (LC-MS/MS). Docetaxel 94-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 24392691-9 2014 KEY FINDINGS: The results confirmed grape seed and green tea as potent inhibitors and milk thistle as moderate inhibitor of CYP3A4-mediated metabolism of BFC, midazolam and docetaxel. 7-benzyloxy-4-trifluoromethylcoumarin 154-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 24392691-9 2014 KEY FINDINGS: The results confirmed grape seed and green tea as potent inhibitors and milk thistle as moderate inhibitor of CYP3A4-mediated metabolism of BFC, midazolam and docetaxel. Midazolam 159-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 24392691-9 2014 KEY FINDINGS: The results confirmed grape seed and green tea as potent inhibitors and milk thistle as moderate inhibitor of CYP3A4-mediated metabolism of BFC, midazolam and docetaxel. Docetaxel 173-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 25141896-6 2014 Time post-transplantation, recipient age, donor CYP3A5 and CYP3A4 genotypes and fluconazole administration significantly influenced tacrolimus apparent clearance while bodyweight influenced volume of distribution. Tacrolimus 132-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 24430948-2 2014 The polymorphic enzyme P450 oxidoreductase (POR) transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH) to cytochrome P450 (CYP) 3A enzymes, which metabolize atorvastatin and simvastatin. NADP 74-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-153 24430948-2 2014 The polymorphic enzyme P450 oxidoreductase (POR) transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH) to cytochrome P450 (CYP) 3A enzymes, which metabolize atorvastatin and simvastatin. NADP 119-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-153 24430948-2 2014 The polymorphic enzyme P450 oxidoreductase (POR) transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH) to cytochrome P450 (CYP) 3A enzymes, which metabolize atorvastatin and simvastatin. Atorvastatin 180-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-153 24430948-2 2014 The polymorphic enzyme P450 oxidoreductase (POR) transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH) to cytochrome P450 (CYP) 3A enzymes, which metabolize atorvastatin and simvastatin. Simvastatin 197-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-153 24974574-4 2014 Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19. Simvastatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 25505590-4 2014 Ketoconazole also inhibited dronedarone metabolism by 89 +- 7%, demonstrating the crucial role of CYP3A in its metabolism. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 24974574-4 2014 Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19. Atorvastatin 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 24974574-4 2014 Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19. Lovastatin 30-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 24974574-4 2014 Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19. Fluvastatin 68-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 25505590-4 2014 Ketoconazole also inhibited dronedarone metabolism by 89 +- 7%, demonstrating the crucial role of CYP3A in its metabolism. Dronedarone 28-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 24974574-4 2014 Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19. Rosuvastatin Calcium 97-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 25505590-5 2014 CYP3A isoforms mostly contributed to N-debutylation while hydroxylation on the butyl-benzofuran moiety was catalyzed by CYP2D6. Nitrogen 37-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 25505590-5 2014 CYP3A isoforms mostly contributed to N-debutylation while hydroxylation on the butyl-benzofuran moiety was catalyzed by CYP2D6. butyl-benzofuran 79-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 24872323-3 2014 Orally administered sorafenib is oxidatively metabolized, predominantly by cytochrome P450 3A4 (CYP3A4), in small-intestinal mucosa or liver. Sorafenib 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-94 24304170-13 2014 CYP3A4 was identified as the dominant CYP isozyme converting gemigliptin to LC15-0636 in recombinant CYP/FMO enzymes. LC15-0444 61-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24304170-13 2014 CYP3A4 was identified as the dominant CYP isozyme converting gemigliptin to LC15-0636 in recombinant CYP/FMO enzymes. LC15-0636 76-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24345815-2 2014 More than 70% of administered CLB is dealkylated to yield N-desmethylclobazam (N-CLB), a pharmacologically active metabolite, by cytochrome P450 (CYP) 3A4 and CYP2C19. Clobazam 30-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-154 24345815-2 2014 More than 70% of administered CLB is dealkylated to yield N-desmethylclobazam (N-CLB), a pharmacologically active metabolite, by cytochrome P450 (CYP) 3A4 and CYP2C19. N-desmethylclobazam 58-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-154 24345815-2 2014 More than 70% of administered CLB is dealkylated to yield N-desmethylclobazam (N-CLB), a pharmacologically active metabolite, by cytochrome P450 (CYP) 3A4 and CYP2C19. n-clb 79-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-154 24872323-3 2014 Orally administered sorafenib is oxidatively metabolized, predominantly by cytochrome P450 3A4 (CYP3A4), in small-intestinal mucosa or liver. Sorafenib 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 24872323-4 2014 We aimed to characterize the CYP3A4-mediated metabolism of sorafenib in HCC patients and explore the contribution of the major metabolite sorafenib N-oxide to adverse effects and therapeutic efficacy. Sorafenib 59-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 24797816-12 2014 Additionally, the level of CYP3A4 and UGT1A9 expression were both notably decreased in the pooled THLMs. thlms 98-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 24871460-4 2014 Our study reveals that ergost-5-en-3beta-ol (4) induces PXR transactivation in HepG2 cells and stimulates the expression of the PXR target gene CYP3A4. campesterol 23-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 24800949-11 2014 Coadministration of pazopanib and lapatinib, weak inhibitors of CYP2C8 and CYP3A4, had an inhibitory effect on paclitaxel clearance. pazopanib 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 24800949-11 2014 Coadministration of pazopanib and lapatinib, weak inhibitors of CYP2C8 and CYP3A4, had an inhibitory effect on paclitaxel clearance. Lapatinib 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 24800949-11 2014 Coadministration of pazopanib and lapatinib, weak inhibitors of CYP2C8 and CYP3A4, had an inhibitory effect on paclitaxel clearance. Paclitaxel 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 24887515-1 2014 INTRODUCTION: We have previously shown that a tag single nucleotide polymorphism (rs10235235), which maps to the CYP3A locus (7q22.1), was associated with a reduction in premenopausal urinary estrone glucuronide levels and a modest reduction in risk of breast cancer in women age <=50 years. Estrone 192-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-118 24887515-1 2014 INTRODUCTION: We have previously shown that a tag single nucleotide polymorphism (rs10235235), which maps to the CYP3A locus (7q22.1), was associated with a reduction in premenopausal urinary estrone glucuronide levels and a modest reduction in risk of breast cancer in women age <=50 years. Glucuronides 200-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-118 24799042-4 2014 The device enables users to manipulate the expression of individual and multiple human metabolizing-enzyme genes (such as CYP3A4, CYP2D6, CYP2C9, CYP1A2, CYP2E1 and UGT1A4) in THLE-2 cell microarrays. thle 176-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 24526611-3 2014 A physiologically based pharmacokinetic (PBPK) model of tacrolimus was proposed, taking into account the body weight, the proportion of fat (P(fat)), hematocrit, lipid fraction of organs, typical intrinsic clearance (CLi(typ)), CYP3A5 genotype of liver donor, plasma unbound fraction of tacrolimus (fu(p)), and concomitant drugs (CYP3A4 inhibitors). Tacrolimus 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 330-336 24637579-5 2014 The metabolism of paclitaxel is mediated primarily by the P450 cytochrome enzymes CYP2C8 and CYP3A, whereas docetaxel is only metabolized by CYP3A4. Paclitaxel 18-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 24477376-7 2014 Ticagrelor is a recently approved P2Y12 receptor antagonist that is subject to drug-drug interactions involving the hepatic cytochrome P450-3A4 enzyme system because of its metabolic elimination pathway. Ticagrelor 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-143 24637579-5 2014 The metabolism of paclitaxel is mediated primarily by the P450 cytochrome enzymes CYP2C8 and CYP3A, whereas docetaxel is only metabolized by CYP3A4. Docetaxel 108-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 24477376-8 2014 This case demonstrates ticagrelor"s drug-drug interaction with phenytoin through a platelet aggregation study and supports the manufacturer recommendation to avoid the combination of ticagrelor with any known inducers of cytochrome P450-3A4 metabolism. Ticagrelor 23-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 221-240 24503628-1 2014 ": evaluation of CYP3A activity with microdoses of midazolam. Midazolam 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-22 24550332-1 2014 Elvitegravir (EVG), an HIV strand transfer integrase inhibitor, is metabolized primarily via cytochrome P450 3A4 (CYP3A) and secondarily via glucuronidation. elvitegravir 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-112 24550332-1 2014 Elvitegravir (EVG), an HIV strand transfer integrase inhibitor, is metabolized primarily via cytochrome P450 3A4 (CYP3A) and secondarily via glucuronidation. elvitegravir 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 24550332-1 2014 Elvitegravir (EVG), an HIV strand transfer integrase inhibitor, is metabolized primarily via cytochrome P450 3A4 (CYP3A) and secondarily via glucuronidation. elvitegravir 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-112 24550332-1 2014 Elvitegravir (EVG), an HIV strand transfer integrase inhibitor, is metabolized primarily via cytochrome P450 3A4 (CYP3A) and secondarily via glucuronidation. elvitegravir 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 24595680-0 2014 4beta-Hydroxycholesterol as an endogenous biomarker of CYP3A activity in cynomolgus monkeys. cholest-5-ene-3,4-diol 0-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 24726088-1 2014 OBJECTIVE: The aim of this study was to examine the effect of ketoconazole, a potent cytochrome P450 (CYP) 3A4 and P-glycoprotein (P-gp) inhibitor, on teneligliptin pharmacokinetics and to evaluate the safety of combined administration of teneligliptin with ketoconazole. Ketoconazole 62-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-110 24726088-1 2014 OBJECTIVE: The aim of this study was to examine the effect of ketoconazole, a potent cytochrome P450 (CYP) 3A4 and P-glycoprotein (P-gp) inhibitor, on teneligliptin pharmacokinetics and to evaluate the safety of combined administration of teneligliptin with ketoconazole. 3-(4-(4-(3-methyl-1-phenyl-1H-pyrazol-5-yl)piperazin-1-yl)pyrrolidin-2-ylcarbonyl)thiazolidine 151-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-110 24726088-13 2014 CONCLUSIONS: Because the exposure to teneligliptin in combined administration with ketoconazole, a potent CYP3A4 and P-gp inhibitor, was less than twice that of administration of teneligliptin alone, it is suggested that combined administration of teneligliptin with drugs and foods that inhibit CYP3A4 should not cause a marked increase in exposure. 3-(4-(4-(3-methyl-1-phenyl-1H-pyrazol-5-yl)piperazin-1-yl)pyrrolidin-2-ylcarbonyl)thiazolidine 37-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 24726088-13 2014 CONCLUSIONS: Because the exposure to teneligliptin in combined administration with ketoconazole, a potent CYP3A4 and P-gp inhibitor, was less than twice that of administration of teneligliptin alone, it is suggested that combined administration of teneligliptin with drugs and foods that inhibit CYP3A4 should not cause a marked increase in exposure. Ketoconazole 83-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 24513655-4 2014 Bedaquiline N-demethylation via CYP3A4 was confirmed as the major pathway in bedaquiline metabolism. bedaquiline 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 24553380-10 2014 Collectively, the data indicate that odanacatib has a long t1/2 on account of its low metabolic intrinsic clearance, and that metabolism (principally mediated by CYP3A) and excretion of intact parent compound account for ~70% and ~30% of the clearance of odanacatib in humans. odanacatib 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-167 24553381-5 2014 The results revealed that CYP1A2, CYP2B6, and CYP3A4 were induced (>2.0-fold) by omeprazole, phenobarbital, and rifampicin, respectively, in all the hepatocyte lots tested at enzyme activity level (23 lots) and mRNA level (8 lots). Omeprazole 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 24553381-5 2014 The results revealed that CYP1A2, CYP2B6, and CYP3A4 were induced (>2.0-fold) by omeprazole, phenobarbital, and rifampicin, respectively, in all the hepatocyte lots tested at enzyme activity level (23 lots) and mRNA level (8 lots). Phenobarbital 96-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 24553381-5 2014 The results revealed that CYP1A2, CYP2B6, and CYP3A4 were induced (>2.0-fold) by omeprazole, phenobarbital, and rifampicin, respectively, in all the hepatocyte lots tested at enzyme activity level (23 lots) and mRNA level (8 lots). Rifampin 115-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 24595680-11 2014 The results suggest that 4beta-hydroxycholesterol can be used as an endogenous biomarker to identify strong CYP3A inducers in cynomolgus monkeys, which may help to evaluate drug-drug interaction potential of drug candidates in preclinical settings. cholest-5-ene-3,4-diol 25-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 24513655-4 2014 Bedaquiline N-demethylation via CYP3A4 was confirmed as the major pathway in bedaquiline metabolism. bedaquiline 77-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 24513655-6 2014 The Km values of CYP2C8, CYP2C19, and CYP3A4 in bedaquiline N-demethylation were 13.1, 21.3, and 8.5 microM, respectively. bedaquiline 48-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 24595680-1 2014 It has been proposed that in humans 4beta-hydroxycholesterol is formed mainly by CYP3A-catalyzed metabolism of cholesterol and thus may serve as an endogenous marker for CYP3A activity. cholest-5-ene-3,4-diol 36-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 24595680-1 2014 It has been proposed that in humans 4beta-hydroxycholesterol is formed mainly by CYP3A-catalyzed metabolism of cholesterol and thus may serve as an endogenous marker for CYP3A activity. cholest-5-ene-3,4-diol 36-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-175 24598282-9 2014 In vitro phenotyping studies demonstrated that multiple cytochrome P450 (P450) isoforms, mainly CYP3A4/5 and CYP1A2, were involved in the metabolism of allitinib. AST 1306 152-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 24595680-1 2014 It has been proposed that in humans 4beta-hydroxycholesterol is formed mainly by CYP3A-catalyzed metabolism of cholesterol and thus may serve as an endogenous marker for CYP3A activity. Cholesterol 49-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 24595680-1 2014 It has been proposed that in humans 4beta-hydroxycholesterol is formed mainly by CYP3A-catalyzed metabolism of cholesterol and thus may serve as an endogenous marker for CYP3A activity. Cholesterol 49-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-175 24595680-3 2014 In the current study, the potential application of 4beta-hydroxycholesterol as an endogenous biomarker of CYP3A in response to drug treatment was evaluated in cynomolgus monkeys. cholest-5-ene-3,4-diol 51-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-111 24595680-4 2014 Following multiple oral administration of rifampicin (a known CYP3A inducer) at 15 mg/kg/d in cynomolgus monkeys, the mean serum 4beta-hydroxycholesterol levels increased 4-fold from the baseline of 55.3 +- 21.7 to 221 +- 53.4 ng/ml. Rifampin 42-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 24595680-4 2014 Following multiple oral administration of rifampicin (a known CYP3A inducer) at 15 mg/kg/d in cynomolgus monkeys, the mean serum 4beta-hydroxycholesterol levels increased 4-fold from the baseline of 55.3 +- 21.7 to 221 +- 53.4 ng/ml. cholest-5-ene-3,4-diol 129-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 24595680-7 2014 This observation correlated with the metabolism of midazolam (a probe substrate of CYP3A activity) monitored in the same study. Midazolam 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 24595680-8 2014 The serum exposure (area under the curve) of midazolam was markedly decreased by ~95%, confirming the induction of CYP3A catalytic activity by rifampicin treatment in monkeys. Midazolam 45-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 24595680-8 2014 The serum exposure (area under the curve) of midazolam was markedly decreased by ~95%, confirming the induction of CYP3A catalytic activity by rifampicin treatment in monkeys. Rifampin 143-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 24468605-1 2014 BACKGROUND: Antiepileptics may affect cortisol metabolism through CYP3A4. Hydrocortisone 38-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 24788541-8 2014 Testosterone, a CYP3A4-specific substrate, was used for detecting the metabolism activity of CYP3A4. Testosterone 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 24604243-0 2014 Pharmacokinetic interactions between the orexin receptor antagonist almorexant and the CYP3A4 inhibitors ketoconazole and diltiazem. Ketoconazole 105-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 24604243-0 2014 Pharmacokinetic interactions between the orexin receptor antagonist almorexant and the CYP3A4 inhibitors ketoconazole and diltiazem. Diltiazem 122-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 24604243-4 2014 Exposure to the phenol metabolites M3 and M8 increased in the presence of the CYP3A4 inhibitors, whereas that to M6 (dealkylated metabolite) decreased. Phenol 16-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 24486455-5 2014 In vitro biotransformation reactions were initiated with NADPH regenerating solutions following initial preincubation of pooled human hepatic or intestinal microsomal protein or human recombinant CYP3A4 supersomes with 1alpha,25(OH)2D3 or midazolam. 1alpha 219-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 196-202 24486455-11 2014 The inhibitory mechanism of aPPD or aPPT for CYP3A4-mediated biotransformation of 1alpha,25(OH)2D3 was competitive in nature (apparent Ki: 1.7-2.9muM). Calcitriol 82-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 24486455-13 2014 In summary, our results suggest that ginsenosides, specifically aPPD and aPPT, inhibit the CYP3A4-mediated catabolism of active vitamin D3 in human liver and intestine, potentially providing additional vitamin D-related benefits to patients with cancer, neurodegenerative and metabolic diseases. Ginsenosides 37-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 24486455-13 2014 In summary, our results suggest that ginsenosides, specifically aPPD and aPPT, inhibit the CYP3A4-mediated catabolism of active vitamin D3 in human liver and intestine, potentially providing additional vitamin D-related benefits to patients with cancer, neurodegenerative and metabolic diseases. Cholecalciferol 128-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 24486455-13 2014 In summary, our results suggest that ginsenosides, specifically aPPD and aPPT, inhibit the CYP3A4-mediated catabolism of active vitamin D3 in human liver and intestine, potentially providing additional vitamin D-related benefits to patients with cancer, neurodegenerative and metabolic diseases. Vitamin D 128-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 24944068-1 2014 OBJECTIVE: Hydrocodone undergoes metabolism via cytochrome P450 (CYP) 3A4 (N-demethylation) to norhydrocodone and via CYP2D6 (O-demethylation) to hydromorphone. Hydrocodone 11-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-73 24944068-1 2014 OBJECTIVE: Hydrocodone undergoes metabolism via cytochrome P450 (CYP) 3A4 (N-demethylation) to norhydrocodone and via CYP2D6 (O-demethylation) to hydromorphone. norhydrocodone 95-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-73 24788541-8 2014 Testosterone, a CYP3A4-specific substrate, was used for detecting the metabolism activity of CYP3A4. Testosterone 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24788541-10 2014 In addition, all the above expression levels in the transfected cell models could be further induced with additional treatment of Rifampicin, a specific inducer for CYP3A4. Rifampin 130-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 24941853-8 2014 Enzymic activity results showed that ginsenoside Rc, Rf, Rb2, F2, and F1 could increase the enzyme activity of CYP3A4 at 48 h (P <0.05). ginsenoside Rc 37-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 24191862-12 2014 Reaction phenotyping showed that CYP3A4, 3A5, 2D6, and 1A1 were mainly responsible for SNX-2112 metabolism. SNX 2112 87-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 24719135-2 2014 CYP3A4 is involved in the metabolism of both clopidogrel and dihydropyridine calcium channel blockers (CCBs). Clopidogrel 45-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24941853-9 2014 CONCLUSION: Ginsenoside Rc, Rf, Rb2, F2, F1, tanshinone I, and isoborneol in DC could induce CYP3A4 enzymes. ginsenoside Rc 12-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24941853-9 2014 CONCLUSION: Ginsenoside Rc, Rf, Rb2, F2, F1, tanshinone I, and isoborneol in DC could induce CYP3A4 enzymes. arginylphenylalanine 28-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24941853-9 2014 CONCLUSION: Ginsenoside Rc, Rf, Rb2, F2, F1, tanshinone I, and isoborneol in DC could induce CYP3A4 enzymes. Fluorine 37-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24941853-9 2014 CONCLUSION: Ginsenoside Rc, Rf, Rb2, F2, F1, tanshinone I, and isoborneol in DC could induce CYP3A4 enzymes. tanshinone 45-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24941853-9 2014 CONCLUSION: Ginsenoside Rc, Rf, Rb2, F2, F1, tanshinone I, and isoborneol in DC could induce CYP3A4 enzymes. isoborneol 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24654690-3 2014 A dual functional hexynylated 17alpha-ethynylestradiol activity-based probe was synthesized for specifically labeling CYP3A4 and then CC-mediated Eu-tagging with an azido-DOTA-Eu complex for CYP3A4 quantification and activity measurement in human liver microsome and serum samples using (153)Eu SUID ICPMS. Ethinyl Estradiol 30-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 24654690-3 2014 A dual functional hexynylated 17alpha-ethynylestradiol activity-based probe was synthesized for specifically labeling CYP3A4 and then CC-mediated Eu-tagging with an azido-DOTA-Eu complex for CYP3A4 quantification and activity measurement in human liver microsome and serum samples using (153)Eu SUID ICPMS. Ethinyl Estradiol 30-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-197 24654690-3 2014 A dual functional hexynylated 17alpha-ethynylestradiol activity-based probe was synthesized for specifically labeling CYP3A4 and then CC-mediated Eu-tagging with an azido-DOTA-Eu complex for CYP3A4 quantification and activity measurement in human liver microsome and serum samples using (153)Eu SUID ICPMS. azido-dota 165-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 24654690-3 2014 A dual functional hexynylated 17alpha-ethynylestradiol activity-based probe was synthesized for specifically labeling CYP3A4 and then CC-mediated Eu-tagging with an azido-DOTA-Eu complex for CYP3A4 quantification and activity measurement in human liver microsome and serum samples using (153)Eu SUID ICPMS. azido-dota 165-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-197 24462213-7 2014 Metabolism study in the human recombinant CYP 3A showed that these lignans had higher affinity to CYP3A than that of FK506, and thus had a stronger CYP3A-mediated metabolism. Lignans 67-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 24474568-3 2014 METHODS: In a modified phase 1 study of sunitinib, patients were stratified into 2 treatment arms based on whether they were receiving therapy with ritonavir, a potent CYP3A4 inhibitor. Ritonavir 148-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 24474568-12 2014 Efavirenz, a potent inducer of CYP3A4, resulted in increased exposure of N-desethyl sunitinib, whereas ritonavir caused decreased exposure of the metabolite. efavirenz 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 24474568-12 2014 Efavirenz, a potent inducer of CYP3A4, resulted in increased exposure of N-desethyl sunitinib, whereas ritonavir caused decreased exposure of the metabolite. SU 12662 73-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 24462213-7 2014 Metabolism study in the human recombinant CYP 3A showed that these lignans had higher affinity to CYP3A than that of FK506, and thus had a stronger CYP3A-mediated metabolism. Lignans 67-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 24462213-7 2014 Metabolism study in the human recombinant CYP 3A showed that these lignans had higher affinity to CYP3A than that of FK506, and thus had a stronger CYP3A-mediated metabolism. Lignans 67-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-153 24462213-7 2014 Metabolism study in the human recombinant CYP 3A showed that these lignans had higher affinity to CYP3A than that of FK506, and thus had a stronger CYP3A-mediated metabolism. Tacrolimus 117-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 24736630-7 2014 Incubations studies with selective chemical inhibitors demonstrated that the metabolism of 20(R)-25-OCH3-PPD was primarily mediated by CYP3A4. 20(r)-25-och3-ppd 91-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 24736630-9 2014 CYP3A4-catalyzed oxygenation metabolism played an important role in the disposition of 25(R)-OCH3-PPD, especially at the C-20 hydroxyl group. (r)-och3-ppd 89-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24462213-7 2014 Metabolism study in the human recombinant CYP 3A showed that these lignans had higher affinity to CYP3A than that of FK506, and thus had a stronger CYP3A-mediated metabolism. Tacrolimus 117-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-153 24462213-8 2014 It was concluded that the blood concentrations of these lignans were decreased and their CYP3A-mediated metabolisms were increased in the presence of FK506 since these lignans had higher affinity to CYP3A. Lignans 56-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 199-204 24462213-8 2014 It was concluded that the blood concentrations of these lignans were decreased and their CYP3A-mediated metabolisms were increased in the presence of FK506 since these lignans had higher affinity to CYP3A. Tacrolimus 150-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-94 24462213-8 2014 It was concluded that the blood concentrations of these lignans were decreased and their CYP3A-mediated metabolisms were increased in the presence of FK506 since these lignans had higher affinity to CYP3A. Tacrolimus 150-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 199-204 24462213-8 2014 It was concluded that the blood concentrations of these lignans were decreased and their CYP3A-mediated metabolisms were increased in the presence of FK506 since these lignans had higher affinity to CYP3A. Lignans 168-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-94 24462213-8 2014 It was concluded that the blood concentrations of these lignans were decreased and their CYP3A-mediated metabolisms were increased in the presence of FK506 since these lignans had higher affinity to CYP3A. Lignans 168-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 199-204 24463070-8 2014 KBA exposed to 1alpha,25-(OH)2 vitamin D3 treated cell monolayer showed the lowest Papp value of 2.01x10(-6) +- 0.02 x 10(-6)cm/s indicating role of CYP3A4 mediated metabolism during KBA transport. 25-(oh)2 vitamin d3 22-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 24733486-7 2014 Furthermore, the CYP3A4 activity in the HNF1alpha-transfected cells could be induced by CYP3A4-specific inducer, rifampicin, and metabolized nifedipine in a dose-dependent manner. Rifampin 113-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 24733486-7 2014 Furthermore, the CYP3A4 activity in the HNF1alpha-transfected cells could be induced by CYP3A4-specific inducer, rifampicin, and metabolized nifedipine in a dose-dependent manner. Rifampin 113-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 24733486-7 2014 Furthermore, the CYP3A4 activity in the HNF1alpha-transfected cells could be induced by CYP3A4-specific inducer, rifampicin, and metabolized nifedipine in a dose-dependent manner. Nifedipine 141-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 24733486-7 2014 Furthermore, the CYP3A4 activity in the HNF1alpha-transfected cells could be induced by CYP3A4-specific inducer, rifampicin, and metabolized nifedipine in a dose-dependent manner. Nifedipine 141-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 24782212-4 2014 Another double-expression vector, pBudCE4.1-optimized CYP 3A4-optimized GST A1, was constructed and then transfected into C3A to establish a stable cell line. pbudce4 34-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-61 24782212-9 2014 Although some C3A cells transfected with pBudCE4.1-optimized CYP 3A4-optimized GST A1 survived, they grew slowly, and were therefore not applicable in clinical practice. pbudce4 41-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-68 24692738-0 2014 Effect of co-administration of ketoconazole, a strong CYP3A inhibitor, on the pharmacokinetics, safety and tolerability of navitoclax, a first-in-class oral Bcl-2 family inhibitor, in cancer patients. Ketoconazole 31-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-59 24727459-1 2014 Poor systemic concentrations of lopinavir (LPV) following oral administration occur due to high cellular efflux by P-glycoprotein (P-gp) and multidrug resistance-associated proteins (MRPs) and extensive metabolism by CYP3A4 enzymes. Lopinavir 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-223 24727459-1 2014 Poor systemic concentrations of lopinavir (LPV) following oral administration occur due to high cellular efflux by P-glycoprotein (P-gp) and multidrug resistance-associated proteins (MRPs) and extensive metabolism by CYP3A4 enzymes. Lopinavir 43-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-223 24705503-4 2014 These studies revealed that phallusiasterol A induces PXR transactivation in HepG2 cells and stimulates the expression of the PXR target genes CYP3A4 and MDR1 in the same cell line. 3,6-dihydroxycholestan-5-yl sulfate 28-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 24817818-0 2014 Effects of EPHX1 and CYP3A4 polymorphisms on carbamazepine metabolism in epileptic patients. Carbamazepine 45-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 24817818-2 2014 Moreover, we reported the genotype frequencies of the CYP3A4*22 (rs 35599367, C>T) variant and its influence on the metabolism of CBZ. Carbamazepine 133-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 24817818-12 2014 Genotype frequencies for the CYP3A4*22 (rs 35599367 C>T) allelic variant were 94% for CC and 6% for CT, with no statistically significant difference in serum CBZ 10,11-epoxide levels between these genotypes 4 hours after administration of the drug (2.6+-1.3 mug/muL and 2.5+-1.2 mug/muL, respectively). Carbon Tetrachloride 103-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 24126681-0 2014 Identification and characterization of a defective CYP3A4 genotype in a kidney transplant patient with severely diminished tacrolimus clearance. Tacrolimus 123-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 24224579-3 2014 Phenprocoumon metabolism is mediated by CYP2C9 and CYP3A enzymes. Phenprocoumon 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 24488374-3 2014 Docetaxel is a widely used anticancer agent that is primarily metabolized by CYP3A4 enzymes and used to treat NADCs. Docetaxel 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 24488374-3 2014 Docetaxel is a widely used anticancer agent that is primarily metabolized by CYP3A4 enzymes and used to treat NADCs. nadcs 110-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 24488374-14 2014 RESULTS: Docetaxel exposure was altered by CYP3A4 inhibitors but not by inducers. Docetaxel 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 24488374-15 2014 The CYP3A4 inducers efavirenz and dexamethasone did not have a significant effect on docetaxel exposure (AUC). efavirenz 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 24488374-16 2014 However, the CYP3A4 inhibitors ritonavir and ketoconazole resulted in a 6.9- and 3.1-fold increase in AUC, respectively. Ritonavir 31-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 24488374-16 2014 However, the CYP3A4 inhibitors ritonavir and ketoconazole resulted in a 6.9- and 3.1-fold increase in AUC, respectively. Ketoconazole 45-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 24488374-18 2014 CONCLUSIONS: Docetaxel exposure was significantly altered by CYP3A4 inhibitors. Docetaxel 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 24452746-3 2014 Atorvastatin is metabolized primarily by CYP3A4 and is a P-gp inhibitor. Atorvastatin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 24126681-7 2014 In addition, the patient harbored inactive CYP3A5*3, resulting in loss of function of the entire CYP3A locus, explaining the deteriorated tacrolimus clearance. Tacrolimus 138-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-48 24476576-2 2014 Because paclitaxel is metabolized by CYP2C8 and CYP3A4, the possibility of drug-drug interactions mediated by enzyme inhibition may exist between the combining agents. Paclitaxel 8-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 24464803-9 2014 Cytochrome P450 (P450) profiling indicated that tofacitinib was mainly metabolized by CYP3A4, with a smaller contribution from CYP2C19. tofacitinib 48-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 24550106-12 2014 Several studies have shown that omeprazole carries a considerable potential for drug interactions because of its high affinity for CYP2C19 and moderate affinity for CYP3A4. Omeprazole 32-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 24476576-4 2014 For reversible inhibition, nilotinib was found to be the most potent inhibitor against both CYP2C8 and CYP3A4, and the inhibition potency could be explained by strong hydrogen binding based on molecular docking simulations and type II binding based on spectral analysis. nilotinib 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 24476576-5 2014 Comparison of K(i) values revealed that the CYP2C8 pathway was more sensitive toward some kinase inhibitors (such as axitinib), while the CYP3A4 pathway was preferentially inhibited by others (such as bosutinib). bosutinib 201-210 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 24476576-7 2014 Further studies showed that axitinib had a K(I) of 0.93 muM and k(inact) of 0.0137 min(-1), and the observed inactivation toward CYP3A4 was probably due to the formation of reactive intermediate(s). Axitinib 28-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 24476576-9 2014 The present results suggest that potent and pathway-dependent inhibition of CYP2C8 and/or CYP3A4 pathways by kinase inhibitors may alter the ratio of paclitaxel metabolites in vivo, and that such changes can be clinically relevant as differential metabolism has been linked to paclitaxel-induced neurotoxicity in cancer patients. Paclitaxel 150-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 24476576-9 2014 The present results suggest that potent and pathway-dependent inhibition of CYP2C8 and/or CYP3A4 pathways by kinase inhibitors may alter the ratio of paclitaxel metabolites in vivo, and that such changes can be clinically relevant as differential metabolism has been linked to paclitaxel-induced neurotoxicity in cancer patients. Paclitaxel 277-287 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 24627099-3 2014 Since mitotane increases cortisol binding globulin (CBG) and induces CYP3A4 activity, high doses of hydrocortisone are thought to be required. Mitotane 6-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 24214373-0 2014 The effect of CYP3A4*1G allele on the pharmacokinetics of atorvastatin in Chinese Han patients with coronary heart disease. Atorvastatin 58-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 24472406-11 2014 Concurrently, midazolam clearance (CYP3A activity) increased by 224% (n = 13, p < 0.05) and further increased after SJW by 374% compared to baseline (n = 13, p < 0.05). Midazolam 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-40 24165884-7 2014 These data suggest that etravirine is a weak CYP3A isozyme inducer and minimally inhibits CYP2C9, 2C19, and P-glycoprotein activity. etravirine 24-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-50 24500275-2 2014 Cytochrome P450 (CYP) 3A4 and 2C19 metabolize diazepam into the active metabolites: nordiazepam, temazepam and oxazepam. Diazepam 46-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-34 24500275-2 2014 Cytochrome P450 (CYP) 3A4 and 2C19 metabolize diazepam into the active metabolites: nordiazepam, temazepam and oxazepam. Nordazepam 84-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-34 24500275-2 2014 Cytochrome P450 (CYP) 3A4 and 2C19 metabolize diazepam into the active metabolites: nordiazepam, temazepam and oxazepam. Temazepam 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-34 24500275-2 2014 Cytochrome P450 (CYP) 3A4 and 2C19 metabolize diazepam into the active metabolites: nordiazepam, temazepam and oxazepam. Oxazepam 111-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-34 24500275-8 2014 Methadone significantly increased temazepam and oxazepam urinary fractions via CYP3A4 inhibition, whereas fluoxetine and esomeprazole increased nordiazepam fractions via CYP2C19 inhibition. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 24405193-0 2014 Longitudinal monitoring of CYP3A activity in patients receiving 3 cycles of itraconazole pulse therapy for onychomycosis. Itraconazole 76-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 24214373-1 2014 The present study aimed to evaluate the impact of CYP3A4*1G allele on the pharmacokinetics of atorvastatin in the Chinese Han patients with coronary heart disease (CHD). Atorvastatin 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 24405193-1 2014 WHAT IS KNOWN AND OBJECTIVE: Itraconazole, a CYP3A inhibitor, is used for the treatment for onychomycosis with a three-cycle pulse therapy over 3 months, but its effects on in vivo CYP3A activity during the entire course remain unknown. Itraconazole 29-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-50 24405193-1 2014 WHAT IS KNOWN AND OBJECTIVE: Itraconazole, a CYP3A inhibitor, is used for the treatment for onychomycosis with a three-cycle pulse therapy over 3 months, but its effects on in vivo CYP3A activity during the entire course remain unknown. Itraconazole 29-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 181-186 24405193-5 2014 WHAT IS NEW AND CONCLUSION: The inhibitory effect of itraconazole pulse therapy on the in vivo CYP3A activity appears clinically relevant at the end of each cycle, but the inhibition resolves, on average, within 3 weeks. Itraconazole 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-100 24525658-0 2014 The influence of the CYP3A4*22 polymorphism on serum concentration of quetiapine in psychiatric patients. Quetiapine Fumarate 70-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 24525658-4 2014 We investigated to which degree the CYP3A4*22 SNP affects serum concentrations of patients receiving quetiapine, a drug exclusively metabolized by CYP3A4. Quetiapine Fumarate 101-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 24525658-4 2014 We investigated to which degree the CYP3A4*22 SNP affects serum concentrations of patients receiving quetiapine, a drug exclusively metabolized by CYP3A4. Quetiapine Fumarate 101-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 24525658-7 2014 RESULTS: Carriers of the CYP3A4*22 allele (*1/*22 and *22/*22, n = 31) had 2.5-fold higher serum levels of quetiapine than did wild-type patients (n = 207; P = 0.03) when using a comparable dose (median, 300 mg/d for both wild-type and carriers; P = 0.67). Quetiapine Fumarate 107-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 24525658-10 2014 CONCLUSION: Being a carrier of the CYP3A4*22 allele increases the serum concentration of quetiapine at comparable doses. Quetiapine Fumarate 89-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 24214373-4 2014 The mean area under the plasma concentration-time curve from 0 to infinity (AUC0- ) of atorvastatin in subjects with the CYP3A4*1G/*1G genotype were 36% or 25% lower than in those with the wild-type or the *1/*1G genotype, respectively. Atorvastatin 88-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 24214373-5 2014 The time to peak plasma concentration (Tmax ) and oral clearance of atorvastatin (CL/F) were significantly different between subjects with the CYP3A4*1G/*1G genotype and the wild-type. Atorvastatin 68-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 24214373-6 2014 The AUC0- for 2-hydroxyatorvastatin in subjects with the CYP3A4*1G/*1G genotype was 44% or 31% lower than in those with the wild-type or the *1/*1G genotype, respectively. 2-hydroxyatorvastatin 15-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 24214373-7 2014 The peak plasma concentration, Tmax and apparent clearance of 2-hydroxyatorvastatin (CL/Fm) were significantly different between subjects with the CYP3A4*1G/*1G genotype and the wild-type. 2-hydroxyatorvastatin 62-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 24214373-8 2014 This study indicates that the CYP3A4*1G allele is associated with the pharmacokinetics of atorvastatin and its metabolites in those Chinese Han patients with CHD after a single oral dose. Atorvastatin 90-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 24589536-5 2014 Ruxolitinib is primarily metabolized by the cytochrome P-450 (CYP) 3A4 isoenzyme system; therefore, if concomitant use with a strong CYP3A4 inhibitor is unavoidable, an initial dosage reduction is warranted. ruxolitinib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-70 24469018-1 2014 OBJECTIVE: This study aimed to investigate whether CYP3A4/5 genetic variants, together with clinical and patient factors, influence serum fentanyl and norfentanyl concentrations and their ratio in cancer pain patients receiving transdermal fentanyl. Fentanyl 138-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 24469018-1 2014 OBJECTIVE: This study aimed to investigate whether CYP3A4/5 genetic variants, together with clinical and patient factors, influence serum fentanyl and norfentanyl concentrations and their ratio in cancer pain patients receiving transdermal fentanyl. norfentanyl 151-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 24469018-1 2014 OBJECTIVE: This study aimed to investigate whether CYP3A4/5 genetic variants, together with clinical and patient factors, influence serum fentanyl and norfentanyl concentrations and their ratio in cancer pain patients receiving transdermal fentanyl. Fentanyl 154-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 24469018-3 2014 Using stepwise linear regression, CYP3A4/5 genetic variability was examined in combination with patient factors relating to organ drug elimination function and ABCB1 genetics for their association with serum fentanyl and norfentanyl concentrations and metabolic ratio (MR) (norfentanyl : fentanyl). Fentanyl 208-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 24469018-8 2014 CYP3A4*22 and CYP3A5*3 genotypes, and multiple clinical factors, combine to influence transdermal fentanyl pharmacokinetics, but accounted for only a small proportion of variability in this study. Fentanyl 98-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24986003-9 2014 Previous antiplatelet agent - clopidogrel is ineffective due to genetic polymorphism in P450 (polymorphism of CYP2C19 and CYP3A4 allele - *1 isoforms in function, *2 and *3 non-functioning alleles) and due to failure of metabolic conversion to active molecule. Clopidogrel 30-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 23629159-1 2014 Efavirenz increases CYP2C19- and CYP3A-mediated omeprazole metabolism. Omeprazole 48-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 25165555-10 2014 Coadministration of erythromycin with other drugs that inhibit or are metabolized by CYP3A4 or with QTc prolonging drugs should be avoided in this setting. Erythromycin 20-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 24741320-2 2014 Modulation of CYP3A4 by flavonoids, such as anthocyanins, has been shown to inhibit the mutagenic activity of mammalian cells. Flavonoids 24-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 24741320-2 2014 Modulation of CYP3A4 by flavonoids, such as anthocyanins, has been shown to inhibit the mutagenic activity of mammalian cells. Anthocyanins 44-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 24741320-3 2014 Considering the previous investigations addressing CYP3A4 inhibition by these substances, we studied the three-dimensional quantitative structure-activity relationship (3D-QSAR) in a series of anthocyanin derivatives as CYP3A4 inhibitors. Anthocyanins 193-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 24741320-3 2014 Considering the previous investigations addressing CYP3A4 inhibition by these substances, we studied the three-dimensional quantitative structure-activity relationship (3D-QSAR) in a series of anthocyanin derivatives as CYP3A4 inhibitors. Anthocyanins 193-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 24589536-5 2014 Ruxolitinib is primarily metabolized by the cytochrome P-450 (CYP) 3A4 isoenzyme system; therefore, if concomitant use with a strong CYP3A4 inhibitor is unavoidable, an initial dosage reduction is warranted. ruxolitinib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 24474302-0 2014 The effect of rifampicin, a prototypical CYP3A4 inducer, on erlotinib pharmacokinetics in healthy subjects. Rifampin 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 24118434-5 2014 EFV was associated with increased DIS inhibition of ALDH activity relative to DIS alone administration possibly as a result of EFV-associated induction of CYP 3A4 which metabolizes the carbamate to DETC-MeSO (which inhibits ALDH). Carbamates 185-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-162 24118434-5 2014 EFV was associated with increased DIS inhibition of ALDH activity relative to DIS alone administration possibly as a result of EFV-associated induction of CYP 3A4 which metabolizes the carbamate to DETC-MeSO (which inhibits ALDH). S-methyl N,N-diethylthiolcarbamate sulfoxide 198-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-162 24118434-6 2014 Conversely, ATV co-administration reduced the effect of DIS on ALDH activity possibly as a result of ATV inhibition of CYP 3A4. Atazanavir Sulfate 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-126 24118434-6 2014 Conversely, ATV co-administration reduced the effect of DIS on ALDH activity possibly as a result of ATV inhibition of CYP 3A4. Disulfiram 56-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-126 24118434-6 2014 Conversely, ATV co-administration reduced the effect of DIS on ALDH activity possibly as a result of ATV inhibition of CYP 3A4. Atazanavir Sulfate 101-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-126 24151189-7 2014 Ketoconazole, a CYP3A inhibitor, blocked the formation of oxygenated metabolites of aPPD in both HIM and HLM in a concentration dependent manner. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-21 23834474-5 2014 For verification, the pregnancy-related changes in the disposition of methadone (cleared by CYP2B6, 3A and 2C19) and glyburide (cleared by CYP3A, 2C9 and 2C19) were predicted. Glyburide 117-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-158 24474302-2 2014 Because erlotinib is metabolized predominately by CYP3A4, co-administration of compounds that increase CYP3A4 activity may alter the efficacy and safety of erlotinib therapy. Erlotinib Hydrochloride 8-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 24474302-2 2014 Because erlotinib is metabolized predominately by CYP3A4, co-administration of compounds that increase CYP3A4 activity may alter the efficacy and safety of erlotinib therapy. Erlotinib Hydrochloride 8-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 24474302-2 2014 Because erlotinib is metabolized predominately by CYP3A4, co-administration of compounds that increase CYP3A4 activity may alter the efficacy and safety of erlotinib therapy. Erlotinib Hydrochloride 156-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 24474302-2 2014 Because erlotinib is metabolized predominately by CYP3A4, co-administration of compounds that increase CYP3A4 activity may alter the efficacy and safety of erlotinib therapy. Erlotinib Hydrochloride 156-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 24474302-3 2014 Two phase I studies were conducted in healthy male subjects to evaluate the effect of pre- or co-administered rifampicin, a CYP3A4 inducer, on the pharmacokinetics of erlotinib. Rifampin 110-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 24474302-11 2014 Doses of >=450 mg erlotinib may be necessary to compensate for concomitant medications with strong CYP3A4 enzyme induction effect. Erlotinib Hydrochloride 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 24378930-5 2014 There are significant interactions between colchicine and CYP3A4 and P-glycoprotein inhibitors, and the colchicine dose must be reduced. Colchicine 104-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 27128460-1 2014 In order to evaluate the potential for CYP3A4 induction by moxidectin, midazolam pharmacokinetic (PK) parameters were compared before and after moxidectin administration. moxidectin 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 24234588-0 2014 Predictive value of CYP3A and ABCB1 phenotyping probes for the pharmacokinetics of sunitinib: the ClearSun study. Sunitinib 83-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-25 24234588-2 2014 In this prospective study cytochrome P450 (CYP) 3A and adenosine triphosphate binding cassette (ABC) B1 phenotypes were correlated to the pharmacokinetics of sunitinib and its active metabolite N-desethylsunitinib. Sunitinib 158-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-50 24234588-2 2014 In this prospective study cytochrome P450 (CYP) 3A and adenosine triphosphate binding cassette (ABC) B1 phenotypes were correlated to the pharmacokinetics of sunitinib and its active metabolite N-desethylsunitinib. SU 12662 194-213 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-50 24335391-6 2014 Oxidation of T-5 by CYP3A5 yields an N-oxide metabolite that is over 100-fold selective over CYP3A4. n-oxide 37-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24696866-7 2014 Elvitegravir undergoes extensive primary metabolism by hepatic and intestinal cytochrome P450 3A (CYP3A) and secondary metabolism by UDP-glucuronosyltransferase 1-1 and 1-3 (UGT1A1/3). elvitegravir 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-96 24335510-4 2014 Following the preparation of microsomes, the kinetic profiles of five known human CYP3A4 (h3A4) substrates (midazolam, testosterone, terfenadine, nifedipine, and triazolam) were determined. Midazolam 108-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 24335510-8 2014 Ketoconazole and troleandomycin showed similar inhibitory potencies toward c3A4 and h3A4, whereas non-h3A4 inhibitors did not inhibit c3A4 activity. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-79 24335510-8 2014 Ketoconazole and troleandomycin showed similar inhibitory potencies toward c3A4 and h3A4, whereas non-h3A4 inhibitors did not inhibit c3A4 activity. Troleandomycin 17-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-79 24346834-6 2014 Faldaprevir is metabolized primarily in the liver by CYP3A4/5 to form M2a and M2b, which are also substrates of efflux transporters (P-glycoprotein and breast cancer resistance protein). faldaprevir 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 24696866-7 2014 Elvitegravir undergoes extensive primary metabolism by hepatic and intestinal cytochrome P450 3A (CYP3A) and secondary metabolism by UDP-glucuronosyltransferase 1-1 and 1-3 (UGT1A1/3). elvitegravir 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 24696866-8 2014 Although boosting it with a strong CYP3A inhibitor such as ritonavir substantially increases its plasma exposure and prolongs its elimination half-life, other combinations or even monotherapy could also be considered. Ritonavir 59-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-40 24405315-12 2014 Regorafenib is mainly metabolized by CYP3A4, and concomitant use of strong inducers/inhibitors of this enzyme should be avoided. regorafenib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 24259679-7 2014 Hyperforin and rifampicin treatment of HepG2 cells cotransfected with human PXR expression vector and a CYP3A4 promoter-reporter construct resulted in potent PXR-dependent induction, whereas all TRPC6-activating compounds failed to show any PXR activation or to antagonize rifampicin-mediated CYP3A4 promoter induction. hyperforin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 24105360-5 2014 Testosterone 6-beta hydroxylation was monitored using high-performance liquid chromatography as an indicator of CYP3A4 catalytic activities. testosterone 6-beta 0-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 24105360-11 2014 CONCLUSION: Our findings suggest that constituents of TCE extract especially protoberberine alkaloids have the potential to interact with cancer chemotherapy agents that are metabolized by CYP3A4 in vivo. Trichloroethylene 54-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 24105360-11 2014 CONCLUSION: Our findings suggest that constituents of TCE extract especially protoberberine alkaloids have the potential to interact with cancer chemotherapy agents that are metabolized by CYP3A4 in vivo. protoberberine alkaloids 77-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 24035278-1 2014 BACKGROUND: To investigate the correlation between CYP3A4/5 activity and clarithromycin metabolism, and between CYP3A activity and CYP3A genotype. Clarithromycin 73-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 24035278-1 2014 BACKGROUND: To investigate the correlation between CYP3A4/5 activity and clarithromycin metabolism, and between CYP3A activity and CYP3A genotype. Clarithromycin 73-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 24035278-2 2014 METHODS: This is an open-label, prospective pharmacokinetic study evaluating CYP3A activity using The Erythromycin Breath Test. Erythromycin 102-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 24035278-9 2014 A linear correlation between the CYP3A4-activity and clarithromycin metabolism was demonstrated (P < 0.05). Clarithromycin 53-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 24259679-7 2014 Hyperforin and rifampicin treatment of HepG2 cells cotransfected with human PXR expression vector and a CYP3A4 promoter-reporter construct resulted in potent PXR-dependent induction, whereas all TRPC6-activating compounds failed to show any PXR activation or to antagonize rifampicin-mediated CYP3A4 promoter induction. hyperforin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 293-299 24259679-7 2014 Hyperforin and rifampicin treatment of HepG2 cells cotransfected with human PXR expression vector and a CYP3A4 promoter-reporter construct resulted in potent PXR-dependent induction, whereas all TRPC6-activating compounds failed to show any PXR activation or to antagonize rifampicin-mediated CYP3A4 promoter induction. Rifampin 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 24259679-7 2014 Hyperforin and rifampicin treatment of HepG2 cells cotransfected with human PXR expression vector and a CYP3A4 promoter-reporter construct resulted in potent PXR-dependent induction, whereas all TRPC6-activating compounds failed to show any PXR activation or to antagonize rifampicin-mediated CYP3A4 promoter induction. Rifampin 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 293-299 24259679-7 2014 Hyperforin and rifampicin treatment of HepG2 cells cotransfected with human PXR expression vector and a CYP3A4 promoter-reporter construct resulted in potent PXR-dependent induction, whereas all TRPC6-activating compounds failed to show any PXR activation or to antagonize rifampicin-mediated CYP3A4 promoter induction. Rifampin 273-283 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 24734312-17 2014 CONCLUSION: This study shows that lomitapide is a weak inhibitor of CYP3A4 and increased the exposure of statin medications. BMS201038 34-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 24078287-10 2014 Moreover, the overexpression of miR-223 significantly reduced CYP3A4-catalyzed testosterone 6beta-hydroxylation activity and CYP2E1-catalyzed chlorzoxazone 6-hydroxylase activity but not CYP1A2-catalyzed 7-ethoxyresorufin O-deethylase activity. testosterone 6beta 79-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 24734312-18 2014 Careful monitoring of adverse events of CYP3A4-metabolized statins should be used when initiating therapy with lomitapide. BMS201038 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 24380838-9 2014 Furthermore, 18beta-GA, DAG, 20(S)-GF1 and Rh1 at 10 muM significantly inhibited CYP3A4/5 activity, while emodin activated the metabolism of midazolam in human liver microsomes. Gallium 19-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 24184159-10 2014 CMPF, hippuric acid and p-cresol have the ability to inhibit CYP3A4 metabolism at clinical concentrations which may correspond to reports of changes in hepatic metabolism in some CRF patients. 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 24184159-10 2014 CMPF, hippuric acid and p-cresol have the ability to inhibit CYP3A4 metabolism at clinical concentrations which may correspond to reports of changes in hepatic metabolism in some CRF patients. hippuric acid 6-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 24184159-10 2014 CMPF, hippuric acid and p-cresol have the ability to inhibit CYP3A4 metabolism at clinical concentrations which may correspond to reports of changes in hepatic metabolism in some CRF patients. 4-cresol 24-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 24380838-9 2014 Furthermore, 18beta-GA, DAG, 20(S)-GF1 and Rh1 at 10 muM significantly inhibited CYP3A4/5 activity, while emodin activated the metabolism of midazolam in human liver microsomes. dehydroandrographolide 24-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 23855261-10 2014 CYP3A4 and FMO3 are the major enzymes responsible for the metabolism of teneligliptin in humans. 3-(4-(4-(3-methyl-1-phenyl-1H-pyrazol-5-yl)piperazin-1-yl)pyrrolidin-2-ylcarbonyl)thiazolidine 72-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24476063-7 2014 Selectivity for aromatic hydroxylation over benzylic hydroxylation of m-xylene-(2)H3 supports a model in which the region near the CYP3A4 active oxidizing species limits substrate dynamics. m-xylene-(2)h3 70-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 23987740-13 2014 But the metabolism of gliquidone in the human liver microsomes was mainly mediated by CYP3A4. gliquidone 22-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 23987740-16 2014 The further study of human recombinant enzymes demonstrated that CYP3A4 was the principal isoform enzyme for the metabolism of gliquidone. gliquidone 127-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 23987740-17 2014 The intrinsic clearance (Vmax/Km) of CYP3A4 during gliquidone metabolism was 3-12 times greater than that of other CYP450 isoforms including CYP2C9, CYP2D6 and CYP2C19. gliquidone 51-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 23987740-19 2014 These findings may assist in valuable prediction of potential interactions of gliquidone with other drugs that are CYP3A4 inhibitors or inducers and help to design more efficacious and safer pharmacotherapy for patients of diabetes mellitus. gliquidone 78-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 24412072-2 2014 The HIV protease inhibitor (PI) ritonavir (RTV) has been widely used as a pharmacoenhancer for other PIs, which are substrates of cytochrome P450 3A (CYP3A). Ritonavir 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-148 24522145-5 2014 CYP3A4*22 carriers showed a significant lower clearance for cyclosporine (-15%), and a trend was observed for everolimus (-7%) and tacrolimus (-16%). Cyclosporine 60-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24522145-5 2014 CYP3A4*22 carriers showed a significant lower clearance for cyclosporine (-15%), and a trend was observed for everolimus (-7%) and tacrolimus (-16%). Everolimus 110-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24522145-5 2014 CYP3A4*22 carriers showed a significant lower clearance for cyclosporine (-15%), and a trend was observed for everolimus (-7%) and tacrolimus (-16%). Tacrolimus 131-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24498291-4 2014 In CYP2C9 and CYP3A4, weak interactions in an overall large active site cavity result in a fairly small binding free energy difference between APAP reactive binding states, consistent with experimental results that show little preference for resulting metabolites. Acetaminophen 143-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 24411125-1 2014 Ritonavir (RTV), an HIV-1 protease inhibitor (PI), is also a potent mechanism-based inhibitor of human cytochrome P450 3A (CYP3A) and has been widely prescribed as a pharmacoenhancer. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-121 24411125-1 2014 Ritonavir (RTV), an HIV-1 protease inhibitor (PI), is also a potent mechanism-based inhibitor of human cytochrome P450 3A (CYP3A) and has been widely prescribed as a pharmacoenhancer. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-128 24411125-1 2014 Ritonavir (RTV), an HIV-1 protease inhibitor (PI), is also a potent mechanism-based inhibitor of human cytochrome P450 3A (CYP3A) and has been widely prescribed as a pharmacoenhancer. Ritonavir 11-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-121 24411125-1 2014 Ritonavir (RTV), an HIV-1 protease inhibitor (PI), is also a potent mechanism-based inhibitor of human cytochrome P450 3A (CYP3A) and has been widely prescribed as a pharmacoenhancer. Ritonavir 11-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-128 24412072-2 2014 The HIV protease inhibitor (PI) ritonavir (RTV) has been widely used as a pharmacoenhancer for other PIs, which are substrates of cytochrome P450 3A (CYP3A). Ritonavir 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 24624624-3 2014 Their pharmacokinetic specificity is the key role of the transporter proteins P-glycoprotein (P-gp) for all these drugs and the metabolism mediated by CYP3A4 for -xabans. xabans 163-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 24412072-2 2014 The HIV protease inhibitor (PI) ritonavir (RTV) has been widely used as a pharmacoenhancer for other PIs, which are substrates of cytochrome P450 3A (CYP3A). Ritonavir 43-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-148 24412072-2 2014 The HIV protease inhibitor (PI) ritonavir (RTV) has been widely used as a pharmacoenhancer for other PIs, which are substrates of cytochrome P450 3A (CYP3A). Ritonavir 43-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 24412072-2 2014 The HIV protease inhibitor (PI) ritonavir (RTV) has been widely used as a pharmacoenhancer for other PIs, which are substrates of cytochrome P450 3A (CYP3A). Monothiopyrophosphoric acid 101-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-148 24412072-2 2014 The HIV protease inhibitor (PI) ritonavir (RTV) has been widely used as a pharmacoenhancer for other PIs, which are substrates of cytochrome P450 3A (CYP3A). Monothiopyrophosphoric acid 101-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 24412072-6 2014 Through these efforts, a potent and selective inhibitor of CYP3A, GS-9350 (cobicistat) with improved physiochemical properties was discovered. Cobicistat 75-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 24160757-5 2014 Clinical pharmacogenetic data further support CYP2C9 as a significant contributor to THC metabolism, and a pharmacokinetic interaction study using ketoconazole with oromucosal cannabis extract further supports CYP3A4 as a significant metabolic pathway for THC and CBD. Ketoconazole 147-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 210-216 24753822-4 2014 Dixon plots of CYP inhibition indicated that thelephoric acid was a competitive inhibitor of CYP1A2 and CYP3A4. thelephoric acid 45-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 24753822-2 2014 In the present study, the inhibitory effects of polyozellin and thelephoric acid on 9 cytochrome P450 (CYP) family members (CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4) were examined in pooled human liver microsomes (HLMs) using a cocktail probe assay. polyozellin 48-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 193-199 24160757-5 2014 Clinical pharmacogenetic data further support CYP2C9 as a significant contributor to THC metabolism, and a pharmacokinetic interaction study using ketoconazole with oromucosal cannabis extract further supports CYP3A4 as a significant metabolic pathway for THC and CBD. Dronabinol 256-259 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 210-216 24160757-5 2014 Clinical pharmacogenetic data further support CYP2C9 as a significant contributor to THC metabolism, and a pharmacokinetic interaction study using ketoconazole with oromucosal cannabis extract further supports CYP3A4 as a significant metabolic pathway for THC and CBD. Cannabidiol 264-267 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 210-216 24301608-0 2014 Amlodipine metabolism in human liver microsomes and roles of CYP3A4/5 in the dihydropyridine dehydrogenation. 1,4-dihydropyridine 77-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 24301608-3 2014 Results from clinical drug-drug interaction studies suggest that CYP3A4/5 mediate metabolism of amlodipine. Amlodipine 96-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 24301608-9 2014 Incubations of amlodipine with HLM in the presence of selective P450 inhibitors showed that both ketoconazole (an inhibitor of CYP3A4/5) and CYP3cide (an inhibitor of CYP3A4) completely blocked the M9 formation, whereas chemical inhibitors of other P450 enzymes had little effect. Amlodipine 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-135 24301608-9 2014 Incubations of amlodipine with HLM in the presence of selective P450 inhibitors showed that both ketoconazole (an inhibitor of CYP3A4/5) and CYP3cide (an inhibitor of CYP3A4) completely blocked the M9 formation, whereas chemical inhibitors of other P450 enzymes had little effect. Amlodipine 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 24301608-9 2014 Incubations of amlodipine with HLM in the presence of selective P450 inhibitors showed that both ketoconazole (an inhibitor of CYP3A4/5) and CYP3cide (an inhibitor of CYP3A4) completely blocked the M9 formation, whereas chemical inhibitors of other P450 enzymes had little effect. Ketoconazole 97-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-135 24301608-9 2014 Incubations of amlodipine with HLM in the presence of selective P450 inhibitors showed that both ketoconazole (an inhibitor of CYP3A4/5) and CYP3cide (an inhibitor of CYP3A4) completely blocked the M9 formation, whereas chemical inhibitors of other P450 enzymes had little effect. Ketoconazole 97-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 24301608-10 2014 Furthermore, metabolism of amlodipine in expressed human P450 enzymes showed that only CYP3A4 had significant activity in amlodipine dehydrogenation. Amlodipine 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 24301608-10 2014 Furthermore, metabolism of amlodipine in expressed human P450 enzymes showed that only CYP3A4 had significant activity in amlodipine dehydrogenation. Amlodipine 122-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 24301608-12 2014 The results from this study suggest that CYP3A4, rather than CYP3A5, plays a key role in metabolic clearance of amlodipine in humans. Amlodipine 112-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 24343782-2 2014 Cobicistat has a lower potential for off-target drug interactions than the standard boosting agent ritonavir, due to its more selective inhibition of CYP3A and lower likelihood for enzymatic induction, and is devoid of anti-HIV activity. Cobicistat 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 24343782-2 2014 Cobicistat has a lower potential for off-target drug interactions than the standard boosting agent ritonavir, due to its more selective inhibition of CYP3A and lower likelihood for enzymatic induction, and is devoid of anti-HIV activity. Ritonavir 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 24332451-6 2014 Coadministering everolimus with strong CYP3A4 and PgP inhibitors increased everolimus Cmin by 10% and 20%, respectively; coadministration with CYP3A4 inducers reduced Cmin by 7%. Everolimus 16-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 24048277-6 2014 Various cutoffs for predicting the likelihood of CYP3A inhibition were evaluated for mechanistic models, and a cutoff of 1.25-fold change in midazolam AUC appears appropriate. Midazolam 141-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 24249597-10 2014 Individuals carrying the CYP3A4*22 T-variant allele have a lower tacrolimus dose requirement than individuals with the CYP3A4*22 CC genotype and this effect appears to be independent of CYP3A5 genotype status. Tacrolimus 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 24249597-10 2014 Individuals carrying the CYP3A4*22 T-variant allele have a lower tacrolimus dose requirement than individuals with the CYP3A4*22 CC genotype and this effect appears to be independent of CYP3A5 genotype status. Tacrolimus 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 24186263-4 2014 METHODS: In vitro inhibition data for AZD2066 were obtained using human liver microsomes and CYP-specific probe substrates. AZD2066 38-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-96 24332451-6 2014 Coadministering everolimus with strong CYP3A4 and PgP inhibitors increased everolimus Cmin by 10% and 20%, respectively; coadministration with CYP3A4 inducers reduced Cmin by 7%. Everolimus 75-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 24161160-4 2014 gov number: NCT00739622) evaluated the interaction between rilpivirine and ethinylestradiol/norethindrone (combination oral contraceptives), which are metabolized by multiple pathways, including CYP3A4. Rilpivirine 59-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 24168324-9 2014 Among CYP1A1, CYP1B1 and CYP3A4 only CYP1A1 responded to low and moderate levels of AFB1. Aflatoxin B1 84-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 24161160-2 2014 OBJECTIVE: Rilpivirine metabolism involves cytochrome P450 3A4 (CYP3A4). Rilpivirine 11-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-62 24161160-4 2014 gov number: NCT00739622) evaluated the interaction between rilpivirine and ethinylestradiol/norethindrone (combination oral contraceptives), which are metabolized by multiple pathways, including CYP3A4. Ethinyl Estradiol 75-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 24161160-2 2014 OBJECTIVE: Rilpivirine metabolism involves cytochrome P450 3A4 (CYP3A4). Rilpivirine 11-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 24161160-4 2014 gov number: NCT00739622) evaluated the interaction between rilpivirine and ethinylestradiol/norethindrone (combination oral contraceptives), which are metabolized by multiple pathways, including CYP3A4. Norethindrone 92-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 24333052-0 2014 Effect of ritonavir-induced cytochrome P450 3A4 inhibition on plasma fentanyl concentrations during patient-controlled epidural labor analgesia: a pharmacokinetic simulation. Ritonavir 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-47 24332840-10 2014 From the numerous perpetrator characteristics, telaprevir"s inhibitor properties, especially of CYP3A4 and P-gp, appear to be the most relevant mechanism for drug interactions. telaprevir 47-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 24290411-2 2014 It is co-administered with low-dose ritonavir, a potent CYP3A inhibitor, to enhance danoprevir pharmacokinetics. Ritonavir 36-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 24290411-2 2014 It is co-administered with low-dose ritonavir, a potent CYP3A inhibitor, to enhance danoprevir pharmacokinetics. danoprevir 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 24290411-3 2014 Ketoconazole is a substrate for and potent selective inhibitor of CYP3A. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 24290411-12 2014 CONCLUSIONS: These results indicate that the effect of potent CYP3A inhibitors, such as ketoconazole, on danoprevir/r pharmacokinetics is not likely to be clinically relevant. danoprevir 105-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 24333052-0 2014 Effect of ritonavir-induced cytochrome P450 3A4 inhibition on plasma fentanyl concentrations during patient-controlled epidural labor analgesia: a pharmacokinetic simulation. Fentanyl 69-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-47 24333052-1 2014 BACKGROUND: Ritonavir inhibition of cytochrome P450 3A4 decreases the elimination clearance of fentanyl by 67%. Ritonavir 12-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-55 24333052-1 2014 BACKGROUND: Ritonavir inhibition of cytochrome P450 3A4 decreases the elimination clearance of fentanyl by 67%. Fentanyl 95-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-55 24333052-2 2014 We used a pharmacokinetic model developed from published data to simulate the effect of sample patient-controlled epidural labor analgesic regimens on plasma fentanyl concentrations in the absence and presence of ritonavir-induced cytochrome P450 3A4 inhibition. Ritonavir 213-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 231-250 24333052-12 2014 CONCLUSION: Our model predicts that even with maximal clinical dosing regimens of epidural fentanyl over 24 h, ritonavir-induced cytochrome P450 3A4 inhibition is unlikely to produce plasma fentanyl concentrations associated with a decrease in minute ventilation. Ritonavir 111-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-148 24038489-6 2014 CYP3A4 activity was assessed by the erythromycin breath test. Erythromycin 36-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24444408-0 2014 CYP3A5 and CYP3A4, but not ABCB1 polymorphisms affect tacrolimus dose-adjusted trough concentrations in kidney transplant recipients. Tacrolimus 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 24242708-8 2014 Inhibition of CYP3A activity using the specific inhibitor ritonavir resulted in alleviation of the anti-proliferative response of VDR ligands in prostate cancer cells. Ritonavir 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 24242708-9 2014 Mass spectrometry revealed that overexpression of CYP3A protein in prostate cancer cells resulted in a significant increase in the oxidative inactivation of testosterone and DHEA to their 6-beta-hydroxy-testosterone and 16-alpha-hydroxy-DHEA metabolites, respectively. Testosterone 157-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 24242708-9 2014 Mass spectrometry revealed that overexpression of CYP3A protein in prostate cancer cells resulted in a significant increase in the oxidative inactivation of testosterone and DHEA to their 6-beta-hydroxy-testosterone and 16-alpha-hydroxy-DHEA metabolites, respectively. Dehydroepiandrosterone 174-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 24242708-9 2014 Mass spectrometry revealed that overexpression of CYP3A protein in prostate cancer cells resulted in a significant increase in the oxidative inactivation of testosterone and DHEA to their 6-beta-hydroxy-testosterone and 16-alpha-hydroxy-DHEA metabolites, respectively. 6 beta-hydroxytestosterone 188-215 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 24242708-9 2014 Mass spectrometry revealed that overexpression of CYP3A protein in prostate cancer cells resulted in a significant increase in the oxidative inactivation of testosterone and DHEA to their 6-beta-hydroxy-testosterone and 16-alpha-hydroxy-DHEA metabolites, respectively. 16-hydroxydehydroepiandrosterone 220-241 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 24061445-2 2014 Both CYP3A5 and CYP3A4 are involved in the metabolism of calcineurin inhibitors and recent data show that POR*28 may explain part of the variability observed in tacrolimus (Tac) pharmacokinetics. Tacrolimus 161-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 24398010-0 2014 The effect of piperine on midazolam plasma concentration in healthy volunteers, a research on the CYP3A-involving metabolism. piperine 14-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 24214410-1 2014 We aim to evaluate the influence of covariates, including cytochrome P450 3A (CYP3A) genetic polymorphisms, on the pharmacokinetics of midazolam (MDZ) in Asian cancer patients, using a population pharmacokinetic approach. Midazolam 135-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-76 24214410-1 2014 We aim to evaluate the influence of covariates, including cytochrome P450 3A (CYP3A) genetic polymorphisms, on the pharmacokinetics of midazolam (MDZ) in Asian cancer patients, using a population pharmacokinetic approach. Midazolam 135-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 24214410-1 2014 We aim to evaluate the influence of covariates, including cytochrome P450 3A (CYP3A) genetic polymorphisms, on the pharmacokinetics of midazolam (MDZ) in Asian cancer patients, using a population pharmacokinetic approach. Midazolam 146-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-76 24214410-1 2014 We aim to evaluate the influence of covariates, including cytochrome P450 3A (CYP3A) genetic polymorphisms, on the pharmacokinetics of midazolam (MDZ) in Asian cancer patients, using a population pharmacokinetic approach. Midazolam 146-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 24214410-2 2014 Pharmacokinetic data were obtained from 24 adult cancer patients who received an intravenous bolus dose of 1 mg MDZ as a CYP3A phenotyping probe, 1-day before starting FOLFIRI chemotherapy. Midazolam 112-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-126 24466356-1 2014 BACKGROUND: The antifungal compound ketoconazole has, in addition to its ability to interfere with fungal ergosterol synthesis, effects upon other enzymes including human CYP3A4, CYP17, lipoxygenase and thromboxane synthetase. Ketoconazole 36-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 23850736-5 2014 We observed that CYP3A4 activity is higher in the 3D HepaRG cultures compared to the 2D HepaRG cultures. heparg 53-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 23850736-5 2014 We observed that CYP3A4 activity is higher in the 3D HepaRG cultures compared to the 2D HepaRG cultures. heparg 88-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 24387788-0 2014 Effects of anthocyanidins and anthocyanins on the expression and catalytic activities of CYP2A6, CYP2B6, CYP2C9, and CYP3A4 in primary human hepatocytes and human liver microsomes. Anthocyanins 11-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 24387788-0 2014 Effects of anthocyanidins and anthocyanins on the expression and catalytic activities of CYP2A6, CYP2B6, CYP2C9, and CYP3A4 in primary human hepatocytes and human liver microsomes. Anthocyanins 30-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 24387788-3 2014 The current study evaluated the effects of anthocyanidins and anthocyanins on the expression and catalytic activity of major drug-metabolizing enzymes CYP2C9, CYP2A6, CYP2B6, and CYP3A4 in primary cultures of human hepatocytes and human liver microsomes. Anthocyanins 62-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 24387788-8 2014 Catalytic activities of CYP2C9, CYP2A6, CYP2B6, and CYP3A4 enzymes were inhibited by all anthocyanidins to different extents (e.g., delphinidin inhibits CYP3A4 by >90% at 100 muM with IC50 = 32 muM). Anthocyanins 89-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 24387788-8 2014 Catalytic activities of CYP2C9, CYP2A6, CYP2B6, and CYP3A4 enzymes were inhibited by all anthocyanidins to different extents (e.g., delphinidin inhibits CYP3A4 by >90% at 100 muM with IC50 = 32 muM). Anthocyanins 89-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 24387788-8 2014 Catalytic activities of CYP2C9, CYP2A6, CYP2B6, and CYP3A4 enzymes were inhibited by all anthocyanidins to different extents (e.g., delphinidin inhibits CYP3A4 by >90% at 100 muM with IC50 = 32 muM). delphinidin 132-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 24387788-8 2014 Catalytic activities of CYP2C9, CYP2A6, CYP2B6, and CYP3A4 enzymes were inhibited by all anthocyanidins to different extents (e.g., delphinidin inhibits CYP3A4 by >90% at 100 muM with IC50 = 32 muM). delphinidin 132-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 24387788-9 2014 Of 21 anthocyanins tested, only cyanidin-3-O-rhamnoside (CYP3A4 by >75% at 100 muM with IC50 = 44 muM) and two glycosides of delphinidin significantly inhibited examined cytochromes P450. cyanidin-3-O-rhamnoside 32-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 24016712-6 2014 Carbofuran formation, representing from 79% to 98% of the total metabolism, was catalyzed predominantly by CYP3A4. Carbofuran 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 24016712-7 2014 The calculated relative contribution of CYP3A4 to carbofuran formation was 93%, while it was 4.4% for CYP2C9. Carbofuran 50-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 24016712-8 2014 The major contribution of CYP3A4 in benfuracarb metabolism was further substantiated by showing a strong correlation with CYP3A4-selective markers midazolam-1"-hydroxylation and omeprazole-sulfoxidation (r=0.885 and 0.772, respectively). benfuracarb 36-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 24016712-8 2014 The major contribution of CYP3A4 in benfuracarb metabolism was further substantiated by showing a strong correlation with CYP3A4-selective markers midazolam-1"-hydroxylation and omeprazole-sulfoxidation (r=0.885 and 0.772, respectively). benfuracarb 36-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 24016712-8 2014 The major contribution of CYP3A4 in benfuracarb metabolism was further substantiated by showing a strong correlation with CYP3A4-selective markers midazolam-1"-hydroxylation and omeprazole-sulfoxidation (r=0.885 and 0.772, respectively). Midazolam 147-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 24016712-8 2014 The major contribution of CYP3A4 in benfuracarb metabolism was further substantiated by showing a strong correlation with CYP3A4-selective markers midazolam-1"-hydroxylation and omeprazole-sulfoxidation (r=0.885 and 0.772, respectively). Midazolam 147-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 24016712-8 2014 The major contribution of CYP3A4 in benfuracarb metabolism was further substantiated by showing a strong correlation with CYP3A4-selective markers midazolam-1"-hydroxylation and omeprazole-sulfoxidation (r=0.885 and 0.772, respectively). Omeprazole 178-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 24016712-9 2014 Carbofuran formation was highly inhibited by the CYP3A inhibitor ketoconazole. Carbofuran 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 24016712-9 2014 Carbofuran formation was highly inhibited by the CYP3A inhibitor ketoconazole. Ketoconazole 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 24398010-0 2014 The effect of piperine on midazolam plasma concentration in healthy volunteers, a research on the CYP3A-involving metabolism. Midazolam 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 24398010-2 2014 Midazolam concentration is applied as a probe to determine the CYP3A enzyme activity. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 24256945-0 2014 Two surfaces of cytochrome b5 with major and minor contributions to CYP3A4-catalyzed steroid and nifedipine oxygenation chemistries. Steroids 85-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 25571290-1 2014 BACKGROUND: Simvastatin is a HMG-CoA reductase Inhibitor and a substrate of CYP3A4. Simvastatin 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 25571290-2 2014 Clarithromycin is a commonly used macrolide antibiotics and a potent inhibitor of CYP3A4. Clarithromycin 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 25571292-2 2014 Verapamil and its active metabolite, norverapamil, are known to be CYP3A4 inhibitors. Verapamil 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 25571292-2 2014 Verapamil and its active metabolite, norverapamil, are known to be CYP3A4 inhibitors. norverapamil 37-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 25571292-3 2014 Co-administration of verapamil with CYP3A4 substrates can alter the pharmacokinetics of the substrates. Verapamil 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 25571292-4 2014 Simvastatin, a commonly used HMG-CoA reductase inhibitor for the treatment of hypercholesterolemia is extensively metabolized by CYP3A4. Simvastatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 25571293-1 2014 BACKGROUND: Simvastatin, a commonly used HMG-CoA reductase inhibitor, is extensively metabolized by CYP3A4. Simvastatin 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 25571293-2 2014 Therefore, co-administration of simvastatin and CYP3A4 inhibitor can affect simvastatin pharmacokinetics. Simvastatin 76-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 25571293-3 2014 Nelfinavir, a protease inhibitor, and its major metabolite (M8) are known to be potent CYP3A4 inhibitors. Nelfinavir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 25332983-0 2014 The role of CYP3A4 in the biotransformation of bile acids and therapeutic implication for cholestasis. Bile Acids and Salts 47-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 25332983-9 2014 The activity of CYP3A4 is also inhibited by accumulated bile acids due to their property of detergent effect. Bile Acids and Salts 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 25332983-12 2014 In this review, we summarise recent progress about the roles of CYP3A4 in the metabolism of bile acids, its regulation and possible implication in the treatment of cholestasis. Bile Acids and Salts 92-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 24296729-3 2014 Amiodarone is metabolized by CYP3A4, CYP2C8 and CYP1A1 to an active metabolite and therefore may be affected by comedications that modulate these isoenzymes. Amiodarone 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 24256945-0 2014 Two surfaces of cytochrome b5 with major and minor contributions to CYP3A4-catalyzed steroid and nifedipine oxygenation chemistries. Nifedipine 97-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 24256945-2 2014 Here, we show that b5 mutations E48G, E49G, D58G, and D65G have reduced capacity to stimulate CYP3A4-catalyzed progesterone and testosterone 6beta-hydroxylation or nifedipine oxidation. Progesterone 111-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 24256945-2 2014 Here, we show that b5 mutations E48G, E49G, D58G, and D65G have reduced capacity to stimulate CYP3A4-catalyzed progesterone and testosterone 6beta-hydroxylation or nifedipine oxidation. testosterone 6beta 128-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 24256945-2 2014 Here, we show that b5 mutations E48G, E49G, D58G, and D65G have reduced capacity to stimulate CYP3A4-catalyzed progesterone and testosterone 6beta-hydroxylation or nifedipine oxidation. Nifedipine 164-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 24256945-8 2014 Our data suggest that a minor population of CYP3A4 molecules remains sensitive to b5 mutation E48G/E49G, consistent with phospholipid-dependent conformational heterogeneity of CYP3A4. Phospholipids 121-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 24256945-8 2014 Our data suggest that a minor population of CYP3A4 molecules remains sensitive to b5 mutation E48G/E49G, consistent with phospholipid-dependent conformational heterogeneity of CYP3A4. Phospholipids 121-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 26161443-0 2014 A chiral HPLC-MS/MS method for simultaneous quantification of warfarin enantiomers and its major hydroxylation metabolites of CYP2C9 and CYP3A4 in human plasma. Warfarin 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 26161443-2 2014 Enantiomeric separation and quantification of warfarin enantiomers and clinically important major hydroxylation metabolites are essential for drug interaction studies and phenotypic characterization of CYP2C9 and CYP3A4, the major cytochrome P450 (CYP) enzymes involved in warfarin metabolism. Warfarin 46-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 213-219 26161443-2 2014 Enantiomeric separation and quantification of warfarin enantiomers and clinically important major hydroxylation metabolites are essential for drug interaction studies and phenotypic characterization of CYP2C9 and CYP3A4, the major cytochrome P450 (CYP) enzymes involved in warfarin metabolism. Warfarin 273-281 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 213-219 24749245-7 2014 Cytochrome b5mc was shown to be capable of stimulating the electrocatalytic activity of CYP3A4 to testosterone. Testosterone 98-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 26161443-3 2014 Here, we describe the development and validation of a chiral high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS)-based quantification of R-warfarin, S-warfarin, S-7-hydroxywarfarin (the major CYP2C9 metabolite) and (9R;10S)-10-hydroxywarfarin (the CYP3A4 metabolite) in human plasma. 7-hydroxywarfarin 186-205 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 273-279 24125115-1 2014 It has been known that cocaine produces its toxic and physiological effects through not only cocaine itself, but also norcocaine formed from cocaine oxidation catalysed by microsomal CYP (cytochrome P450) 3A4 in the human liver. Cocaine 23-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-208 24125115-1 2014 It has been known that cocaine produces its toxic and physiological effects through not only cocaine itself, but also norcocaine formed from cocaine oxidation catalysed by microsomal CYP (cytochrome P450) 3A4 in the human liver. norcocaine 118-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-208 24369269-1 2014 Telaprevir (TVR) is a protease inhibitor used in combination with pegylated interferon alfa-2b and ribavirin for hepatitis C, and TVR strongly inhibits CYP3A4 and CYP3A5. telaprevir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 24369269-1 2014 Telaprevir (TVR) is a protease inhibitor used in combination with pegylated interferon alfa-2b and ribavirin for hepatitis C, and TVR strongly inhibits CYP3A4 and CYP3A5. telaprevir 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 24369269-3 2014 Before initiation of triple therapy, all patients switched from tacrolimus to cyclosporine, which has a lower inhibitory effect on CYP3A4 and CYP3A5 than tacrolimus. Tacrolimus 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 24369269-3 2014 Before initiation of triple therapy, all patients switched from tacrolimus to cyclosporine, which has a lower inhibitory effect on CYP3A4 and CYP3A5 than tacrolimus. Cyclosporine 78-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 24575309-9 2014 Since ranolazine is a documented P-GP and CYP3A inhibitor, and sirolimus a known substrate for both pathways, it is proposed that ranolazine inhibition of P-GP and CYP3A4 contributed to the significant elevation in sirolimus exposure. Ranolazine 130-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 23772874-6 2014 CONCLUSION: The correlation with unbound midazolam clearance suggests that either score predicts the metabolic capacity of CYP3A, the most relevant drug metabolizing enzyme subfamily in humans. Midazolam 41-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-128 24149944-2 2014 Since sunitinib is metabolized by cytochrome P450(CYP)3A4, variability in the activity of this enzyme may explain a considerable proportion of this inter-patient variability. Sunitinib 6-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-57 24149944-3 2014 Midazolam is widely used as a phenotyping probe to assess CYP3A4-activity. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 23738582-3 2014 METHODS: We assessed the effect of the OATP and CYP3A inhibitor clarithromycin on bosentan pharmacokinetics at steady state and concurrently quantified changes of CYP3A activity using midazolam as a probe drug. Bosentan 82-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 23738582-6 2014 Clarithromycin also reduced CYP3A activity (midazolam clearance) in all participants; however, these changes were not correlated to the changes of bosentan clearance. Clarithromycin 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 23772874-3 2014 METHODS: Midazolam was used as a CYP3A probe and its pharmacokinetics were analyzed in 24 patients with mild to severe liver cirrhosis (n = 4, 10 and 10 with CP class A, B and C, respectively) and six patients without liver disease. Midazolam 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 24575309-9 2014 Since ranolazine is a documented P-GP and CYP3A inhibitor, and sirolimus a known substrate for both pathways, it is proposed that ranolazine inhibition of P-GP and CYP3A4 contributed to the significant elevation in sirolimus exposure. Ranolazine 6-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 24575309-9 2014 Since ranolazine is a documented P-GP and CYP3A inhibitor, and sirolimus a known substrate for both pathways, it is proposed that ranolazine inhibition of P-GP and CYP3A4 contributed to the significant elevation in sirolimus exposure. Ranolazine 130-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 24575309-9 2014 Since ranolazine is a documented P-GP and CYP3A inhibitor, and sirolimus a known substrate for both pathways, it is proposed that ranolazine inhibition of P-GP and CYP3A4 contributed to the significant elevation in sirolimus exposure. Sirolimus 215-224 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 24389597-2 2014 We verified if the pharmacodynamic effects of CYP3A4-metabolized statins (atorvastatin) and non-CYP3A4-metabolized statins (pitavastatin) differ in patients with coronary artery disease (CAD) treated with DAPT. Atorvastatin 74-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 24492588-0 2014 Synthesis and biological activity of 1alpha,2alpha,25-trihydroxyvitamin D3: active metabolite of 2alpha-(3-hydroxypropoxy)-1alpha,25-dihydroxyvitamin D3 by human CYP3A4. 2alpha,25-trihydroxyvitamin d3 44-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 24492588-0 2014 Synthesis and biological activity of 1alpha,2alpha,25-trihydroxyvitamin D3: active metabolite of 2alpha-(3-hydroxypropoxy)-1alpha,25-dihydroxyvitamin D3 by human CYP3A4. 2ALPHA-(3-HYDROXYPROPOXY)-1ALPHA,25-DIHYDROXYVITAMIN D3 97-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 24107805-0 2014 Impact of CYP2D6 and CYP3A4 genetic polymorphism on combined cholinesterase inhibitors and memantine treatment in mild to moderate Alzheimer"s disease. Memantine 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 24092799-0 2014 Priapism induced by boceprevir-CYP3A4 inhibition and alpha-adrenergic blockade: case report. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 20-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 24092799-2 2014 A drug-drug interaction is the suspected cause whereby CYP3A4 inhibition by boceprevir led to increased exposures of doxazosin, tamsulosin, and/or quetiapine, resulting in additional alpha-adrenergic blockade. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 76-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 24092799-2 2014 A drug-drug interaction is the suspected cause whereby CYP3A4 inhibition by boceprevir led to increased exposures of doxazosin, tamsulosin, and/or quetiapine, resulting in additional alpha-adrenergic blockade. Doxazosin 117-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 24092799-2 2014 A drug-drug interaction is the suspected cause whereby CYP3A4 inhibition by boceprevir led to increased exposures of doxazosin, tamsulosin, and/or quetiapine, resulting in additional alpha-adrenergic blockade. Tamsulosin 128-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 24092799-2 2014 A drug-drug interaction is the suspected cause whereby CYP3A4 inhibition by boceprevir led to increased exposures of doxazosin, tamsulosin, and/or quetiapine, resulting in additional alpha-adrenergic blockade. Quetiapine Fumarate 147-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 27128230-1 2014 Sirolimus, metabolized primarily by intestinal and hepatic CYP3A4, is a substrate for P-glycoprotein. Sirolimus 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 27128230-2 2014 CYP3A4 inducers would be expected to decrease sirolimus exposure. Sirolimus 46-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 27128230-3 2014 This open-label, nonrandomized study investigated effects of CYP3A4 induction, by rifampin, on sirolimus pharmacokinetics. Rifampin 82-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 27128230-3 2014 This open-label, nonrandomized study investigated effects of CYP3A4 induction, by rifampin, on sirolimus pharmacokinetics. Sirolimus 95-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 27128233-2 2014 Tofacitinib is predominantly metabolized by cytochrome P450 (CYP) 3A4 and to a lesser extent by CYP2C19. tofacitinib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-69 27128233-3 2014 Two Phase 1, randomized, open-label, single sequence studies in 24 healthy subjects (12 per study) characterized the effects of fluconazole (moderate CYP3A4/potent CYP2C19 inhibitor) and ketoconazole (potent CYP3A4 inhibitor) on tofacitinib pharmacokinetics. Fluconazole 128-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 27128233-11 2014 Co-administration of moderate to potent CYP3A4 inhibitors is likely to increase the systemic exposure of tofacitinib and thus may warrant dosage adjustments or restrictions. tofacitinib 105-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 25429674-3 2014 Fluconazole, itraconazole, and voriconazole were relatively less potent inhibitors of CYP3A5 than of CYP3A4. Fluconazole 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 25429674-3 2014 Fluconazole, itraconazole, and voriconazole were relatively less potent inhibitors of CYP3A5 than of CYP3A4. Itraconazole 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 25429674-3 2014 Fluconazole, itraconazole, and voriconazole were relatively less potent inhibitors of CYP3A5 than of CYP3A4. Voriconazole 31-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 25429674-4 2014 The inhibitory effects of fluconazole, itraconazole, ketoconazole, and voriconazole against CYP3A4 and CYP3A5 seemed to be correlated with their dissociation constants for CYP51 (lanosterol 14alpha-demethylase) from Candida albicans. Fluconazole 26-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 25429674-4 2014 The inhibitory effects of fluconazole, itraconazole, ketoconazole, and voriconazole against CYP3A4 and CYP3A5 seemed to be correlated with their dissociation constants for CYP51 (lanosterol 14alpha-demethylase) from Candida albicans. Itraconazole 39-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 25429674-4 2014 The inhibitory effects of fluconazole, itraconazole, ketoconazole, and voriconazole against CYP3A4 and CYP3A5 seemed to be correlated with their dissociation constants for CYP51 (lanosterol 14alpha-demethylase) from Candida albicans. Ketoconazole 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 25429674-4 2014 The inhibitory effects of fluconazole, itraconazole, ketoconazole, and voriconazole against CYP3A4 and CYP3A5 seemed to be correlated with their dissociation constants for CYP51 (lanosterol 14alpha-demethylase) from Candida albicans. Voriconazole 71-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 25429674-5 2014 In in vivo pharmacokinetic studies, itraconazole was found to be a potent clinically important inhibitor of CYP3A4/5 substrates, and fluconazole and voriconazole increased the blood/plasma concentrations of not only CYP3A4/5 substrates but also CYP2C9 substrates. Itraconazole 36-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 25429674-5 2014 In in vivo pharmacokinetic studies, itraconazole was found to be a potent clinically important inhibitor of CYP3A4/5 substrates, and fluconazole and voriconazole increased the blood/plasma concentrations of not only CYP3A4/5 substrates but also CYP2C9 substrates. Itraconazole 36-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-222 25429674-5 2014 In in vivo pharmacokinetic studies, itraconazole was found to be a potent clinically important inhibitor of CYP3A4/5 substrates, and fluconazole and voriconazole increased the blood/plasma concentrations of not only CYP3A4/5 substrates but also CYP2C9 substrates. Fluconazole 133-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 25429674-5 2014 In in vivo pharmacokinetic studies, itraconazole was found to be a potent clinically important inhibitor of CYP3A4/5 substrates, and fluconazole and voriconazole increased the blood/plasma concentrations of not only CYP3A4/5 substrates but also CYP2C9 substrates. Fluconazole 133-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-222 25429674-5 2014 In in vivo pharmacokinetic studies, itraconazole was found to be a potent clinically important inhibitor of CYP3A4/5 substrates, and fluconazole and voriconazole increased the blood/plasma concentrations of not only CYP3A4/5 substrates but also CYP2C9 substrates. Voriconazole 149-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 25429674-5 2014 In in vivo pharmacokinetic studies, itraconazole was found to be a potent clinically important inhibitor of CYP3A4/5 substrates, and fluconazole and voriconazole increased the blood/plasma concentrations of not only CYP3A4/5 substrates but also CYP2C9 substrates. Voriconazole 149-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-222 24068654-2 2014 Here, the potential pharmacokinetic interaction between SJW and the sensitive CYP3A4 substrate docetaxel was investigated. Docetaxel 95-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 24805065-0 2014 Ritonavir analogues as a probe for deciphering the cytochrome P450 3A4 inhibitory mechanism. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-70 24805065-3 2014 Currently, the CYP3A4 inhibitor ritonavir and its derivative cobicistat are prescribed to HIV patients as pharmacoenhancers. Ritonavir 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 24805065-3 2014 Currently, the CYP3A4 inhibitor ritonavir and its derivative cobicistat are prescribed to HIV patients as pharmacoenhancers. Cobicistat 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 24805065-5 2014 To unravel the structural basis of CYP3A4 inhibition, we compared the binding modes of ritonavir and ten analogues using biochemical, mutagenesis and x-ray crystallography techniques. Ritonavir 87-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 24805065-6 2014 This review summarizes our findings on the relative contribution of the heme-ligating moiety, side chains and the terminal group of ritonavir-like molecules to the ligand binding process, and highlights strategies for a structure-guided design of CYP3A4 inactivators. Heme 72-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 247-253 24805065-6 2014 This review summarizes our findings on the relative contribution of the heme-ligating moiety, side chains and the terminal group of ritonavir-like molecules to the ligand binding process, and highlights strategies for a structure-guided design of CYP3A4 inactivators. Ritonavir 132-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 247-253 24107805-1 2014 AIM: The impact of CYP2D6 and CYP3A4 polymorphism on the steady-state plasma concentrations and therapeutic outcome of donepezil monotherapy and combination therapy in Alzheimer"s disease (AD) patients. Donepezil 119-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 24131672-11 2014 These results show that DS is a good representative substrate of MDZ and TST primarily due to their shared, large binding regions on CYP3A. schizandrin A 24-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-138 23965645-5 2014 When CYP3A4/5 polymorphisms were assessed by a mixture model, extensive metabolizers yielded a decrease in simvastatin bioavailability of 81% and a decrease in simvastatin clearance by 4.6 times as compared to poor metabolizers. Simvastatin 107-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 5-11 23965645-5 2014 When CYP3A4/5 polymorphisms were assessed by a mixture model, extensive metabolizers yielded a decrease in simvastatin bioavailability of 81% and a decrease in simvastatin clearance by 4.6 times as compared to poor metabolizers. Simvastatin 160-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 5-11 24131672-4 2014 CYP3A4 and CYP3A5 were found to be the major isoforms involved in the monohydroxylation of DS. schizandrin A 91-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24131672-12 2014 Therefore, DS is an attractive candidate as a novel CYP3A probe substrate for predicting the metabolic modifications in CYP3A activity. schizandrin A 11-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-57 24191259-0 2014 Studies on the role of metabolic activation in tyrosine kinase inhibitor-dependent hepatotoxicity: induction of CYP3A4 enhances the cytotoxicity of lapatinib in HepaRG cells. Lapatinib 148-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 24131672-12 2014 Therefore, DS is an attractive candidate as a novel CYP3A probe substrate for predicting the metabolic modifications in CYP3A activity. schizandrin A 11-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-125 24191259-2 2014 Lapatinib is extensively metabolized by cytochrome P450 3A4/5 to yield an O-debenzylated metabolite, which can undergo further oxidation to a reactive quinone imine. Lapatinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-59 24484539-5 2014 Among the substrates that are preferably metabolized by CYP3A4, including carebastine, itraconazole, haloperidol, and fluvastatin, the former three compounds were found to closely dock to the heme region of CYP3A4 but not to that of CYP3A5. Fluvastatin 118-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 24191259-2 2014 Lapatinib is extensively metabolized by cytochrome P450 3A4/5 to yield an O-debenzylated metabolite, which can undergo further oxidation to a reactive quinone imine. quinone imine 151-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-59 24191259-3 2014 A recent clinical study reported that concomitant use of lapatinib with dexamethasone increased the incidence of hepatotoxicity in metastatic breast cancer patients treated with lapatinib, and so we hypothesized that induction of CYP3A enhances the bioactivation of lapatinib to reactive intermediates that contribute to hepatotoxicity. Lapatinib 57-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-235 24191259-3 2014 A recent clinical study reported that concomitant use of lapatinib with dexamethasone increased the incidence of hepatotoxicity in metastatic breast cancer patients treated with lapatinib, and so we hypothesized that induction of CYP3A enhances the bioactivation of lapatinib to reactive intermediates that contribute to hepatotoxicity. Dexamethasone 72-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-235 24191259-3 2014 A recent clinical study reported that concomitant use of lapatinib with dexamethasone increased the incidence of hepatotoxicity in metastatic breast cancer patients treated with lapatinib, and so we hypothesized that induction of CYP3A enhances the bioactivation of lapatinib to reactive intermediates that contribute to hepatotoxicity. Lapatinib 178-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-235 24191259-3 2014 A recent clinical study reported that concomitant use of lapatinib with dexamethasone increased the incidence of hepatotoxicity in metastatic breast cancer patients treated with lapatinib, and so we hypothesized that induction of CYP3A enhances the bioactivation of lapatinib to reactive intermediates that contribute to hepatotoxicity. Lapatinib 178-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-235 24191259-4 2014 Therefore, we examined the effect of CYP3A4 induction on the cytotoxicity and metabolism of lapatinib in the HepaRG human hepatic cell line. Lapatinib 92-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 24191259-5 2014 Differentiated HepaRG cells were pretreated with dexamethasone (100 muM) or the prototypical CYP3A4 inducer rifampicin (4 muM) for 72 hours, followed by incubation with lapatinib (0-100 muM) for 24 hours. Rifampin 108-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24191259-7 2014 Induction of CYP3A4 by dexamethasone or rifampicin enhanced lapatinib-induced cytotoxicity, compared with treatment with lapatinib alone. Dexamethasone 23-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 24191259-7 2014 Induction of CYP3A4 by dexamethasone or rifampicin enhanced lapatinib-induced cytotoxicity, compared with treatment with lapatinib alone. Lapatinib 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 24406279-5 2014 On the other hand, in order to explain the differences in the clinical response to CBZ, genetic polymorphisms in phase I (CYP3A4, CYP3A5 and EPHX1) and phase II (UGT2B7) metabolising enzymes have been assessed; additionally, the influence of transporters (ABCB1 and ABCC2), receptors (PXR) and other drug targets (voltage- gated Na+ channels) in CBZ clinical response has been evaluated. Carbamazepine 83-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 24484539-5 2014 Among the substrates that are preferably metabolized by CYP3A4, including carebastine, itraconazole, haloperidol, and fluvastatin, the former three compounds were found to closely dock to the heme region of CYP3A4 but not to that of CYP3A5. carebastine 74-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 24484539-5 2014 Among the substrates that are preferably metabolized by CYP3A4, including carebastine, itraconazole, haloperidol, and fluvastatin, the former three compounds were found to closely dock to the heme region of CYP3A4 but not to that of CYP3A5. carebastine 74-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 24484539-5 2014 Among the substrates that are preferably metabolized by CYP3A4, including carebastine, itraconazole, haloperidol, and fluvastatin, the former three compounds were found to closely dock to the heme region of CYP3A4 but not to that of CYP3A5. Itraconazole 87-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 24484539-5 2014 Among the substrates that are preferably metabolized by CYP3A4, including carebastine, itraconazole, haloperidol, and fluvastatin, the former three compounds were found to closely dock to the heme region of CYP3A4 but not to that of CYP3A5. Itraconazole 87-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 24484539-5 2014 Among the substrates that are preferably metabolized by CYP3A4, including carebastine, itraconazole, haloperidol, and fluvastatin, the former three compounds were found to closely dock to the heme region of CYP3A4 but not to that of CYP3A5. Haloperidol 101-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 24484539-5 2014 Among the substrates that are preferably metabolized by CYP3A4, including carebastine, itraconazole, haloperidol, and fluvastatin, the former three compounds were found to closely dock to the heme region of CYP3A4 but not to that of CYP3A5. Haloperidol 101-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 24191259-7 2014 Induction of CYP3A4 by dexamethasone or rifampicin enhanced lapatinib-induced cytotoxicity, compared with treatment with lapatinib alone. Lapatinib 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 24484539-5 2014 Among the substrates that are preferably metabolized by CYP3A4, including carebastine, itraconazole, haloperidol, and fluvastatin, the former three compounds were found to closely dock to the heme region of CYP3A4 but not to that of CYP3A5. Fluvastatin 118-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 24191259-11 2014 Collectively, these data suggest that CYP3A4 induction potentiates lapatinib-induced hepatotoxicity via increased reactive metabolite formation. Lapatinib 67-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 24484539-5 2014 Among the substrates that are preferably metabolized by CYP3A4, including carebastine, itraconazole, haloperidol, and fluvastatin, the former three compounds were found to closely dock to the heme region of CYP3A4 but not to that of CYP3A5. Heme 192-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 24522199-1 2014 The effects of genetic polymorphisms of ABCB1 C3435T, POR*28, CYP3A4*1G and CYP3A5*3 variants and gender relating to metabolism on the exposure and response of amlodipine in Chinese hypertensive patients were determined. Amlodipine 160-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 24484539-5 2014 Among the substrates that are preferably metabolized by CYP3A4, including carebastine, itraconazole, haloperidol, and fluvastatin, the former three compounds were found to closely dock to the heme region of CYP3A4 but not to that of CYP3A5. Heme 192-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 24695277-3 2014 Sequential metabolic reactions by Phase I and then Phase II enzymes were found in diclofenac [CYP2C9 and UDP-glucuronyltransferases (UGTs)], midazolam (CYP3A4 and UGTs) and propranolol (CYP1A2/2D6 and UGTs). Propranolol 173-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 24484539-6 2014 The ligand-CYP3A5 interaction energies (U values) for vincristine, R- and S-verapamil, and beta-endosulfan were considerably lower than the corresponding ligand-CYP3A4 interaction energies; these substrates also had lower reported Michaelis constants (km) for CYP3A5 than for CYP3A4. Vincristine 54-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 24739523-5 2014 To validate these CVs, variability in the AUC of CYP2C19 substrates lansoprazole and rabeprazole, partially metabolized by CYP3A4 in EMs and IMs, were simulated using the CV in CL(int,h) for CYP2C19 EMs and IMs and 33% of the CV previously reported for CYP3A4. Rabeprazole 85-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 24484539-6 2014 The ligand-CYP3A5 interaction energies (U values) for vincristine, R- and S-verapamil, and beta-endosulfan were considerably lower than the corresponding ligand-CYP3A4 interaction energies; these substrates also had lower reported Michaelis constants (km) for CYP3A5 than for CYP3A4. Vincristine 54-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 276-282 24484539-6 2014 The ligand-CYP3A5 interaction energies (U values) for vincristine, R- and S-verapamil, and beta-endosulfan were considerably lower than the corresponding ligand-CYP3A4 interaction energies; these substrates also had lower reported Michaelis constants (km) for CYP3A5 than for CYP3A4. r- and s-verapamil 67-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 24825095-9 2014 CONCLUSIONS: Lurasidone PK is altered by strong cytochrome P450 (CYP) 3A4 inhibitors or inducers, and coadministration is contraindicated; whereas moderate CYP3A4 inhibitors have less effect, and lurasidone dosage restrictions are recommended. Lurasidone Hydrochloride 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 25029082-13 2014 CONCLUSIONS: The significant difference in absorption of domperidone on pretreatment with silymarin is due to the inhibition of P-glycoprotein and CYP3A. Domperidone 57-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-152 24484539-6 2014 The ligand-CYP3A5 interaction energies (U values) for vincristine, R- and S-verapamil, and beta-endosulfan were considerably lower than the corresponding ligand-CYP3A4 interaction energies; these substrates also had lower reported Michaelis constants (km) for CYP3A5 than for CYP3A4. r- and s-verapamil 67-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 276-282 25029082-13 2014 CONCLUSIONS: The significant difference in absorption of domperidone on pretreatment with silymarin is due to the inhibition of P-glycoprotein and CYP3A. Silymarin 90-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-152 24484539-6 2014 The ligand-CYP3A5 interaction energies (U values) for vincristine, R- and S-verapamil, and beta-endosulfan were considerably lower than the corresponding ligand-CYP3A4 interaction energies; these substrates also had lower reported Michaelis constants (km) for CYP3A5 than for CYP3A4. Endosulfan 91-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 276-282 25029082-14 2014 Silymarin, which inhibits CYP3A4, should be contraindicated for domperidone. Silymarin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 24484539-9 2014 Molecular docking simulation could partly explain the differences of the affinities (km) of the substrates for CYP3A4 and CYP3A5 based on the accessibility of substrates to the heme moiety of CYP3A molecules. Heme 177-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 24492672-4 2014 Intravenous administration of Ad-E4-122aT-hCYP3A4 at a dose of 2 x 10(11) virus particles/mouse produced a mouse exhibiting human CYP3A4 activity at a level similar to that in the human liver, as shown in the dexamethasone metabolic experiment using liver microsomes. Dexamethasone 209-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-49 24492672-4 2014 Intravenous administration of Ad-E4-122aT-hCYP3A4 at a dose of 2 x 10(11) virus particles/mouse produced a mouse exhibiting human CYP3A4 activity at a level similar to that in the human liver, as shown in the dexamethasone metabolic experiment using liver microsomes. Dexamethasone 209-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 24096683-1 2014 PURPOSE: Dolutegravir (DTG), an unboosted HIV integrase inhibitor (INI), is metabolized by UGT1A1 and to a minor extent by CYP3A. dolutegravir 9-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-128 24096683-1 2014 PURPOSE: Dolutegravir (DTG), an unboosted HIV integrase inhibitor (INI), is metabolized by UGT1A1 and to a minor extent by CYP3A. dolutegravir 23-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-128 25061471-12 2014 Fisetin showed moderate inhibition of CYP2D6 and weak inhibition of CYP3A4. fisetin 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 24711855-3 2014 Dextromethorphan was used as a common marker for measuring metabolic activity of CYP2D6 and CYP3A4 enzymes. Dextromethorphan 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 24674673-8 2014 Multiple factors may affect CYP3A expression and activity, such as inducers like rifampicin, phenobarbital, 3-methylcholantrene, beta-naphtoflavone, and dexamethasone. Phenobarbital 93-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 24295085-7 2014 Substrates, inhibitors or inducers of UGT1A1 and CYP3A may also affect the pharmacokinetic profile of indacaterol. indacaterol 102-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 24674673-8 2014 Multiple factors may affect CYP3A expression and activity, such as inducers like rifampicin, phenobarbital, 3-methylcholantrene, beta-naphtoflavone, and dexamethasone. 3-methylcholantrene 108-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 24674673-8 2014 Multiple factors may affect CYP3A expression and activity, such as inducers like rifampicin, phenobarbital, 3-methylcholantrene, beta-naphtoflavone, and dexamethasone. Rifampin 81-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 24674673-8 2014 Multiple factors may affect CYP3A expression and activity, such as inducers like rifampicin, phenobarbital, 3-methylcholantrene, beta-naphtoflavone, and dexamethasone. beta-naphtoflavone 129-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 24674673-8 2014 Multiple factors may affect CYP3A expression and activity, such as inducers like rifampicin, phenobarbital, 3-methylcholantrene, beta-naphtoflavone, and dexamethasone. Dexamethasone 153-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 24990333-9 2014 CONCLUSION: Combining agents that are mainly metabolized by CYP3A4 such as LPZ elevates the blood concentrations of TAC and CSA, which could leading to adverse events. Lansoprazole 75-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 24696691-4 2014 Midazolam is hydroxylated by CYP3A4 and CYP3A5; the activities of these enzymes surge in the liver in the first weeks of life and thus the metabolic rate of midazolam is lower in neonates than in adults. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 24696691-4 2014 Midazolam is hydroxylated by CYP3A4 and CYP3A5; the activities of these enzymes surge in the liver in the first weeks of life and thus the metabolic rate of midazolam is lower in neonates than in adults. Midazolam 157-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 24990333-9 2014 CONCLUSION: Combining agents that are mainly metabolized by CYP3A4 such as LPZ elevates the blood concentrations of TAC and CSA, which could leading to adverse events. Cyclosporine 124-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 24033383-1 2014 BACKGROUND AND AIM: The pharmacokinetics of tacrolimus (Tac) differ among individuals, and genetic polymorphisms of cytochrome P-450 (CYP) 3A4, CYP3A5, and ABCB1 are thought to be involved. Tacrolimus 44-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-142 24157377-0 2014 Marsdenia tenacissima extract inhibits gefitinib metabolism in vitro by interfering with human hepatic CYP3A4 and CYP2D6 enzymes. Gefitinib 39-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 24055701-1 2014 (Z)-Endoxifen (4-hydroxy-N-desmethyltamoxifen), an active metabolite generated via actions of CYP3A4/5 and CYP2D6, is a more potent selective estrogen receptor modulator (SERM) than tamoxifen. 4-hydroxy-N-desmethyltamoxifen 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 24055701-1 2014 (Z)-Endoxifen (4-hydroxy-N-desmethyltamoxifen), an active metabolite generated via actions of CYP3A4/5 and CYP2D6, is a more potent selective estrogen receptor modulator (SERM) than tamoxifen. 4-hydroxy-N-desmethyltamoxifen 15-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 24055701-1 2014 (Z)-Endoxifen (4-hydroxy-N-desmethyltamoxifen), an active metabolite generated via actions of CYP3A4/5 and CYP2D6, is a more potent selective estrogen receptor modulator (SERM) than tamoxifen. Tamoxifen 36-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 25341568-3 2014 Resveratrol is now being discussed as a novel agent that is capable of attenuating the PXR-inducible expression of the CYP3A4 gene, although the mechanistic explanation has not been determined. Resveratrol 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 24157377-6 2014 Gefitinib undergoes hepatic metabolism predominantly through human cytochrome P450 (CYP) 3A4 and CYP2D6 enzymes. Gefitinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-92 24157377-11 2014 Human hepatoma HepG2 cells were used to investigate the effect of gefitinib alone or in combination with MTE on CYP3A4 and CYP2D6 mRNA and protein expression. Gefitinib 66-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 24157377-11 2014 Human hepatoma HepG2 cells were used to investigate the effect of gefitinib alone or in combination with MTE on CYP3A4 and CYP2D6 mRNA and protein expression. methylthioethanol 105-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 24157377-13 2014 The co-administration of MTE with gefitinib significantly decreased the in vitro intrinsic clearance (Clint) of gefitinib by 2.6 and 4.0-fold for CYP2D6 and CYP3A4, respectively, but did not affect other CYP450s. methylthioethanol 25-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 24157377-13 2014 The co-administration of MTE with gefitinib significantly decreased the in vitro intrinsic clearance (Clint) of gefitinib by 2.6 and 4.0-fold for CYP2D6 and CYP3A4, respectively, but did not affect other CYP450s. Gefitinib 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 24157377-13 2014 The co-administration of MTE with gefitinib significantly decreased the in vitro intrinsic clearance (Clint) of gefitinib by 2.6 and 4.0-fold for CYP2D6 and CYP3A4, respectively, but did not affect other CYP450s. Gefitinib 112-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 24157377-14 2014 CYP2D6 and CYP3A4 mRNA and protein expression in human hepatoma HepG2 cells were greatly reduced in the combined gefitinib and MTE treatment. Gefitinib 113-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 24157377-14 2014 CYP2D6 and CYP3A4 mRNA and protein expression in human hepatoma HepG2 cells were greatly reduced in the combined gefitinib and MTE treatment. methylthioethanol 127-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 24157377-15 2014 CONCLUSION: We demonstrate that MTE inhibits gefitinib metabolism by interfering with CYP3A4 and CYP2D6. methylthioethanol 32-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 24157377-15 2014 CONCLUSION: We demonstrate that MTE inhibits gefitinib metabolism by interfering with CYP3A4 and CYP2D6. Gefitinib 45-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 24157377-16 2014 Meanwhile, MTE combined with gefitinib down-regulates the mRNA and protein expression of CYP3A4 and CYP2D6 in the HepG2 cells. Gefitinib 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 24527031-3 2014 Cytochrome P-450 isoenzymes CYP3A4 and CYP3A5 and protein P-glycoprotein (P-gp) are involved in CyA bioavailability. Cyclosporine 96-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 25343299-5 2014 Cedrol also markedly inhibited CYP3A4-mediated midazolam hydroxylation with a Ki value of 3.4 muM, whereas beta-cedrene and thujopsene moderately blocked CYP3A4. cedrol 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 25343291-5 2014 CYP3A4 and CYP3A5 were only involved in the formation of M1, whereas CYP2B6 and CYP2C19 were responsible for all metabolic reactions of sibutramine. sibutramine 136-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 25343299-9 2014 These in vitro results indicate that cedrol, beta-cedrene, and thujopsene need to be examined for potential pharmacokinetic drug interactions in vivo due to their potent inhibition of CYP2B6 and CYP3A4. cedrol 37-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 25343299-5 2014 Cedrol also markedly inhibited CYP3A4-mediated midazolam hydroxylation with a Ki value of 3.4 muM, whereas beta-cedrene and thujopsene moderately blocked CYP3A4. Midazolam 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 25343299-9 2014 These in vitro results indicate that cedrol, beta-cedrene, and thujopsene need to be examined for potential pharmacokinetic drug interactions in vivo due to their potent inhibition of CYP2B6 and CYP3A4. cedrene 45-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 25343299-5 2014 Cedrol also markedly inhibited CYP3A4-mediated midazolam hydroxylation with a Ki value of 3.4 muM, whereas beta-cedrene and thujopsene moderately blocked CYP3A4. cedrene 107-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 25343299-5 2014 Cedrol also markedly inhibited CYP3A4-mediated midazolam hydroxylation with a Ki value of 3.4 muM, whereas beta-cedrene and thujopsene moderately blocked CYP3A4. thujopsene 124-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 25343299-9 2014 These in vitro results indicate that cedrol, beta-cedrene, and thujopsene need to be examined for potential pharmacokinetic drug interactions in vivo due to their potent inhibition of CYP2B6 and CYP3A4. thujopsene 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 27485194-1 2014 A quantitative structure-activity relationship analysis of the inhibitory activity of structurally diverse compounds on recombinant human CYP3A4 is presented using a bilinear approach based on our previously developed LinBiExp model. linbiexp 218-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 24739263-0 2014 Increased levels of fatty acids contributed to induction of hepatic CYP3A4 activity induced by diabetes - in vitro evidence from HepG2 cell and Fa2N-4 cell lines. Fatty Acids 20-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 24739263-5 2014 It was found that only fatty acids concentration-dependently up-regulated CYP3A4 activity, and the induction by fatty acids was further confirmed in Fa2N-4 cells. Fatty Acids 23-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 24739263-7 2014 In addition, effects of pharmacological inhibitors on fatty acid-induced CYP3A4 activity were studied. Fatty Acids 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 24739263-8 2014 The results indicated that the induction of CYP3A4 activity by oleic acid may be partly via AMPK-, PKC-, and NF-kappaB-dependent pathways, whereas that by palmitic acid was possibly associated with the PKC-dependent pathway. Oleic Acid 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 24739263-8 2014 The results indicated that the induction of CYP3A4 activity by oleic acid may be partly via AMPK-, PKC-, and NF-kappaB-dependent pathways, whereas that by palmitic acid was possibly associated with the PKC-dependent pathway. Palmitic Acid 155-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 24739263-9 2014 In conclusion, the increased levels of fatty acids may be one of the reasons leading to the elevated function and expression of CYP3A4 under diabetic conditions. Fatty Acids 39-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 27485194-3 2014 Strongest inhibitory activity is likely to occur for compounds close to an optimal size, which is roughly that of the well-know CYP3A4-inhibitor ketoconazole. Ketoconazole 145-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 24240480-2 2014 Quetiapine is metabolized by CYP3A enzymes including CYP3A5 and is a substrate of P-glycoprotein, an efflux drug transporter encoded by the ABCB1 gene. Quetiapine Fumarate 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-34 24531557-3 2014 Ergotamine, typically used to treat migraine, has less than 5% bioavailability due to extensive first-pass metabolism by cytochrome P450 3A4 (CYP3A4). Ergotamine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-140 25495409-6 2014 CYP3A4*1G and CYP3A5*3 could influence CBZ metabolism, while POR*28 had no effect on it. Carbamazepine 39-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24794907-10 2014 Dasatinib is metabolized in humans markedly by CYP3A4 to active metabolites and by phase II drug-metabolizing enzymes, such as UDP glucuronosyltransferase. Dasatinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 24756798-6 2014 The metabolization of ruxolitinib through CYP3A4 needs to be considered particularly if co-administered with potent CYP3A4 inhibitors. ruxolitinib 22-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 24756798-6 2014 The metabolization of ruxolitinib through CYP3A4 needs to be considered particularly if co-administered with potent CYP3A4 inhibitors. ruxolitinib 22-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 24379677-11 2014 The interaction with simvastatin seems mainly driven by CYP3A4 inhibition at the intestinal level, whereas the interaction with atorvastatin is more due to hepatic CYP3A4 inhibition. Simvastatin 21-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 24379677-11 2014 The interaction with simvastatin seems mainly driven by CYP3A4 inhibition at the intestinal level, whereas the interaction with atorvastatin is more due to hepatic CYP3A4 inhibition. Atorvastatin 128-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 24379677-12 2014 The interaction of CYP3A4 inhibitor with simvastatin has been more pronounced compared with atorvastatin. Simvastatin 41-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 24379677-12 2014 The interaction of CYP3A4 inhibitor with simvastatin has been more pronounced compared with atorvastatin. Atorvastatin 92-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 24379677-13 2014 From the current data, atorvastatin seems to be a safer CYP3A4-statin for comedication with DHP-CCB. Atorvastatin 23-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 24379677-13 2014 From the current data, atorvastatin seems to be a safer CYP3A4-statin for comedication with DHP-CCB. dhp-ccb 92-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 24379677-15 2014 Amlodipine may have interactions with CYP3A5 in addition to CYP3A4, which may explain its particular characteristics in comparison with other DHP-CCBs. Amlodipine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 24794908-8 2014 Gefitinib is metabolized extensively in the liver into five metabolites by cytochrome P450s, primarily by CYP3A4 and to a lesser extent by CYP3A5 and CYP2D6. Gefitinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 24531557-3 2014 Ergotamine, typically used to treat migraine, has less than 5% bioavailability due to extensive first-pass metabolism by cytochrome P450 3A4 (CYP3A4). Ergotamine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 24656020-1 2014 BACKGROUND: The bioavailability of oral tacrolimus is influenced by enterocyte metabolism, which involves CYP3A and P-glycoprotein. Tacrolimus 40-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-111 24346990-3 2013 Clarithromycin is an inhibitor of CYP3A4 and azithromycin is not, which makes comparisons between these 2 macrolide antibiotics useful in assessing clinically important drug interactions. Clarithromycin 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 24085192-4 2014 Eleven drugs exhibited lower EC50 values in cells transfected with CYP3A4 (THLE-3A4 cells) than in THLE-Null cells; 10 of these drugs (91%) caused human liver injury. thle 75-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 23883428-5 2014 The present study was designed to systematically investigate the performance of human cryopreserved hepatocytes in suspension to predict fraction metabolized via CYP3A (fmCYP3A) by assessing the ketoconazole sensitive intrinsic clearance (CLint) for five prototypical CYP3A substrates with varying degree of CYP3A dependent CLint in twelve individual hepatocyte batches. Ketoconazole 195-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-167 23883428-5 2014 The present study was designed to systematically investigate the performance of human cryopreserved hepatocytes in suspension to predict fraction metabolized via CYP3A (fmCYP3A) by assessing the ketoconazole sensitive intrinsic clearance (CLint) for five prototypical CYP3A substrates with varying degree of CYP3A dependent CLint in twelve individual hepatocyte batches. Ketoconazole 195-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-176 23883428-5 2014 The present study was designed to systematically investigate the performance of human cryopreserved hepatocytes in suspension to predict fraction metabolized via CYP3A (fmCYP3A) by assessing the ketoconazole sensitive intrinsic clearance (CLint) for five prototypical CYP3A substrates with varying degree of CYP3A dependent CLint in twelve individual hepatocyte batches. Ketoconazole 195-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-176 24376769-1 2013 Effector-induced allosteric transitions in cytochrome P450 3A4 (CYP3A4) were investigated by luminescence resonance energy transfer (LRET) between two SH-reactive probes attached to various pairs of distantly located cysteine residues, namely the double-cysteine mutants CYP3A4(C64/C468), CYP3A4(C377/C468) and CYP3A4(C64/C121). Cysteine 217-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-62 24376769-1 2013 Effector-induced allosteric transitions in cytochrome P450 3A4 (CYP3A4) were investigated by luminescence resonance energy transfer (LRET) between two SH-reactive probes attached to various pairs of distantly located cysteine residues, namely the double-cysteine mutants CYP3A4(C64/C468), CYP3A4(C377/C468) and CYP3A4(C64/C121). Cysteine 217-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 24376769-1 2013 Effector-induced allosteric transitions in cytochrome P450 3A4 (CYP3A4) were investigated by luminescence resonance energy transfer (LRET) between two SH-reactive probes attached to various pairs of distantly located cysteine residues, namely the double-cysteine mutants CYP3A4(C64/C468), CYP3A4(C377/C468) and CYP3A4(C64/C121). Cysteine 254-262 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-62 24376769-1 2013 Effector-induced allosteric transitions in cytochrome P450 3A4 (CYP3A4) were investigated by luminescence resonance energy transfer (LRET) between two SH-reactive probes attached to various pairs of distantly located cysteine residues, namely the double-cysteine mutants CYP3A4(C64/C468), CYP3A4(C377/C468) and CYP3A4(C64/C121). Cysteine 254-262 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 24127648-1 2013 Both currently approved DAAs, the protease inhibitors (PIs) telaprevir (TVR) and boceprevir (BOC), are substrates and inhibitors of P-glycoprotein and the cytochrome P450 3A4, which are regularly involved in DDIs. daas 24-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-174 24184833-7 2013 The result indicated that the formation of each metabolite of alisol A was mainly catalyzed by CYP3A4 enzyme. alisol A 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 24127648-1 2013 Both currently approved DAAs, the protease inhibitors (PIs) telaprevir (TVR) and boceprevir (BOC), are substrates and inhibitors of P-glycoprotein and the cytochrome P450 3A4, which are regularly involved in DDIs. telaprevir 72-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-174 24127648-1 2013 Both currently approved DAAs, the protease inhibitors (PIs) telaprevir (TVR) and boceprevir (BOC), are substrates and inhibitors of P-glycoprotein and the cytochrome P450 3A4, which are regularly involved in DDIs. telaprevir 60-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-174 24127648-1 2013 Both currently approved DAAs, the protease inhibitors (PIs) telaprevir (TVR) and boceprevir (BOC), are substrates and inhibitors of P-glycoprotein and the cytochrome P450 3A4, which are regularly involved in DDIs. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 81-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-174 24060875-0 2013 Induction of influx and efflux transporters and cytochrome P450 3A4 in primary human hepatocytes by rifampin, rifabutin, and rifapentine. Rifampin 100-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-67 24127648-1 2013 Both currently approved DAAs, the protease inhibitors (PIs) telaprevir (TVR) and boceprevir (BOC), are substrates and inhibitors of P-glycoprotein and the cytochrome P450 3A4, which are regularly involved in DDIs. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 93-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-174 24060875-0 2013 Induction of influx and efflux transporters and cytochrome P450 3A4 in primary human hepatocytes by rifampin, rifabutin, and rifapentine. Rifabutin 110-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-67 24060875-0 2013 Induction of influx and efflux transporters and cytochrome P450 3A4 in primary human hepatocytes by rifampin, rifabutin, and rifapentine. rifapentine 125-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-67 24060875-4 2013 Rifampin and rifabutin significantly induced CYP3A4 (80-fold and 20-fold, respectively) in primary human hepatocytes. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 24060875-4 2013 Rifampin and rifabutin significantly induced CYP3A4 (80-fold and 20-fold, respectively) in primary human hepatocytes. Rifabutin 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 24060875-6 2013 Rifapentine induced CYP3A4 in hepatocytes from 3 of 6 donors. rifapentine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 23773422-0 2013 Epidemiology of CYP3A4-mediated clopidogrel drug-drug interactions and their clinical consequences. Clopidogrel 32-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 24312617-4 2013 We investigated four CYP subfamilies (CYP1A, CYP2D, CYP2C, and CYP3A) that are involved in 90% of all metabolic drug transformations and identified four amino acid interaction networks associated with specific CYP functionalities, i.e., membrane binding, heme binding, catalytic activity, and dimerization. Heme 255-259 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 23773422-2 2013 The objective of this study was to evaluate the prevalence and clinical consequences of potential drug-drug interactions of clopidogrel with drugs affecting CYP3A4 activity. Clopidogrel 124-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 23773422-5 2013 RESULTS: In the nationwide analysis, 6.1%, 1.0%, and 20.8% of the clopidogrel-treated patients were exposed to concomitant use of CYP3A4 inhibitors, CYP3A4 inducers, and atorvastatin, respectively. Clopidogrel 66-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 23773422-5 2013 RESULTS: In the nationwide analysis, 6.1%, 1.0%, and 20.8% of the clopidogrel-treated patients were exposed to concomitant use of CYP3A4 inhibitors, CYP3A4 inducers, and atorvastatin, respectively. Clopidogrel 66-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 23773422-12 2013 CYP3A4 inhibitors and atorvastatin may reduce bleedings in clopidogrel users. Clopidogrel 59-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24085261-0 2013 Investigation into CYP3A4-mediated drug-drug interactions on midostaurin in healthy volunteers. midostaurin 61-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 24085261-4 2013 METHODS: Three phase I studies in healthy volunteers evaluated the effects of a CYP3A4 inhibitor (ketoconazole 400 mg daily for 10 days) or CYP3A4 inducer (rifampicin 600 mg daily for 14 days) on concentrations of midostaurin and its metabolites following a single 50-mg dose of midostaurin and the effects of midostaurin as a single dose (100 mg) and multiple doses (50 mg twice daily) on midazolam (a sensitive CYP3A4 probe) concentration. midostaurin 214-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 23974086-8 2013 RESULTS: In vitro, the CYP3A4*22 allele resulted in approximately 20% lower metabolic rates of SRL (P = 0.0411). Sirolimus 95-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 24085261-6 2013 RESULTS: Inhibition of CYP3A4 by ketoconazole increased midostaurin exposure more than tenfold, and induction of CYP3A4 by rifampicin decreased midostaurin exposure by more than tenfold. Ketoconazole 33-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 24085261-6 2013 RESULTS: Inhibition of CYP3A4 by ketoconazole increased midostaurin exposure more than tenfold, and induction of CYP3A4 by rifampicin decreased midostaurin exposure by more than tenfold. midostaurin 56-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 24085261-6 2013 RESULTS: Inhibition of CYP3A4 by ketoconazole increased midostaurin exposure more than tenfold, and induction of CYP3A4 by rifampicin decreased midostaurin exposure by more than tenfold. Rifampin 123-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 24085261-6 2013 RESULTS: Inhibition of CYP3A4 by ketoconazole increased midostaurin exposure more than tenfold, and induction of CYP3A4 by rifampicin decreased midostaurin exposure by more than tenfold. midostaurin 144-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 24085261-8 2013 CONCLUSION: The pharmacokinetics of midostaurin and its metabolites was affected substantially by ketoconazole and rifampicin, suggesting that midostaurin is a sensitive CYP3A4 substrate. midostaurin 36-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 24085261-8 2013 CONCLUSION: The pharmacokinetics of midostaurin and its metabolites was affected substantially by ketoconazole and rifampicin, suggesting that midostaurin is a sensitive CYP3A4 substrate. Ketoconazole 98-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 24085261-8 2013 CONCLUSION: The pharmacokinetics of midostaurin and its metabolites was affected substantially by ketoconazole and rifampicin, suggesting that midostaurin is a sensitive CYP3A4 substrate. Rifampin 115-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 24085261-8 2013 CONCLUSION: The pharmacokinetics of midostaurin and its metabolites was affected substantially by ketoconazole and rifampicin, suggesting that midostaurin is a sensitive CYP3A4 substrate. midostaurin 143-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 23974699-5 2013 Seven-day rifampicin administration increased CYP2C19 and CYP3A enzyme activities. Rifampin 10-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 23974699-6 2013 The induced CYP2C19 and CYP3A activities remained elevated at 4 days after rifampicin discontinuation and returned to baseline levels 8 days after rifampicin discontinuation. Rifampin 75-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 23974699-6 2013 The induced CYP2C19 and CYP3A activities remained elevated at 4 days after rifampicin discontinuation and returned to baseline levels 8 days after rifampicin discontinuation. Rifampin 147-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 24085261-2 2013 In vitro studies showed that midostaurin is predominantly metabolized by cytochrome P450 3A4 (CYP3A4) and that midostaurin inhibits and/or induces the same enzyme. midostaurin 29-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-92 24085261-2 2013 In vitro studies showed that midostaurin is predominantly metabolized by cytochrome P450 3A4 (CYP3A4) and that midostaurin inhibits and/or induces the same enzyme. midostaurin 29-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 24085261-3 2013 Here, we address the clinical relevance of CYP3A4-related drug-drug interactions with midostaurin as either a "victim" or "perpetrator." midostaurin 86-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 24085261-4 2013 METHODS: Three phase I studies in healthy volunteers evaluated the effects of a CYP3A4 inhibitor (ketoconazole 400 mg daily for 10 days) or CYP3A4 inducer (rifampicin 600 mg daily for 14 days) on concentrations of midostaurin and its metabolites following a single 50-mg dose of midostaurin and the effects of midostaurin as a single dose (100 mg) and multiple doses (50 mg twice daily) on midazolam (a sensitive CYP3A4 probe) concentration. midostaurin 214-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 23785064-0 2013 Stereoselective inhibition of CYP2C19 and CYP3A4 by fluoxetine and its metabolite: implications for risk assessment of multiple time-dependent inhibitor systems. Fluoxetine 52-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 23785064-3 2013 Fluoxetine was chosen as the model drug to evaluate the role of TDI metabolites in DDI prediction because it is a TDI of both CYP3A4 and CYP2C19 with a circulating N-dealkylated inhibitory metabolite, norfluoxetine. Fluoxetine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 23785064-5 2013 Only (S)-fluoxetine and (R)-norfluoxetine were TDIs of CYP3A4, with (R)-norfluoxetine being the most potent (K(I) = 8 muM, and k(inact,app) = 0.011 min(-1)). Fluoxetine 5-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 23785064-5 2013 Only (S)-fluoxetine and (R)-norfluoxetine were TDIs of CYP3A4, with (R)-norfluoxetine being the most potent (K(I) = 8 muM, and k(inact,app) = 0.011 min(-1)). (R)-Norfluoxetine 24-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 23785064-5 2013 Only (S)-fluoxetine and (R)-norfluoxetine were TDIs of CYP3A4, with (R)-norfluoxetine being the most potent (K(I) = 8 muM, and k(inact,app) = 0.011 min(-1)). (R)-Norfluoxetine 68-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 23785064-6 2013 Based on in-vitro-to-in-vivo predictions, (S)-norfluoxetine plays the most important role in in vivo CYP2C19 DDIs, whereas (R)-norfluoxetine is most important in CYP3A4 DDIs. (R)-Norfluoxetine 123-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 23770199-6 2013 Clopidogrel (10 and 100 muM) was also toxic for HepG2 cells expressing human CYP3A4 (HepG2/CYP3A4) and HepG2 cells co-incubated with CYP3A4 supersomes (HepG2/CYP3A4 supersome), but not for wild-type HepG2 cells (HepG2/wt). Clopidogrel 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 24338455-12 2013 CONCLUSIONS: CYP3A4 and CYP3A5 may contribute to salt-sensitive hypertension in human which may act as biomarkers for this disease. Salts 49-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 23770199-6 2013 Clopidogrel (10 and 100 muM) was also toxic for HepG2 cells expressing human CYP3A4 (HepG2/CYP3A4) and HepG2 cells co-incubated with CYP3A4 supersomes (HepG2/CYP3A4 supersome), but not for wild-type HepG2 cells (HepG2/wt). Clopidogrel 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 23770199-6 2013 Clopidogrel (10 and 100 muM) was also toxic for HepG2 cells expressing human CYP3A4 (HepG2/CYP3A4) and HepG2 cells co-incubated with CYP3A4 supersomes (HepG2/CYP3A4 supersome), but not for wild-type HepG2 cells (HepG2/wt). Clopidogrel 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 23770199-7 2013 Clopidogrel (100 muM) decreased the cellular glutathione content in HepG2/CYP3A4 supersome and triggered an oxidative stress reaction (10 and 100 microM) in HepG2/CYP3A4, but not in HepG2/wt. Clopidogrel 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 23770199-7 2013 Clopidogrel (100 muM) decreased the cellular glutathione content in HepG2/CYP3A4 supersome and triggered an oxidative stress reaction (10 and 100 microM) in HepG2/CYP3A4, but not in HepG2/wt. Clopidogrel 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 23770199-6 2013 Clopidogrel (10 and 100 muM) was also toxic for HepG2 cells expressing human CYP3A4 (HepG2/CYP3A4) and HepG2 cells co-incubated with CYP3A4 supersomes (HepG2/CYP3A4 supersome), but not for wild-type HepG2 cells (HepG2/wt). Clopidogrel 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 23770199-7 2013 Clopidogrel (100 muM) decreased the cellular glutathione content in HepG2/CYP3A4 supersome and triggered an oxidative stress reaction (10 and 100 microM) in HepG2/CYP3A4, but not in HepG2/wt. Glutathione 45-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 24102384-3 2013 Erythromycin, a macrolide antibiotic, has been shown to be a moderate CYP3A4 inhibitor. Erythromycin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 23770199-8 2013 Glutathione depletion significantly increased the cytotoxicity of clopidogrel (10 and 100 microM) in HepG2/CYP3A4 supersome. Glutathione 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 23770199-8 2013 Glutathione depletion significantly increased the cytotoxicity of clopidogrel (10 and 100 microM) in HepG2/CYP3A4 supersome. Clopidogrel 66-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 23770199-9 2013 Co-incubation with 1 muM ketoconazole or 10mM glutathione almost completely prevented the cytotoxic effect of clopidogrel in HepG2/CYP3A4 and HepG2/CYP3A4 supersome. Ketoconazole 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 23770199-9 2013 Co-incubation with 1 muM ketoconazole or 10mM glutathione almost completely prevented the cytotoxic effect of clopidogrel in HepG2/CYP3A4 and HepG2/CYP3A4 supersome. Ketoconazole 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 23770199-9 2013 Co-incubation with 1 muM ketoconazole or 10mM glutathione almost completely prevented the cytotoxic effect of clopidogrel in HepG2/CYP3A4 and HepG2/CYP3A4 supersome. Glutathione 46-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 23770199-9 2013 Co-incubation with 1 muM ketoconazole or 10mM glutathione almost completely prevented the cytotoxic effect of clopidogrel in HepG2/CYP3A4 and HepG2/CYP3A4 supersome. Glutathione 46-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 23770199-9 2013 Co-incubation with 1 muM ketoconazole or 10mM glutathione almost completely prevented the cytotoxic effect of clopidogrel in HepG2/CYP3A4 and HepG2/CYP3A4 supersome. Clopidogrel 110-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 23770199-9 2013 Co-incubation with 1 muM ketoconazole or 10mM glutathione almost completely prevented the cytotoxic effect of clopidogrel in HepG2/CYP3A4 and HepG2/CYP3A4 supersome. Clopidogrel 110-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 23770199-10 2013 HepG2/CYP3A4 incubated with 100 muM clopidogrel showed mitochondrial damage and cytochrome c release, eventually promoting apoptosis and/or necrosis. Clopidogrel 36-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 23770199-12 2013 In conclusion, clopidogrel incubated with CYP3A4 is associated with the formation of metabolites that are toxic for hepatocytes and can be trapped by glutathione. Clopidogrel 15-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 23770199-12 2013 In conclusion, clopidogrel incubated with CYP3A4 is associated with the formation of metabolites that are toxic for hepatocytes and can be trapped by glutathione. Glutathione 150-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 23770199-13 2013 High CYP3A4 activity and low cellular glutathione stores may be risk factors for clopidogrel-associated hepatocellular toxicity. Clopidogrel 81-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 5-11 23996211-1 2013 Celecoxib is metabolized by enzymes of the cytochrome P450 (CYP450) superfamily, mainly CYP2C9 and CYP3A4. Celecoxib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 24102384-12 2013 This indicates that inhibition of CYP3A4 impacted rate and extent of absorption of UPA and also its metabolism by slowing the elimination of its metabolite PGL4002. pgl4002 156-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 23089673-1 2013 We investigated the effects of pharmacogenetic variations and efavirenz pharmacokinetics on inter-individual differences in the extent of CYP3A induction by efavirenz using 4beta-hydroxycholesterol/cholesterol (4beta-OHC/Chol) as a marker for CYP3A induction. cholest-5-ene-3,4-diol 173-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-143 24161162-0 2013 Impact of CYP3A and ABCB1 polymorphisms on the pharmacokinetics and pharmacodynamics of fentanyl. Fentanyl 88-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 23089673-1 2013 We investigated the effects of pharmacogenetic variations and efavirenz pharmacokinetics on inter-individual differences in the extent of CYP3A induction by efavirenz using 4beta-hydroxycholesterol/cholesterol (4beta-OHC/Chol) as a marker for CYP3A induction. Cholesterol 186-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-143 23089673-1 2013 We investigated the effects of pharmacogenetic variations and efavirenz pharmacokinetics on inter-individual differences in the extent of CYP3A induction by efavirenz using 4beta-hydroxycholesterol/cholesterol (4beta-OHC/Chol) as a marker for CYP3A induction. 4beta-ohc 211-220 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-143 23089673-1 2013 We investigated the effects of pharmacogenetic variations and efavirenz pharmacokinetics on inter-individual differences in the extent of CYP3A induction by efavirenz using 4beta-hydroxycholesterol/cholesterol (4beta-OHC/Chol) as a marker for CYP3A induction. chol 221-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-143 25505570-9 2013 Additional studies were done to ascertain if ajulemic acid can inhibit the activities of five principal human cytochrome P450 isozymes; CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4/5. lenabasum 45-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-181 23916407-1 2013 Verapamil and its major metabolite norverapamil were identified to be both mechanism-based inhibitors and substrates of CYP3A and reported to have non-linear pharmacokinetics in clinic. Verapamil 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-125 23916407-3 2013 The results showed that S-isomers were more preferential to be metabolized than R-isomers for both verapamil and norverapamil, and their inhibitory effects on CYP3A activity were also stereoselective with S-isomers more potent than R-isomers. norverapamil 113-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-164 23916407-8 2013 Finally, the developed semi-PBPK model was further applied to predict drug-drug interactions (DDI) between verapamil and other three CYP3A substrates including midazolam, simvastatin, and cyclosporine A. Verapamil 107-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-138 23981337-0 2013 Enhanced intestinal absorption of etoposide by self-microemulsifying drug delivery systems: roles of P-glycoprotein and cytochrome P450 3A inhibition. Etoposide 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-138 23981337-1 2013 Etoposide is recognized as a dual P-glycoprotein (P-gp) and cytochrome P450 3A (CYP3A) substrate drug with poor water-solubility. Etoposide 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-78 23916407-1 2013 Verapamil and its major metabolite norverapamil were identified to be both mechanism-based inhibitors and substrates of CYP3A and reported to have non-linear pharmacokinetics in clinic. norverapamil 35-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-125 23981337-1 2013 Etoposide is recognized as a dual P-glycoprotein (P-gp) and cytochrome P450 3A (CYP3A) substrate drug with poor water-solubility. Etoposide 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-85 23916407-3 2013 The results showed that S-isomers were more preferential to be metabolized than R-isomers for both verapamil and norverapamil, and their inhibitory effects on CYP3A activity were also stereoselective with S-isomers more potent than R-isomers. Verapamil 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-164 23981337-1 2013 Etoposide is recognized as a dual P-glycoprotein (P-gp) and cytochrome P450 3A (CYP3A) substrate drug with poor water-solubility. Water 112-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-85 26835051-5 2013 Physicians will have to consider the pharmacokinetic effect of drugs and co-morbidities when prescribing NOACs - plasma levels of NOACs may be affected by P-glycoprotein (P-gp) substrates, as well as cytochrome P450 (CYP3A4) inducers or inhibitors. noacs 105-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-223 23981337-6 2013 In vitro Caco-2 cell models were applied to study the effects of P-gp and CYP3A inhibition by SMEDDS on the cellular accumulation of etoposide. Etoposide 133-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-79 23988488-9 2013 Using the relative activity factor approach, the hepatic clearance was calculated to be 27 and 73% for 2-O-demethylation by CYP1A2 and CYP3A4, 82, 3, and 15% for 9-O-demethylation by CYP1A2, CYP2C19, and CYP2D6, and finally <1 and 99% for N-demethylation by CYP2D6 and CYP3A4. hippuric acid 103-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 23988488-9 2013 Using the relative activity factor approach, the hepatic clearance was calculated to be 27 and 73% for 2-O-demethylation by CYP1A2 and CYP3A4, 82, 3, and 15% for 9-O-demethylation by CYP1A2, CYP2C19, and CYP2D6, and finally <1 and 99% for N-demethylation by CYP2D6 and CYP3A4. Nitrogen 242-243 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 24027778-3 2013 Direct electron transfer (DET) between CYP3A4 and CNFs was observed at a formal potential of -0.302 V. The electrocatalytic reduction current increased with the addition of drugs including testosterone and quinidine. Testosterone 189-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 24027778-3 2013 Direct electron transfer (DET) between CYP3A4 and CNFs was observed at a formal potential of -0.302 V. The electrocatalytic reduction current increased with the addition of drugs including testosterone and quinidine. Quinidine 206-215 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 24027778-4 2013 In contrast, the reduction current was greatly suppressed in the presence of ketoconazole, which is a CYP3A4 inhibitor. Ketoconazole 77-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 24056704-11 2013 CONCLUSION: GLS4 is a sensitive substrate of CYP3A. Morphothiadin 12-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-50 24056704-12 2013 CYP3A inhibitors or inducers cause considerable change of GLS4 plasma concentrations in dogs, which should be considered in clinical practice. Morphothiadin 58-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 24259602-6 2013 Phase I DDI studies have reported pharmacokinetic DDIs mediated by P-gp alone (dabigatran etexilate) or in combination with CYP3A4 enzymes (rivaroxaban and apixaban). Rivaroxaban 140-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 24259602-9 2013 DDI studies involving rifampicin suggest that rivaroxaban and apixaban should be avoided when strong inducers of P-gp and CYP3A4 are used concurrently. Rivaroxaban 46-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 24259602-9 2013 DDI studies involving rifampicin suggest that rivaroxaban and apixaban should be avoided when strong inducers of P-gp and CYP3A4 are used concurrently. apixaban 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 24259602-10 2013 Concomitant use of apixaban and strong dual inhibitors of P-gp and CYP3A4 should be avoided or the dose reduced. apixaban 19-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 23929629-0 2013 Time-dependent inhibition of CYP3A4 by sertraline, a selective serotonin reuptake inhibitor. Sertraline 39-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 23929629-5 2013 The study examined whether sertraline produces time-dependent inhibition of CYP3A4 and/or other P450 enzymes. Sertraline 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 23929629-6 2013 Incubation of human liver microsomes with sertraline in the presence of NADPH resulted in marked decreases in testosterone 6beta-hydroxylation activities, indicating that sertraline metabolism leads to CYP3A4 inactivation. Sertraline 42-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 202-208 23929629-6 2013 Incubation of human liver microsomes with sertraline in the presence of NADPH resulted in marked decreases in testosterone 6beta-hydroxylation activities, indicating that sertraline metabolism leads to CYP3A4 inactivation. NADP 72-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 202-208 26835051-5 2013 Physicians will have to consider the pharmacokinetic effect of drugs and co-morbidities when prescribing NOACs - plasma levels of NOACs may be affected by P-glycoprotein (P-gp) substrates, as well as cytochrome P450 (CYP3A4) inducers or inhibitors. noacs 130-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-223 23929629-6 2013 Incubation of human liver microsomes with sertraline in the presence of NADPH resulted in marked decreases in testosterone 6beta-hydroxylation activities, indicating that sertraline metabolism leads to CYP3A4 inactivation. Sertraline 171-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 202-208 23929629-10 2013 This is the first report indicating that sertraline produced time-dependent inhibition of CYP3A4, which may be associated with MI complex formation. Sertraline 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 23394826-10 2013 Furthermore, in clinical studies the sensitive CYP3A4 substrate probe midazolam is often used to determine pharmacokinetic interactions. Midazolam 70-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 23394826-11 2013 Results of these clinical studies with midazolam are used to predict pharmacokinetic interactions with other drugs metabolized by CYP3A4. Midazolam 39-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 23394826-14 2013 In clinical studies using midazolam or anticancer drugs (irinotecan and imatinib) as known CYP3A4 substrates in combination with SJW, decreased plasma levels of these drugs were observed, which was expected as a consequence of CYP3A4 induction. Midazolam 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 23394826-14 2013 In clinical studies using midazolam or anticancer drugs (irinotecan and imatinib) as known CYP3A4 substrates in combination with SJW, decreased plasma levels of these drugs were observed, which was expected as a consequence of CYP3A4 induction. Midazolam 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 227-233 23394826-14 2013 In clinical studies using midazolam or anticancer drugs (irinotecan and imatinib) as known CYP3A4 substrates in combination with SJW, decreased plasma levels of these drugs were observed, which was expected as a consequence of CYP3A4 induction. Irinotecan 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 23394826-14 2013 In clinical studies using midazolam or anticancer drugs (irinotecan and imatinib) as known CYP3A4 substrates in combination with SJW, decreased plasma levels of these drugs were observed, which was expected as a consequence of CYP3A4 induction. Irinotecan 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 227-233 23394826-14 2013 In clinical studies using midazolam or anticancer drugs (irinotecan and imatinib) as known CYP3A4 substrates in combination with SJW, decreased plasma levels of these drugs were observed, which was expected as a consequence of CYP3A4 induction. Imatinib Mesylate 72-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 23394826-14 2013 In clinical studies using midazolam or anticancer drugs (irinotecan and imatinib) as known CYP3A4 substrates in combination with SJW, decreased plasma levels of these drugs were observed, which was expected as a consequence of CYP3A4 induction. Imatinib Mesylate 72-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 227-233 23394826-21 2013 At last, midazolam as a model substrate for CYP3A4, has convincingly shown to correctly predict clinical interactions between CAM and anticancer drugs. Midazolam 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 23784264-5 2013 midazolam after 10 days of pretreatment with 600 mg of rifampicin once daily (CYP3A-induced phase). Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 23824675-11 2013 Dolutegravir"s major and minor metabolic pathways are uridine diphosphate glucuronosyltransferase 1A1 and cytochrome P450 (CYP)-3A4, respectively, and it neither induces nor inhibits CYP isoenzymes. dolutegravir 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-131 23868281-3 2013 BTs using orally or intravenously administered selective non-radioactive (13)C-labeled probes to non-invasively evaluate dihydropyrimidine dehydrogenase, cytochrome P450 (CYP) 3A4, and CYP2D6 enzyme activity have been published. Carbon-13 73-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-179 23872824-0 2013 A randomised study of the effect of danoprevir/ritonavir or ritonavir on substrates of cytochrome P450 (CYP) 3A and 2C9 in chronic hepatitis C patients using a drug cocktail. danoprevir 36-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-111 24100879-9 2013 The selective cytochrome P450 3A4 inhibitor cobicistat is a better tolerated alternative to ritonavir for pharmacokinetic "boosting", but may also result in clinically undesirable drug interactions. Cobicistat 44-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-33 23872824-0 2013 A randomised study of the effect of danoprevir/ritonavir or ritonavir on substrates of cytochrome P450 (CYP) 3A and 2C9 in chronic hepatitis C patients using a drug cocktail. Ritonavir 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-111 23807564-5 2013 Thus, a clinical study in healthy Chinese subjects was conducted to investigate the impact of PXR polymorphisms on repaglinide (an endogenous marker for CYP3A4 activity) pharmacokinetics used alone or in combination with a PXR inducer, flucloxacillin. repaglinide 115-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 23872824-0 2013 A randomised study of the effect of danoprevir/ritonavir or ritonavir on substrates of cytochrome P450 (CYP) 3A and 2C9 in chronic hepatitis C patients using a drug cocktail. Ritonavir 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-111 24164611-4 2013 Situations discussed that result in a reduction in clearance will include: multiple organ failure in critically ill, patients with non-functioning CYP2D6 and CYP2C8/9 alleles, and CYP3A4 drug interactions with erythromycin and clarithromycin. Erythromycin 210-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 23872824-8 2013 CONCLUSIONS: Substantial inhibition of CYP3A- and modest induction of CYP2C9- activity were observed with danoprevir/r and low-dose ritonavir. danoprevir 106-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 23872824-8 2013 CONCLUSIONS: Substantial inhibition of CYP3A- and modest induction of CYP2C9- activity were observed with danoprevir/r and low-dose ritonavir. Ritonavir 132-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 24256019-12 2013 Therefore, statins metabolized through CYP3A4 (simvastatin, lovastatin and atorvastatin) are the ones with the highest number of clinically relevant interactions. Simvastatin 47-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 24256019-12 2013 Therefore, statins metabolized through CYP3A4 (simvastatin, lovastatin and atorvastatin) are the ones with the highest number of clinically relevant interactions. Lovastatin 60-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 24256019-12 2013 Therefore, statins metabolized through CYP3A4 (simvastatin, lovastatin and atorvastatin) are the ones with the highest number of clinically relevant interactions. Atorvastatin 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 23631744-15 2013 Inhibition of organic anion transporting polypeptide 1B1 by CP-778875 (IC50 = 2.14 +- 0.40 muM) could be the dominant cause of the pharmacokinetic interaction as CP-778875 did not exhibit significant inhibition of cytochrome P450 3A4/3A5, multidrug resistant protein 1 or breast cancer resistant protein, which are also involved in the hepatobiliary disposition of atorvastatin. 5-(N-(4-((4-ethylbenzyl)thio)phenyl)sulfamoyl)-2-methylbenzoic acid 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 214-233 23766489-1 2013 OBJECTIVES: Voriconazole exhibits non-linear pharmacokinetics in adults and is said to be mainly metabolized by CYP2C19 and CYP3A4 to voriconazole-N-oxide. Voriconazole 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 23766489-1 2013 OBJECTIVES: Voriconazole exhibits non-linear pharmacokinetics in adults and is said to be mainly metabolized by CYP2C19 and CYP3A4 to voriconazole-N-oxide. Voriconazole N-Oxide 134-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 24026006-1 2013 Bufalin 5beta-hydroxylation was found to be an isoform-specific biotransformation probe substrate for cytochrome P450 3A4 (CYP3A4). bufalin 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-121 24026006-1 2013 Bufalin 5beta-hydroxylation was found to be an isoform-specific biotransformation probe substrate for cytochrome P450 3A4 (CYP3A4). bufalin 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 23845848-5 2013 Metabolism by CYP3A4 is only known for dihydrodiol metabolites of PAH but not for their parent compounds. Polycyclic Aromatic Hydrocarbons 66-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 23845848-6 2013 In the present study, a CYP3A4 reporter gene assay, requiring the overexpression of PXR, was used to investigate whether the PAH parent compounds BaP, benzo[c]phenanthrene (BcP) and dibenzo[a,l]pyrene (DBalP) as well as their corresponding phase I metabolites, the respective dihydrodiols and diol epoxides, can induce CYP3A4 promoter activity. Polycyclic Aromatic Hydrocarbons 125-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 23845848-6 2013 In the present study, a CYP3A4 reporter gene assay, requiring the overexpression of PXR, was used to investigate whether the PAH parent compounds BaP, benzo[c]phenanthrene (BcP) and dibenzo[a,l]pyrene (DBalP) as well as their corresponding phase I metabolites, the respective dihydrodiols and diol epoxides, can induce CYP3A4 promoter activity. Benzo(a)pyrene 146-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 23845848-6 2013 In the present study, a CYP3A4 reporter gene assay, requiring the overexpression of PXR, was used to investigate whether the PAH parent compounds BaP, benzo[c]phenanthrene (BcP) and dibenzo[a,l]pyrene (DBalP) as well as their corresponding phase I metabolites, the respective dihydrodiols and diol epoxides, can induce CYP3A4 promoter activity. benzo(c)phenanthrene 173-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 23845848-6 2013 In the present study, a CYP3A4 reporter gene assay, requiring the overexpression of PXR, was used to investigate whether the PAH parent compounds BaP, benzo[c]phenanthrene (BcP) and dibenzo[a,l]pyrene (DBalP) as well as their corresponding phase I metabolites, the respective dihydrodiols and diol epoxides, can induce CYP3A4 promoter activity. dibenzo(a,l)pyrene 182-200 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 23845848-6 2013 In the present study, a CYP3A4 reporter gene assay, requiring the overexpression of PXR, was used to investigate whether the PAH parent compounds BaP, benzo[c]phenanthrene (BcP) and dibenzo[a,l]pyrene (DBalP) as well as their corresponding phase I metabolites, the respective dihydrodiols and diol epoxides, can induce CYP3A4 promoter activity. dibenzo(a,l)pyrene 202-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 23845848-6 2013 In the present study, a CYP3A4 reporter gene assay, requiring the overexpression of PXR, was used to investigate whether the PAH parent compounds BaP, benzo[c]phenanthrene (BcP) and dibenzo[a,l]pyrene (DBalP) as well as their corresponding phase I metabolites, the respective dihydrodiols and diol epoxides, can induce CYP3A4 promoter activity. trans-1,2-dihydro-1,2-naphthalenediol 276-288 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 23845848-6 2013 In the present study, a CYP3A4 reporter gene assay, requiring the overexpression of PXR, was used to investigate whether the PAH parent compounds BaP, benzo[c]phenanthrene (BcP) and dibenzo[a,l]pyrene (DBalP) as well as their corresponding phase I metabolites, the respective dihydrodiols and diol epoxides, can induce CYP3A4 promoter activity. diol epoxides 293-306 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 23845848-7 2013 BaP, BcP and their dihydrodiols were found to significantly activate the CYP3A4 promoter. Benzo(a)pyrene 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 23845848-7 2013 BaP, BcP and their dihydrodiols were found to significantly activate the CYP3A4 promoter. benzo(c)phenanthrene 5-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 23845848-7 2013 BaP, BcP and their dihydrodiols were found to significantly activate the CYP3A4 promoter. trans-1,2-dihydro-1,2-naphthalenediol 19-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 23845848-8 2013 Moreover, activation of PXR by all four compounds was detected by using a PXR transactivation assay, supporting that PXR mediates CYP3A4 induction by PAH. Polycyclic Aromatic Hydrocarbons 150-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 23845848-9 2013 Taken together, these results show that both PAH parent compounds as well as their phase I metabolites induce CYP3A4 promoter via the transcription factor PXR. Polycyclic Aromatic Hydrocarbons 45-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 23939663-0 2013 Reduced exposure variability of the CYP3A substrate simvastatin by dose individualization to CYP3A activity. Simvastatin 52-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 23939663-0 2013 Reduced exposure variability of the CYP3A substrate simvastatin by dose individualization to CYP3A activity. Simvastatin 52-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 23939663-1 2013 This study aimed to demonstrate that the dose of a CYP3A substrate (simvastatin) can be adapted individually on the basis of CYP3A activity as assessed by midazolam metabolic clearance. Simvastatin 68-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 23939663-1 2013 This study aimed to demonstrate that the dose of a CYP3A substrate (simvastatin) can be adapted individually on the basis of CYP3A activity as assessed by midazolam metabolic clearance. Simvastatin 68-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-130 23939663-1 2013 This study aimed to demonstrate that the dose of a CYP3A substrate (simvastatin) can be adapted individually on the basis of CYP3A activity as assessed by midazolam metabolic clearance. Midazolam 155-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 23939663-1 2013 This study aimed to demonstrate that the dose of a CYP3A substrate (simvastatin) can be adapted individually on the basis of CYP3A activity as assessed by midazolam metabolic clearance. Midazolam 155-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-130 23939663-2 2013 In 18 healthy participants individual CYP3A activity was quantified using midazolam metabolic clearance both alone and during CYP3A inhibition with 40 mg ritonavir. Midazolam 74-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 23939663-2 2013 In 18 healthy participants individual CYP3A activity was quantified using midazolam metabolic clearance both alone and during CYP3A inhibition with 40 mg ritonavir. Ritonavir 154-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 23939663-7 2013 CYP3A activity-based dose adaptation can be used to reduce interindividual variability in simvastatin exposure. Simvastatin 90-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 23845848-0 2013 Polycyclic aromatic hydrocarbons stimulate human CYP3A4 promoter activity via PXR. Polycyclic Aromatic Hydrocarbons 0-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 23845848-3 2013 Recently, it was shown that the PAH benzo[a]pyrene (BaP) can induce CYP3A4 as well. Polycyclic Aromatic Hydrocarbons 32-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 23845848-3 2013 Recently, it was shown that the PAH benzo[a]pyrene (BaP) can induce CYP3A4 as well. [a]pyrene 41-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 23845848-3 2013 Recently, it was shown that the PAH benzo[a]pyrene (BaP) can induce CYP3A4 as well. Benzo(a)pyrene 52-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 23845848-5 2013 Metabolism by CYP3A4 is only known for dihydrodiol metabolites of PAH but not for their parent compounds. trans-1,2-dihydro-1,2-naphthalenediol 39-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 23846873-2 2013 We reported previously that MC treatment triggers a pronounced downregulation, particularly at the protein level, of mouse hepatic Cyp3a11, a counterpart of the key human drug-metabolizing enzyme CYP3A4. Methylcholanthrene 28-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 196-202 23703578-6 2013 Drug-drug interactions are dependent on statins" pharmacokinetic profile: simvastatin, lovastatin and atorvastatin are metabolized through cytochrome P450 (CYP) 3A, while the metabolism of the other statins is independent of this CYP. Simvastatin 74-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-163 23703578-6 2013 Drug-drug interactions are dependent on statins" pharmacokinetic profile: simvastatin, lovastatin and atorvastatin are metabolized through cytochrome P450 (CYP) 3A, while the metabolism of the other statins is independent of this CYP. Lovastatin 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-163 23703578-6 2013 Drug-drug interactions are dependent on statins" pharmacokinetic profile: simvastatin, lovastatin and atorvastatin are metabolized through cytochrome P450 (CYP) 3A, while the metabolism of the other statins is independent of this CYP. Atorvastatin 102-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-163 23703578-10 2013 All HIV PIs except nelfinavir are coadministered with a low dose of ritonavir, a potent CYP3A inhibitor to improve their pharmacokinetic properties. Ritonavir 68-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-93 23703578-11 2013 Cobicistat is a new potent CYP3A inhibitor that is combined with elvitegravir and will be combined with HIV-PIs in the future. Cobicistat 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 23703578-11 2013 Cobicistat is a new potent CYP3A inhibitor that is combined with elvitegravir and will be combined with HIV-PIs in the future. elvitegravir 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 23703578-12 2013 The HCV-PIs boceprevir and telaprevir are both, to different extents, inhibitors of CYP3A. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-89 23703578-12 2013 The HCV-PIs boceprevir and telaprevir are both, to different extents, inhibitors of CYP3A. telaprevir 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-89 23703578-14 2013 Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated. Simvastatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 23703578-14 2013 Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated. Simvastatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 23703578-14 2013 Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated. Lovastatin 16-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 23703578-14 2013 Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated. Lovastatin 16-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 23703578-14 2013 Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated. Ritonavir 141-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 23892274-1 2013 AIM: 20(S)-Ginsenoside Rh2 (Rh2) has shown potent inhibition on P-glycoprotein (P-gp), while most HIV protease inhibitors are both substrates and inhibitors of P-gp and CYP3A4. ginsenoside Rh2 11-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 23892274-1 2013 AIM: 20(S)-Ginsenoside Rh2 (Rh2) has shown potent inhibition on P-glycoprotein (P-gp), while most HIV protease inhibitors are both substrates and inhibitors of P-gp and CYP3A4. rh2 23-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 23928571-8 2013 The significant lapatinib-docetaxel interaction is likely CYP3A4-mediated, suggesting that caution should be exercised when this combination is administered, particularly to patients with compromised CYP3A activity, and recipients should be monitored closely for enhanced toxicity, particularly for adverse effects on the intestine. Lapatinib 16-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 23928571-8 2013 The significant lapatinib-docetaxel interaction is likely CYP3A4-mediated, suggesting that caution should be exercised when this combination is administered, particularly to patients with compromised CYP3A activity, and recipients should be monitored closely for enhanced toxicity, particularly for adverse effects on the intestine. Docetaxel 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 23852652-5 2013 Roles for CYP3A4, CYP2C9, CYP2C19 and CYP2B6 in the metabolism of ospemifene and its two main metabolites, 4--hydroxyospemifene and 4"-hydroxyospemifene, were confirmed. Ospemifene 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 23852652-5 2013 Roles for CYP3A4, CYP2C9, CYP2C19 and CYP2B6 in the metabolism of ospemifene and its two main metabolites, 4--hydroxyospemifene and 4"-hydroxyospemifene, were confirmed. 4-hydroxyospemifene 107-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 23852652-5 2013 Roles for CYP3A4, CYP2C9, CYP2C19 and CYP2B6 in the metabolism of ospemifene and its two main metabolites, 4--hydroxyospemifene and 4"-hydroxyospemifene, were confirmed. 4-hydroxyospemifene 132-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 23852652-7 2013 CONCLUSIONS: The clinical pharmacokinetic findings and in vitro data suggest that CYP3A4 is important for ospemifene metabolism, but other CYP isoforms and metabolic pathways also contribute. Ospemifene 106-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 23852652-8 2013 Strong CYP3A or CYP2C9 inducers (e.g. rifampicin) would be expected to decrease the exposure to ospemifene. Rifampin 38-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-12 23852652-8 2013 Strong CYP3A or CYP2C9 inducers (e.g. rifampicin) would be expected to decrease the exposure to ospemifene. Ospemifene 96-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-12 23852652-9 2013 Ospemifene should be used with caution when coadministered with the modest CYP3A inhibitor ketoconazole and should not be coadministered with the potent CYP3A/CYP2C9/CYP2C19 inhibitor fluconazole. Ospemifene 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 23886699-0 2013 The effect of ritonavir on human CYP2B6 catalytic activity: heme modification contributes to the mechanism-based inactivation of CYP2B6 and CYP3A4 by ritonavir. Ritonavir 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 23886699-0 2013 The effect of ritonavir on human CYP2B6 catalytic activity: heme modification contributes to the mechanism-based inactivation of CYP2B6 and CYP3A4 by ritonavir. Heme 60-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 23886699-0 2013 The effect of ritonavir on human CYP2B6 catalytic activity: heme modification contributes to the mechanism-based inactivation of CYP2B6 and CYP3A4 by ritonavir. Ritonavir 150-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 23886699-7 2013 Here, we provide evidence that RTV inactivation of CYP3A4 is due to heme destruction with the formation of a heme-protein adduct. Heme 68-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 23886699-7 2013 Here, we provide evidence that RTV inactivation of CYP3A4 is due to heme destruction with the formation of a heme-protein adduct. Heme 109-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 23886699-9 2013 Furthermore, LC-MS/MS analysis revealed that both CYP3A4 and human liver microsomes form an RTV-glutathione conjugate having a MH+ at m/z 858 during metabolism of RTV, suggesting the formation of an isocyanate intermediate leading to formation of the conjugate. Ritonavir 92-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 23886699-9 2013 Furthermore, LC-MS/MS analysis revealed that both CYP3A4 and human liver microsomes form an RTV-glutathione conjugate having a MH+ at m/z 858 during metabolism of RTV, suggesting the formation of an isocyanate intermediate leading to formation of the conjugate. Glutathione 96-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 23886699-9 2013 Furthermore, LC-MS/MS analysis revealed that both CYP3A4 and human liver microsomes form an RTV-glutathione conjugate having a MH+ at m/z 858 during metabolism of RTV, suggesting the formation of an isocyanate intermediate leading to formation of the conjugate. Ritonavir 163-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 23886699-9 2013 Furthermore, LC-MS/MS analysis revealed that both CYP3A4 and human liver microsomes form an RTV-glutathione conjugate having a MH+ at m/z 858 during metabolism of RTV, suggesting the formation of an isocyanate intermediate leading to formation of the conjugate. Isocyanates 199-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 23703578-14 2013 Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated. Ritonavir 141-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 23703578-14 2013 Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated. telaprevir 216-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 23703578-14 2013 Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated. telaprevir 216-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 23703578-14 2013 Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 230-240 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 23703578-14 2013 Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 230-240 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 23703578-15 2013 Atorvastatin is also a CYP3A substrate, but less potent drug-drug interactions have been reported with CYP3A inhibitors. Atorvastatin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-28 23703578-15 2013 Atorvastatin is also a CYP3A substrate, but less potent drug-drug interactions have been reported with CYP3A inhibitors. Atorvastatin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 23748747-1 2013 PURPOSE: We assessed the effect of cytochrome P450 (CYP) 3A4 and the OATP1B1 inhibitor clarithromycin on ambrisentan steady-state kinetics and its relationship to the SLCO1B1 15 haplotype in healthy volunteers. ambrisentan 105-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-60 24114622-10 2013 Moreover, concomitant use with strong CYP3A4 inhibitors (such as ketoconazole, itraconazole, clarithromycin, ritonavir, telithromycin, etc.) Ketoconazole 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 24114622-10 2013 Moreover, concomitant use with strong CYP3A4 inhibitors (such as ketoconazole, itraconazole, clarithromycin, ritonavir, telithromycin, etc.) Itraconazole 79-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 24114622-10 2013 Moreover, concomitant use with strong CYP3A4 inhibitors (such as ketoconazole, itraconazole, clarithromycin, ritonavir, telithromycin, etc.) Ritonavir 109-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 24114622-10 2013 Moreover, concomitant use with strong CYP3A4 inhibitors (such as ketoconazole, itraconazole, clarithromycin, ritonavir, telithromycin, etc.) telithromycin 120-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 23913028-1 2013 Erlotinib is approved for the treatment of non-small cell lung and pancreatic cancers, and is metabolized by CYP3A4. Erlotinib Hydrochloride 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 23748748-0 2013 Concentration effect relationship of CYP3A inhibition by ritonavir in humans. Ritonavir 57-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-42 23748748-1 2013 PURPOSE: To investigate the dose and concentration dependency of CYP3A inhibition by ritonavir using the established limited sampling strategy with midazolam for CYP3A activity. Ritonavir 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 23748748-1 2013 PURPOSE: To investigate the dose and concentration dependency of CYP3A inhibition by ritonavir using the established limited sampling strategy with midazolam for CYP3A activity. Ritonavir 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-167 23748748-1 2013 PURPOSE: To investigate the dose and concentration dependency of CYP3A inhibition by ritonavir using the established limited sampling strategy with midazolam for CYP3A activity. Midazolam 148-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 23748748-3 2013 Single ascending doses of ritonavir (0.1-300 mg) were evaluated for CYP3A inhibition in two cohorts using midazolam as a marker substance. Ritonavir 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 23748748-4 2013 RESULTS: Ritonavir administered as a single oral dose produced a dose-dependent CYP3A inhibition with an ID50 of 3.4 mg. Ritonavir 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-85 23748748-7 2013 CONCLUSIONS: Ritonavir shows a dose and concentration effect relationship of CYP3A inhibition. Ritonavir 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 23876819-1 2013 Deoxyelephantopin was evaluated for its effects on the expression of mRNAs encoding CYP1A2, CYP2D6 and CYP3A4, and protein expression and resultant enzymatic activity. deoxyelephantopin 0-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 23876819-7 2013 In silico docking simulation showed that deoxyelephantopin has a weak interaction with CYP3A4 enzyme and it minimally affects the metabolism of CYP3A4 substrates. deoxyelephantopin 41-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 23876819-7 2013 In silico docking simulation showed that deoxyelephantopin has a weak interaction with CYP3A4 enzyme and it minimally affects the metabolism of CYP3A4 substrates. deoxyelephantopin 41-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 23857299-7 2013 Cimetidine and famotidine both inhibited CYP3A4-mediated formation of noroxycodone and CYP2D6-mediated formation of oxymorphone, and famotidine inhibited CYP3A4-mediated formation of R- and S-EDDP, but IC50s were so high that only >10x therapeutic concentrations may have potential for reversible in vivo inhibition. Cimetidine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 23857299-7 2013 Cimetidine and famotidine both inhibited CYP3A4-mediated formation of noroxycodone and CYP2D6-mediated formation of oxymorphone, and famotidine inhibited CYP3A4-mediated formation of R- and S-EDDP, but IC50s were so high that only >10x therapeutic concentrations may have potential for reversible in vivo inhibition. Cimetidine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 23857299-7 2013 Cimetidine and famotidine both inhibited CYP3A4-mediated formation of noroxycodone and CYP2D6-mediated formation of oxymorphone, and famotidine inhibited CYP3A4-mediated formation of R- and S-EDDP, but IC50s were so high that only >10x therapeutic concentrations may have potential for reversible in vivo inhibition. Famotidine 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 23857299-7 2013 Cimetidine and famotidine both inhibited CYP3A4-mediated formation of noroxycodone and CYP2D6-mediated formation of oxymorphone, and famotidine inhibited CYP3A4-mediated formation of R- and S-EDDP, but IC50s were so high that only >10x therapeutic concentrations may have potential for reversible in vivo inhibition. noroxycodone 70-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 23857299-7 2013 Cimetidine and famotidine both inhibited CYP3A4-mediated formation of noroxycodone and CYP2D6-mediated formation of oxymorphone, and famotidine inhibited CYP3A4-mediated formation of R- and S-EDDP, but IC50s were so high that only >10x therapeutic concentrations may have potential for reversible in vivo inhibition. Famotidine 133-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 23857299-7 2013 Cimetidine and famotidine both inhibited CYP3A4-mediated formation of noroxycodone and CYP2D6-mediated formation of oxymorphone, and famotidine inhibited CYP3A4-mediated formation of R- and S-EDDP, but IC50s were so high that only >10x therapeutic concentrations may have potential for reversible in vivo inhibition. r- and s-eddp 183-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 23857299-9 2013 Omeprazole, esomeprazole and pantoprazole had greater effects on CYP3A4-mediated reactions, whereas lansoprazole was selective for CYP2D6-mediated formation of oxymorphone. Omeprazole 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 23857299-9 2013 Omeprazole, esomeprazole and pantoprazole had greater effects on CYP3A4-mediated reactions, whereas lansoprazole was selective for CYP2D6-mediated formation of oxymorphone. Esomeprazole 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 23857299-9 2013 Omeprazole, esomeprazole and pantoprazole had greater effects on CYP3A4-mediated reactions, whereas lansoprazole was selective for CYP2D6-mediated formation of oxymorphone. Pantoprazole 29-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 24028620-0 2013 Baicalin pharmacokinetic profile of absorption process using novel in-vitro model: cytochrome P450 3A4-induced Caco-2 cell monolayers combined with rat intestinal rinse fluids. baicalin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-102 24028620-2 2013 METHODS: The effects of BG on intestinal cytochrome P450 3A4 (CYP3A) protein/mRNA expression, activity and permeability glycoprotein (P-gp) were evaluated in CYP3A4-induced Caco-2 cell monolayers or rats. O(6)-benzylguanine 24-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-60 24174816-6 2013 RESULTS: Assessment using recombinant enzymes showed that mitragynine gave the strongest inhibitory effect on CYP2D6 with an IC50 value of 0.45+-0.33 mM, followed by CYP2C9 and CYP3A4 with IC50 values of 9.70+-4.80 and 41.32+-6.74 muM respectively. mitragynine 58-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 24174816-7 2013 Positive inhibitors appropriate for CYP2C9, CYP2D6, and CYP3A4 which are sulfaphenazole, quinidine and ketoconazole were used respectively. Sulfaphenazole 73-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 24174816-11 2013 On the other hand, mitragynine inhibits CYP3A4 competitively with a Ki value of 379.18 muM. mitragynine 19-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 23729226-3 2013 Because netupitant may be used with a variety of drugs, which may be substrates of CYP3A4, two studies were designed to establish the potential risk for drug-drug interaction with three different CYP3A4 substrates: midazolam, erythromycin, and dexamethasone. netupitant 8-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 23729226-8 2013 RESULTS: Netupitant, by inhibiting the CYP3A4, increased the C max and AUCinf of midazolam by 40 and 144 %, respectively, and the C max and AUCinf of erythromycin by 30 %. Midazolam 81-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 24052064-0 2013 Impact of CYP3A4*22 allele on tacrolimus pharmacokinetics in early period after renal transplantation: toward updated genotype-based dosage guidelines. Tacrolimus 30-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 23729226-10 2013 CONCLUSIONS: The results of these studies suggest that netupitant is a moderate inhibitor of CYP3A4 and therefore, co-administration with drugs that are substrates of CYP3A4 may require dose adjustments. netupitant 55-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24052064-1 2013 BACKGROUND: Tacrolimus (Tac) metabolism is mainly mediated by the cytochrome P450 3A (CYP3A) subfamily. Tacrolimus 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-84 24052064-1 2013 BACKGROUND: Tacrolimus (Tac) metabolism is mainly mediated by the cytochrome P450 3A (CYP3A) subfamily. Tacrolimus 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 23729226-10 2013 CONCLUSIONS: The results of these studies suggest that netupitant is a moderate inhibitor of CYP3A4 and therefore, co-administration with drugs that are substrates of CYP3A4 may require dose adjustments. netupitant 55-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 167-173 23748441-2 2013 Netupitant, a new highly selective NK1 RA, is both a substrate for and a moderate inhibitor of CYP3A4. netupitant 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 24052064-10 2013 During the second week after transplantation, CrCl was on average 9.5 mL/min higher for CYP3A4*22 carriers compared with CYP3A4*1/*1 patients (P = 0.007), suggesting that Tac overexposure in CYP3A4*22 carriers might provide a renal function benefit. crcl 46-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 23682612-5 2013 In this study, we investigated the effects of methanol, ethanol, acetonitrile and dimethyl sulfoxide (1% to 4%) on the assessment of km, Vmax and Clint for the metabolism of midazolam via CYP3A4 to 1-hydroxymidazolam and the metabolism of caffeine to paraxanthine via CYP1A2 using expressed enzymes in vitro. acetonitrile 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-194 23770984-5 2013 RESULTS: All three gingerols potently inhibited CYP2C9 activity, exerted moderate inhibition on CYP2C19 and CYP3A4, and weak inhibion on CYP2D6. gingerol 19-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 23682612-5 2013 In this study, we investigated the effects of methanol, ethanol, acetonitrile and dimethyl sulfoxide (1% to 4%) on the assessment of km, Vmax and Clint for the metabolism of midazolam via CYP3A4 to 1-hydroxymidazolam and the metabolism of caffeine to paraxanthine via CYP1A2 using expressed enzymes in vitro. Dimethyl Sulfoxide 82-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-194 23682612-5 2013 In this study, we investigated the effects of methanol, ethanol, acetonitrile and dimethyl sulfoxide (1% to 4%) on the assessment of km, Vmax and Clint for the metabolism of midazolam via CYP3A4 to 1-hydroxymidazolam and the metabolism of caffeine to paraxanthine via CYP1A2 using expressed enzymes in vitro. Midazolam 174-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-194 23682612-5 2013 In this study, we investigated the effects of methanol, ethanol, acetonitrile and dimethyl sulfoxide (1% to 4%) on the assessment of km, Vmax and Clint for the metabolism of midazolam via CYP3A4 to 1-hydroxymidazolam and the metabolism of caffeine to paraxanthine via CYP1A2 using expressed enzymes in vitro. 1-hydroxymethylmidazolam 198-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-194 23682612-5 2013 In this study, we investigated the effects of methanol, ethanol, acetonitrile and dimethyl sulfoxide (1% to 4%) on the assessment of km, Vmax and Clint for the metabolism of midazolam via CYP3A4 to 1-hydroxymidazolam and the metabolism of caffeine to paraxanthine via CYP1A2 using expressed enzymes in vitro. Caffeine 239-247 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-194 23682612-5 2013 In this study, we investigated the effects of methanol, ethanol, acetonitrile and dimethyl sulfoxide (1% to 4%) on the assessment of km, Vmax and Clint for the metabolism of midazolam via CYP3A4 to 1-hydroxymidazolam and the metabolism of caffeine to paraxanthine via CYP1A2 using expressed enzymes in vitro. 1,7-dimethylxanthine 251-263 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-194 24086247-0 2013 Modeling of rifampicin-induced CYP3A4 activation dynamics for the prediction of clinical drug-drug interactions from in vitro data. Rifampin 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 24086247-3 2013 Rifampicin is a well-known CYP3A4 inducer, and is commonly used as a positive control for evaluating the CYP3A4 induction potential of test compounds. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 24086247-3 2013 Rifampicin is a well-known CYP3A4 inducer, and is commonly used as a positive control for evaluating the CYP3A4 induction potential of test compounds. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 24086247-4 2013 Herein, we report the compilation of in vitro induction data for CYP3A4 by rifampicin in human hepatocytes, and the transcription/translation model developed for this enzyme using an extended least squares method that can account for inherent inter-individual variability. Rifampin 75-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 24058572-4 2013 Hepatic CYP3A activity was measured via midazolam hydroxylation in human liver microsomes. Midazolam 40-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-13 24448021-2 2013 However, large variability exists in Ki reported for ketoconazole with midazolam, a model inhibitor-substrate pair for CYP3A. Ketoconazole 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-124 24448021-2 2013 However, large variability exists in Ki reported for ketoconazole with midazolam, a model inhibitor-substrate pair for CYP3A. Midazolam 71-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-124 23707768-0 2013 Piperine activates human pregnane X receptor to induce the expression of cytochrome P450 3A4 and multidrug resistance protein 1. piperine 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-92 23707768-3 2013 Here, we studied, whether piperine (PIP), a major component extracted from the widely-used daily spice black pepper, could induce PXR-mediated expression of cytochrome P450 3A4 (CYP3A4) and multidrug resistance protein 1 (MDR1). piperine 26-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-176 23707768-3 2013 Here, we studied, whether piperine (PIP), a major component extracted from the widely-used daily spice black pepper, could induce PXR-mediated expression of cytochrome P450 3A4 (CYP3A4) and multidrug resistance protein 1 (MDR1). piperine 26-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 23707768-3 2013 Here, we studied, whether piperine (PIP), a major component extracted from the widely-used daily spice black pepper, could induce PXR-mediated expression of cytochrome P450 3A4 (CYP3A4) and multidrug resistance protein 1 (MDR1). piperine 36-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-176 23707768-3 2013 Here, we studied, whether piperine (PIP), a major component extracted from the widely-used daily spice black pepper, could induce PXR-mediated expression of cytochrome P450 3A4 (CYP3A4) and multidrug resistance protein 1 (MDR1). piperine 36-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 23707768-4 2013 Our results showed that PIP activated human PXR (hPXR)-mediated CYP3A4 and MDR1 expression in human hepatocytes, intestine cells, and a mouse model; PIP activated hPXR by recruiting its coactivator SRC-1 in both cellular and cell-free systems; PIP bound to the hPXR ligand binding domain in a competitive ligand binding assay in vitro. piperine 24-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 23707768-5 2013 The dichotomous effects of PIP on induction of CYP3A4 and MDR1 expression observed here and inhibition of their activity reported elsewhere challenges the potential use of PIP as a bioavailability enhancer and suggests that caution should be taken in PIP consumption during drug treatment in patients, particularly those who favor daily pepper spice or rely on certain pepper remedies. piperine 27-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 24422406-1 2013 OBJECTIVE: To define the effect of Curculiginis Rhizoma and its active ingredient orcinol glucoside on PXR-CYP3A of L02 cells in normal and deficiency-cold states, in order to lay a foundation for studies on the mechanism of efficacy expression differentiation of Curculiginis Rhizoma in different states. Orcinol glucoside 82-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-112 24422406-5 2013 Aqueous extracts from Curculiginis Rhizoma could significantly reduce PXR protein expression of L02 cells in normal state, while orcinol glucoside could significantly reduce CYP3A activity and PXR protein expression of L02 cells in normal state. Orcinol glucoside 129-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-179 24422406-6 2013 Meanwhile, aqueous extracts from Curculiginis Rhizoma could significantly increase CYP3A activity and PXR protein expression of L02 cells in deficiency-cold state, while orcinol glucoside could significantly reduce CYP3A activity and increase PXR protein expression of L02 cells in deficiency-cold state. Orcinol glucoside 170-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-220 23928187-7 2013 Interestingly, we found that the compounds that bind directly to PXR, as revealed in an intrinsic tryptophan fluorescence assay, modulate CYP3A4 promoter activity differentially in HepG2 cells. Tryptophan 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 23770984-6 2013 8-Gingerol was the most potent in inhibition of P450 enzymes with IC50 values of 6.8, 12.5, 8.7, and 42.7 mumol/L for CYP2C9, CYP2C19, CYP3A4, and CYP2D6, respectively. 8-gingerol 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 23770984-7 2013 By comparing the effects of gingerols on CYP3A4 with three different fluorescent substrate probes, it was demonstrated that the inhibition of gingerols on CYP3A4 had no substrate-dependence. gingerol 142-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 23770984-8 2013 In HepG2 cells, 8-gingerol and 10-gingerol inhibited, but 6-gingerol induced mRNA expression of CYP3A4. gingerol 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 23770984-9 2013 CONCLUSION: 6-, 8-, and 10-gingerol suppress human cytochrome P450 activity, while 8- and 10-gingerol inhibit CYP3A4 expression. 8- and 10-gingerol 83-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 23674377-0 2013 Development and validation of a LC-MS/MS method for the in vitro analysis of 1-hydroxymidazolam in human liver microsomes: application for determining CYP3A4 inhibition in complex matrix mixtures. 1-hydroxymethylmidazolam 77-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 23287855-4 2013 In vitro analysis suggested that the purified CYP102A5 metabolizes typical substrates of human CYP2C9, CYP2D6, CYP2E1, and CYP3A4, such as coumarin, propranolol, aniline, chlorzoxazone, p-nitrophenol, and nifedipine. Propranolol 149-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 23287855-4 2013 In vitro analysis suggested that the purified CYP102A5 metabolizes typical substrates of human CYP2C9, CYP2D6, CYP2E1, and CYP3A4, such as coumarin, propranolol, aniline, chlorzoxazone, p-nitrophenol, and nifedipine. aniline 162-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 23287855-4 2013 In vitro analysis suggested that the purified CYP102A5 metabolizes typical substrates of human CYP2C9, CYP2D6, CYP2E1, and CYP3A4, such as coumarin, propranolol, aniline, chlorzoxazone, p-nitrophenol, and nifedipine. Chlorzoxazone 171-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 23287855-4 2013 In vitro analysis suggested that the purified CYP102A5 metabolizes typical substrates of human CYP2C9, CYP2D6, CYP2E1, and CYP3A4, such as coumarin, propranolol, aniline, chlorzoxazone, p-nitrophenol, and nifedipine. 4-nitrophenol 186-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 23287855-4 2013 In vitro analysis suggested that the purified CYP102A5 metabolizes typical substrates of human CYP2C9, CYP2D6, CYP2E1, and CYP3A4, such as coumarin, propranolol, aniline, chlorzoxazone, p-nitrophenol, and nifedipine. Nifedipine 205-215 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 23073537-7 2013 Basal expression of CYP3A4 protein in HepG2-PGC-1alpha cells was increased but rifampicin-inducible expression of CYP3A4 protein was lowered in comparison with parent HepG2 cells. Rifampin 79-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 23674377-2 2013 To evaluate changes in the activity of CYP3A4 in patients, levels of 1-hydroxymidazolam in plasma are often determined with liquid chromatography-quadrupole mass spectrometry (LC-MS/MS). 1-hydroxymethylmidazolam 69-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 23674377-10 2013 Furthermore, the applicability of this assay for the determination of CYP3A4 inhibition in complex matrix mixtures was successfully demonstrated in an in vitro experiment in which CYP3A4 inhibition by known CAM (beta-carotene, green tea, milk thistle and St. John"s wort) was determined. beta Carotene 212-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 23674377-10 2013 Furthermore, the applicability of this assay for the determination of CYP3A4 inhibition in complex matrix mixtures was successfully demonstrated in an in vitro experiment in which CYP3A4 inhibition by known CAM (beta-carotene, green tea, milk thistle and St. John"s wort) was determined. beta Carotene 212-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 23653047-4 2013 OBJECTIVE: The primary objective of this study was to develop a coupled dynamic model for the interaction of the CYP3A inhibitor voriconazole and the prototypical CYP3A substrate midazolam. Voriconazole 129-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-118 23305158-7 2013 A significant increase in rivaroxaban exposure was demonstrated with the strong CYP3A4, P-gp/Bcrp (ABCG2) inhibitors (and potential CYP2J2 inhibitors) ketoconazole (158% increase [95% CI 136%, 182%] for a 400 mg once daily dose) and ritonavir (153% increase [95% CI 134%, 174%]). Rivaroxaban 26-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 23305158-7 2013 A significant increase in rivaroxaban exposure was demonstrated with the strong CYP3A4, P-gp/Bcrp (ABCG2) inhibitors (and potential CYP2J2 inhibitors) ketoconazole (158% increase [95% CI 136%, 182%] for a 400 mg once daily dose) and ritonavir (153% increase [95% CI 134%, 174%]). Ketoconazole 151-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 23305158-7 2013 A significant increase in rivaroxaban exposure was demonstrated with the strong CYP3A4, P-gp/Bcrp (ABCG2) inhibitors (and potential CYP2J2 inhibitors) ketoconazole (158% increase [95% CI 136%, 182%] for a 400 mg once daily dose) and ritonavir (153% increase [95% CI 134%, 174%]). Ritonavir 233-242 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 23305158-8 2013 CONCLUSIONS: Results suggest that rivaroxaban may be co-administered with CYP3A4 and/or P-gp substrates/moderate inhibitors, but not with strong combined CYP3A4, P-gp and Bcrp (ABCG2) inhibitors (mainly comprising azole-antimycotics, apart from fluconazole, and HIV protease inhibitors), which are multi-pathway inhibitors of rivaroxaban clearance and elimination. Rivaroxaban 34-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 23677771-14 2013 In the presence of ketoconazole, a strong CYP3A4/5 inhibitor, axitinib C max and AUC increased by 1.5- and 2-fold, respectively, whereas co-administration of rifampin, a strong CYP3A4/5 inducer, resulted in a 71 and 79 % decrease in the C max and AUC , respectively. Ketoconazole 19-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 23677771-14 2013 In the presence of ketoconazole, a strong CYP3A4/5 inhibitor, axitinib C max and AUC increased by 1.5- and 2-fold, respectively, whereas co-administration of rifampin, a strong CYP3A4/5 inducer, resulted in a 71 and 79 % decrease in the C max and AUC , respectively. Axitinib 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 23677771-14 2013 In the presence of ketoconazole, a strong CYP3A4/5 inhibitor, axitinib C max and AUC increased by 1.5- and 2-fold, respectively, whereas co-administration of rifampin, a strong CYP3A4/5 inducer, resulted in a 71 and 79 % decrease in the C max and AUC , respectively. Rifampin 159-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 23305158-3 2013 METHODS: The pharmacokinetic effects of substrates or inhibitors of CYP3A4, P-gp and Bcrp (ABCG2) on rivaroxaban were studied in healthy volunteers. Rivaroxaban 101-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 23712757-2 2013 Danoprevir is a substrate of cytochrome P450 3A4, and the organic anion transporting polypeptides (OATP) 1B1 and 1B3. danoprevir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-48 23653047-4 2013 OBJECTIVE: The primary objective of this study was to develop a coupled dynamic model for the interaction of the CYP3A inhibitor voriconazole and the prototypical CYP3A substrate midazolam. Voriconazole 129-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-168 23653047-4 2013 OBJECTIVE: The primary objective of this study was to develop a coupled dynamic model for the interaction of the CYP3A inhibitor voriconazole and the prototypical CYP3A substrate midazolam. Midazolam 179-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-118 23653047-4 2013 OBJECTIVE: The primary objective of this study was to develop a coupled dynamic model for the interaction of the CYP3A inhibitor voriconazole and the prototypical CYP3A substrate midazolam. Midazolam 179-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-168 23657159-1 2013 Cytochrome P450 (CYP) 3A4 is considered the most important enzyme in imatinib biotransformation. Imatinib Mesylate 69-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-25 23664723-2 2013 Gefitinib is metabolized by cytochrome P450 (CYP) enzymes--including CYP3A4/5, CYP1A1, and CYP2D6--in the liver. Gefitinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 23664723-9 2013 However, in 7 patients taking CYP3A4-inhibitory drugs, rechallenge of gefitinib again caused hepatotoxicity in 4 patients with allele *5 or *10 but not in 3 patients with normal alleles (P = .029). Gefitinib 70-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 23664723-11 2013 CONCLUSION: Reduced function of CYP2D6 may partly account for gefitinib-induced hepatotoxicity when CYP3A4 is inhibited. Gefitinib 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 23780963-6 2013 In HLMs, the intrinsic clearance of vinorelbine metabolism was highly correlated with CYP3A4 activity, and there was no significant difference in intrinsic clearance between CYP3A5 high and low expressers. Vinorelbine 36-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 23780963-7 2013 When radiolabeled vinorelbine substrate was used, there were clear qualitative differences in metabolite formation fingerprints between CYP3A4+b5 and CYP3A5+b5 as determined by NMR and mass spectrometry analysis. Vinorelbine 18-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 23780963-0 2013 The relative contributions of CYP3A4 and CYP3A5 to the metabolism of vinorelbine. Vinorelbine 69-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 23780963-8 2013 One major metabolite (M2), a didehydro-vinorelbine, was present in both recombinant and microsomal systems but was more abundant in CYP3A4+b5 incubations. didehydro-vinorelbine 29-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 23780963-2 2013 Vincristine, a related vinca alkaloid, is 9-fold more efficiently metabolized by CYP3A5 than by CYP3A4 in vitro. Vincristine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 23780963-2 2013 Vincristine, a related vinca alkaloid, is 9-fold more efficiently metabolized by CYP3A5 than by CYP3A4 in vitro. Vinca Alkaloids 23-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 23780963-3 2013 This study quantified the relative contribution of CYP3A4 and CYP3A5 to the metabolism of vinorelbine in vitro using cDNA-expressed human cytochrome P450s (P450s) and human liver microsomes (HLMs). Vinorelbine 90-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 23824607-5 2013 We determined the inhibitory ability of norendoxifen against important drug-metabolizing cytochrome P450 enzymes, including CYP1A2, CYP2A6, CYP3A4, CYP3A5, and CYP2C19, to establish the potency of norendoxifen as a potential cause of drug-drug interactions. N,N-didesmethyl-4-hydroxytamoxifen 40-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 23780963-9 2013 We conclude that despite the equivalent efficiency of recombinant CYP3A4 and CYP3A5 in vinorelbine metabolism the polymorphic expression of CYP3A5, as shown by the kinetics with HLMs, may have a minimal effect on systemic clearance of vinorelbine. Vinorelbine 87-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 23824607-7 2013 The inhibitory abilities of E-, mixed, and Z-norendoxifen against recombinant aromatase (CYP19), CYP1A2, CYP3A4, CYP3A5, and CYP2C19 were tested using microsomal incubations. N,N-didesmethyl-4-hydroxytamoxifen 43-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 23780963-4 2013 CYP3A4 and CYP3A5 were identified as the P450s capable of oxidizing vinorelbine using a panel of human enzymes and selective P450 inhibitors in HLMs. Vinorelbine 68-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23780963-5 2013 For CYP3A4 coexpressed with cytochrome b5 (CYP3A4+b5) and CYP3A5+b5, the Michaelis-Menten constants for vinorelbine were 2.6 and 3.6 muM, respectively, but the Vmax of 1.4 pmol/min/pmol was common to both enzymes. Vinorelbine 104-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 23780963-5 2013 For CYP3A4 coexpressed with cytochrome b5 (CYP3A4+b5) and CYP3A5+b5, the Michaelis-Menten constants for vinorelbine were 2.6 and 3.6 muM, respectively, but the Vmax of 1.4 pmol/min/pmol was common to both enzymes. Vinorelbine 104-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 23903277-3 2013 CYP2C19 and CYP3A4/5 are the principal contributors in the two-step hepatic oxidation of clopidgrel. clopidgrel 89-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 24086951-4 2013 Pomalidomide is extensively metabolized, mainly by the cytochrome P450 3A4 and 1A2 pathways. pomalidomide 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-82 23669408-7 2013 In addition, canthaxanthin weakly inhibited CYP2C19 and CYP3A4/5, with IC50 values of 10.9 and 13.9 muM, respectively. Canthaxanthin 13-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 23669408-8 2013 Zeaxanthin weakly inhibited CYP3A4/5, with an IC50 of 15.5 muM. Zeaxanthins 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 23903277-6 2013 Lipophilic statins, such as atorvastatin, are predominantly metabolized by CYP3A4 and may interfere with CYP activation of clopidogrel, contrary to what happens with hydrophilic statins, such as rosuvastin or pravastatin. Atorvastatin 28-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 24137426-3 2013 The present study evaluated the effect of fucoxanthin on the expression and enzymatic activity of the major xenobiotic metabolizing enzymes, CYP1A1, CYP1A2 and CYP3A4. fucoxanthin 42-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 23436703-3 2013 I discuss here further instances of gene-gene-drug interactions, including a proposed dynamic effect on statin therapy by genetic variants in both a transporter (SLCO1B1) and a metabolizing enzyme (CYP3A4) in liver cells, the main target site where statins block cholesterol synthesis. Cholesterol 263-274 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 198-204 23801357-2 2013 In vitro studies suggested that metabolism of ponatinib is partially mediated by CYP3A4. ponatinib 46-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 23801357-3 2013 The effects of CYP3A4 inhibition on the pharmacokinetics of ponatinib and its CYP3A4-mediated metabolite, AP24567, were evaluated in a single-center, randomized, two-period, two-sequence crossover study in healthy volunteers. ponatinib 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 23833241-3 2013 In this study, we evaluated the effect of renal function on CYP3A activity after kidney transplantation in patients with end-stage renal disease (ESRD) by measuring the change in CYP3A activity using plasma concentration of 4beta-hydroxycholesterol as a biomarker. cholest-5-ene-3,4-diol 224-248 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 24137426-5 2013 Fucoxanthin also inhibited the enzyme activity of CYP1A2 and CYP3A4 in a dose-dependent manner in vitro. fucoxanthin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 23230007-2 2013 Quetiapine is predominantly metabolised by cytochrome P450 3A4 (CYP3A4) and to a lesser extent by CYP2D6. Quetiapine Fumarate 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-62 24024898-1 2013 BACKGROUND & AIM: In vitro studies have identified both midazolam and tacrolimus as dual CYP3A4 and CYP3A5 substrates. Midazolam 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24024898-1 2013 BACKGROUND & AIM: In vitro studies have identified both midazolam and tacrolimus as dual CYP3A4 and CYP3A5 substrates. Tacrolimus 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24024898-7 2013 Furthermore, these data suggest that midazolam is to be considered as a phenotypic probe for in vivo CYP3A4 activity rather than combined CYP3A4 and CYP3A5 activity. Midazolam 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 23230007-2 2013 Quetiapine is predominantly metabolised by cytochrome P450 3A4 (CYP3A4) and to a lesser extent by CYP2D6. Quetiapine Fumarate 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 23230007-4 2013 The aim of the present study is to evaluate if the use of high dosages of quetiapine in some patients, as compared to patients treated with a dosage in the licensed range (up to 800 mg/day), could be explained by a high activity of CYP3A4 and/or of CYP2D6. Quetiapine Fumarate 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 232-238 23230007-5 2013 CYP3A4 activities were determined using the midazolam metabolic ratio in 21 bipolar and schizoaffective bipolar patients genotyped for CYP2D6. Midazolam 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23905516-11 2013 In other systems, such as iNOS and CYP3A4 (where the HXC-Fe motif is not found), a somewhat larger conformational change would be necessary to recuit a nearby histidine. Histidine 159-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 23850985-3 2013 We found that both sesquiterpenes (1-30 muM) greatly induced expression of CYP2B6 and CYP3A4 but not CYP1A2 mRNAs in human primary hepatocytes (HPHs). Sesquiterpenes 19-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 23850985-6 2013 CYP inhibition studies with pooled human liver microsomes (HLMs) indicated that zederone and germacrone moderately inhibited CYP2B6 and CYP3A4 activities in vitro, with IC50 values below 10 muM. zederone 80-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 23850985-6 2013 CYP inhibition studies with pooled human liver microsomes (HLMs) indicated that zederone and germacrone moderately inhibited CYP2B6 and CYP3A4 activities in vitro, with IC50 values below 10 muM. germacrone 93-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 23707193-3 2013 Brucine was incubated with HLMs or CYP3A4 and then analysed by Liquid chromatography/mass spectrometry. brucine 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 23707193-7 2013 Furthermore, brucine significantly inhibited the CYP3A4-catalyzed midazolam 1"-hydroxylation (Ki=2.14muM) at a concentration lower than 10muM, but no obvious inhibitory effects were observed on other CYP substrates (IC50>50muM). Midazolam 66-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 23707193-5 2013 CYP3A4 may be the major enzyme responsible for brucine metabolism in HLMs, other human isoforms of CYP showed minimal or no effect on brucine metabolism. brucine 47-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23707193-6 2013 The inhibitory action of brucine was observed in CYP3A4 for the 1"-hydroxylation of midazolam, with inhibitory concentration 50 (IC50) of 8.4-fold higher than specific inhibitors in HLMs. brucine 25-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 23707193-6 2013 The inhibitory action of brucine was observed in CYP3A4 for the 1"-hydroxylation of midazolam, with inhibitory concentration 50 (IC50) of 8.4-fold higher than specific inhibitors in HLMs. Midazolam 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 23707193-7 2013 Furthermore, brucine significantly inhibited the CYP3A4-catalyzed midazolam 1"-hydroxylation (Ki=2.14muM) at a concentration lower than 10muM, but no obvious inhibitory effects were observed on other CYP substrates (IC50>50muM). brucine 13-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 23859149-2 2013 Via a combination of ligand- and structure-based approaches, a series of dual inhibitors were designed leading to the 2-(3-pyridyl)naphthalenes 10 and 11 with strong inhibition of both enzymes (IC50 values around 20 nM) and excellent selectivities over CYP11B1, CYP19, and CYP3A4. 2-(3-pyridyl)naphthalenes 118-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 273-279 24019753-0 2013 Association of CYP3A4/5, ABCB1 and ABCC2 polymorphisms and clinical outcomes of Thai breast cancer patients treated with tamoxifen. Tamoxifen 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-23 23965431-0 2013 Effects of decreased vitamin D and accumulated uremic toxin on human CYP3A4 activity in patients with end-stage renal disease. Vitamin D 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 23965431-2 2013 For instance, the concentration of erythromycin, a substrate of cytochrome P450 3A4 (CYP3A4), has been reported to be elevated in patients with end-stage renal disease. Erythromycin 35-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-83 23965431-2 2013 For instance, the concentration of erythromycin, a substrate of cytochrome P450 3A4 (CYP3A4), has been reported to be elevated in patients with end-stage renal disease. Erythromycin 35-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 23965431-9 2013 Furthermore, addition of 1,25-dihydroxyvitamin D to uremic serum partially restored the serum effect on CYP3A4 expression. 1,25-dihydroxyvitamin D 25-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 23965431-10 2013 The present study suggests that the decrease of 1,25-dihydroxyvitamin D and the accumulation of uremic toxins contributed to the decreased hepatic clearance of CYP3A4 substrates in patients with end-stage renal disease. 1,25-dihydroxyvitamin D 48-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 23687222-1 2013 OBJECTIVE: Nevirapine is metabolized by cytochrome P450 (CYP) 2B6 and CYP3A4. Nevirapine 11-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 23689718-1 2013 This study assessed the safety, tolerability, and pharmacokinetic interaction between PA-824, a novel antitubercular nitroimidazo-oxazine, and midazolam, a CYP3A4 substrate, in 14 healthy adult male and female subjects. Midazolam 143-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 23822632-6 2013 The results show that CYP3A4-dependent metabolism of the more hydrophilic atorvastatin acid was dependent on OATP1B1 uptake and influenced by MDR1 efflux. Atorvastatin 74-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 23732466-0 2013 CYP3A4-catalyzed simvastatin metabolism as a non-invasive marker of small intestinal health in celiac disease. Simvastatin 17-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23689718-2 2013 The study followed up on observations in vitro that PA-824 caused weak and time-dependent inhibition of CYP3A4. pretomanid 52-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 23568224-5 2013 This study aimed to investigate the magnitude of a possible effect of a potent CYP3A4 inhibitor, ketoconazole, on the pharmacokinetics of macitentan. Ketoconazole 97-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 23898066-9 2013 These findings indicate that co-administration of cimetidine alters the pharmacokinetics of sunitinib probably due to inhibition of CYP3A4, suggesting the possibility that cimetidine should be used carefully for patients with cancer being treated with sunitinib therapy. Cimetidine 50-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 23898066-9 2013 These findings indicate that co-administration of cimetidine alters the pharmacokinetics of sunitinib probably due to inhibition of CYP3A4, suggesting the possibility that cimetidine should be used carefully for patients with cancer being treated with sunitinib therapy. Sunitinib 92-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 23732298-8 2013 In conclusion, the present results suggest that sterol-sensitive LXRalpha positively regulates the basal expression of CYP3A4 but suppresses the xenobiotic/PXR-dependent CYP3A4 expression in human hepatocytes. Sterols 48-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 23732298-8 2013 In conclusion, the present results suggest that sterol-sensitive LXRalpha positively regulates the basal expression of CYP3A4 but suppresses the xenobiotic/PXR-dependent CYP3A4 expression in human hepatocytes. Sterols 48-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 23732299-2 2013 Cytochrome P450 (CYP) 3A4 converts sorafenib to multiple metabolites that have been detected in patient plasma. Sorafenib 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-25 23876492-7 2013 Atorvastatin concentration was associated with SLCO1B1 c.388A>G (P<0.01) and c.521T>C (P<0.05) and 4beta-hydroxycholesterol, a CYP3A activity marker (adjusted R(2)=0.47). Atorvastatin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-144 23884060-1 2013 Boceprevir and telaprevir are inhibitors and substrates of the cytochrome P450 3A4 family. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-82 23884060-1 2013 Boceprevir and telaprevir are inhibitors and substrates of the cytochrome P450 3A4 family. telaprevir 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-82 23568224-5 2013 This study aimed to investigate the magnitude of a possible effect of a potent CYP3A4 inhibitor, ketoconazole, on the pharmacokinetics of macitentan. macitentan 138-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 23568224-9 2013 CONCLUSIONS: Although macitentan metabolism is indeed affected by CYP3A4 inhibition, the changes are not considered to be clinically significant and macitentan can be administered concomitantly with CYP3A4 inhibitors without need for dose adjustment. macitentan 22-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 23568224-9 2013 CONCLUSIONS: Although macitentan metabolism is indeed affected by CYP3A4 inhibition, the changes are not considered to be clinically significant and macitentan can be administered concomitantly with CYP3A4 inhibitors without need for dose adjustment. macitentan 149-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 199-205 23936594-1 2013 CYP3A4 is a key enzyme involved in the metabolism of numerous compounds, such as paclitaxel, and its activity shows an extensive inter-individual variation which can influence treatment response. Paclitaxel 81-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23674608-0 2013 Comparison of endogenous 4beta-hydroxycholesterol with midazolam as markers for CYP3A4 induction by rifampicin. cholest-5-ene-3,4-diol 25-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 23674608-0 2013 Comparison of endogenous 4beta-hydroxycholesterol with midazolam as markers for CYP3A4 induction by rifampicin. Rifampin 100-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 23674608-5 2013 The CYP3A4 induction could be detected even at the lowest dose of rifampicin (10 mg) via the estimated midazolam clearance, the 4beta-hydroxycholesterol ratio (both P < 0.01), and the 6beta-hydroxycortisol ratio (P < 0.05). Rifampin 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 23674608-5 2013 The CYP3A4 induction could be detected even at the lowest dose of rifampicin (10 mg) via the estimated midazolam clearance, the 4beta-hydroxycholesterol ratio (both P < 0.01), and the 6beta-hydroxycortisol ratio (P < 0.05). Midazolam 103-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 23674608-5 2013 The CYP3A4 induction could be detected even at the lowest dose of rifampicin (10 mg) via the estimated midazolam clearance, the 4beta-hydroxycholesterol ratio (both P < 0.01), and the 6beta-hydroxycortisol ratio (P < 0.05). 4beta 128-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 23674608-5 2013 The CYP3A4 induction could be detected even at the lowest dose of rifampicin (10 mg) via the estimated midazolam clearance, the 4beta-hydroxycholesterol ratio (both P < 0.01), and the 6beta-hydroxycortisol ratio (P < 0.05). Hydroxycholesterols 134-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 23674608-5 2013 The CYP3A4 induction could be detected even at the lowest dose of rifampicin (10 mg) via the estimated midazolam clearance, the 4beta-hydroxycholesterol ratio (both P < 0.01), and the 6beta-hydroxycortisol ratio (P < 0.05). 6 beta-hydroxycortisol 187-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 23674609-12 2013 In conclusion, silybin and isosilybin might be suitable candidates to design potent PXR antagonists to prevent drug-drug interactions via CYP3A4 in cancer patients. Silybin 15-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 23674609-12 2013 In conclusion, silybin and isosilybin might be suitable candidates to design potent PXR antagonists to prevent drug-drug interactions via CYP3A4 in cancer patients. isosilybin 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 23441978-1 2013 OBJECTIVES: Etravirine is a substrate and inducer of cytochrome P450 (CYP) 3A and a substrate and inhibitor of CYP2C9 and CYPC2C19. etravirine 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-77 23441978-2 2013 Darunavir/ritonavir is a substrate and inhibitor of CYP3A. Darunavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-57 23441978-2 2013 Darunavir/ritonavir is a substrate and inhibitor of CYP3A. Ritonavir 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-57 23441978-3 2013 Artemether and lumefantrine are primarily metabolized by CYP3A; artemether is also metabolized to a lesser extent by CYP2B6, CYP2C9 and CYP2C19. Artemether, Lumefantrine Drug Combination 0-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 23936594-2 2013 The study"s purpose was to investigate the potential predictive role of a CYP3A4 profile (CYP3A4*1B, rs2740574 and CYP3A4*22, rs35599367) in serous ovarian cancer patients treated with first-line chemotherapy (paclitaxel and cisplatin or carboplatin), after cytoreductive surgery. Paclitaxel 210-220 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 23936594-2 2013 The study"s purpose was to investigate the potential predictive role of a CYP3A4 profile (CYP3A4*1B, rs2740574 and CYP3A4*22, rs35599367) in serous ovarian cancer patients treated with first-line chemotherapy (paclitaxel and cisplatin or carboplatin), after cytoreductive surgery. Cisplatin 225-234 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 23936594-2 2013 The study"s purpose was to investigate the potential predictive role of a CYP3A4 profile (CYP3A4*1B, rs2740574 and CYP3A4*22, rs35599367) in serous ovarian cancer patients treated with first-line chemotherapy (paclitaxel and cisplatin or carboplatin), after cytoreductive surgery. Carboplatin 238-249 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 23879227-5 2013 TVR also inhibits hepatic CYP3A4 that are responsible for metabolizing methadone. Methadone 71-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 23720017-5 2013 For a theoretical drug metabolized 50% by each of CYP2D6 and CYP3A4 pathways at birth, co-administration of ketoconazole (3 mg/kg) resulted in a 1.65-fold difference between inhibited versus uninhibited AUC compared to 2.4-fold in 1 year olds and 3.2-fold in adults. Ketoconazole 108-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 23733622-0 2013 Cancer cachexia raises the plasma concentration of oxymorphone through the reduction of CYP3A but not CYP2D6 in oxycodone-treated patients. Oxymorphone 51-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-93 23733622-10 2013 In conclusion, cancer cachexia raised the plasma exposures of oxycodone and oxymorphone through the reduction of CYP3A but not CYP2D6. Oxycodone 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-118 23733622-10 2013 In conclusion, cancer cachexia raised the plasma exposures of oxycodone and oxymorphone through the reduction of CYP3A but not CYP2D6. Oxymorphone 76-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-118 23574377-1 2013 WHAT IS KNOWN AND OBJECTIVE: Tacrolimus has a narrow therapeutic index and shows large interindividual variations in pharmacokinetics, which may be partly explained by genetic variability in metabolic enzymes of the cytochrome P450 (mainly CYP3A4 and CYP3A5) and transport P-glycoprotein (encoded by the ABCB1 gene). Tacrolimus 29-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 240-246 23778326-0 2013 A search for new CYP3A4 variants as determinants of tacrolimus dose requirements in renal-transplanted patients. Tacrolimus 52-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 23930676-7 2013 CONCLUSION: The minor alleles of the PPARA rs4253728 and rs4823613 polymorphisms are associated with a better total and LDL-cholesterol-lowering response to simvastatin, possibly through influence on CYP3A4. Cholesterol 124-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 23930676-7 2013 CONCLUSION: The minor alleles of the PPARA rs4253728 and rs4823613 polymorphisms are associated with a better total and LDL-cholesterol-lowering response to simvastatin, possibly through influence on CYP3A4. Simvastatin 157-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 23778326-1 2013 The CYP3A5*3 and CYP3A4*1B alleles have been related with tacrolimus (Tac) dose requirements. Tacrolimus 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 23851904-7 2013 Administration of the CYP3A4 inducer rifampicin produced distinct differences in CYP3A4 and CYP11B1, CYP19A1, HSD11B, and HSD17B, which were indicated by their heat map-visualized steroid signatures. Rifampin 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 23545481-6 2013 Estimated CLint for phthalic acid production by hCYP3A4 was 24.5 muL nmol CYP(-1)min(-1) while it was continuously produced by rCYP2C6 and 3A2 via passive mechanism. phthalic acid 20-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-55 22634058-7 2013 CYP3A4 activity was moderately inhibited by fenvalerate and potently by alpha-cypermethrin. fenvalerate 44-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22634058-7 2013 CYP3A4 activity was moderately inhibited by fenvalerate and potently by alpha-cypermethrin. cypermethrin 72-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22634058-8 2013 The correlations between IC50 values obtained from the N-in-one and single substrate approaches were highly significant for CYP2Cs (r(2)=0.94), CYP3A4, omeprazole-sulfoxidation, (r(2)=0.89), followed by CYP1A2 and CYP2B6 (r(2)=0.82), and CYP2D6 (r(2)=0.80). n-in-one 55-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 23851904-7 2013 Administration of the CYP3A4 inducer rifampicin produced distinct differences in CYP3A4 and CYP11B1, CYP19A1, HSD11B, and HSD17B, which were indicated by their heat map-visualized steroid signatures. Rifampin 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 23851904-7 2013 Administration of the CYP3A4 inducer rifampicin produced distinct differences in CYP3A4 and CYP11B1, CYP19A1, HSD11B, and HSD17B, which were indicated by their heat map-visualized steroid signatures. Steroids 180-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 23851904-7 2013 Administration of the CYP3A4 inducer rifampicin produced distinct differences in CYP3A4 and CYP11B1, CYP19A1, HSD11B, and HSD17B, which were indicated by their heat map-visualized steroid signatures. Steroids 180-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 23851904-8 2013 CONCLUSIONS: This CYP-mediated steroid signature profile allows simultaneous assessment of CYP1A, CYP1B, CYP2C, CYP3A, CYP11B, CYP17A, CYP19A, and CYP21A in urine samples. Steroids 31-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-117 23922954-3 2013 In this descriptive study, correlations were examined between concentrations of tamoxifen metabolites and genotypes for CYP2D6, CYP3A4, CYP3A5, SULT1A1, SULT1A2 and SULT1E1 in 135 patients with estrogen receptor-positive breast cancer. Tamoxifen 80-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 23651100-0 2013 Pivotal role of P450-P450 interactions in CYP3A4 allostery: the case of alpha-naphthoflavone. alpha-naphthoflavone 72-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 23884207-0 2013 Development of a Physiologically-Based Pharmacokinetic Model for Sirolimus: Predicting Bioavailability Based on Intestinal CYP3A Content. Sirolimus 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-128 23808489-1 2013 Hydroisoindoline 2 has been previously identified as a potent, brain-penetrant NK1 receptor antagonist with a long duration of action and improved profile of CYP3A4 inhibition and induction compared to aprepitant. hydroisoindoline 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 23651100-1 2013 We investigated the relationship between oligomerization of CYP3A4 (cytochrome P450 3A4) and its response to ANF (alpha-naphthoflavone), a prototypical heterotropic activator. alpha-naphthoflavone 114-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 23651100-1 2013 We investigated the relationship between oligomerization of CYP3A4 (cytochrome P450 3A4) and its response to ANF (alpha-naphthoflavone), a prototypical heterotropic activator. alpha-naphthoflavone 114-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-87 23651100-2 2013 The addition of ANF resulted in over a 2-fold increase in the rate of CYP3A4-dependent debenzylation of 7-BFC [7-benzyloxy-4-(trifluoromethyl)coumarin] in HLM (human liver microsomes), but failed to produce activation in BD Supersomes or Baculosomes containing recombinant CYP3A4 and NADPH-CPR (cytochrome P450 reductase). 7-benzyloxy-4-trifluoromethylcoumarin 104-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 23688499-0 2013 Pregnane X receptor dependent up-regulation of CYP2C9 and CYP3A4 in tumor cells by antitumor acridine agents, C-1748 and C-1305, selectively diminished under hypoxia. Acridines 93-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 23651100-2 2013 The addition of ANF resulted in over a 2-fold increase in the rate of CYP3A4-dependent debenzylation of 7-BFC [7-benzyloxy-4-(trifluoromethyl)coumarin] in HLM (human liver microsomes), but failed to produce activation in BD Supersomes or Baculosomes containing recombinant CYP3A4 and NADPH-CPR (cytochrome P450 reductase). 7-benzyloxy-4-trifluoromethylcoumarin 104-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 273-279 23651100-2 2013 The addition of ANF resulted in over a 2-fold increase in the rate of CYP3A4-dependent debenzylation of 7-BFC [7-benzyloxy-4-(trifluoromethyl)coumarin] in HLM (human liver microsomes), but failed to produce activation in BD Supersomes or Baculosomes containing recombinant CYP3A4 and NADPH-CPR (cytochrome P450 reductase). 7-benzyloxy-4-trifluoromethylcoumarin 111-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 23688499-0 2013 Pregnane X receptor dependent up-regulation of CYP2C9 and CYP3A4 in tumor cells by antitumor acridine agents, C-1748 and C-1305, selectively diminished under hypoxia. 9-(2'-hydroxyethylamino)-4-methyl-1-nitroacridine 110-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 23688499-0 2013 Pregnane X receptor dependent up-regulation of CYP2C9 and CYP3A4 in tumor cells by antitumor acridine agents, C-1748 and C-1305, selectively diminished under hypoxia. C 1305 121-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 23688499-6 2013 C-1748-mediated CYP3A4 and CYP2C9 mRNA induction equal to rifampicin occurred at extremely low concentrations (0.001 and 0.01muM), whereas 10muM C-1305 induced three-times higher CYP3A4 and CYP2C9 mRNA levels than rifampicin did. 9-(2'-hydroxyethylamino)-4-methyl-1-nitroacridine 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 23688499-6 2013 C-1748-mediated CYP3A4 and CYP2C9 mRNA induction equal to rifampicin occurred at extremely low concentrations (0.001 and 0.01muM), whereas 10muM C-1305 induced three-times higher CYP3A4 and CYP2C9 mRNA levels than rifampicin did. 9-(2'-hydroxyethylamino)-4-methyl-1-nitroacridine 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 23651100-2 2013 The addition of ANF resulted in over a 2-fold increase in the rate of CYP3A4-dependent debenzylation of 7-BFC [7-benzyloxy-4-(trifluoromethyl)coumarin] in HLM (human liver microsomes), but failed to produce activation in BD Supersomes or Baculosomes containing recombinant CYP3A4 and NADPH-CPR (cytochrome P450 reductase). baculosomes 238-249 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 23746300-0 2013 Dissecting cytochrome P450 3A4-ligand interactions using ritonavir analogues. Ritonavir 57-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-30 23751364-5 2013 Consequently, slight enantioselectivity was found for the CYP3A4 metabolism of verapamil. Verapamil 79-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 23847265-1 2013 OBJECTIVE: Clarithromycin strongly inhibits enzyme cytochrome P450 3A4, preventing the metabolism of some other drugs, while azithromycin is a weak inhibitor. Clarithromycin 11-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-70 23746300-1 2013 Cytochrome P450 3A4 (CYP3A4) inhibitors ritonavir and cobicistat, currently administered to HIV patients as pharmacoenhancers, were designed on the basis of the chemical structure/activity relationships rather than the CYP3A4 crystal structure. Ritonavir 40-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 23746300-1 2013 Cytochrome P450 3A4 (CYP3A4) inhibitors ritonavir and cobicistat, currently administered to HIV patients as pharmacoenhancers, were designed on the basis of the chemical structure/activity relationships rather than the CYP3A4 crystal structure. Ritonavir 40-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 23746300-1 2013 Cytochrome P450 3A4 (CYP3A4) inhibitors ritonavir and cobicistat, currently administered to HIV patients as pharmacoenhancers, were designed on the basis of the chemical structure/activity relationships rather than the CYP3A4 crystal structure. Cobicistat 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 23746300-1 2013 Cytochrome P450 3A4 (CYP3A4) inhibitors ritonavir and cobicistat, currently administered to HIV patients as pharmacoenhancers, were designed on the basis of the chemical structure/activity relationships rather than the CYP3A4 crystal structure. Cobicistat 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 23746300-1 2013 Cytochrome P450 3A4 (CYP3A4) inhibitors ritonavir and cobicistat, currently administered to HIV patients as pharmacoenhancers, were designed on the basis of the chemical structure/activity relationships rather than the CYP3A4 crystal structure. Cobicistat 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 23733841-16 2013 CONCLUSIONS: Methadone caused concentration-dependent autoinduction of methadone N-demethylation in human hepatocytes, related to induction of CYP2B6 and CYP3A4 mRNA expression, protein expression, and catalytic activity. Methadone 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 21790905-3 2013 Methadone metabolism is attributed primarily to cytochrome P450 enzymes CYP3A4, CYP2B6 and CYP2D6. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 23733841-3 2013 Although methadone N-demethylation is catalyzed in vitro by cytochrome P4502B6 (CYP2B6) and CYP3A4, and clearance in vivo depends on CYP2B6, mechanism(s) of autoinduction are incompletely understood. Methadone 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 23774830-6 2013 The enzyme kinetic studies showed that the initial metabolic step in humans, the N-deethylation, was catalyzed by CYP2B6 and CYP3A4. Nitrogen 81-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 23673446-1 2013 PURPOSE: Sorafenib is primarily metabolized in the liver, by CYP3A4-mediated oxidation and UGT1A9-mediated glucuronidation. Sorafenib 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 23673446-3 2013 Here, we report a pharmacokinetic interaction between sorafenib and the CYP3A4 inducer prednisolone in a patient with hepatocellular carcinoma (HCC). Sorafenib 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 23790595-7 2013 Importantly, we show that by better understanding the effect of clinical variables such as age, renal function, dosing interval, and drug metabolism (CYP3A4) and transport (P-glycoprotein), we might be able to better predict the risk for sub- and supratherapeutic anticoagulation response and individualize OAC selection and dosing. SDZ 33-243 307-310 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 23673446-3 2013 Here, we report a pharmacokinetic interaction between sorafenib and the CYP3A4 inducer prednisolone in a patient with hepatocellular carcinoma (HCC). Prednisolone 87-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 23512668-2 2013 In this analysis we studied the maturation of in vivo CYP3A-mediated clearance of midazolam, as model drug, from preterm neonates of 26 weeks gestational age (GA) to adults. Midazolam 82-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-59 23620487-0 2013 Inhibition of CYP2C19 and CYP3A4 by omeprazole metabolites and their contribution to drug-drug interactions. Omeprazole 36-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 23870610-1 2013 BACKGROUND: In vitro studies have demonstrated that ticagrelor, an oral antiplatelet agent, is a substrate, activator, and inhibitor of cytochrome P450 (CYP) 3A. Ticagrelor 52-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-160 23584886-0 2013 Optimization of drug-drug interaction study design: comparison of minimal physiologically based pharmacokinetic models on prediction of CYP3A inhibition by ketoconazole. Ketoconazole 156-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-141 23584886-1 2013 Ketoconazole is a potent CYP3A inhibitor used to assess the contribution of CYP3A to drug clearance and quantify the increase in drug exposure due to a strong inhibitor. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-30 23553423-2 2013 Telaprevir is well absorbed with fatty food, moderately protein bound (59-76 %) with a large volume of distribution (~252 L), primarily metabolized by cytochrome P450 (CYP) 3A4 and P-glycoprotein, and is largely excreted into feces. telaprevir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-176 23553423-6 2013 Telaprevir is a substrate and/or inhibitor of CYP3A4 and P-glycoprotein, and drug-drug interaction studies in humans have focused on these pathways. telaprevir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 23620487-4 2013 In addition omeprazole, omeprazole sulfone, and 5"-O-desmethylomeprazole were time dependent inhibitors (TDI) of CYP2C19, whereas omeprazole and 5"-O-desmethylomeprazole were found to be TDIs of CYP3A4. omeprazole sulfone 24-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 23584886-1 2013 Ketoconazole is a potent CYP3A inhibitor used to assess the contribution of CYP3A to drug clearance and quantify the increase in drug exposure due to a strong inhibitor. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 23620487-1 2013 The aim of this study was to evaluate the contribution of metabolites to drug-drug interactions (DDI) using the inhibition of CYP2C19 and CYP3A4 by omeprazole and its metabolites as a model. Omeprazole 148-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 23584886-2 2013 Physiologically based pharmacokinetic (PBPK) models have been used to evaluate treatment regimens resulting in maximal CYP3A inhibition by ketoconazole but have reached different conclusions. Ketoconazole 139-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-124 23584886-6 2013 On the basis of model 1, ketoconazole (400 mg QD) for at least 3 days and substrate administration within 2 hours is required for maximal CYP3A inhibition. Ketoconazole 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-143 23584886-7 2013 Ketoconazole treatment regimens that use 200 mg BID underestimate the systemic fraction metabolized by CYP3A (0.86 versus 0.90) for midazolam. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 23584886-7 2013 Ketoconazole treatment regimens that use 200 mg BID underestimate the systemic fraction metabolized by CYP3A (0.86 versus 0.90) for midazolam. Midazolam 132-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 23620487-4 2013 In addition omeprazole, omeprazole sulfone, and 5"-O-desmethylomeprazole were time dependent inhibitors (TDI) of CYP2C19, whereas omeprazole and 5"-O-desmethylomeprazole were found to be TDIs of CYP3A4. 5"-o-desmethylomeprazole 48-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 23620487-4 2013 In addition omeprazole, omeprazole sulfone, and 5"-O-desmethylomeprazole were time dependent inhibitors (TDI) of CYP2C19, whereas omeprazole and 5"-O-desmethylomeprazole were found to be TDIs of CYP3A4. 5"-o-desmethylomeprazole 145-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 23620487-6 2013 Identifying omeprazole as a TDI of both CYP2C19 and CYP3A4 was the most important factor in DDI risk assessment. Omeprazole 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 23620487-8 2013 On the basis of inactivation data, CYP2C19 and CYP3A4 inhibition by omeprazole would be sufficient to identify risk, but metabolites were predicted to contribute 30-63% to the in vivo hepatic interactions. Omeprazole 68-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 23743505-10 2013 With a panel of recombinant human cytochrome P450s (CYPs), CYP2C18 and CYP3A4 produced the most noroxycodone, whereas CYP2D6 produced the most oxymorphone. noroxycodone 96-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 24063896-7 2013 Because it is a substrate and potent inhibitor of CYP3A4 and glycoprotein P, telaprevir has multiple drug-drug interactions. telaprevir 77-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 23565891-6 2013 Evidence supporting the effect of substrates, inhibitor or inducers for drug specific metabolizing enzymes in anti-Parkinson"s disease drug response includes CYP1A2 in the response to ropinirole and rasagiline, and CYP3A4 in the response to bromocriptine, lisuride, pergolide and cabergoline. Bromocriptine 241-254 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-221 22271348-11 2013 A comparison of rat CYP3A1 with human CYP3A4 suggests that cysteines 64 and 378 reside along the substrate channel, remote from the active site. Cysteine 59-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 23743505-10 2013 With a panel of recombinant human cytochrome P450s (CYPs), CYP2C18 and CYP3A4 produced the most noroxycodone, whereas CYP2D6 produced the most oxymorphone. Oxymorphone 143-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 23670789-2 2013 This open-label, fixed-sequence, 3-period study was intended to evaluate the potential of anacetrapib to be a victim of OATP1B1/3 inhibition and strong CYP3A induction using acute and chronic dosing of rifampin, respectively, as a probe. anacetrapib 90-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-157 22985909-2 2013 This review focuses on two aspects: regulation of CYP3A4 expression by vitamin D and metabolism of vitamin D by CYP3A4. Vitamin D 71-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 22985909-2 2013 This review focuses on two aspects: regulation of CYP3A4 expression by vitamin D and metabolism of vitamin D by CYP3A4. Vitamin D 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 22985909-4 2013 The interplay between vitamin D and CYP3A4 provides new insights into our understanding of how enzyme induction can contribute to vitamin D deficiency. Vitamin D 130-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 23778904-1 2013 BACKGROUND: Clarithromycin and erythromycin, but not azithromycin, inhibit cytochrome P450 isoenzyme 3A4 (CYP3A4), and inhibition increases blood concentrations of statins that are metabolized by CYP3A4. Clarithromycin 12-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-104 23837477-0 2013 CYP3A4*22 and CYP3A combined genotypes both correlate with tacrolimus disposition in pediatric heart transplant recipients. Tacrolimus 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23837477-0 2013 CYP3A4*22 and CYP3A combined genotypes both correlate with tacrolimus disposition in pediatric heart transplant recipients. Tacrolimus 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 23837477-1 2013 BACKGROUND: Tacrolimus metabolism depends on CYP3A4 and CYP3A5. Tacrolimus 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 23837477-2 2013 We aimed to determine the relationship between the CYP3A4*22 polymorphism and combined CYP3A genotypes with tacrolimus disposition in pediatric heart transplant recipients. Tacrolimus 108-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 23837477-2 2013 We aimed to determine the relationship between the CYP3A4*22 polymorphism and combined CYP3A genotypes with tacrolimus disposition in pediatric heart transplant recipients. Tacrolimus 108-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 23837477-6 2013 RESULTS: CYP3A4*22 carriers needed 30% less tacrolimus (p = 0.016) to reach similar target concentrations compared with CYP3A4*1/*1 (n = 56) carriers. Tacrolimus 44-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 23837477-7 2013 Poor CYP3A metabolizers required 17% (p = 0.023) less tacrolimus than intermediate and 48% less (p < 0.0001) than extensive metabolizers. Tacrolimus 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 5-10 23837477-9 2013 CONCLUSION: Analysis of CYP3A4*22, either alone or in combination with CYP3A5*3, may help towards individualization of tacrolimus therapy in pediatric heart transplant patients. Tacrolimus 119-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 23252722-4 2013 Based on these results, it is likely that the primary factor responsible for the low oral bioavailability of doxorubicin is the limited intestinal absorption, rather than the CYP3A4-mediated first-pass metabolism. Doxorubicin 109-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 23252722-9 2013 Taken together, the present study demonstrated that the limited and paracellular intestinal absorption of doxorubicin was a major factor responsible for its low oral bioavailability, restricting the role of CYP3A4-mediated first-pass metabolism and P-gp-mediated efflux. Doxorubicin 106-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 23278282-8 2013 CYP3A4*1B carriers and CYP3A5 expressers, independently or when assessed as a combined CYP3A4-3A5 genotype, had significantly lower dose-normalized pre-dose (C0/dose) and 2-hour post-dose (C2/dose) concentrations of tacrolimus and metabolites. Tacrolimus 216-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-9 23278282-8 2013 CYP3A4*1B carriers and CYP3A5 expressers, independently or when assessed as a combined CYP3A4-3A5 genotype, had significantly lower dose-normalized pre-dose (C0/dose) and 2-hour post-dose (C2/dose) concentrations of tacrolimus and metabolites. Tacrolimus 216-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23278282-11 2013 Genetic polymorphism of CYP3A5 or CYP3A4 influence tacrolimus or metabolites dose-normalized concentrations but not metabolite to parent concentration ratios. Tacrolimus 51-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 23640974-0 2013 CYP3A4*22 genotype and systemic exposure affect paclitaxel-induced neurotoxicity. Paclitaxel 48-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23640974-6 2013 Genetic variants of paclitaxel pharmacokinetics tested were CYP3A4*22, CYP2C8*3, CYP2C8*4, and ABCB1 3435 C>T. The association between CYP3A4*22 and neurotoxicity observed in the exploratory cohort was validated in an independent patient cohort (n = 239). Paclitaxel 20-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 23640974-6 2013 Genetic variants of paclitaxel pharmacokinetics tested were CYP3A4*22, CYP2C8*3, CYP2C8*4, and ABCB1 3435 C>T. The association between CYP3A4*22 and neurotoxicity observed in the exploratory cohort was validated in an independent patient cohort (n = 239). Paclitaxel 20-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 23640974-13 2013 In this study, female CYP3A4*22 carriers had increased risk of developing severe neurotoxicity during paclitaxel therapy. Paclitaxel 102-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 23778904-1 2013 BACKGROUND: Clarithromycin and erythromycin, but not azithromycin, inhibit cytochrome P450 isoenzyme 3A4 (CYP3A4), and inhibition increases blood concentrations of statins that are metabolized by CYP3A4. Clarithromycin 12-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 23778904-1 2013 BACKGROUND: Clarithromycin and erythromycin, but not azithromycin, inhibit cytochrome P450 isoenzyme 3A4 (CYP3A4), and inhibition increases blood concentrations of statins that are metabolized by CYP3A4. Clarithromycin 12-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 196-202 23778904-1 2013 BACKGROUND: Clarithromycin and erythromycin, but not azithromycin, inhibit cytochrome P450 isoenzyme 3A4 (CYP3A4), and inhibition increases blood concentrations of statins that are metabolized by CYP3A4. Erythromycin 31-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-104 23778904-1 2013 BACKGROUND: Clarithromycin and erythromycin, but not azithromycin, inhibit cytochrome P450 isoenzyme 3A4 (CYP3A4), and inhibition increases blood concentrations of statins that are metabolized by CYP3A4. Erythromycin 31-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 23778904-1 2013 BACKGROUND: Clarithromycin and erythromycin, but not azithromycin, inhibit cytochrome P450 isoenzyme 3A4 (CYP3A4), and inhibition increases blood concentrations of statins that are metabolized by CYP3A4. Erythromycin 31-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 196-202 23778904-11 2013 CONCLUSION: In older adults, coprescription of clarithromycin or erythromycin with a statin that is metabolized by CYP3A4 increases the risk for statin toxicity. Clarithromycin 47-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 23778904-11 2013 CONCLUSION: In older adults, coprescription of clarithromycin or erythromycin with a statin that is metabolized by CYP3A4 increases the risk for statin toxicity. Erythromycin 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 23686600-4 2013 Crizotinib is metabolized and excreted after O-dealkylation by cytochrome P-450 (CYP) isoenzyme 3A4/5; as crizotinib is also an inhibitor of CYP3A4/5, its use entails a high potential for drug interactions, including confirmed interactions with ketoconazole and rifampin that can alter crizotinib pharmacokinetics. Crizotinib 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 23686600-4 2013 Crizotinib is metabolized and excreted after O-dealkylation by cytochrome P-450 (CYP) isoenzyme 3A4/5; as crizotinib is also an inhibitor of CYP3A4/5, its use entails a high potential for drug interactions, including confirmed interactions with ketoconazole and rifampin that can alter crizotinib pharmacokinetics. Crizotinib 106-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 23583259-8 2013 Rilpivirine, etravirine, and efavirenz, but not nevirapine or delavirdine, were identified as agonists of hPXR, as assessed in mechanistic experiments, and inducers of CYP3A4, as determined in primary cultures of human hepatocytes. etravirine 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 23604525-6 2013 Clomiphene, tamoxifen and toremifene were biotransformed to 22, 23 and 18 metabolites respectively, these phase I reactions being catalyzed mainly by CYP3A4 and CYP2D6 isoforms and, to a lesser degree, by CYP3A5, CYP2B6, CYP2C9, CYP2C19 isoforms. Clomiphene 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 23604525-6 2013 Clomiphene, tamoxifen and toremifene were biotransformed to 22, 23 and 18 metabolites respectively, these phase I reactions being catalyzed mainly by CYP3A4 and CYP2D6 isoforms and, to a lesser degree, by CYP3A5, CYP2B6, CYP2C9, CYP2C19 isoforms. Tamoxifen 12-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 23604525-6 2013 Clomiphene, tamoxifen and toremifene were biotransformed to 22, 23 and 18 metabolites respectively, these phase I reactions being catalyzed mainly by CYP3A4 and CYP2D6 isoforms and, to a lesser degree, by CYP3A5, CYP2B6, CYP2C9, CYP2C19 isoforms. Toremifene 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 23583259-6 2013 Rilpivirine, etravirine, and efavirenz, but not nevirapine or delavirdine, increased hPXR target gene (CYP3A4) expression in primary cultures of human hepatocytes. Rilpivirine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 23571542-3 2013 Due to EFV"s induction of cytochrome P450 3A4, the metabolic enzyme responsible for BDQ biotransformation, the drugs are expected to interact. bedaquiline 84-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-45 23583259-6 2013 Rilpivirine, etravirine, and efavirenz, but not nevirapine or delavirdine, increased hPXR target gene (CYP3A4) expression in primary cultures of human hepatocytes. etravirine 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 23583259-8 2013 Rilpivirine, etravirine, and efavirenz, but not nevirapine or delavirdine, were identified as agonists of hPXR, as assessed in mechanistic experiments, and inducers of CYP3A4, as determined in primary cultures of human hepatocytes. efavirenz 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 23491640-10 2013 Finally, analysis of the frontal cortex of chronic alcohol abusers revealed elevated expression of CYP3A4 in microsomal but not mitochondrial fractions; CYP3A5 expression was unchanged. Alcohols 51-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 23583259-6 2013 Rilpivirine, etravirine, and efavirenz, but not nevirapine or delavirdine, increased hPXR target gene (CYP3A4) expression in primary cultures of human hepatocytes. efavirenz 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 23583259-8 2013 Rilpivirine, etravirine, and efavirenz, but not nevirapine or delavirdine, were identified as agonists of hPXR, as assessed in mechanistic experiments, and inducers of CYP3A4, as determined in primary cultures of human hepatocytes. Rilpivirine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 23116485-1 2013 AIM: To investigate the effects of the cytochrome P450 3A4 (CYP3A4) inhibitor ketoconazole on the pharmacokinetics (PK) and pharmacodynamics of fluticasone furoate (FF) and vilanterol trifenatate (VI). Ketoconazole 78-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 23116485-1 2013 AIM: To investigate the effects of the cytochrome P450 3A4 (CYP3A4) inhibitor ketoconazole on the pharmacokinetics (PK) and pharmacodynamics of fluticasone furoate (FF) and vilanterol trifenatate (VI). fluticasone furoate 144-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-58 23116485-1 2013 AIM: To investigate the effects of the cytochrome P450 3A4 (CYP3A4) inhibitor ketoconazole on the pharmacokinetics (PK) and pharmacodynamics of fluticasone furoate (FF) and vilanterol trifenatate (VI). fluticasone furoate 144-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 23116485-12 2013 Co-administration of FF/VI with strong CYP3A4 inhibitors has the potential to increase systemic exposure to both fluticasone furoate and vilanterol, which could lead to an increase in the potential for adverse reactions. fluticasone furoate 113-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 23116485-12 2013 Co-administration of FF/VI with strong CYP3A4 inhibitors has the potential to increase systemic exposure to both fluticasone furoate and vilanterol, which could lead to an increase in the potential for adverse reactions. vilanterol 137-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 23163400-0 2013 The CYP3A4*22 allele affects the predictive value of a pharmacogenetic algorithm predicting tacrolimus predose concentrations. Tacrolimus 92-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 23636448-1 2013 PURPOSE: The metabolism of pazopanib is primarily mediated by CYP3A4. pazopanib 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 23636448-3 2013 This study evaluated the effect of a potent CYP3A4 inhibitor, ketoconazole, and the proton pump inhibitor esomeprazole on the pharmacokinetics and safety of pazopanib and its metabolites. pazopanib 157-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 23636448-10 2013 CONCLUSIONS: Concomitant use of pazopanib with a strong CYP3A4 inhibitor should be avoided. pazopanib 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 23509226-13 2013 Apatinib was metabolized primarily by CYP3A4/5 and, to a lesser extent, by CYP2D6, CYP2C9, and CYP2E1. apatinib 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 23530020-0 2013 Prilocaine- and lidocaine-induced methemoglobinemia is caused by human carboxylesterase-, CYP2E1-, and CYP3A4-mediated metabolic activation. Prilocaine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 23530020-0 2013 Prilocaine- and lidocaine-induced methemoglobinemia is caused by human carboxylesterase-, CYP2E1-, and CYP3A4-mediated metabolic activation. Lidocaine 16-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 23550066-1 2013 Ketamine is primarily metabolized to norketamine by hepatic CYP2B6 and CYP3A4-mediated N-demethylation. Ketamine 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 23530020-11 2013 Collectively, we found that the metabolites produced by human CES-, CYP2E1-, and CYP3A4-mediated metabolism were involved in prilocaine- and lidocaine-induced methemoglobinemia. Prilocaine 125-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 23530020-11 2013 Collectively, we found that the metabolites produced by human CES-, CYP2E1-, and CYP3A4-mediated metabolism were involved in prilocaine- and lidocaine-induced methemoglobinemia. Lidocaine 141-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 23550066-1 2013 Ketamine is primarily metabolized to norketamine by hepatic CYP2B6 and CYP3A4-mediated N-demethylation. norketamine 37-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 23550066-1 2013 Ketamine is primarily metabolized to norketamine by hepatic CYP2B6 and CYP3A4-mediated N-demethylation. Nitrogen 87-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 23242004-1 2013 PURPOSE: Tramadol is mainly metabolized by the cytochrome P450 (CYP) 2D6, CYP2B6 and CYP3A4 enzymes. Tramadol 9-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 24252527-4 2013 Rilpivirine is metabolized by cytochrome P450 (CYP) 3A and consequently potential interactions should be considered when it is administered with P450 (CYP) 3A inducers or inhibitors. Rilpivirine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-54 23511711-0 2013 A nanogram dose of the CYP3A probe substrate midazolam to evaluate drug interactions. Midazolam 45-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-28 23511711-1 2013 The objective of the study was to establish an in vivo method for assessing cytochrome P450 3A (CYP3A) activity using therapeutically inert nanogram doses of midazolam. Midazolam 158-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-94 23334403-0 2013 Almorexant effects on CYP3A4 activity studied by its simultaneous and time-separated administration with simvastatin and atorvastatin. Simvastatin 105-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 23511711-1 2013 The objective of the study was to establish an in vivo method for assessing cytochrome P450 3A (CYP3A) activity using therapeutically inert nanogram doses of midazolam. Midazolam 158-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-101 23511711-3 2013 We then evaluated the interactions with the CYP3A inhibitor ketoconazole (400 mg q.d.) Ketoconazole 60-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-49 23511711-9 2013 This is the first study showing that midazolam pharmacokinetics is linear in a 30,000-fold concentration range, and therefore that nano- and microgram doses of midazolam can reliably predict the pharmacokinetics of midazolam in therapeutic doses and can be used to assess CYP3A activity even in the presence of strong CYP3A inhibitors. Midazolam 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 272-277 23511711-9 2013 This is the first study showing that midazolam pharmacokinetics is linear in a 30,000-fold concentration range, and therefore that nano- and microgram doses of midazolam can reliably predict the pharmacokinetics of midazolam in therapeutic doses and can be used to assess CYP3A activity even in the presence of strong CYP3A inhibitors. Midazolam 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 318-323 23511711-9 2013 This is the first study showing that midazolam pharmacokinetics is linear in a 30,000-fold concentration range, and therefore that nano- and microgram doses of midazolam can reliably predict the pharmacokinetics of midazolam in therapeutic doses and can be used to assess CYP3A activity even in the presence of strong CYP3A inhibitors. Midazolam 160-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 272-277 23511711-9 2013 This is the first study showing that midazolam pharmacokinetics is linear in a 30,000-fold concentration range, and therefore that nano- and microgram doses of midazolam can reliably predict the pharmacokinetics of midazolam in therapeutic doses and can be used to assess CYP3A activity even in the presence of strong CYP3A inhibitors. Midazolam 160-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 318-323 24252529-5 2013 Coadministration of RPV with drugs that increase gastric pH, such as omeprazole, or those inducing CYP3A4, such as rifampicin, can significantly reduce RPV concentrations and is contraindicated. Rifampin 115-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 24252529-6 2013 The concomitant use of RPV with a CYP3A4 inhibitor (such as clarithromycin) can increase RPV concentrations. Clarithromycin 60-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 23511711-9 2013 This is the first study showing that midazolam pharmacokinetics is linear in a 30,000-fold concentration range, and therefore that nano- and microgram doses of midazolam can reliably predict the pharmacokinetics of midazolam in therapeutic doses and can be used to assess CYP3A activity even in the presence of strong CYP3A inhibitors. Midazolam 160-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 272-277 23334403-0 2013 Almorexant effects on CYP3A4 activity studied by its simultaneous and time-separated administration with simvastatin and atorvastatin. Atorvastatin 121-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 23511711-9 2013 This is the first study showing that midazolam pharmacokinetics is linear in a 30,000-fold concentration range, and therefore that nano- and microgram doses of midazolam can reliably predict the pharmacokinetics of midazolam in therapeutic doses and can be used to assess CYP3A activity even in the presence of strong CYP3A inhibitors. Midazolam 160-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 318-323 23334403-10 2013 This suggests that the observed interaction of almorexant with simvastatin is mainly caused by intestinal CYP3A4 inhibition, whereas the interaction with atorvastatin is more due to hepatic CYP3A4 inhibition. Simvastatin 63-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 22996801-3 2013 Vinflunine is metabolized through CYP3A4 and mainly eliminated via the feces. vinflunine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 23557867-0 2013 CYP3A4/5 polymorphisms affect the blood level of cyclosporine and tacrolimus in Chinese renal transplant recipients. Cyclosporine 49-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23557867-0 2013 CYP3A4/5 polymorphisms affect the blood level of cyclosporine and tacrolimus in Chinese renal transplant recipients. Tacrolimus 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23557867-2 2013 We approached the effect of the CYP3A4*18B and CYP3A5*3 polymorphisms and haplotypes on the whole blood cyclosporine or tacrolimus concentration in Chinese renal transplant patients during the first month after transplantation. Cyclosporine 104-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 23557867-5 2013 RESULTS: Both CYP3A4*18B and CYP3A5*3 polymorphisms affected the tacrolimus dose-adjusted trough concentration (C0/D). Tacrolimus 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 23557867-10 2013 CONCLUSIONS: Genetic polymorphisms of CYP3A5*3 and CYP3A4*18B may be partly responsible in large interindividual variability of cyclosporine and tacrolimus blood levels in Chinese renal transplant patients during the first month after transplantation. Cyclosporine 128-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 23557867-10 2013 CONCLUSIONS: Genetic polymorphisms of CYP3A5*3 and CYP3A4*18B may be partly responsible in large interindividual variability of cyclosporine and tacrolimus blood levels in Chinese renal transplant patients during the first month after transplantation. Tacrolimus 145-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 23557867-11 2013 A patient carried combined genotype of CYP3A4*1/*1-CYP3A5* 3/*3 might require lower tacrolimus doses to achieve target concentration levels. Tacrolimus 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 23500771-4 2013 The results showed that SAG was a potent noncompetitive inhibitor of CYP2C8 activity (Ki=8.9 muM), and competitive inhibitor of CYP1A2, CYP2C9 and CYP3A4 activities (Ki=2.7, 3.8 and 2.0 muM, respectively). sanguinarine 24-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 23500771-5 2013 Furthermore, SAG exhibited time- and NADPH-dependent inhibition towards CYP1A2 and CYP3A4 with KI/kinact values of 13.3/0.087 and 5.58/0.029 min(-1) muM(-1), respectively. sanguinarine 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 23500771-5 2013 Furthermore, SAG exhibited time- and NADPH-dependent inhibition towards CYP1A2 and CYP3A4 with KI/kinact values of 13.3/0.087 and 5.58/0.029 min(-1) muM(-1), respectively. NADP 37-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 23500771-7 2013 In vitro-in vivo extrapolation (IV-IVE) from HLM data showed that more than 35.9% of CYP1A2, CYP2C9, CYP2C8 and CYP3A4 activities in vivo could be inhibited by SAG, suggesting that harmful DDIs could occur when SAG or its medical preparations are co-administered with drugs primarily cleared by these CYP isoforms. sanguinarine 160-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 23500771-7 2013 In vitro-in vivo extrapolation (IV-IVE) from HLM data showed that more than 35.9% of CYP1A2, CYP2C9, CYP2C8 and CYP3A4 activities in vivo could be inhibited by SAG, suggesting that harmful DDIs could occur when SAG or its medical preparations are co-administered with drugs primarily cleared by these CYP isoforms. sanguinarine 211-214 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 23585187-3 2013 The effect of LCL161 on CYP3A4/5 (CYP3A) activity was investigated in vitro and in a clinical study. LCL161 14-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-32 23585187-3 2013 The effect of LCL161 on CYP3A4/5 (CYP3A) activity was investigated in vitro and in a clinical study. LCL161 14-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 23290512-0 2013 Fluticasone propionate pharmacogenetics: CYP3A4*22 polymorphism and pediatric asthma control. Fluticasone 0-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 23454087-7 2013 The selective CYP3A inhibitor ketoconazole induced greater DA relaxation than cimetidine, whereas famotidine and other H2 antagonists with less CYP inhibitory effects caused less dilation. Ketoconazole 30-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 23562850-2 2013 We have previously shown that silencing mediator for retinoid and thyroid receptors (SMRT) interacts with SXR even in the presence of rifampicin on cytochrome P450 monooxygenase 3A4 (CYP3A4) promoter in HepG2 cells. Rifampin 134-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-181 23510058-0 2013 Evaluation of the effects of single-nucleotide polymorphisms in CYP3A4 and CYP4F2 on stable phenprocoumon and acenocoumarol maintenance doses. single-nucleotide 29-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 23510058-0 2013 Evaluation of the effects of single-nucleotide polymorphisms in CYP3A4 and CYP4F2 on stable phenprocoumon and acenocoumarol maintenance doses. Phenprocoumon 92-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 23384967-2 2013 CYP3A4 enzyme is essential in the hydroxylation of steroid hormones and is regulated by PXR. Steroids 51-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23384967-4 2013 Both BPA and DES (10-50muM) caused a significant activation of the CYP3A4 promoter via the PXR in the DPX2 human hepatoma cell line. bisphenol A 5-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 23666577-4 2013 O-demethylation is catalyzed by the highly polymorphic CYP2D6 and N-demethylation by several enzymes, CYP2C19, CYP2C9, and CYP3A4. Nitrogen 66-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 23256623-8 2013 CYP1A2 was primarily involved in hydroxylation of the quinolone moiety (M1 and M3), while CYP3A4 was mainly responsible for hydroxylation of the quinazoline moiety of luotonin A (M2 and M4) in human liver microsomes. Quinazolines 145-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 23256623-8 2013 CYP1A2 was primarily involved in hydroxylation of the quinolone moiety (M1 and M3), while CYP3A4 was mainly responsible for hydroxylation of the quinazoline moiety of luotonin A (M2 and M4) in human liver microsomes. luotonin A 167-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 23565802-0 2013 Fluoxetine inhibition of CYP3A4 potentiating adrenal suppression and peptic ulcer disease from intra-articular triamcinolone injections. Fluoxetine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 23565802-0 2013 Fluoxetine inhibition of CYP3A4 potentiating adrenal suppression and peptic ulcer disease from intra-articular triamcinolone injections. Triamcinolone 111-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 23384967-4 2013 Both BPA and DES (10-50muM) caused a significant activation of the CYP3A4 promoter via the PXR in the DPX2 human hepatoma cell line. Diethylstilbestrol 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 23384967-6 2013 BPA and DES treated DPX2 cells demonstrated increased expression of CYP3A4 mRNA, and increased enzyme activity. bisphenol A 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 23384967-7 2013 In summary, BPA, in concentrations relevant to current safety levels of human exposure, activates the human PXR and demonstrates an increase in CYP3A4 mRNA expression and enzyme activity. bisphenol A 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 23750331-10 2013 Evaluation of the PKs of THC/CBD spray alone and in combination with CYP450 inhibitors/inducers suggests that all analytes are substrates for the isoenzyme CYP3A4, but not CYP2C19. Dronabinol 25-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 23750331-10 2013 Evaluation of the PKs of THC/CBD spray alone and in combination with CYP450 inhibitors/inducers suggests that all analytes are substrates for the isoenzyme CYP3A4, but not CYP2C19. Cannabidiol 29-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 23387445-0 2013 Phase I and II metabolism and MRP2-mediated export of bosentan in a MDCKII-OATP1B1-CYP3A4-UGT1A1-MRP2 quadruple-transfected cell line. Bosentan 54-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 23090875-3 2013 Unlike paclitaxel, docetaxel is extensively metabolized by CYP3A4 and its oral bioavailability can be enhanced in mice and humans by coadministration of the potent CYP3A inhibitor ritonavir. Ritonavir 180-189 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 23090875-13 2013 Mouse liver microsomes metabolized paclitaxel far less efficiently than human or CYP3A4-transgenic liver microsomes, revealing much lower efficiency of paclitaxel metabolism by mouse than by human CYP3As. Paclitaxel 152-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 23090875-14 2013 Accordingly, ritonavir could enhance the oral bioavailability of paclitaxel in CYP3A4-humanized mice, despite the fact that these mice are P-gp-proficient. Ritonavir 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 23090875-14 2013 Accordingly, ritonavir could enhance the oral bioavailability of paclitaxel in CYP3A4-humanized mice, despite the fact that these mice are P-gp-proficient. Paclitaxel 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 23090875-15 2013 Our results show that CYP3A4 inhibition most likely underlies the boosting effect of ritonavir on oral paclitaxel bioavailability in humans. Ritonavir 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 23090875-15 2013 Our results show that CYP3A4 inhibition most likely underlies the boosting effect of ritonavir on oral paclitaxel bioavailability in humans. Paclitaxel 103-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 23090875-16 2013 Furthermore, CYP3A4-humanized mice allow improved understanding of CYP3A4-mediated paclitaxel metabolism in humans. Paclitaxel 83-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 23090875-16 2013 Furthermore, CYP3A4-humanized mice allow improved understanding of CYP3A4-mediated paclitaxel metabolism in humans. Paclitaxel 83-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 23586711-0 2013 Pyridine-substituted desoxyritonavir is a more potent inhibitor of cytochrome P450 3A4 than ritonavir. pyridine 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-86 23586711-0 2013 Pyridine-substituted desoxyritonavir is a more potent inhibitor of cytochrome P450 3A4 than ritonavir. desoxyritonavir 21-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-86 23586711-0 2013 Pyridine-substituted desoxyritonavir is a more potent inhibitor of cytochrome P450 3A4 than ritonavir. Ritonavir 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-86 23586711-1 2013 Utilization of the cytochrome P450 3A4 (CYP3A4) inhibitor ritonavir as a pharmacoenhancer for anti-HIV drugs revolutionized the treatment of HIV infection. Ritonavir 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-38 23586711-1 2013 Utilization of the cytochrome P450 3A4 (CYP3A4) inhibitor ritonavir as a pharmacoenhancer for anti-HIV drugs revolutionized the treatment of HIV infection. Ritonavir 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 23586711-2 2013 However, owing to ritonavir-related complications, there is a need for development of new CYP3A4 inhibitors with improved pharmacochemical properties, which requires a full understanding of the CYP3A4 inactivation mechanisms and the unraveling of possible inhibitor binding modes. Ritonavir 18-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 23586711-3 2013 We investigated the mechanism of CYP3A4 interaction with three desoxyritonavir analogues, containing the heme-ligating imidazole, oxazole, or pyridine group instead of the thiazole moiety (compounds 1, 2, and 3, respectively). desoxyritonavir 63-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 23586711-3 2013 We investigated the mechanism of CYP3A4 interaction with three desoxyritonavir analogues, containing the heme-ligating imidazole, oxazole, or pyridine group instead of the thiazole moiety (compounds 1, 2, and 3, respectively). Heme 105-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 23586711-3 2013 We investigated the mechanism of CYP3A4 interaction with three desoxyritonavir analogues, containing the heme-ligating imidazole, oxazole, or pyridine group instead of the thiazole moiety (compounds 1, 2, and 3, respectively). imidazole 119-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 23586711-3 2013 We investigated the mechanism of CYP3A4 interaction with three desoxyritonavir analogues, containing the heme-ligating imidazole, oxazole, or pyridine group instead of the thiazole moiety (compounds 1, 2, and 3, respectively). Oxazoles 130-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 23586711-3 2013 We investigated the mechanism of CYP3A4 interaction with three desoxyritonavir analogues, containing the heme-ligating imidazole, oxazole, or pyridine group instead of the thiazole moiety (compounds 1, 2, and 3, respectively). pyridine 142-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 23586711-5 2013 Additionally, Ser119 was identified as a key residue assisting binding of ritonavir-like inhibitors, which emphasizes the importance of polar interactions in the CYP3A4-ligand association. Ritonavir 74-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 23090875-3 2013 Unlike paclitaxel, docetaxel is extensively metabolized by CYP3A4 and its oral bioavailability can be enhanced in mice and humans by coadministration of the potent CYP3A inhibitor ritonavir. Docetaxel 19-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 23580071-0 2013 CYP3A4 and seasonal variation in vitamin D status in addition to CYP2D6 contribute to therapeutic endoxifen level during tamoxifen therapy. 4-hydroxy-N-desmethyltamoxifen 98-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23580071-0 2013 CYP3A4 and seasonal variation in vitamin D status in addition to CYP2D6 contribute to therapeutic endoxifen level during tamoxifen therapy. Tamoxifen 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23580071-5 2013 Regression analysis indicated that besides CYP2D6, the recently described CYP3A4*22 genotype, seasonal variation, and concomitant use of CYP2D6-inhibiting antidepressants were significant predictors of endoxifen concentration. 4-hydroxy-N-desmethyltamoxifen 202-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 23431112-5 2013 The results suggest that ABT-384 is a sensitive substrate of CYP3A. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 25-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-66 23404373-0 2013 Metabolism-dependent inhibition of CYP3A4 by lapatinib: evidence for formation of a metabolic intermediate complex with a nitroso/oxime metabolite formed via a nitrone intermediate. Lapatinib 45-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 23404373-0 2013 Metabolism-dependent inhibition of CYP3A4 by lapatinib: evidence for formation of a metabolic intermediate complex with a nitroso/oxime metabolite formed via a nitrone intermediate. nitroso/oxime 122-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 23469989-3 2013 The aim of the present study was to explore the role of tagging single nucleotide polymorphisms (tSNPs) of CYP3A4, CYP2C9 and CYP2C19 in the risk of ATLI in a population-based anti-TB treatment cohort. Terbium 181-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 23404373-0 2013 Metabolism-dependent inhibition of CYP3A4 by lapatinib: evidence for formation of a metabolic intermediate complex with a nitroso/oxime metabolite formed via a nitrone intermediate. nitrones 160-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 23393219-0 2013 Quantitative prediction of repaglinide-rifampicin complex drug interactions using dynamic and static mechanistic models: delineating differential CYP3A4 induction and OATP1B1 inhibition potential of rifampicin. repaglinide 27-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 23605691-4 2013 Oxycodone is primarily metabolized in the liver by the cytochrome P450 (CYP) enzymes with CYP3A as the major metabolic pathway and CYP2D6 as the minor metabolic pathway to noroxycodone, oxymorphone and noroxymorphone. Oxycodone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 23393219-1 2013 Repaglinide is mainly metabolized by cytochrome P450 enzymes CYP2C8 and CYP3A4, and it is also a substrate to a hepatic uptake transporter, organic anion transporting polypeptide (OATP)1B1. repaglinide 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 23404373-4 2013 We describe an approach combining heme iron oxidation with potassium ferricyanide and metabolite profiling to probe the mechanism of MI complex-based CYP3A4 inactivation by the secondary alkylamine drug lapatinib. Heme 34-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 23404373-4 2013 We describe an approach combining heme iron oxidation with potassium ferricyanide and metabolite profiling to probe the mechanism of MI complex-based CYP3A4 inactivation by the secondary alkylamine drug lapatinib. Iron 39-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 23404373-4 2013 We describe an approach combining heme iron oxidation with potassium ferricyanide and metabolite profiling to probe the mechanism of MI complex-based CYP3A4 inactivation by the secondary alkylamine drug lapatinib. potassium ferricyanide 59-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 23404373-4 2013 We describe an approach combining heme iron oxidation with potassium ferricyanide and metabolite profiling to probe the mechanism of MI complex-based CYP3A4 inactivation by the secondary alkylamine drug lapatinib. alkylamine 187-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 23404373-4 2013 We describe an approach combining heme iron oxidation with potassium ferricyanide and metabolite profiling to probe the mechanism of MI complex-based CYP3A4 inactivation by the secondary alkylamine drug lapatinib. Lapatinib 203-212 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 23404373-5 2013 Ten metabolites formed from lapatinib by CYP3A4-mediated heteroatom dealkylation, C-hydroxylation, N-oxygenation with or without further oxidation, or a combination thereof, were detected by accurate mass spectrometry. Lapatinib 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 23404373-6 2013 The abundance of one metabolite, the N-dealkylated nitroso/oxime lapatinib metabolite (M9), correlated directly with the prevalence or the disruption of the MI complex with CYP3A4. Nitrogen 37-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 23404373-6 2013 The abundance of one metabolite, the N-dealkylated nitroso/oxime lapatinib metabolite (M9), correlated directly with the prevalence or the disruption of the MI complex with CYP3A4. nitroso/oxime lapatinib 51-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 23404373-9 2013 Our findings support the mechanism of lapatinib CYP3A4 inactivation as MI complex formation with the nitroso metabolite formed through the secondary hydroxylamine and nitrone pathway, rather than by N-dealkylation to the primary amine followed by N-hydroxylation and dehydrogenation as is usually assumed. Lapatinib 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 23404373-9 2013 Our findings support the mechanism of lapatinib CYP3A4 inactivation as MI complex formation with the nitroso metabolite formed through the secondary hydroxylamine and nitrone pathway, rather than by N-dealkylation to the primary amine followed by N-hydroxylation and dehydrogenation as is usually assumed. nitroso 101-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 23404373-9 2013 Our findings support the mechanism of lapatinib CYP3A4 inactivation as MI complex formation with the nitroso metabolite formed through the secondary hydroxylamine and nitrone pathway, rather than by N-dealkylation to the primary amine followed by N-hydroxylation and dehydrogenation as is usually assumed. Hydroxylamine 149-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 23404373-9 2013 Our findings support the mechanism of lapatinib CYP3A4 inactivation as MI complex formation with the nitroso metabolite formed through the secondary hydroxylamine and nitrone pathway, rather than by N-dealkylation to the primary amine followed by N-hydroxylation and dehydrogenation as is usually assumed. nitrones 167-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 23404373-9 2013 Our findings support the mechanism of lapatinib CYP3A4 inactivation as MI complex formation with the nitroso metabolite formed through the secondary hydroxylamine and nitrone pathway, rather than by N-dealkylation to the primary amine followed by N-hydroxylation and dehydrogenation as is usually assumed. Amines 157-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 23404373-9 2013 Our findings support the mechanism of lapatinib CYP3A4 inactivation as MI complex formation with the nitroso metabolite formed through the secondary hydroxylamine and nitrone pathway, rather than by N-dealkylation to the primary amine followed by N-hydroxylation and dehydrogenation as is usually assumed. Nitrogen 199-200 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 23605691-11 2013 Simultaneous inhibition of both CYP3A and CYP2D6 results in increased oxycodone concentrations and such a combination should be avoided. Oxycodone 70-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-37 23557865-3 2013 The aim of this study was to investigate the association between postoperative fentanyl consumption and genetic polymorphisms of mu-opioid receptor (OPRM1), ABCB1 (gene encoding P-glycoprotein), CYP3A4 and CYP3A5 in Korean patients. Fentanyl 79-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 23131857-0 2013 Evaluation of limited sampling models for prediction of oral midazolam AUC for CYP3A phenotyping and drug interaction studies. Midazolam 61-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-84 23131857-9 2013 CONCLUSION: A four-sampling point limited sampling strategy to predict the oral midazolam AUC for CYP3A phenotyping is proposed. Midazolam 80-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 23428312-8 2013 In LS180 cells, rilpivirine induced mRNA expression of ABCB1, CYP3A4 and UGT1A3, whereas ABCC1, ABCC2, ABCG2, OATP1B1 and UGT1A9 were not induced. Rilpivirine 16-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 23381968-1 2013 In this study, we assessed the effects of clopidogrel and clarithromycin, known CYP2B6 and CYP3A inhibitors, respectively, on the enantioselective disposition of racemic sibutramine in conjunction with CYP2B6 polymorphisms in humans. sibutramine 170-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-96 23212742-0 2013 Enhancement of hepatic 4-hydroxylation of 25-hydroxyvitamin D3 through CYP3A4 induction in vitro and in vivo: implications for drug-induced osteomalacia. Calcifediol 42-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 23212742-2 2013 Human CYP24A1, CYP3A4, and CYP27B1 catalyze the inactivation and activation of vitamin D and have been implicated in the adverse drug response. Vitamin D 79-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 23212742-4 2013 With human hepatocytes, treatment with phenobarbital, hyperforin, carbamazepine, and rifampin significantly increased the levels of CYP3A4, but not CYP24A1 or CYP27B1 mRNA. Phenobarbital 39-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 23212742-4 2013 With human hepatocytes, treatment with phenobarbital, hyperforin, carbamazepine, and rifampin significantly increased the levels of CYP3A4, but not CYP24A1 or CYP27B1 mRNA. hyperforin 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 23212742-4 2013 With human hepatocytes, treatment with phenobarbital, hyperforin, carbamazepine, and rifampin significantly increased the levels of CYP3A4, but not CYP24A1 or CYP27B1 mRNA. Carbamazepine 66-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 23212742-4 2013 With human hepatocytes, treatment with phenobarbital, hyperforin, carbamazepine, and rifampin significantly increased the levels of CYP3A4, but not CYP24A1 or CYP27B1 mRNA. Rifampin 85-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 23212742-6 2013 This inductive effect was blocked by the addition of 6",7"-dihydroxybergamottin, a selective CYP3A4 inhibitor. 6',7'-dihydroxybergamottin 53-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 23381968-6 2013 These results suggest that the enantioselective disposition of sibutramine and its active metabolites are influenced by the altered genetic and environmental factors of CYP2B6 and CYP3A activity in vivo. sibutramine 63-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-185 23512537-6 2013 CYP3A4 and CYP3A5 metabolized BDP via hydroxylation ([M4] and [M6]) and dehydrogenation ([M5]) at similar rates; CYP3A7 did not metabolize BDP. Beclomethasone 30-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23512537-11 2013 These studies show that CYP3A4 and CYP3A5 metabolize BDP to inactive metabolites and suggest that differences in the expression or function of these enzymes in the lung and/or liver could influence BDP disposition in humans. Beclomethasone 53-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 22767428-5 2013 CYP3A4, CYP2C9 and CYP1A2 were identified to be the main CYP isoforms involved in the metabolism of evodiamine in human liver microsomes. evodiamine 100-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23947183-4 2013 Tacrolimus is mainly metabolized by cytochrome P450 isozymes, CYP3A4 and CYP3A5, expressed in the intestine as well as in the liver. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 23459029-2 2013 The aim of this study was to examine the association between tacrolimus pharmacokinetic variability and CYP3A4 and CYP3A5 genotypes by a population pharmacokinetic analysis based on routine drug monitoring data in adult renal transplant recipients. Tacrolimus 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 23459029-8 2013 The apparent clearance of tacrolimus was about two-fold higher in kidney transplant patients with higher enzymatic activity of CYP3A5*1 and CYP3A4*1G (with the CYP3A5*1/*1 or *1/*3 and CYP3A4*1/*1G or CYP3A4*1G/*1G) compared with those with lower enzymatic activity (CYP3A5*3/*3 and CYP3A4*1/*1). Tacrolimus 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 23459029-8 2013 The apparent clearance of tacrolimus was about two-fold higher in kidney transplant patients with higher enzymatic activity of CYP3A5*1 and CYP3A4*1G (with the CYP3A5*1/*1 or *1/*3 and CYP3A4*1/*1G or CYP3A4*1G/*1G) compared with those with lower enzymatic activity (CYP3A5*3/*3 and CYP3A4*1/*1). Tacrolimus 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 23459029-8 2013 The apparent clearance of tacrolimus was about two-fold higher in kidney transplant patients with higher enzymatic activity of CYP3A5*1 and CYP3A4*1G (with the CYP3A5*1/*1 or *1/*3 and CYP3A4*1/*1G or CYP3A4*1G/*1G) compared with those with lower enzymatic activity (CYP3A5*3/*3 and CYP3A4*1/*1). Tacrolimus 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 23459029-8 2013 The apparent clearance of tacrolimus was about two-fold higher in kidney transplant patients with higher enzymatic activity of CYP3A5*1 and CYP3A4*1G (with the CYP3A5*1/*1 or *1/*3 and CYP3A4*1/*1G or CYP3A4*1G/*1G) compared with those with lower enzymatic activity (CYP3A5*3/*3 and CYP3A4*1/*1). Tacrolimus 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 23459029-9 2013 CONCLUSION: This is the first study to extensively determine the effect of CYP3A4*1G and CYP3A5*3 genetic polymorphisms and hematocrit value on tacrolimus pharmacokinetics in Chinese renal transplant recipients. Tacrolimus 144-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 23459029-10 2013 The findings suggest that CYP3A5*3 and CYP3A4*1G polymorphisms and hematocrit are determinant factors in the apparent clearance of tacrolimus. Tacrolimus 131-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 23478147-1 2013 Starting from 11beta-HSD1 inhibitors that were active ex vivo but with Cyp 3A4 liability, we obtained a new series of adamantane ureas displaying potent inhibition of both human and rodent 11beta-HSD1 enzymes, devoid of Cyp 3A4 interactions, and rationally designed to provide long-lasting inhibition in target tissues. adamantane ureas 118-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-78 23434495-8 2013 Principal component analysis of the metabolite formation profile of dPA also revealed the highest similarity between CYP3A4 and HLMs. dpa 68-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 23434495-9 2013 Both quercetin (CYP2C8 inhibitor) and ketoconazole (CYP3A4 inhibitor) showed 60-100% inhibition of M1-M4 and M6 formations in HLMs, while M5 formation was mainly inhibited by alpha-naphthoflavone (CYP1A2 inhibitor, 70-80%) and quercetin (90%). Ketoconazole 38-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 23434495-9 2013 Both quercetin (CYP2C8 inhibitor) and ketoconazole (CYP3A4 inhibitor) showed 60-100% inhibition of M1-M4 and M6 formations in HLMs, while M5 formation was mainly inhibited by alpha-naphthoflavone (CYP1A2 inhibitor, 70-80%) and quercetin (90%). alpha-naphthoflavone 175-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 23434495-9 2013 Both quercetin (CYP2C8 inhibitor) and ketoconazole (CYP3A4 inhibitor) showed 60-100% inhibition of M1-M4 and M6 formations in HLMs, while M5 formation was mainly inhibited by alpha-naphthoflavone (CYP1A2 inhibitor, 70-80%) and quercetin (90%). Quercetin 227-236 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 23434495-11 2013 These findings shed a light on main involvement of CYP3A4 in human hepatic elimination of APs, indicating potential drug interactions. aps 90-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 23361230-10 2013 They were also involved in the N-demethylation of the analogue methamphetamine and CYP2C19, CYP2D6, and CYP3A4 in its ring hydroxylation. Nitrogen 31-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 23473235-2 2013 Through insightful design, we hoped to discover and synthesize a new series of small molecule inhibitors that could attenuate CYP3A4 time-dependent inhibition commonly observed with the THQ scaffold, maintain or improve aqueous solubility and oral absorption, reduce free drug clearance, and selectively increase mTOR potency. thq 186-189 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 23582127-4 2013 Treatment with multiple substrates of cytochrome P450 3A4 combined with inhibition of the enzyme by fluconazole impairs metabolism and thereby increase plasma concentrations of vincristine, which is considered to be the main reason for the neurotoxic side effects. Vincristine 177-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-57 23361230-10 2013 They were also involved in the N-demethylation of the analogue methamphetamine and CYP2C19, CYP2D6, and CYP3A4 in its ring hydroxylation. Methamphetamine 63-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 23357765-10 2013 CYP3A4 was the major isoform involved in arbidol metabolism, whereas the other P450s and flavin-containing monooxygenases (FMOs) played minor roles. umifenovir 41-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23357765-11 2013 These results indicated possible drug interactions between arbidol and CYP3A4 inhibitors and inducers. umifenovir 59-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 22943633-1 2013 AIM: The present study evaluated the possibility of drug interactions involving blueberry juice (BBJ) and substrate drugs whose clearance is dependent on cytochromes P4503A (CYP3A) and P4502C9 (CYP2C9). blueberry juice 80-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-179 23617933-2 2013 The CYP3A4*18, CYP3A5*3, and MDR1-3435 variant alleles are very important, particularly in tacrolimus metabolism in organ transplant rejection. Tacrolimus 91-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 23126373-13 2013 Multiple enzymes, mainly CYP3A4/5 and CYP1A1/2, are involved in famitinib metabolic clearance. famitinib 64-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 22943633-1 2013 AIM: The present study evaluated the possibility of drug interactions involving blueberry juice (BBJ) and substrate drugs whose clearance is dependent on cytochromes P4503A (CYP3A) and P4502C9 (CYP2C9). epacadostat 97-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-179 22943633-2 2013 METHODS: A 50:50 mixture of lowbush and highbush BBJ was evaluated in vitro as an inhibitor of CYP3A activity (hydroxylation of triazolam and dealkylation of buspirone) and of CYP2C9 activity (flurbiprofen hydroxylation) using human liver microsomes. epacadostat 49-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-100 22943633-2 2013 METHODS: A 50:50 mixture of lowbush and highbush BBJ was evaluated in vitro as an inhibitor of CYP3A activity (hydroxylation of triazolam and dealkylation of buspirone) and of CYP2C9 activity (flurbiprofen hydroxylation) using human liver microsomes. Triazolam 128-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-100 22943633-4 2013 RESULTS: BBJ inhibited CYP3A and CYP2C9 activity in vitro, with 50% inhibitory concentrations (IC50 ) of less than 2%, but without evidence of mechanism-based (irreversible) inhibition. epacadostat 9-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-28 22943633-6 2013 In clinical studies, GFJ significantly increased area under the plasma concentration-time curve (AUC) for the CYP3A substrate buspirone. Buspirone 126-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-115 23408070-6 2013 It has a t(1/2) of 6-8 h. Donepezil and galantamine are mainly metabolised by cytochrome P450 (CYP) 2D6 and CYP3A4 in the liver. Galantamine 40-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 27121666-7 2013 In conclusion, diltiazem markedly affected the pharmacokinetics of ACT-077825, probably via inhibition of CYP3A4 activity, without changing its safety and tolerability profile in healthy male subjects. Diltiazem 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 23408070-6 2013 It has a t(1/2) of 6-8 h. Donepezil and galantamine are mainly metabolised by cytochrome P450 (CYP) 2D6 and CYP3A4 in the liver. Donepezil 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 23340957-0 2013 Identification of the active components in Shenmai injection that differentially affect Cyp3a4-mediated 1"-hydroxylation and 4-hydroxylation of midazolam. Midazolam 144-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 23845193-6 2013 The complete inhibition of the CYP2C9 and CYP3A4 mediated metabolic pathway of glibenclamide through sorafenib might have resulted in a rapid accumulation of glibenclamide. Glyburide 79-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 23845193-6 2013 The complete inhibition of the CYP2C9 and CYP3A4 mediated metabolic pathway of glibenclamide through sorafenib might have resulted in a rapid accumulation of glibenclamide. Sorafenib 101-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 23845193-6 2013 The complete inhibition of the CYP2C9 and CYP3A4 mediated metabolic pathway of glibenclamide through sorafenib might have resulted in a rapid accumulation of glibenclamide. Glyburide 158-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 23340957-2 2013 In our previous study, SMI was shown to differentially affect CYP3A4-mediated 1"-hydroxylation and 4-hydroxylation of midazolam (MDZ). Midazolam 129-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 23386704-0 2013 Serum levels of 25-hydroxyvitamin D and the CYP3A biomarker 4beta-hydroxycholesterol in a high-dose vitamin D supplementation study. cholest-5-ene-3,4-diol 60-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-49 23340957-9 2013 We conclude that PXT is the constituent of SMI responsible for the differential effects on CYP3A4-mediated 1"-hydroxylation and 4-hydroxylation of MDZ. Midazolam 147-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 23616950-1 2013 Cobicistat is a novel cytochrome P450 3A4 (CYP3A4) inhibitor in advanced clinical evaluation for use as a pharmacoenhancer of antiretroviral drugs. Cobicistat 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-41 23386704-1 2013 The primary aim was to study the relationship between individual serum levels of 25-hydroxyvitamin D and 4beta-hydroxycholesterol, which is an endogenous biomarker of the drug-metabolizing CYP3A enzymes. 25-hydroxyvitamin D 81-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-194 23386704-1 2013 The primary aim was to study the relationship between individual serum levels of 25-hydroxyvitamin D and 4beta-hydroxycholesterol, which is an endogenous biomarker of the drug-metabolizing CYP3A enzymes. cholest-5-ene-3,4-diol 105-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-194 23386704-11 2013 However, the negative correlation between CRP and 4beta-hydroxycholesterol supports earlier experimental results that inflammation may suppress hepatic CYP3A activity, a finding of potentially high clinical relevance that warrants further exploration. cholest-5-ene-3,4-diol 50-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-157 23616950-1 2013 Cobicistat is a novel cytochrome P450 3A4 (CYP3A4) inhibitor in advanced clinical evaluation for use as a pharmacoenhancer of antiretroviral drugs. Cobicistat 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 23093043-9 2013 Co-administration of strong CYP3A/P-glycoprotein inducers with ticagrelor should be discouraged. Ticagrelor 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 23426978-1 2013 The selective mammalian target of rapamycin (mTOR) inhibitor everolimus has demonstrated competitive inhibition of cytochrome P450 enzyme (CYP) 3A4 in vitro; however, its influence on CYP3A4 activity in humans is unknown. Everolimus 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-147 23426978-1 2013 The selective mammalian target of rapamycin (mTOR) inhibitor everolimus has demonstrated competitive inhibition of cytochrome P450 enzyme (CYP) 3A4 in vitro; however, its influence on CYP3A4 activity in humans is unknown. Everolimus 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 23426978-6 2013 These results suggest everolimus may affect the bioavailability, but not the systemic clearance, of orally coadministered CYP3A4 substrate drugs. Everolimus 22-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 23512128-8 2013 After irreversible chemical inhibition of the proton pump, such as occurs with pantoprazole, the recovery of the protein of the pump has a half-life of around 50 h. Cytochrome P450 (CYP) 2C19 and to a lesser degree CYP3A4 clear the PPIs metabolically. Pantoprazole 79-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-221 23137766-3 2013 With the advent of the direct-acting antivirals telaprevir and boceprevir, which are both substrates and inhibitors of the cytochrome P450 (CYP) 3A iso-enzyme, knowledge and awareness of drug-drug interactions have become a cornerstone in the evaluation of patients starting and continuing HCV combination therapy. telaprevir 48-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-147 23137766-3 2013 With the advent of the direct-acting antivirals telaprevir and boceprevir, which are both substrates and inhibitors of the cytochrome P450 (CYP) 3A iso-enzyme, knowledge and awareness of drug-drug interactions have become a cornerstone in the evaluation of patients starting and continuing HCV combination therapy. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-147 23681436-5 2013 Rilpivirine is predominantly metabolized by cytochrome P450 3A4. Rilpivirine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-63 23503455-1 2013 BACKGROUND: The frequently prescribed antidementia drug galantamine is extensively metabolized by the enzymes cytochrome P450 (CYP) 2D6 and CYP3A and is a substrate of the P-glycoprotein. Galantamine 56-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-145 23153057-3 2013 The cocktail strategy (in situ incubation) was used to assess the induction of CYP1A2, CYP2B6, CYP2C9 and CYP3A4 by using the recommended probe substrate, i.e. phenacetin, bupropion, diclofenac and midazolam, respectively. Bupropion 172-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 23307906-12 2013 Larger studies with stronger study designs are needed to clarify potential drug-vitamin D interactions, especially for drugs metabolized by cytochrome P450 3A4 (CYP3A4). Vitamin D 80-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-159 23307906-12 2013 Larger studies with stronger study designs are needed to clarify potential drug-vitamin D interactions, especially for drugs metabolized by cytochrome P450 3A4 (CYP3A4). Vitamin D 80-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 23462027-4 2013 MAIN OUTCOME MEASURES: Colchicine is metabolized via cytochrome P450 3A4 (CYP3A4); therefore, coadministration with agents that inhibit this isoenzyme can produce elevated colchicine plasma concentrations, resulting in severe and sometimes fatal adverse events. Colchicine 23-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-72 27536444-5 2013 METHODS: The ability of 4-AP to inhibit CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4/5 in a direct and time-dependent manner was evaluated using pooled human liver microsomes. 4-Aminopyridine 24-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 23361102-0 2013 Impact of OATP1B1, MDR1, and CYP3A4 expression in liver and intestine on interpatient pharmacokinetic variability of atorvastatin in obese subjects. Atorvastatin 117-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 23361102-7 2013 In conclusion, this study suggests that OATP1B1 phenotype is more important than CYP3A4 and MDR1 phenotypes for the individual pharmacokinetic variability of atorvastatin. Atorvastatin 158-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 23364483-0 2013 CYP3A and ABCB1 genetic polymorphisms on the pharmacokinetics and pharmacodynamics of tacrolimus and its metabolites (M-I and M-III). Tacrolimus 86-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 23462027-4 2013 MAIN OUTCOME MEASURES: Colchicine is metabolized via cytochrome P450 3A4 (CYP3A4); therefore, coadministration with agents that inhibit this isoenzyme can produce elevated colchicine plasma concentrations, resulting in severe and sometimes fatal adverse events. Colchicine 23-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 23462027-4 2013 MAIN OUTCOME MEASURES: Colchicine is metabolized via cytochrome P450 3A4 (CYP3A4); therefore, coadministration with agents that inhibit this isoenzyme can produce elevated colchicine plasma concentrations, resulting in severe and sometimes fatal adverse events. Colchicine 172-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-72 23462027-4 2013 MAIN OUTCOME MEASURES: Colchicine is metabolized via cytochrome P450 3A4 (CYP3A4); therefore, coadministration with agents that inhibit this isoenzyme can produce elevated colchicine plasma concentrations, resulting in severe and sometimes fatal adverse events. Colchicine 172-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 23462027-8 2013 Other antibiotics that are strong CYP3A4 inhibitors include itraconazole and telithromycin, whereas erythromycin and fluconazole are moderate inhibitors of the isoenzyme CYP3A4. Itraconazole 60-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 23462027-8 2013 Other antibiotics that are strong CYP3A4 inhibitors include itraconazole and telithromycin, whereas erythromycin and fluconazole are moderate inhibitors of the isoenzyme CYP3A4. Erythromycin 100-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 23462027-8 2013 Other antibiotics that are strong CYP3A4 inhibitors include itraconazole and telithromycin, whereas erythromycin and fluconazole are moderate inhibitors of the isoenzyme CYP3A4. Fluconazole 117-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 23462027-9 2013 Coadministration of CYP3A4 inhibitors (particularly clarithromycin) and colchicine has resulted in acute colchicine toxicity manifested by severe gastrointestional toxicity, bone marrow suppression, multiorgan failure, and death. Clarithromycin 52-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 23462027-9 2013 Coadministration of CYP3A4 inhibitors (particularly clarithromycin) and colchicine has resulted in acute colchicine toxicity manifested by severe gastrointestional toxicity, bone marrow suppression, multiorgan failure, and death. Colchicine 105-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 23462027-10 2013 CONCLUSION: Pharmacist awareness of potentially clinically significant interactions between colchicine and antibiotics that inhibit CYP3A4 can help to ensure the efficacy of colchicine is realized while mitigating serious toxicities and minimizing the risk of adverse events. Colchicine 92-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 23462027-10 2013 CONCLUSION: Pharmacist awareness of potentially clinically significant interactions between colchicine and antibiotics that inhibit CYP3A4 can help to ensure the efficacy of colchicine is realized while mitigating serious toxicities and minimizing the risk of adverse events. Colchicine 174-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 23293300-5 2013 In human hepatocytes, BOC inhibited CYP3A-mediated metabolism of midazolam, OATP1B-mediated hepatic uptake of pitavastatin, and both the uptake and metabolism of atorvastatin. Midazolam 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 23238784-5 2013 Within 14 days of culture, the HepaRG-AMC-BALs contained highly polarized viable liver-like tissue with heterogeneous expression of CYP3A4. heparg 31-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 23238784-5 2013 Within 14 days of culture, the HepaRG-AMC-BALs contained highly polarized viable liver-like tissue with heterogeneous expression of CYP3A4. amc-bals 38-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 23238784-7 2013 The CYP3A4 activity could be induced 2-fold by rifampicin, whereas CYP2C9 activity remained equally high. Rifampin 47-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 23297297-7 2013 Inhibition experiments using pooled human liver microsomes confirmed the major role of CYP3A4 in hepatic bioactivation of clozapine. Clozapine 122-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 23297297-11 2013 Therefore, interindividual differences and drug-drug interactions at the level of CYP3A4 might be factors determining exposure of hepatic tissue to reactive clozapine metabolites. Clozapine 157-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 22777148-4 2013 The formation of 1"-hydroxymidazolam in biopsy tissue and the serum 1"-hydroxymidazolam:midazolam ratio were indicators of intestinal and hepatic CYP3A activity, respectively. Midazolam 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-151 22777148-5 2013 RESULTS: Intestinal CYP3A activity decreased by 64 % (p = 0.0029) following the first dose of clarithromycin, but hepatic CYP3A activity did not significantly decrease. Clarithromycin 94-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-25 22777148-0 2013 Rate of onset of inhibition of gut-wall and hepatic CYP3A by clarithromycin. Clarithromycin 61-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-57 23381958-1 2013 BACKGROUND AND OBJECTIVE: The cytochrome P450 (CYP) enzyme, CYP3A4, metabolizes ACT-178882, a new direct renin inhibitor. MK-1597 80-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 22777148-6 2013 Repeated dosing of clarithromycin caused a significant decrease in hepatic CYP3A activity (p = 0.005), while intestinal activity showed little further decline. Clarithromycin 19-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 23381958-2 2013 This study investigated the effect of diltiazem, a moderate inhibitor of CYP3A4, on the single-dose pharmacokinetics of ACT-178882 in healthy subjects. Diltiazem 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 22777148-1 2013 AIMS: To determine the extent and time-course of hepatic and intestinal cytochrome P450 3A (CYP3A) inactivation due to the mechanism-based inhibitor clarithromycin. Clarithromycin 149-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-90 22777148-1 2013 AIMS: To determine the extent and time-course of hepatic and intestinal cytochrome P450 3A (CYP3A) inactivation due to the mechanism-based inhibitor clarithromycin. Clarithromycin 149-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-97 22777148-8 2013 CONCLUSIONS: Following the administration of clarithromycin, the onset of hepatic CYP3A inactivation is delayed compared to that of intestinal CYP3A. Clarithromycin 45-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-87 22777148-4 2013 The formation of 1"-hydroxymidazolam in biopsy tissue and the serum 1"-hydroxymidazolam:midazolam ratio were indicators of intestinal and hepatic CYP3A activity, respectively. 1-hydroxymethylmidazolam 17-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-151 22777148-9 2013 The time-course of drug-drug interactions due to clarithromycin will vary with the relative contribution of intestinal and hepatic CYP3A to the clearance and bioavailability of a victim substrate. Clarithromycin 49-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-136 22777148-4 2013 The formation of 1"-hydroxymidazolam in biopsy tissue and the serum 1"-hydroxymidazolam:midazolam ratio were indicators of intestinal and hepatic CYP3A activity, respectively. 1-hydroxymethylmidazolam 68-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-151 22968811-5 2013 Midazolam served as a marker substance of CYP3A activity using an established limited sampling strategy. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 22945461-4 2013 Each participant had already completed a 14 days course of St John"s Wort to induce CYP3A4, which was quantified through the metabolic ratio of exogenous 3-hydroxyquinine to quinine. 3-hydroxyquinidine 154-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 22968811-0 2013 Effect of the CYP3A inhibitor ketoconazole on the PXR-mediated induction of CYP3A activity. Ketoconazole 30-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 22886152-2 2013 We have investigated the effect of polymorphisms in the CYP3A and ABCB1 genes on CsA pharmacokinetics, acute rejection incidence and drug-related side effects in renal transplant recipients METHODS: The presence of CYP3A5*3, CYP3A4*1B and ABCB1 C1236T, G2677T/A and C3435T polymorphisms was assessed in 68 patients and retrospectively associated with pharmacokinetic and clinical parameters at 1 week and 1, 5 and 12 months after transplantation. Cyclosporine 81-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 22968811-6 2013 RESULTS: After 8 days of simultaneous ketoconazole and St John"s wort administration, CYP3A-mediated midazolam metabolism was strongly inhibited (81 % decrease in clearance). Ketoconazole 38-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 22968811-0 2013 Effect of the CYP3A inhibitor ketoconazole on the PXR-mediated induction of CYP3A activity. Ketoconazole 30-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 22968811-1 2013 PURPOSE: The aim of this clinical study was to investigate a previously proposed mechanism of ketoconazole-mediated inhibition of cytochrome P450 3A (CYP3A) induction. Ketoconazole 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-148 22968811-6 2013 RESULTS: After 8 days of simultaneous ketoconazole and St John"s wort administration, CYP3A-mediated midazolam metabolism was strongly inhibited (81 % decrease in clearance). Midazolam 101-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 22968811-1 2013 PURPOSE: The aim of this clinical study was to investigate a previously proposed mechanism of ketoconazole-mediated inhibition of cytochrome P450 3A (CYP3A) induction. Ketoconazole 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 22968811-7 2013 Following the induction of CYP3A with St John"s wort (6.6-fold increase in clearance on day 8), a single dose of ketoconazole strongly inhibited midazolam metabolism to the same degree (82 % decrease in clearance in relation to baseline). Ketoconazole 113-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 22968811-4 2013 In the second phase, we studied the inhibitory effect of a single dose of ketoconazole directly at the enzyme level during CYP3A induction by St John"s wort. Ketoconazole 74-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-128 22968811-9 2013 These results apparently contradict the in vitro results where ketoconazole showed an inhibitory effect on the transcription of CYP3A genes. Ketoconazole 63-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-133 22968811-10 2013 CONCLUSIONS: Ketoconazole is a strong inhibitor of CYP3A, also when used concomitantly with St John"s wort. Ketoconazole 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 22990330-0 2013 Pharmacokinetic interactions of almorexant with midazolam and simvastatin, two CYP3A4 model substrates, in healthy male subjects. almorexant 32-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 22990330-1 2013 PURPOSE: Pre-clinical experiments have shown that almorexant, a dual orexin receptor antagonist, is able to inhibit cytochrome P450 3A4 (CYP3A4). almorexant 50-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-135 22990330-1 2013 PURPOSE: Pre-clinical experiments have shown that almorexant, a dual orexin receptor antagonist, is able to inhibit cytochrome P450 3A4 (CYP3A4). almorexant 50-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 23361846-1 2013 Methadone N-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 (CYP2B6) and CYP3A4, but clinical disposition is often attributed to CYP3A4. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 23716885-7 2013 CONCLUSIONS: There would be an accumulation of aripiprazole when coadministered with fluvoxamine, a known inhibitor of CYP3A4, leading to hepatic damage and reduction in aripiprazole when administered along with carbamazepine. Fluvoxamine 85-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 23716885-1 2013 OBJECTIVES: Aripiprazole, a new atypical antipsychotic drug extensively metabolized by enzyme CYP3A4, is found to produce asymptomatic elevation of serum transaminase levels on long-term treatment. Aripiprazole 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 23716885-6 2013 The coadministration of aripiprazole with carbamazepine leads to significant decrease in blood concentration of aripiprazole possibly due to induction of enzyme CYP3A4 resulting in loss or reduction of clinical efficacy. Aripiprazole 24-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 23716885-6 2013 The coadministration of aripiprazole with carbamazepine leads to significant decrease in blood concentration of aripiprazole possibly due to induction of enzyme CYP3A4 resulting in loss or reduction of clinical efficacy. Carbamazepine 42-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 23716885-6 2013 The coadministration of aripiprazole with carbamazepine leads to significant decrease in blood concentration of aripiprazole possibly due to induction of enzyme CYP3A4 resulting in loss or reduction of clinical efficacy. Aripiprazole 112-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 23716885-7 2013 CONCLUSIONS: There would be an accumulation of aripiprazole when coadministered with fluvoxamine, a known inhibitor of CYP3A4, leading to hepatic damage and reduction in aripiprazole when administered along with carbamazepine. Aripiprazole 47-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 23407222-2 2013 Isoniazid (INH) inhibits CYP3A4, which metabolises nevirapine (NVP). Isoniazid 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 23407222-2 2013 Isoniazid (INH) inhibits CYP3A4, which metabolises nevirapine (NVP). Nevirapine 51-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 23492463-4 2013 Ranolazine is a weak inhibitor of CYP3A4 known to increase the serum level of simvastatin and its active metabolite 2-fold. Ranolazine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 23492463-4 2013 Ranolazine is a weak inhibitor of CYP3A4 known to increase the serum level of simvastatin and its active metabolite 2-fold. Simvastatin 78-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 23361846-1 2013 Methadone N-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 (CYP2B6) and CYP3A4, but clinical disposition is often attributed to CYP3A4. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 24023447-3 2013 One of them is clopidogrel drug-drug interaction with CYP2C19 and CYP3A4 enzyme inhibitors. Clopidogrel 15-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 25505649-2 2013 Artemether is a substrate of CYP3A4 and CYP2B6, antiretrovirals such as efavirenz induce these enzymes and have the potential to reduce artemether pharmacokinetic exposure. Artemether 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 25505649-2 2013 Artemether is a substrate of CYP3A4 and CYP2B6, antiretrovirals such as efavirenz induce these enzymes and have the potential to reduce artemether pharmacokinetic exposure. efavirenz 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 25505649-2 2013 Artemether is a substrate of CYP3A4 and CYP2B6, antiretrovirals such as efavirenz induce these enzymes and have the potential to reduce artemether pharmacokinetic exposure. Artemether 136-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 24023447-10 2013 The use of the potential CYP3A4 inhibitors - lipophilic statins and CCB - was increased after the prescription of clopidogrel too. Clopidogrel 114-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 24023447-12 2013 CONCLUSION: In the primary health care practices, it is revealed that there is co-medication of clopidogrel with weak CYP3A4 inhibitors, such as lipophilic statins and amlodipine, and with the moderate CYP2C19 inhibitor - omeprazole. Clopidogrel 96-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 23264496-5 2013 The PXR ligand rifampicin further increased the expression of CYP3A4, and siRNA-mediated knock-down of PXR in confluent cells resulted in decreased CYP3A4 expression. Rifampin 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 23264496-9 2013 Moreover, the CDK inhibitor roscovitine stimulated the expression of CYP3A4. Roscovitine 28-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 23324807-0 2013 Impact of POR*28 on the clinical pharmacokinetics of CYP3A phenotyping probes midazolam and erythromycin. Midazolam 78-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 23295386-4 2013 Furthermore, a humanized CYP3A4/3A7 mouse model showed in vivo induction of CYP3A4 mRNA and protein by [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]acetic acid (WY14,643) in liver but not in intestine, whereas hepatic occupancy of PBRs by PPARalpha was ligand independent. pirinixic acid 103-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 23295386-4 2013 Furthermore, a humanized CYP3A4/3A7 mouse model showed in vivo induction of CYP3A4 mRNA and protein by [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]acetic acid (WY14,643) in liver but not in intestine, whereas hepatic occupancy of PBRs by PPARalpha was ligand independent. pirinixic acid 103-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 23295386-4 2013 Furthermore, a humanized CYP3A4/3A7 mouse model showed in vivo induction of CYP3A4 mRNA and protein by [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]acetic acid (WY14,643) in liver but not in intestine, whereas hepatic occupancy of PBRs by PPARalpha was ligand independent. wy14 161-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 23295386-4 2013 Furthermore, a humanized CYP3A4/3A7 mouse model showed in vivo induction of CYP3A4 mRNA and protein by [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]acetic acid (WY14,643) in liver but not in intestine, whereas hepatic occupancy of PBRs by PPARalpha was ligand independent. wy14 161-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 23295386-4 2013 Furthermore, a humanized CYP3A4/3A7 mouse model showed in vivo induction of CYP3A4 mRNA and protein by [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]acetic acid (WY14,643) in liver but not in intestine, whereas hepatic occupancy of PBRs by PPARalpha was ligand independent. pbrs 231-235 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 23295386-4 2013 Furthermore, a humanized CYP3A4/3A7 mouse model showed in vivo induction of CYP3A4 mRNA and protein by [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]acetic acid (WY14,643) in liver but not in intestine, whereas hepatic occupancy of PBRs by PPARalpha was ligand independent. pbrs 231-235 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 23295386-6 2013 Interestingly, the common phospholipid 1-palmitoyl-2-oleoyl-sn-glycerol-3-phosphocholine (16:0/18:1-PC), previously proposed to reflect nutritional status and shown to be a specific endogenous ligand of PPARalpha, induced CYP3A4 (up to 4-fold) and other biotransformation genes in hepatocytes with similar selectivity and potency as WY14,643. phospholipid 1-palmitoyl-2-oleoyl-sn-glycerol-3-phosphocholine 26-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 222-228 23313934-1 2013 The present study aimed to investigate the effect of cytochrome P450 3A4 (CYP3A4)*18B polymorphisms and the interaction of the micro opioid receptor gene (OPRM1) A118G and CYP3A4*18B polymorphisms on postoperative fentanyl analgesia in Chinese Han patients undergoing radical gastrectomy. Fentanyl 238-246 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 196-202 23313934-6 2013 In the first 48 h following surgery, patients in the CYP3A4*18B/*18B group consumed significantly less fentanyl compared with patients in the *1/*1 group (P=0.032). Fentanyl 115-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 23313934-9 2013 Results demonstrated that 48 h following surgery, patients with the CYP3A4*18B/*18B genotype required less fentanyl than patients with the CYP3A4*1/*1 genotype to control pain. Fentanyl 119-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 23313934-10 2013 Additionally, the combined genotype of CYP3A4*18B and OPRM1 A118G may affect fentanyl doses administered for pain control, but not postoperative nausea, vomiting and dizziness. Fentanyl 89-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 23254912-1 2013 Etoposide, used for the treatment of breast cancer, is mainly metabolized via hepatic cytochrome P450 (CYP) 3A4 in humans and is also a substrate for p-glycoprotein (P-gp). Etoposide 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-123 23324807-0 2013 Impact of POR*28 on the clinical pharmacokinetics of CYP3A phenotyping probes midazolam and erythromycin. Erythromycin 92-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 23324807-3 2013 The aim of the present study was to determine the in vivo impact of the POR*28 allele on the pharmacokinetics of the classic CYP3A phenotyping probes midazolam and erythromycin. Midazolam 150-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-130 23324807-3 2013 The aim of the present study was to determine the in vivo impact of the POR*28 allele on the pharmacokinetics of the classic CYP3A phenotyping probes midazolam and erythromycin. Erythromycin 164-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-130 23324807-4 2013 Whereas midazolam is metabolized by both CYP3A4 and CYP3A5, erythromycin is exclusively oxidized by CYP3A4. Midazolam 8-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 23324807-4 2013 Whereas midazolam is metabolized by both CYP3A4 and CYP3A5, erythromycin is exclusively oxidized by CYP3A4. Erythromycin 60-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 23481136-1 2013 BACKGROUND AND AIMS: Tacrolimus is a macrolide immunosuppressant used for prevention of allograft rejection in organ transplantation and metabolized in the liver and intestine by cytochrome P450 3A4 (CYP3A4) enzyme. Tacrolimus 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-198 23481136-1 2013 BACKGROUND AND AIMS: Tacrolimus is a macrolide immunosuppressant used for prevention of allograft rejection in organ transplantation and metabolized in the liver and intestine by cytochrome P450 3A4 (CYP3A4) enzyme. Tacrolimus 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 23481136-1 2013 BACKGROUND AND AIMS: Tacrolimus is a macrolide immunosuppressant used for prevention of allograft rejection in organ transplantation and metabolized in the liver and intestine by cytochrome P450 3A4 (CYP3A4) enzyme. Macrolides 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-198 23481136-1 2013 BACKGROUND AND AIMS: Tacrolimus is a macrolide immunosuppressant used for prevention of allograft rejection in organ transplantation and metabolized in the liver and intestine by cytochrome P450 3A4 (CYP3A4) enzyme. Macrolides 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 23102508-4 2013 Miltirone showed moderate inhibition on CYP1A2 (IC(50)=1.73 muM) and CYP2C9 (IC(50)=8.61 muM), and weak inhibition on CYP2D6 (IC(50)=30.20 muM) and CYP3A4 (IC(50)=33.88 muM). miltirone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 23274770-2 2013 Mitragynine, an euphoric compound was evaluated for its effects on the expression of mRNAs encoding CYP1A2, CYP2D6 and CYP3A4 and protein expression and resultant enzymatic activity. mitragynine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 23274770-5 2013 The effects of mitragynine on human CYP3A4 protein expression were determined using an optimized hCYP3A4-HepG2 cell-based assay. mitragynine 15-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 23274770-6 2013 An in silico computational method to predict the binding conformation of mitragynine to the active site of the CYP3A4 enzyme was performed and further validated using in vitro CYP3A4 inhibition assays. mitragynine 73-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 23724652-6 2013 Forscolin was metabolized by CYP3A4 in human liver microsomes. forscolin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 23724652-7 2013 There was definite inhibition on CYP3A4 at the concentrations of forscolin between 0.1 ng x mL(-1) and 5 microg x mL(-1). forscolin 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 23179081-0 2013 Mitotane induces CYP3A4 expression via activation of the steroid and xenobiotic receptor. Mitotane 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 23179081-5 2013 Although the precise mechanism of these interactions is not well understood, cytochrome P450 mono-oxygenase 3A4 (CYP3A4) is a key enzyme to inactivate both glucocorticoids and sunitinib. Sunitinib 176-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-111 23274770-6 2013 An in silico computational method to predict the binding conformation of mitragynine to the active site of the CYP3A4 enzyme was performed and further validated using in vitro CYP3A4 inhibition assays. mitragynine 73-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 23353592-7 2013 Using commercial kits macitentan was demonstrated to be a moderate inhibitor of CYP3A4 and CYP2C19. macitentan 22-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 23179081-5 2013 Although the precise mechanism of these interactions is not well understood, cytochrome P450 mono-oxygenase 3A4 (CYP3A4) is a key enzyme to inactivate both glucocorticoids and sunitinib. Sunitinib 176-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 23102508-5 2013 Enzyme kinetic studies showed that miltirone competitively inhibited CYP2C9 (K(i)=1.48 muM), and displayed mixed type inhibitions on CYP1A2, CYP2D6 and CYP3A4 with K(i) values of 3.17 muM, 24.25 muM and 35.09 muM, respectively. miltirone 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 23179081-11 2013 Mitotane increased CYP3A4 mRNA levels, which was attenuated by SXR knockdown. Mitotane 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 22937971-2 2013 These prodrugs can be used for targeting into gut wall, since these types of cyclic phosphates are known to be activated mainly by CYP3A forms, which are expressed not only in the liver but also in the small intestine and to a lesser extent in the colon. cyclic phosphates 77-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-136 23179081-12 2013 Finally, we showed that mitotane increased CYP3A4 enzyme activity. Mitotane 24-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 23179081-13 2013 We conclude that mitotane can induce CYP3A4 gene expression and suggest that mitotane is used cautiously due to its drug-drug interactions. Mitotane 17-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 23238299-2 2013 This study demonstrates that chelidonine and an alkaloid extract from Chelidonium majus, which contains protoberberine and benzo[c]phenanthridine alkaloids, has the ability to overcome MDR of different cancer cell lines through interaction with ABC-transporters, CYP3A4 and GST, by induction of apoptosis, and cytotoxic effects. chelidonine 29-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 263-269 23238299-2 2013 This study demonstrates that chelidonine and an alkaloid extract from Chelidonium majus, which contains protoberberine and benzo[c]phenanthridine alkaloids, has the ability to overcome MDR of different cancer cell lines through interaction with ABC-transporters, CYP3A4 and GST, by induction of apoptosis, and cytotoxic effects. Alkaloids 48-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 263-269 23238299-2 2013 This study demonstrates that chelidonine and an alkaloid extract from Chelidonium majus, which contains protoberberine and benzo[c]phenanthridine alkaloids, has the ability to overcome MDR of different cancer cell lines through interaction with ABC-transporters, CYP3A4 and GST, by induction of apoptosis, and cytotoxic effects. benzo[c]phenanthridine alkaloids 123-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 263-269 23238299-4 2013 In addition, chelidonine and the alkaloid extract inhibited the activity of the drug modifying enzymes CYP3A4 and GST in a dose-dependent manner. chelidonine 13-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 23238299-4 2013 In addition, chelidonine and the alkaloid extract inhibited the activity of the drug modifying enzymes CYP3A4 and GST in a dose-dependent manner. Alkaloids 33-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 23238299-8 2013 Treatment of Caco-2 cells with 50 mug/ml alkaloid extract and 50 muM chelidonine for up to 48 h resulted in a significant decrease in mRNA levels of P-gp/MDR1, MRP1, BCRP, CYP3A4, GST, and hPXR and in a significant increase in caspase-3 and caspase-8 mRNA. Alkaloids 41-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 23238299-8 2013 Treatment of Caco-2 cells with 50 mug/ml alkaloid extract and 50 muM chelidonine for up to 48 h resulted in a significant decrease in mRNA levels of P-gp/MDR1, MRP1, BCRP, CYP3A4, GST, and hPXR and in a significant increase in caspase-3 and caspase-8 mRNA. chelidonine 69-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 22642697-0 2013 The effect of CYP3A inhibitors and inducers on the pharmacokinetics of telaprevir in healthy volunteers. telaprevir 71-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 22900583-9 2013 Midazolam metabolic ratio (MR) dramatically decreased in presence of ritonavir (6.7 +- 2.6 versus 0.13 +- 0.07) reflecting an almost complete inhibition of CYP3A4, whereas omeprazole, flurbiprofen and bupropion MR were not affected. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 22900583-9 2013 Midazolam metabolic ratio (MR) dramatically decreased in presence of ritonavir (6.7 +- 2.6 versus 0.13 +- 0.07) reflecting an almost complete inhibition of CYP3A4, whereas omeprazole, flurbiprofen and bupropion MR were not affected. Ritonavir 69-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 22900583-10 2013 These data demonstrate that ritonavir is able to block prasugrel CYP3A4 bioactivation. Ritonavir 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 22725836-2 2013 Previous in vitro studies indicate that curcuminoids and piperine (a black pepper derivative that enhances curcuminoid bioavailability) could inhibit human CYP3A, CYP2C9, UGT and SULT dependent drug metabolism. curcuminoids 40-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-161 22642697-9 2013 CONCLUSION: CYP3A inducers, rifampicin and efavirenz, can reduce telaprevir exposure to varying degrees based on their potency. Rifampin 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 22725836-2 2013 Previous in vitro studies indicate that curcuminoids and piperine (a black pepper derivative that enhances curcuminoid bioavailability) could inhibit human CYP3A, CYP2C9, UGT and SULT dependent drug metabolism. piperine 57-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-161 22725836-2 2013 Previous in vitro studies indicate that curcuminoids and piperine (a black pepper derivative that enhances curcuminoid bioavailability) could inhibit human CYP3A, CYP2C9, UGT and SULT dependent drug metabolism. curcuminoid 40-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-161 22803519-2 2013 The aim of this study was to determine the effect of rifampicin, a CYP3A4 inducer, on the plasma pharmacokinetics of eribulin in patients with solid tumours. Rifampin 53-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 22803519-12 2013 CONCLUSIONS: These results indicate that eribulin mesylate may be safely co-administered with compounds that are CYP3A4 inducers. eribulin 41-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 22642697-9 2013 CONCLUSION: CYP3A inducers, rifampicin and efavirenz, can reduce telaprevir exposure to varying degrees based on their potency. efavirenz 43-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 22642697-9 2013 CONCLUSION: CYP3A inducers, rifampicin and efavirenz, can reduce telaprevir exposure to varying degrees based on their potency. telaprevir 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 23319370-4 2013 C-1311-mediated CYP3A4 activity modulation and the effect of CYP3A4 overexpression on C-1311 metabolism have also been examined. C 1311 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 23203815-11 2013 5-Hydroxy pomalidomide, the notable oxidative metabolite, was formed primarily via CYP1A2 and CYP3A4. 5-hydroxy pomalidomide 0-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 23319370-4 2013 C-1311-mediated CYP3A4 activity modulation and the effect of CYP3A4 overexpression on C-1311 metabolism have also been examined. C 1311 86-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 23319370-7 2013 C-1311 metabolism was very low in both hepatoma cell lines and slightly influenced by CYP3A4 expression. C 1311 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 23129213-5 2013 Crizotinib E(max) and EC(50) for CYP3A4 induction (measured as mRNA expression) were estimated as 6.4- to 29-fold and 0.47 to 3.1 microM, respectively. Crizotinib 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 23319370-8 2013 Interestingly, in HepG2 cells, C-1311 was an effective modulator of CYP3A4 enzymatic activity, being the inhibitor of this isoenzyme in Hep3A4 cells. C 1311 31-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 23319370-11 2013 Although CYP3A4 did not influence C-1311 metabolism, changes in CYP3A4 levels affected the C-1311-induced response in hepatoma cells. C 1311 91-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 23319370-12 2013 Therefore, inter-patient differences in CYP3A4 levels should be considered when assessing the potential therapeutic effects of C-1311. C 1311 127-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 23292752-9 2013 Since both are substrates, co-administration of rivaroxaban and apixaban with strong cytochrome P450 (CYP) 3A4 and permeability glycoprotein (P-gp) inhibitors and inducers can result in substantial changes in plasma concentrations due to altered clearance rates; consequently, their concomitant use is contraindicated and caution is required when used concomitantly with strong CYP3A4 and P-gp inducers. Rivaroxaban 48-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 378-384 23292752-9 2013 Since both are substrates, co-administration of rivaroxaban and apixaban with strong cytochrome P450 (CYP) 3A4 and permeability glycoprotein (P-gp) inhibitors and inducers can result in substantial changes in plasma concentrations due to altered clearance rates; consequently, their concomitant use is contraindicated and caution is required when used concomitantly with strong CYP3A4 and P-gp inducers. apixaban 64-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 378-384 22837389-4 2013 The results showed that estradiol enhances CYP2A6, CYP2B6, and CYP3A4 expression, whereas progesterone induces CYP2A6, CYP2B6, CYP2C8, CYP3A4, and CYP3A5 expression. Estradiol 24-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 22837389-4 2013 The results showed that estradiol enhances CYP2A6, CYP2B6, and CYP3A4 expression, whereas progesterone induces CYP2A6, CYP2B6, CYP2C8, CYP3A4, and CYP3A5 expression. Progesterone 90-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 23129213-0 2013 Prediction of crizotinib-midazolam interaction using the Simcyp population-based simulator: comparison of CYP3A time-dependent inhibition between human liver microsomes versus hepatocytes. Crizotinib 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-111 23139378-4 2013 The plasma concentration profiles of repaglinide were then analyzed by a PBPK model, together with those of the inhibitors, assuming a competitive inhibition of CYP3A4 by itraconazole, mechanism-based inhibition of CYP2C8 by gemfibrozil glucuronide, and inhibition of organic anion transporting polypeptide (OATP) 1B1 by gemfibrozil and its glucuronide. Itraconazole 171-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 23143891-5 2013 In this work, the metabolism of four frequently prescribed inhaled GCs, triamcinolone acetonide, flunisolide, budesonide, and fluticasone propionate, by the CYP3A family of enzymes was studied to identify differences in their rates of clearance and to identify their metabolites. Triamcinolone Acetonide 72-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-162 23143891-5 2013 In this work, the metabolism of four frequently prescribed inhaled GCs, triamcinolone acetonide, flunisolide, budesonide, and fluticasone propionate, by the CYP3A family of enzymes was studied to identify differences in their rates of clearance and to identify their metabolites. flunisolide 97-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-162 23175666-0 2013 Intraindividual and interindividual variabilities in endogenous cortisol 6beta-hydroxylation clearance as an index for in vivo CYP3A phenotyping in humans. cortisol 6beta 64-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 23143891-5 2013 In this work, the metabolism of four frequently prescribed inhaled GCs, triamcinolone acetonide, flunisolide, budesonide, and fluticasone propionate, by the CYP3A family of enzymes was studied to identify differences in their rates of clearance and to identify their metabolites. Budesonide 110-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-162 23175666-1 2013 This study was designed to evaluate the in vivo activity of cytochrome P450 3A (CYP3A) in 49 healthy Japanese subjects aged 22-58 years using endogenous cortisol 6beta-hydroxylation clearance [CLm(6beta)], a novel biomarker for CYP3A phenotyping. cortisol 6beta 153-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-78 23175666-1 2013 This study was designed to evaluate the in vivo activity of cytochrome P450 3A (CYP3A) in 49 healthy Japanese subjects aged 22-58 years using endogenous cortisol 6beta-hydroxylation clearance [CLm(6beta)], a novel biomarker for CYP3A phenotyping. cortisol 6beta 153-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-85 23143891-5 2013 In this work, the metabolism of four frequently prescribed inhaled GCs, triamcinolone acetonide, flunisolide, budesonide, and fluticasone propionate, by the CYP3A family of enzymes was studied to identify differences in their rates of clearance and to identify their metabolites. Fluticasone 126-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-162 23143891-9 2013 In contrast, flunisolide was only metabolized via CYP3A4, with no significant turnover by CYP3A5 or CYP3A7. flunisolide 13-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 23175666-2 2013 CLm(6beta) in the 49 healthy subjects was 2.40 +- 0.79 ml/min with an approximately 4-fold interindividual variability of CYP3A activity. clm 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-127 23404385-16 2013 This is the first study to report the genetic polymorphism of CYP3A5 in a North Indian population and its association with urinary 6beta-OH-CS/CS ratio reflecting the CYP3A phenotypes. 6 beta-hydroxycortisol 131-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 23175666-2 2013 CLm(6beta) in the 49 healthy subjects was 2.40 +- 0.79 ml/min with an approximately 4-fold interindividual variability of CYP3A activity. 6beta 4-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-127 23175667-2 2013 Tacrolimus is mainly metabolized via CYP3A4/5, whereas CYP2C19 and CYP3A4/5 are responsible for omeprazole metabolism. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-45 23175667-2 2013 Tacrolimus is mainly metabolized via CYP3A4/5, whereas CYP2C19 and CYP3A4/5 are responsible for omeprazole metabolism. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 23223499-2 2013 Placental growth hormone (PGH), estrogens (primarily 17beta-estradiol), cortisol, and progesterone have the potential to modulate CYP3A activity. GH2 protein, human 26-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-135 23223499-2 2013 Placental growth hormone (PGH), estrogens (primarily 17beta-estradiol), cortisol, and progesterone have the potential to modulate CYP3A activity. Estradiol 53-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-135 23223499-2 2013 Placental growth hormone (PGH), estrogens (primarily 17beta-estradiol), cortisol, and progesterone have the potential to modulate CYP3A activity. Hydrocortisone 72-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-135 23223499-2 2013 Placental growth hormone (PGH), estrogens (primarily 17beta-estradiol), cortisol, and progesterone have the potential to modulate CYP3A activity. Progesterone 86-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-135 23223499-5 2013 Of all the hormones, cortisol was the most potent inducer of CYP3A activity and CYP3A4, CYP3A5 mRNA expression. Hydrocortisone 21-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-66 23223499-5 2013 Of all the hormones, cortisol was the most potent inducer of CYP3A activity and CYP3A4, CYP3A5 mRNA expression. Hydrocortisone 21-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 23223499-6 2013 The combination of PGH/growth hormone and cortisol induced CYP3A activity and expression significantly more than did cortisol alone. GH2 protein, human 19-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 23223499-6 2013 The combination of PGH/growth hormone and cortisol induced CYP3A activity and expression significantly more than did cortisol alone. Hydrocortisone 42-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 23320989-7 2013 Cariprazine is metabolized by CYP3A4 and to a lesser extent by CYP2D6. cariprazine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 23404385-16 2013 This is the first study to report the genetic polymorphism of CYP3A5 in a North Indian population and its association with urinary 6beta-OH-CS/CS ratio reflecting the CYP3A phenotypes. Hydrocortisone 140-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 23071008-1 2013 Induction of the cytochrome P450 (CYP) family of enzymes by coadministered compounds can result in drug-drug interactions, as in the case of the coadministration of rifampicin with many CYP3A substrates, including midazolam. Rifampin 165-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 186-191 23071008-1 2013 Induction of the cytochrome P450 (CYP) family of enzymes by coadministered compounds can result in drug-drug interactions, as in the case of the coadministration of rifampicin with many CYP3A substrates, including midazolam. Midazolam 214-223 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 186-191 23071008-7 2013 The E(max) and EC(50) values in two separate lots of hepatocytes for CYP3A induction by rifampicin in a 96-well format were similar when discrete probe was compared with the probe cocktail. Rifampin 88-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 23188647-0 2013 Flavonoids and polymer derivatives as CYP3A4 inhibitors for improved oral drug bioavailability. Flavonoids 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 23436267-8 2013 This finding suggests that the inhibition of P-gp by ketoconazole, along with its effect on CYP3A4, needs to be considered when designing a DDI study of ketoconazole with a victim drug that is a dual substrate. Ketoconazole 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 23436267-8 2013 This finding suggests that the inhibition of P-gp by ketoconazole, along with its effect on CYP3A4, needs to be considered when designing a DDI study of ketoconazole with a victim drug that is a dual substrate. Ketoconazole 153-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 23188647-4 2013 Comparing results obtained from a known CYP3A4 inhibitor, verapamil, the flavonoids inhibited felodipine metabolism. Verapamil 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 23188647-4 2013 Comparing results obtained from a known CYP3A4 inhibitor, verapamil, the flavonoids inhibited felodipine metabolism. Flavonoids 73-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 23188647-4 2013 Comparing results obtained from a known CYP3A4 inhibitor, verapamil, the flavonoids inhibited felodipine metabolism. Felodipine 94-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 23188647-5 2013 In-depth computational analysis of these flavonoids in terms of CYP3A4 binding, sequencing, and affinity, computational biomimetism was employed to validate the potential CYP3A4 inhibitors. Flavonoids 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 23188647-5 2013 In-depth computational analysis of these flavonoids in terms of CYP3A4 binding, sequencing, and affinity, computational biomimetism was employed to validate the potential CYP3A4 inhibitors. Flavonoids 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 23318278-9 2013 The clobazam C/D ratio has the potential to measure the contribution of CYP3A4 activity to the clearance of clobazam from the body. Clobazam 4-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 23073666-0 2013 Effect of the fluoroquinolone antibacterial agent DX-619 on the apparent formation and renal clearances of 6beta-hydroxycortisol, an endogenous probe for CYP3A4 inhibition, in healthy subjects. 6 beta-hydroxycortisol 107-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 23073666-1 2013 PURPOSE: To examine the effect of the fluoroquinolone DX-619 on CYP3A4 and urinary excretion of 6beta-hydroxycortisol, an endogenous probe of hepatic CYP3A4 activity, in healthy subjects. Fluoroquinolones 38-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 23073666-5 2013 RESULTS: DX-619 was a mechanism-based inhibitor of CYP3A4, with K(I) and k(inact) of 67.9 +- 7.3 mumol/l and 0.0730 +- 0.0033 min(-1), respectively. DX 619 9-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 23073666-6 2013 Pharmacokinetic simulation suggested in vivo relevance of CYP3A4 inhibition by DX-619. DX 619 79-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 23073666-10 2013 CONCLUSIONS: DX-619 caused a moderate inhibition of hepatic CYP3A4-mediated formation and significant inhibition of MATE-mediated efflux of 6beta-hydroxycortisol into urine. DX 619 13-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 23318278-4 2013 Clobazam is mainly metabolized by a cytochrome P450 (CYP) isoenzyme, CYP3A4, to its active metabolite, N-desmethylclobazam. Clobazam 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 23318278-9 2013 The clobazam C/D ratio has the potential to measure the contribution of CYP3A4 activity to the clearance of clobazam from the body. Clobazam 108-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 23318278-4 2013 Clobazam is mainly metabolized by a cytochrome P450 (CYP) isoenzyme, CYP3A4, to its active metabolite, N-desmethylclobazam. N-desmethylclobazam 103-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 23408444-1 2013 The P-gp/MDR1 multidrug transporter mediates detoxification of numerous drugs, including colchicine, and CYP3A4 is key to the biotransformation of colchicine. Colchicine 89-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 22830982-7 2013 Furthermore, the RTqPCR analysis showed that the drugs acted as inductors leading to overexpression of mRNA levels when compared to post-thawing values (such as for HNF4alpha, PXR and CYP3A4 by dextromethorpahn and omeprazole). dextromethorpahn 194-210 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 23408444-1 2013 The P-gp/MDR1 multidrug transporter mediates detoxification of numerous drugs, including colchicine, and CYP3A4 is key to the biotransformation of colchicine. Colchicine 147-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 23480152-7 2013 Perampanel has high oral bioavailability, dose-proportional kinetics, and undergoes oxidative metabolism, primarily via CYP3A4, followed by glucuronidation. perampanel 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 23107770-2 2013 The oral bioavailability of tacrolimus varies greatly between individuals and depends largely on the activity of both the cytochrome P450 3A (CYP3A) subfamily and P-glycoprotein (P-gp). Tacrolimus 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-140 23107770-2 2013 The oral bioavailability of tacrolimus varies greatly between individuals and depends largely on the activity of both the cytochrome P450 3A (CYP3A) subfamily and P-glycoprotein (P-gp). Tacrolimus 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-147 23107770-3 2013 The possible influence of single nucleotide polymorphisms (SNPs) of CYP3A subfamily and P-gp (MDR-1) in liver transplant recipients has recently been indicated as one of the most important variables affecting the pharmacokinetics of tacrolimus and the renal injury induced by tacrolimus. Tacrolimus 233-243 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 23107770-3 2013 The possible influence of single nucleotide polymorphisms (SNPs) of CYP3A subfamily and P-gp (MDR-1) in liver transplant recipients has recently been indicated as one of the most important variables affecting the pharmacokinetics of tacrolimus and the renal injury induced by tacrolimus. Tacrolimus 276-286 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 23160340-0 2013 CYP3A4 overexpression enhances the cytotoxicity of the antitumor triazoloacridinone derivative C-1305 in CHO cells. triazoloacridinone 65-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23160340-0 2013 CYP3A4 overexpression enhances the cytotoxicity of the antitumor triazoloacridinone derivative C-1305 in CHO cells. C 1305 95-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23160340-1 2013 AIM: To examine how the higher expression level of CYP3A4 isoenzyme influenced the cytotoxicity of the antitumor triazoloacridinone derivative C-1305 in Chinese hamster ovary (CHO) cells. triazoloacridinone 113-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 23160340-1 2013 AIM: To examine how the higher expression level of CYP3A4 isoenzyme influenced the cytotoxicity of the antitumor triazoloacridinone derivative C-1305 in Chinese hamster ovary (CHO) cells. C 1305 143-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 23234359-11 2013 Preincubation of THLE-3A4 cells with the cytochrome P450 3A4 inhibitor ritonavir blocked the selective toxicity of rimonabant to these cells. Ritonavir 71-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-60 23234359-11 2013 Preincubation of THLE-3A4 cells with the cytochrome P450 3A4 inhibitor ritonavir blocked the selective toxicity of rimonabant to these cells. Rimonabant 115-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-60 23234359-13 2013 We conclude that the potent toxicity of rimonabant in THLE-3A4 cells occurs by a mechanistic sequence, which is initiated by cytochrome P450 3A4 mediated formation of a highly cytotoxic reactive iminium ion metabolite that binds covalently to cellular proteins. Rimonabant 40-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-144 23480152-8 2013 The terminal half-life (t1/2 ) in humans is 105 h; however, in the presence of a strong CYP3A4 inducer (such as carbamazepine), the t1/2 can be reduced. Carbamazepine 112-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 24110489-3 2013 We aimed to develop a biologically relevant pharmacokinetic model of lopinavir with a description of a CYP3A4-mediated first pass metabolism and enterohepatic circulation (EHC). Lopinavir 69-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 24292054-3 2013 In our study, the kinetics of CYP3A4-catalyzed carbamazepine 10,11-epoxidation in human liver microsomes was sigmoidal and fitted to the Hill equation, revealing the S50 value of 358 microM, n of 2.0, and the Vmax value of 463 pmol/min/mg. Carbamazepine 47-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 24189425-2 2013 The concentration/dose (C/D) ratio of tacrolimus in patients carrying graft liver with CYP3A4*1/*1 was significantly higher during 7 d after surgery than in that with CYP3A4*1/*1G (214 vs. 157 [ng/mL]/[mg/kg/day], p<0.01). Tacrolimus 38-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 25011542-2 2013 Docetaxel is metabolized by cytochrome P450 3A4 (CYP3A4). Docetaxel 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-47 24189425-8 2013 Thus, we elucidated that CYP3A4*1G genotype in the intestine was an important indicator of the pharmacokinetics of tacrolimus, whereas this genotype in the graft liver tended to influence the frequency of acute cellular rejection after transplantation. Tacrolimus 115-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 23407140-9 2013 However, this benefit may in part be driven by an increased efficacy of CYP3A4-metabolized statins on top of ticagrelor and/or from the inappropriate dose restriction of simvastatin and lovastatin in the clopidogrel arm. Ticagrelor 109-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 23257955-4 2013 Since fentanyl is predominantly metabolized by the drug-metabolizing enzyme cytochrome P450 (CYP) 3A4 in the liver, its concentration may vary in cases of physiologically reduced CYP3A4 activity in the liver (liver disease and aging) or on co-administration of drugs. Fentanyl 6-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-101 23257955-4 2013 Since fentanyl is predominantly metabolized by the drug-metabolizing enzyme cytochrome P450 (CYP) 3A4 in the liver, its concentration may vary in cases of physiologically reduced CYP3A4 activity in the liver (liver disease and aging) or on co-administration of drugs. Fentanyl 6-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 25011542-2 2013 Docetaxel is metabolized by cytochrome P450 3A4 (CYP3A4). Docetaxel 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 25011542-3 2013 Clarithromycin, a potent inhibitor of CYP3A4, is occasionally used in combination with docetaxel. Clarithromycin 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 23001793-5 2013 Ketoconazole (inhibitor of CYP3A4/5) inhibited metabolism of (-)-THP or (+)-THP at same degree, whereas the inhibition of fluvoxamine (inhibitor of CYP1A2) on metabolism of (+)-THP was greater than that of (-)-THP; moreover, the metabolic rate of (+)-THP was 5.3-fold of (-)-THP in recombinant human CYP1A2. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-35 23762720-0 2013 Glossopharyngeal Dystonia Secondary to a Lurasidone-Fluoxetine CYP-3A4 Interaction. Lurasidone Hydrochloride 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-70 23762720-3 2013 In this case, we report a glossopharyngeal dystonia secondary to a lurasidone-fluoxetine CYP-3A4 interaction to highlight the importance of maintaining an index of suspicion for laryngeal dystonia, a potentially fatal dystonia. Lurasidone Hydrochloride 67-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-96 23762720-3 2013 In this case, we report a glossopharyngeal dystonia secondary to a lurasidone-fluoxetine CYP-3A4 interaction to highlight the importance of maintaining an index of suspicion for laryngeal dystonia, a potentially fatal dystonia. Fluoxetine 78-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-96 23400261-0 2013 CYP3A4 genetic status may be associated with increased vulnerability to the inhibitory effect of calcium-channel blockers on clopidogrel. Clopidogrel 125-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23400261-1 2013 BACKGROUND: Calcium-channel blockers (CCBs) inhibit the CYP3A4 enzyme, which is involved in clopidogrel activation. Clopidogrel 92-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 23400261-3 2013 We investigated the relationship between CYP3A4 genotype and the inhibitory effect of CCBs on clopidogrel response. Clopidogrel 94-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 23400261-11 2013 The number of CYP3A4 (IVS10+12G>A) A-alleles may be associated with an increased vulnerability to the effects of CCBs on clopidogrel response variation. Clopidogrel 124-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 23001793-5 2013 Ketoconazole (inhibitor of CYP3A4/5) inhibited metabolism of (-)-THP or (+)-THP at same degree, whereas the inhibition of fluvoxamine (inhibitor of CYP1A2) on metabolism of (+)-THP was greater than that of (-)-THP; moreover, the metabolic rate of (+)-THP was 5.3-fold of (-)-THP in recombinant human CYP1A2. tetrahydropalmatine 61-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-35 23001793-5 2013 Ketoconazole (inhibitor of CYP3A4/5) inhibited metabolism of (-)-THP or (+)-THP at same degree, whereas the inhibition of fluvoxamine (inhibitor of CYP1A2) on metabolism of (+)-THP was greater than that of (-)-THP; moreover, the metabolic rate of (+)-THP was 5.3-fold of (-)-THP in recombinant human CYP1A2. tetrahydropalmatine 72-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-35 22971642-10 2013 Furthermore, cyp isoforms other than CYP3A, which contribute to the metabolism of saquinavir in humans, are involved in the metabolism of saquinavir in mice. Saquinavir 82-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-42 23028140-7 2013 In the beginning of imatinib treatment, the fractions of its hepatic clearance mediated by CYP2C8 and CYP3A4 were predicted to approximate 40 and 60%, respectively. Imatinib Mesylate 20-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 23028140-8 2013 During long-term treatment with imatinib 400 mg once or twice daily, up to 65 or 75% of its hepatic elimination was predicted to occur via CYP2C8, and only about 35 or 25% by CYP3A4, due to dose- and time-dependent autoinactivation of CYP3A4 by imatinib. Imatinib Mesylate 32-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 23028140-8 2013 During long-term treatment with imatinib 400 mg once or twice daily, up to 65 or 75% of its hepatic elimination was predicted to occur via CYP2C8, and only about 35 or 25% by CYP3A4, due to dose- and time-dependent autoinactivation of CYP3A4 by imatinib. Imatinib Mesylate 32-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 235-241 23028140-9 2013 Thus, although CYP2C8 and CYP3A4 are the main enzymes in imatinib metabolism in vitro, in silico predictions indicate that imatinib inhibits its own CYP3A4-mediated metabolism, assigning a key role for CYP2C8. Imatinib Mesylate 57-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 23028140-9 2013 Thus, although CYP2C8 and CYP3A4 are the main enzymes in imatinib metabolism in vitro, in silico predictions indicate that imatinib inhibits its own CYP3A4-mediated metabolism, assigning a key role for CYP2C8. Imatinib Mesylate 123-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 23073735-8 2013 Thorough investigations of the biotransformation of AZD3839 have been performed to find the reactive pathway causing the TDI of CYP3A4, and are presented here. AZD3839 52-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 22971642-10 2013 Furthermore, cyp isoforms other than CYP3A, which contribute to the metabolism of saquinavir in humans, are involved in the metabolism of saquinavir in mice. Saquinavir 138-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-42 23118326-6 2013 A clinical DDI study was conducted in patients with solid tumors to evaluate the effect of carfilzomib on CYP3A activity. carfilzomib 91-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-111 23028140-0 2013 Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response. Imatinib Mesylate 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 23118326-11 2013 Carfilzomib showed direct and time-dependent inhibition of CYP3A in human liver microsome preparations and exposure to carfilzomib resulted in reductions in CYP3A and 1A2 gene expression in cultured human hepatocytes. carfilzomib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 23118326-11 2013 Carfilzomib showed direct and time-dependent inhibition of CYP3A in human liver microsome preparations and exposure to carfilzomib resulted in reductions in CYP3A and 1A2 gene expression in cultured human hepatocytes. carfilzomib 119-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-170 23257392-0 2013 Mechanism-based inhibition of CYP1A1 and CYP3A4 by the furanocoumarin chalepensin. Furocoumarins 55-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 23257392-0 2013 Mechanism-based inhibition of CYP1A1 and CYP3A4 by the furanocoumarin chalepensin. 3-(alpha,alpha-dimethylallyl)psoralen 70-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 23028140-1 2013 Recent data suggest that the role of CYP3A4 in imatinib metabolism is smaller than presumed. Imatinib Mesylate 47-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 23028140-5 2013 In vitro, CYP2C8 inhibitors and CYP3A4 inhibitors inhibited the depletion of 0.1 microM imatinib by 45 and 80%, respectively, and the formation of the main metabolite of imatinib, N-desmethylimatinib, by >50%. Imatinib Mesylate 88-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 23257392-1 2013 The cytochrome P450 (P450, CYP) 2A6 inhibitor chalepensin was found to inhibit human CYP1A1, CYP1A2, CYP2A13, CYP2C9, CYP2D6, CYP2E1, and CYP3A4 to different extents. 3-(alpha,alpha-dimethylallyl)psoralen 46-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 23028140-5 2013 In vitro, CYP2C8 inhibitors and CYP3A4 inhibitors inhibited the depletion of 0.1 microM imatinib by 45 and 80%, respectively, and the formation of the main metabolite of imatinib, N-desmethylimatinib, by >50%. Imatinib Mesylate 170-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 23028140-5 2013 In vitro, CYP2C8 inhibitors and CYP3A4 inhibitors inhibited the depletion of 0.1 microM imatinib by 45 and 80%, respectively, and the formation of the main metabolite of imatinib, N-desmethylimatinib, by >50%. N-desmethylimatinib 180-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 23257392-2 2013 CYP1A1 and CYP3A4 underwent pronounced mechanism-based inactivation by chalepensin and had the smallest IC50 ratios of inhibition with NADPH-fortified pre-incubation (IC50(+)) to that without pre-incubation (IC50(-)). 3-(alpha,alpha-dimethylallyl)psoralen 71-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 23028140-6 2013 Likewise, recombinant CYP2C8 and CYP3A4 metabolized imatinib extensively, whereas other isoforms had minor effect on imatinib concentrations. Imatinib Mesylate 52-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 23257392-2 2013 CYP1A1 and CYP3A4 underwent pronounced mechanism-based inactivation by chalepensin and had the smallest IC50 ratios of inhibition with NADPH-fortified pre-incubation (IC50(+)) to that without pre-incubation (IC50(-)). NADP 135-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 23364258-0 2013 Active eosinophilic esophagitis is associated with impaired elimination of budesonide by cytochrome P450 3A enzymes. Budesonide 75-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-107 23257392-6 2013 Cytosol-supported glutathione conjugation protected CYP3A4 but not CYP1A1 against the inactivation by chalepensin. Glutathione 18-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 23257392-6 2013 Cytosol-supported glutathione conjugation protected CYP3A4 but not CYP1A1 against the inactivation by chalepensin. 3-(alpha,alpha-dimethylallyl)psoralen 102-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 23257392-8 2013 The high epoxidation activities of CYP1A1, CYP2A6, and CYP3A4 were in agreement with their pronounced susceptibilities to mechanism-based inactivation by chalepensin. 3-(alpha,alpha-dimethylallyl)psoralen 154-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 23257392-9 2013 Considering both the IC50 values and inactivation kinetic parameters, the threshold concentrations of chalepensin for potential drug interactions through inhibition of CYP2A6 and CYP3A4 were estimated to be consistently low. 3-(alpha,alpha-dimethylallyl)psoralen 102-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 23268924-5 2013 In human liver microsomes, IC50 values of GTE were 5.9, 4.5, 48.7, 25.1 and 13.8 microg/mL, for CYP2B6, CYP2C8, CYP2C19, CYP2D6 and CYP3A, respectively. epigallocatechin gallate 42-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-137 23268924-7 2013 In human intestinal microsomes, IC50 values of GTE and EGCG for CYP3A were 18.4 microg/mL and 31.1 microM, respectively. epigallocatechin gallate 47-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 23268924-7 2013 In human intestinal microsomes, IC50 values of GTE and EGCG for CYP3A were 18.4 microg/mL and 31.1 microM, respectively. epigallocatechin gallate 55-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 23268924-8 2013 EGCG moderately inhibited CYP3A activity in a noncompetitive manner. epigallocatechin gallate 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-31 23268924-9 2013 These results suggest that green tea catechins cause clinically relevant interactions with substrates for CYP2B6 and CYP2C8 in addition to CYP3A. Catechin 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-144 23364258-2 2013 Safety of budesonide is based on high elimination by cytochrome P450 3A (CYP3A) enzymes. Budesonide 10-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-71 23314529-2 2013 Metabolism of certain statins involves the cytochrome P450 3A (CYP3A) enzymes, and CYP3A4*22 significantly influences the dose needed for achieving optimal lipid control for atorvastatin, simvastatin, and lovastatin. Atorvastatin 174-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 23314529-2 2013 Metabolism of certain statins involves the cytochrome P450 3A (CYP3A) enzymes, and CYP3A4*22 significantly influences the dose needed for achieving optimal lipid control for atorvastatin, simvastatin, and lovastatin. Atorvastatin 174-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 23268924-2 2013 The objective of the present study was to evaluate the effects of green tea extract (GTE, total catechins 86.5%, w/w) and (-)-epigallocatechin-3-gallate (EGCG) on the activities of CYP2B6, CYP2C8, CYP2C19, CYP2D6 and CYP3A in vitro, using pooled human liver and intestinal microsomes. epigallocatechin gallate 85-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-222 23268924-2 2013 The objective of the present study was to evaluate the effects of green tea extract (GTE, total catechins 86.5%, w/w) and (-)-epigallocatechin-3-gallate (EGCG) on the activities of CYP2B6, CYP2C8, CYP2C19, CYP2D6 and CYP3A in vitro, using pooled human liver and intestinal microsomes. epigallocatechin gallate 122-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-222 23268924-2 2013 The objective of the present study was to evaluate the effects of green tea extract (GTE, total catechins 86.5%, w/w) and (-)-epigallocatechin-3-gallate (EGCG) on the activities of CYP2B6, CYP2C8, CYP2C19, CYP2D6 and CYP3A in vitro, using pooled human liver and intestinal microsomes. epigallocatechin gallate 154-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-222 23314529-2 2013 Metabolism of certain statins involves the cytochrome P450 3A (CYP3A) enzymes, and CYP3A4*22 significantly influences the dose needed for achieving optimal lipid control for atorvastatin, simvastatin, and lovastatin. Simvastatin 188-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 23314529-2 2013 Metabolism of certain statins involves the cytochrome P450 3A (CYP3A) enzymes, and CYP3A4*22 significantly influences the dose needed for achieving optimal lipid control for atorvastatin, simvastatin, and lovastatin. Simvastatin 188-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 23314529-2 2013 Metabolism of certain statins involves the cytochrome P450 3A (CYP3A) enzymes, and CYP3A4*22 significantly influences the dose needed for achieving optimal lipid control for atorvastatin, simvastatin, and lovastatin. Lovastatin 205-215 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 23364258-2 2013 Safety of budesonide is based on high elimination by cytochrome P450 3A (CYP3A) enzymes. Budesonide 10-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 23314529-2 2013 Metabolism of certain statins involves the cytochrome P450 3A (CYP3A) enzymes, and CYP3A4*22 significantly influences the dose needed for achieving optimal lipid control for atorvastatin, simvastatin, and lovastatin. Lovastatin 205-215 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 23385314-3 2013 Efavirenz was a moderate inhibitor of CYP2C9 (K(i) = 19.46 microM) and CYP2C19 (K(i) = 21.31 microM); and a weak inhibitor of CYP3A (K(i) = 40.33 microM). efavirenz 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-131 23364258-10 2013 CONCLUSION: Active EoE is associated with reduced elimination of budesonide via CYP3A, the major subfamily of drug-metabolizing enzymes in humans. Budesonide 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-85 24166670-2 2013 BI 11634 is a factor Xa inhibitor in drug development and its interaction with CYP3A4 was evaluated. N-(1-(5-chloro-1H-benzimidazol-2-yl)-2-methoxyethyl)-3-methyl-4-(3-oxo-4-morpholinyl)benzamide 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 23629743-5 2013 These results are consistent with those of molecular docking simulations, where paclitaxel could not access the CYP2C8 catalytic site in the presence of nilotinib, but the binding of midazolam, a substrate of CYP3A4, to the catalytic site of CYP3A4 was not affected by nilotinib. Paclitaxel 80-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 209-215 23629743-5 2013 These results are consistent with those of molecular docking simulations, where paclitaxel could not access the CYP2C8 catalytic site in the presence of nilotinib, but the binding of midazolam, a substrate of CYP3A4, to the catalytic site of CYP3A4 was not affected by nilotinib. Paclitaxel 80-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 242-248 23514827-5 2013 In this study, we quantitatively investigated the inhibition kinetics of MBI inhibitors, erythromycin and clarithromycin, on the CYP3A4 variants CYP3A4.1, 4.2, 4.7, 4.16, and 4.18. Erythromycin 89-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 23514827-5 2013 In this study, we quantitatively investigated the inhibition kinetics of MBI inhibitors, erythromycin and clarithromycin, on the CYP3A4 variants CYP3A4.1, 4.2, 4.7, 4.16, and 4.18. Erythromycin 89-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 23514827-5 2013 In this study, we quantitatively investigated the inhibition kinetics of MBI inhibitors, erythromycin and clarithromycin, on the CYP3A4 variants CYP3A4.1, 4.2, 4.7, 4.16, and 4.18. Clarithromycin 106-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 23514827-5 2013 In this study, we quantitatively investigated the inhibition kinetics of MBI inhibitors, erythromycin and clarithromycin, on the CYP3A4 variants CYP3A4.1, 4.2, 4.7, 4.16, and 4.18. Clarithromycin 106-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 23514827-6 2013 The activity of CYP3A4 was assessed using testosterone 6beta-hydroxylation with recombinant CYP3A4. testosterone 6beta 42-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 23629743-5 2013 These results are consistent with those of molecular docking simulations, where paclitaxel could not access the CYP2C8 catalytic site in the presence of nilotinib, but the binding of midazolam, a substrate of CYP3A4, to the catalytic site of CYP3A4 was not affected by nilotinib. Midazolam 183-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 209-215 23514827-7 2013 Both erythromycin and clarithromycin decreased the activity of CYP3A4 in a time-dependent manner. Erythromycin 5-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 23629743-5 2013 These results are consistent with those of molecular docking simulations, where paclitaxel could not access the CYP2C8 catalytic site in the presence of nilotinib, but the binding of midazolam, a substrate of CYP3A4, to the catalytic site of CYP3A4 was not affected by nilotinib. Midazolam 183-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 242-248 24166670-5 2013 Inhibition of the CYP3A4-mediated metabolism of BI 11634 by quinidine was further evaluated. Quinidine 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 23629743-5 2013 These results are consistent with those of molecular docking simulations, where paclitaxel could not access the CYP2C8 catalytic site in the presence of nilotinib, but the binding of midazolam, a substrate of CYP3A4, to the catalytic site of CYP3A4 was not affected by nilotinib. nilotinib 269-278 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 209-215 23514827-7 2013 Both erythromycin and clarithromycin decreased the activity of CYP3A4 in a time-dependent manner. Clarithromycin 22-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 23514827-8 2013 The maximum inactivation rate constants, k(inact,max), of erythromycin for CYP3A4.2 and CYP3A4.7 were 0.5-fold that for CYP3A4.1, while that for CYP3A4.16 and CYP3A4.18 were similar to that for CYP3A4.1. Erythromycin 58-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 23514827-8 2013 The maximum inactivation rate constants, k(inact,max), of erythromycin for CYP3A4.2 and CYP3A4.7 were 0.5-fold that for CYP3A4.1, while that for CYP3A4.16 and CYP3A4.18 were similar to that for CYP3A4.1. Erythromycin 58-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 24166670-6 2013 RESULTS: From the reaction phenotyping studies, it was shown that the metabolism of BI 11634 in HLM was inhibited by ketoconazole and quinidine, well-accepted specific inhibitors of CYP3A4 and CYP2D6, respectively. Bismuth 84-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 182-188 23514827-8 2013 The maximum inactivation rate constants, k(inact,max), of erythromycin for CYP3A4.2 and CYP3A4.7 were 0.5-fold that for CYP3A4.1, while that for CYP3A4.16 and CYP3A4.18 were similar to that for CYP3A4.1. Erythromycin 58-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 23514827-8 2013 The maximum inactivation rate constants, k(inact,max), of erythromycin for CYP3A4.2 and CYP3A4.7 were 0.5-fold that for CYP3A4.1, while that for CYP3A4.16 and CYP3A4.18 were similar to that for CYP3A4.1. Erythromycin 58-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 24166670-6 2013 RESULTS: From the reaction phenotyping studies, it was shown that the metabolism of BI 11634 in HLM was inhibited by ketoconazole and quinidine, well-accepted specific inhibitors of CYP3A4 and CYP2D6, respectively. Ketoconazole 117-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 182-188 23514827-8 2013 The maximum inactivation rate constants, k(inact,max), of erythromycin for CYP3A4.2 and CYP3A4.7 were 0.5-fold that for CYP3A4.1, while that for CYP3A4.16 and CYP3A4.18 were similar to that for CYP3A4.1. Erythromycin 58-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 23514827-8 2013 The maximum inactivation rate constants, k(inact,max), of erythromycin for CYP3A4.2 and CYP3A4.7 were 0.5-fold that for CYP3A4.1, while that for CYP3A4.16 and CYP3A4.18 were similar to that for CYP3A4.1. Erythromycin 58-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 23514827-9 2013 The K(I) values of erythromycin for CYP3A4.2, 4.7, 4.16, and 4.18 were 1.2-, 0.4-, 2.2- and 0.72-fold those of CYP3A4.1, respectively. Erythromycin 19-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 23514827-9 2013 The K(I) values of erythromycin for CYP3A4.2, 4.7, 4.16, and 4.18 were 1.2-, 0.4-, 2.2- and 0.72-fold those of CYP3A4.1, respectively. Erythromycin 19-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 24166670-6 2013 RESULTS: From the reaction phenotyping studies, it was shown that the metabolism of BI 11634 in HLM was inhibited by ketoconazole and quinidine, well-accepted specific inhibitors of CYP3A4 and CYP2D6, respectively. Quinidine 134-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 182-188 24166670-8 2013 Additional studies confirmed that BI 11634 was metabolized by CYP3A4 to form one major metabolite and this reaction was inhibited by quinidine with a Ki of 7 microM. N-(1-(5-chloro-1H-benzimidazol-2-yl)-2-methoxyethyl)-3-methyl-4-(3-oxo-4-morpholinyl)benzamide 34-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 24166670-8 2013 Additional studies confirmed that BI 11634 was metabolized by CYP3A4 to form one major metabolite and this reaction was inhibited by quinidine with a Ki of 7 microM. Quinidine 133-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 24166670-9 2013 CONCLUSIONS: These data indicated that BI 11634 may interact with CYP3A4 similar to nifedipine. N-(1-(5-chloro-1H-benzimidazol-2-yl)-2-methoxyethyl)-3-methyl-4-(3-oxo-4-morpholinyl)benzamide 39-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 24166670-10 2013 CYP3A4 substrates have been categorized into three subgroups, including a stand-alone subgroup for dihydropyridine calcium channel blockers such as nifedipine and felodipine. Nifedipine 148-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24166670-10 2013 CYP3A4 substrates have been categorized into three subgroups, including a stand-alone subgroup for dihydropyridine calcium channel blockers such as nifedipine and felodipine. Felodipine 163-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24166670-12 2013 The specificity of quinidine as a CYP2D6 inhibitor is questionable as it can also significantly inhibit CYP3A4-mediated metabolism of some compounds. Quinidine 19-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 24379885-1 2013 We recently reported that Praeruptorin C effectively transactivated the mRNA, protein expression, and catalytic activity of CYP3A4 via the CAR-mediated pathway, but whether and how PC could affect the expression and catalytic activity of CYP3A4 via PXR pathway remains unknown. pc 181-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 238-244 24223062-0 2013 Opposite Effects of Single-Dose and Multidose Administration of the Ethanol Extract of Danshen on CYP3A in Healthy Volunteers. Ethanol 68-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 24223062-1 2013 The aim of this study was to investigate the effect of single- and multidose administration of the ethanol extract of danshen on in vivo CYP3A activity in healthy volunteers. Ethanol 99-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-142 24379885-5 2013 These findings suggest that PC can significantly upregulate CYP3A level via the PXR-mediated pathway, and this should be taken into consideration to predict any potential herb-drug interactions between PC, Qianhu, and the other coadministered drugs. pc 28-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 24223062-7 2013 The in vitro study showed that dihydrotanshinone I in the extract could inhibit CYP3A, while tanshinone IIA and cryptotanshinone could induce CYP3A. dhts 31-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-85 24223062-7 2013 The in vitro study showed that dihydrotanshinone I in the extract could inhibit CYP3A, while tanshinone IIA and cryptotanshinone could induce CYP3A. tanshinone 93-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-147 23162091-0 2013 Mitotane therapy in adrenocortical cancer induces CYP3A4 and inhibits 5alpha-reductase, explaining the need for personalized glucocorticoid and androgen replacement. Mitotane 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 24223062-7 2013 The in vitro study showed that dihydrotanshinone I in the extract could inhibit CYP3A, while tanshinone IIA and cryptotanshinone could induce CYP3A. cryptotanshinone 112-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-147 23137182-6 2013 When saxagliptin is used in combination with a strong inhibitor of CYP3A4/A5, reduction in the daily dosage is recommended. saxagliptin 5-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 22505343-7 2013 The reduced risk from ibuprofen use was limited to individuals carrying the T allele of a single nucleotide polymorphism (rs4646450) compared to those who did not use ibuprofen and did not carry the T allele in the CYP3A locus, providing new evidence that this association might be modified by polymorphisms in genes that metabolize ibuprofen. Ibuprofen 22-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-220 23162091-7 2013 RESULTS: We found a sharp increase in the excretion of 6beta-hydroxycortisol over cortisol (P < 0.001), indicative of a strong induction of the major drug-metabolizing enzyme cytochrome P450 3A4. 6 beta-hydroxycortisol 55-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-197 23162091-7 2013 RESULTS: We found a sharp increase in the excretion of 6beta-hydroxycortisol over cortisol (P < 0.001), indicative of a strong induction of the major drug-metabolizing enzyme cytochrome P450 3A4. Hydrocortisone 68-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-197 23162091-12 2013 CONCLUSIONS: Cytochrome P450 3A4 induction by mitotane results in rapid inactivation of more than 50% of administered hydrocortisone, explaining the need for doubling hydrocortisone replacement in mitotane-treated patients. Mitotane 46-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-32 23162091-12 2013 CONCLUSIONS: Cytochrome P450 3A4 induction by mitotane results in rapid inactivation of more than 50% of administered hydrocortisone, explaining the need for doubling hydrocortisone replacement in mitotane-treated patients. Hydrocortisone 118-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-32 23162091-12 2013 CONCLUSIONS: Cytochrome P450 3A4 induction by mitotane results in rapid inactivation of more than 50% of administered hydrocortisone, explaining the need for doubling hydrocortisone replacement in mitotane-treated patients. Hydrocortisone 167-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-32 23162091-12 2013 CONCLUSIONS: Cytochrome P450 3A4 induction by mitotane results in rapid inactivation of more than 50% of administered hydrocortisone, explaining the need for doubling hydrocortisone replacement in mitotane-treated patients. Mitotane 197-205 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-32 23400742-1 2013 The nonnucleoside reverse transcriptase inhibitor etravirine, approved for use in treatment-experienced, HIV-1-infected patients, is a substrate and inducer of cytochrome P450 (CYP) 3A4 and a substrate and inhibitor of CYP2C9/CYP2C19. etravirine 50-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-185 23958198-3 2013 Based on in vitro evidence cranberry juice is an inhibitor of CYP enzymes and at higher amounts as potent as ketoconazole (CYP3A) and fluconazole (CYP2C9). Ketoconazole 109-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-128 23525057-7 2013 Due to inhibition of CYP3A4 and P-glycoprotein, significant drug-drug interactions are possible with telaprevir. telaprevir 101-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 23400746-6 2013 This is consistent with the in vitro results, in which fimasartan is a substrate of CYP3A and OATP1B1. fimasartan 55-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-89 23665933-5 2013 Liver microsomes genotyped as CYP3A4*1/*22 (n = 4) showed significantly lower CYP3A-dependent dextromethorphan N-demethylation, midazolam 1"-hydroxylation, and testosterone 6beta-hydroxylation activities, as well as lower expression levels of CYP3A protein (28% of control), compared with those of the CYP3A4*1/*1 group (n = 19). Midazolam 128-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 23548184-7 2013 Ritonavir exhibits strong inhibition of hepatic enzyme CYP 3A4, which is part of the major metabolic pathway of most glucocorticoids. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-62 22982757-5 2013 The metabolism of O2C3 was significantly inhibited by ketoconazole, and the recombinant human CYP3A4 converted O2C3 to 1alpha,2alpha,25(OH)(3)D(3), which suggests that CYP3A4 is responsible for the metabolism of O2C3 in human liver. o2c3 18-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 22982757-5 2013 The metabolism of O2C3 was significantly inhibited by ketoconazole, and the recombinant human CYP3A4 converted O2C3 to 1alpha,2alpha,25(OH)(3)D(3), which suggests that CYP3A4 is responsible for the metabolism of O2C3 in human liver. o2c3 18-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 24382036-7 2013 Use of carbamazepine, a CYP3A4 inducer, probably led to an increased clearance of rivaroxaban resulting in pulmonary embolisms. Rivaroxaban 82-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 23841924-3 2013 The metabolism and bioavailability of cyclosporin can be significantly and persistently influenced through induction of CYP3A4 caused by the concomitant use of rifampicin. Cyclosporine 38-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 23665933-5 2013 Liver microsomes genotyped as CYP3A4*1/*22 (n = 4) showed significantly lower CYP3A-dependent dextromethorphan N-demethylation, midazolam 1"-hydroxylation, and testosterone 6beta-hydroxylation activities, as well as lower expression levels of CYP3A protein (28% of control), compared with those of the CYP3A4*1/*1 group (n = 19). Dextromethorphan 94-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 23665933-5 2013 Liver microsomes genotyped as CYP3A4*1/*22 (n = 4) showed significantly lower CYP3A-dependent dextromethorphan N-demethylation, midazolam 1"-hydroxylation, and testosterone 6beta-hydroxylation activities, as well as lower expression levels of CYP3A protein (28% of control), compared with those of the CYP3A4*1/*1 group (n = 19). Dextromethorphan 94-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-35 23665933-5 2013 Liver microsomes genotyped as CYP3A4*1/*22 (n = 4) showed significantly lower CYP3A-dependent dextromethorphan N-demethylation, midazolam 1"-hydroxylation, and testosterone 6beta-hydroxylation activities, as well as lower expression levels of CYP3A protein (28% of control), compared with those of the CYP3A4*1/*1 group (n = 19). Dextromethorphan 94-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 23665933-5 2013 Liver microsomes genotyped as CYP3A4*1/*22 (n = 4) showed significantly lower CYP3A-dependent dextromethorphan N-demethylation, midazolam 1"-hydroxylation, and testosterone 6beta-hydroxylation activities, as well as lower expression levels of CYP3A protein (28% of control), compared with those of the CYP3A4*1/*1 group (n = 19). Midazolam 128-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-35 23665933-5 2013 Liver microsomes genotyped as CYP3A4*1/*22 (n = 4) showed significantly lower CYP3A-dependent dextromethorphan N-demethylation, midazolam 1"-hydroxylation, and testosterone 6beta-hydroxylation activities, as well as lower expression levels of CYP3A protein (28% of control), compared with those of the CYP3A4*1/*1 group (n = 19). Testosterone 160-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 23665933-5 2013 Liver microsomes genotyped as CYP3A4*1/*22 (n = 4) showed significantly lower CYP3A-dependent dextromethorphan N-demethylation, midazolam 1"-hydroxylation, and testosterone 6beta-hydroxylation activities, as well as lower expression levels of CYP3A protein (28% of control), compared with those of the CYP3A4*1/*1 group (n = 19). Testosterone 160-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-35 23665933-5 2013 Liver microsomes genotyped as CYP3A4*1/*22 (n = 4) showed significantly lower CYP3A-dependent dextromethorphan N-demethylation, midazolam 1"-hydroxylation, and testosterone 6beta-hydroxylation activities, as well as lower expression levels of CYP3A protein (28% of control), compared with those of the CYP3A4*1/*1 group (n = 19). Testosterone 160-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 24382036-7 2013 Use of carbamazepine, a CYP3A4 inducer, probably led to an increased clearance of rivaroxaban resulting in pulmonary embolisms. Carbamazepine 7-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 23841924-3 2013 The metabolism and bioavailability of cyclosporin can be significantly and persistently influenced through induction of CYP3A4 caused by the concomitant use of rifampicin. Rifampin 160-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 24143101-4 2013 Lurasidone is rapidly absorbed (time to maximum plasma concentration: 1-3 hours), metabolized mainly by CYP3A4 and eliminated by hepatic metabolism. Lurasidone Hydrochloride 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 22917556-4 2012 13-Hydroxyellipticine, the metabolite forming the major ellipticine-DNA adduct, was generated mainly by CYP3A4 and 1A1, followed by CYP2D6>2C19>1B1>1A2>2E1 and >2C9. 13-hydroxyellipticine 0-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-118 23252946-0 2013 Associations between the genotypes and phenotype of CYP3A and the lipid response to simvastatin in Chinese patients with hypercholesterolemia. Simvastatin 84-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-57 23252947-2 2013 MATERIALS & METHODS: Twenty-five SNPs within seven CBZ pathway genes, namely CYP3A4, CYP3A5, EPHX1, NR1I2, UGT2B7, ABCB1 and ABCC2, were analyzed for association with CBZ pharmacokinetics in 90 epilepsy patients. Carbamazepine 55-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 23153560-6 2013 Midazolam as an in vivo phenotype marker of CYP3A was administered before and after each treatment arm. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-49 23153560-7 2013 Rifampicin alone decreased midazolam AUC by 70%, indicative of the expected increase in CYP3A4 activity. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 23153560-7 2013 Rifampicin alone decreased midazolam AUC by 70%, indicative of the expected increase in CYP3A4 activity. Midazolam 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 23153560-9 2013 Treatment with SFN alone also did not affect CYP3A4 activity in the cohort as a whole, although in the subset with the highest basal CYP3A4 activity there was a statistically significant increase in midazolam AUC (i.e., decrease in CYP3A4 activity). sulforaphane 15-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 23153560-9 2013 Treatment with SFN alone also did not affect CYP3A4 activity in the cohort as a whole, although in the subset with the highest basal CYP3A4 activity there was a statistically significant increase in midazolam AUC (i.e., decrease in CYP3A4 activity). sulforaphane 15-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 23153560-9 2013 Treatment with SFN alone also did not affect CYP3A4 activity in the cohort as a whole, although in the subset with the highest basal CYP3A4 activity there was a statistically significant increase in midazolam AUC (i.e., decrease in CYP3A4 activity). Midazolam 199-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 23153560-9 2013 Treatment with SFN alone also did not affect CYP3A4 activity in the cohort as a whole, although in the subset with the highest basal CYP3A4 activity there was a statistically significant increase in midazolam AUC (i.e., decrease in CYP3A4 activity). Midazolam 199-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 23016756-0 2012 Reaction of human cytochrome P450 3A4 with peroxynitrite: nitrotyrosine formation on the proximal side impairs its interaction with NADPH-cytochrome P450 reductase. Peroxynitrous Acid 43-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-37 23016756-0 2012 Reaction of human cytochrome P450 3A4 with peroxynitrite: nitrotyrosine formation on the proximal side impairs its interaction with NADPH-cytochrome P450 reductase. 3-nitrotyrosine 58-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-37 23016756-1 2012 The reaction of peroxynitrite (PN) with purified human cytochrome P450 3A4 (CYP3A4) resulted in the loss of the reduced-CO difference spectrum, but the absolute absorption spectrum of the heme was not significantly altered. Peroxynitrous Acid 16-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-74 23252947-3 2013 RESULTS: The CYP3A4*1B SNP was significantly associated with CBZ clearance. Carbamazepine 61-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 23252948-5 2013 A new CYP3A4 allele (CYP3A4*22; rs35599367 C>T in intron 6) with a frequency of 5-7% in the Caucasian population was recently discovered through its association with low hepatic CYP3A4 expression and CYP3A4 activity, and showing effects on statin, tacrolimus and cyclosporine metabolism. Tacrolimus 251-261 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 23252948-5 2013 A new CYP3A4 allele (CYP3A4*22; rs35599367 C>T in intron 6) with a frequency of 5-7% in the Caucasian population was recently discovered through its association with low hepatic CYP3A4 expression and CYP3A4 activity, and showing effects on statin, tacrolimus and cyclosporine metabolism. Tacrolimus 251-261 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 23252948-5 2013 A new CYP3A4 allele (CYP3A4*22; rs35599367 C>T in intron 6) with a frequency of 5-7% in the Caucasian population was recently discovered through its association with low hepatic CYP3A4 expression and CYP3A4 activity, and showing effects on statin, tacrolimus and cyclosporine metabolism. Tacrolimus 251-261 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 23252948-5 2013 A new CYP3A4 allele (CYP3A4*22; rs35599367 C>T in intron 6) with a frequency of 5-7% in the Caucasian population was recently discovered through its association with low hepatic CYP3A4 expression and CYP3A4 activity, and showing effects on statin, tacrolimus and cyclosporine metabolism. Tacrolimus 251-261 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 23252948-5 2013 A new CYP3A4 allele (CYP3A4*22; rs35599367 C>T in intron 6) with a frequency of 5-7% in the Caucasian population was recently discovered through its association with low hepatic CYP3A4 expression and CYP3A4 activity, and showing effects on statin, tacrolimus and cyclosporine metabolism. Cyclosporine 266-278 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 23252948-5 2013 A new CYP3A4 allele (CYP3A4*22; rs35599367 C>T in intron 6) with a frequency of 5-7% in the Caucasian population was recently discovered through its association with low hepatic CYP3A4 expression and CYP3A4 activity, and showing effects on statin, tacrolimus and cyclosporine metabolism. Cyclosporine 266-278 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 23252948-5 2013 A new CYP3A4 allele (CYP3A4*22; rs35599367 C>T in intron 6) with a frequency of 5-7% in the Caucasian population was recently discovered through its association with low hepatic CYP3A4 expression and CYP3A4 activity, and showing effects on statin, tacrolimus and cyclosporine metabolism. Cyclosporine 266-278 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 23252948-5 2013 A new CYP3A4 allele (CYP3A4*22; rs35599367 C>T in intron 6) with a frequency of 5-7% in the Caucasian population was recently discovered through its association with low hepatic CYP3A4 expression and CYP3A4 activity, and showing effects on statin, tacrolimus and cyclosporine metabolism. Cyclosporine 266-278 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 23327575-0 2013 CYP3A4 intron 6 C>T SNP (CYP3A4*22) encodes lower CYP3A4 activity in cancer patients, as measured with probes midazolam and erythromycin. Midazolam 113-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23327575-0 2013 CYP3A4 intron 6 C>T SNP (CYP3A4*22) encodes lower CYP3A4 activity in cancer patients, as measured with probes midazolam and erythromycin. Midazolam 113-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 23327575-0 2013 CYP3A4 intron 6 C>T SNP (CYP3A4*22) encodes lower CYP3A4 activity in cancer patients, as measured with probes midazolam and erythromycin. Midazolam 113-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 23327575-0 2013 CYP3A4 intron 6 C>T SNP (CYP3A4*22) encodes lower CYP3A4 activity in cancer patients, as measured with probes midazolam and erythromycin. Erythromycin 127-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23327575-0 2013 CYP3A4 intron 6 C>T SNP (CYP3A4*22) encodes lower CYP3A4 activity in cancer patients, as measured with probes midazolam and erythromycin. Erythromycin 127-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 23327575-0 2013 CYP3A4 intron 6 C>T SNP (CYP3A4*22) encodes lower CYP3A4 activity in cancer patients, as measured with probes midazolam and erythromycin. Erythromycin 127-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 23327575-4 2013 RESULTS: The MDZ metabolic ratio (1 -OH-MDZ:MDZ) was 20.7% (95% CI: -36.2 to -6.2) lower for CYP3A4*22 carriers compared with CYP3A4*1/*1 patients (p = 0.01). Midazolam 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 23327575-4 2013 RESULTS: The MDZ metabolic ratio (1 -OH-MDZ:MDZ) was 20.7% (95% CI: -36.2 to -6.2) lower for CYP3A4*22 carriers compared with CYP3A4*1/*1 patients (p = 0.01). Midazolam 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 23327575-4 2013 RESULTS: The MDZ metabolic ratio (1 -OH-MDZ:MDZ) was 20.7% (95% CI: -36.2 to -6.2) lower for CYP3A4*22 carriers compared with CYP3A4*1/*1 patients (p = 0.01). 1 -oh-mdz 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 23327575-4 2013 RESULTS: The MDZ metabolic ratio (1 -OH-MDZ:MDZ) was 20.7% (95% CI: -36.2 to -6.2) lower for CYP3A4*22 carriers compared with CYP3A4*1/*1 patients (p = 0.01). 1 -oh-mdz 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 23327575-4 2013 RESULTS: The MDZ metabolic ratio (1 -OH-MDZ:MDZ) was 20.7% (95% CI: -36.2 to -6.2) lower for CYP3A4*22 carriers compared with CYP3A4*1/*1 patients (p = 0.01). Midazolam 40-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 23327575-6 2013 CYP3A4 erythromycin N-demethylation activity was 40% lower in CYP3A4*22 carriers compared with CYP3A4*1/*1 patients (p = 0.032). erythromycin n 7-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23327575-6 2013 CYP3A4 erythromycin N-demethylation activity was 40% lower in CYP3A4*22 carriers compared with CYP3A4*1/*1 patients (p = 0.032). erythromycin n 7-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 23327575-6 2013 CYP3A4 erythromycin N-demethylation activity was 40% lower in CYP3A4*22 carriers compared with CYP3A4*1/*1 patients (p = 0.032). erythromycin n 7-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22917556-9 2012 CYP3A4 and 1A1 in the presence of cytochrome b(5) are mainly responsible for bioactivation of ellipticine to DNA adduct 1 (formed by ellipticine-13-ylium from 13-hydroxyellipticine), while 12-hydroxyellipticine generated during the CYP2C19-mediated ellipticine oxidation is the predominant metabolite forming ellipticine-12-ylium that generates ellipticine-DNA adduct 2. ellipticine 133-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-14 22917556-9 2012 CYP3A4 and 1A1 in the presence of cytochrome b(5) are mainly responsible for bioactivation of ellipticine to DNA adduct 1 (formed by ellipticine-13-ylium from 13-hydroxyellipticine), while 12-hydroxyellipticine generated during the CYP2C19-mediated ellipticine oxidation is the predominant metabolite forming ellipticine-12-ylium that generates ellipticine-DNA adduct 2. ellipticine-12-ylium 309-329 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-14 22917556-9 2012 CYP3A4 and 1A1 in the presence of cytochrome b(5) are mainly responsible for bioactivation of ellipticine to DNA adduct 1 (formed by ellipticine-13-ylium from 13-hydroxyellipticine), while 12-hydroxyellipticine generated during the CYP2C19-mediated ellipticine oxidation is the predominant metabolite forming ellipticine-12-ylium that generates ellipticine-DNA adduct 2. ellipticine 133-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-14 22917556-12 2012 In liver CYP3A4 is the predominant ellipticine activating CYP species, which is expected to result in efficient metabolism after oral ingestion of ellipticine in humans. ellipticine 35-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 22917556-12 2012 In liver CYP3A4 is the predominant ellipticine activating CYP species, which is expected to result in efficient metabolism after oral ingestion of ellipticine in humans. ellipticine 147-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 23016756-1 2012 The reaction of peroxynitrite (PN) with purified human cytochrome P450 3A4 (CYP3A4) resulted in the loss of the reduced-CO difference spectrum, but the absolute absorption spectrum of the heme was not significantly altered. Peroxynitrous Acid 16-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 23016756-1 2012 The reaction of peroxynitrite (PN) with purified human cytochrome P450 3A4 (CYP3A4) resulted in the loss of the reduced-CO difference spectrum, but the absolute absorption spectrum of the heme was not significantly altered. Peroxynitrous Acid 31-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-74 23016756-1 2012 The reaction of peroxynitrite (PN) with purified human cytochrome P450 3A4 (CYP3A4) resulted in the loss of the reduced-CO difference spectrum, but the absolute absorption spectrum of the heme was not significantly altered. Peroxynitrous Acid 31-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 23016756-1 2012 The reaction of peroxynitrite (PN) with purified human cytochrome P450 3A4 (CYP3A4) resulted in the loss of the reduced-CO difference spectrum, but the absolute absorption spectrum of the heme was not significantly altered. Heme 188-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-74 23016756-1 2012 The reaction of peroxynitrite (PN) with purified human cytochrome P450 3A4 (CYP3A4) resulted in the loss of the reduced-CO difference spectrum, but the absolute absorption spectrum of the heme was not significantly altered. Heme 188-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 23016756-2 2012 The loss of 7-benzyloxy-4-(trifluoromethyl)coumarin (BFC) O-debenzylation activity of CYP3A4 was concentration-dependent with respect to PN, and the loss of BFC activity supported by NADPH-cytochrome P450 reductase (CPR) was much greater than that supported by tert-butyl hydroperoxide. 7-benzyloxy-4-trifluoromethylcoumarin 12-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 23016756-2 2012 The loss of 7-benzyloxy-4-(trifluoromethyl)coumarin (BFC) O-debenzylation activity of CYP3A4 was concentration-dependent with respect to PN, and the loss of BFC activity supported by NADPH-cytochrome P450 reductase (CPR) was much greater than that supported by tert-butyl hydroperoxide. 7-benzyloxy-4-trifluoromethylcoumarin 53-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 23016756-2 2012 The loss of 7-benzyloxy-4-(trifluoromethyl)coumarin (BFC) O-debenzylation activity of CYP3A4 was concentration-dependent with respect to PN, and the loss of BFC activity supported by NADPH-cytochrome P450 reductase (CPR) was much greater than that supported by tert-butyl hydroperoxide. tert-Butylhydroperoxide 261-285 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 23016756-3 2012 Moreover, the PN-treated CYP3A4 exhibited a reduced-CO spectrum when reduced by CPR that was much smaller than when it was reduced by dithionite. Dithionite 134-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 23016756-6 2012 PN-treated CYP3A4 was digested by trypsin and endoproteinase Glu C, and nitrotyrosine formation was then determined by using electrospray ionization-liquid chromatography-tandem mass spectrometry. Peroxynitrous Acid 0-2 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 23016756-8 2012 Using the GRAMM-X docking program, the structure for the CYP3A4-CPR complex shows that Tyr99, Tyr347, and Tyr430 are on the proximal side of CYP3A4 and are in close contact with three acidic residues in the FMN domain of CPR, suggesting that modification of one or more of these tyrosine residues by PN may influence CPR binding or the transfer of electrons to CYP3A4. Tyrosine 279-287 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 23016756-8 2012 Using the GRAMM-X docking program, the structure for the CYP3A4-CPR complex shows that Tyr99, Tyr347, and Tyr430 are on the proximal side of CYP3A4 and are in close contact with three acidic residues in the FMN domain of CPR, suggesting that modification of one or more of these tyrosine residues by PN may influence CPR binding or the transfer of electrons to CYP3A4. Tyrosine 279-287 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 23016756-8 2012 Using the GRAMM-X docking program, the structure for the CYP3A4-CPR complex shows that Tyr99, Tyr347, and Tyr430 are on the proximal side of CYP3A4 and are in close contact with three acidic residues in the FMN domain of CPR, suggesting that modification of one or more of these tyrosine residues by PN may influence CPR binding or the transfer of electrons to CYP3A4. Tyrosine 279-287 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 22917556-4 2012 13-Hydroxyellipticine, the metabolite forming the major ellipticine-DNA adduct, was generated mainly by CYP3A4 and 1A1, followed by CYP2D6>2C19>1B1>1A2>2E1 and >2C9. ellipticine 10-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-118 22917556-9 2012 CYP3A4 and 1A1 in the presence of cytochrome b(5) are mainly responsible for bioactivation of ellipticine to DNA adduct 1 (formed by ellipticine-13-ylium from 13-hydroxyellipticine), while 12-hydroxyellipticine generated during the CYP2C19-mediated ellipticine oxidation is the predominant metabolite forming ellipticine-12-ylium that generates ellipticine-DNA adduct 2. ellipticine 94-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-14 22917556-9 2012 CYP3A4 and 1A1 in the presence of cytochrome b(5) are mainly responsible for bioactivation of ellipticine to DNA adduct 1 (formed by ellipticine-13-ylium from 13-hydroxyellipticine), while 12-hydroxyellipticine generated during the CYP2C19-mediated ellipticine oxidation is the predominant metabolite forming ellipticine-12-ylium that generates ellipticine-DNA adduct 2. ellipticine-13-ylium 133-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-14 22917556-9 2012 CYP3A4 and 1A1 in the presence of cytochrome b(5) are mainly responsible for bioactivation of ellipticine to DNA adduct 1 (formed by ellipticine-13-ylium from 13-hydroxyellipticine), while 12-hydroxyellipticine generated during the CYP2C19-mediated ellipticine oxidation is the predominant metabolite forming ellipticine-12-ylium that generates ellipticine-DNA adduct 2. 13-hydroxyellipticine 159-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-14 22917556-9 2012 CYP3A4 and 1A1 in the presence of cytochrome b(5) are mainly responsible for bioactivation of ellipticine to DNA adduct 1 (formed by ellipticine-13-ylium from 13-hydroxyellipticine), while 12-hydroxyellipticine generated during the CYP2C19-mediated ellipticine oxidation is the predominant metabolite forming ellipticine-12-ylium that generates ellipticine-DNA adduct 2. 12-hydroxyellipticine 189-210 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-14 23217392-1 2012 BACKGROUND: Cyclosporin A (CsA) is a substrate of both cytochrome P450 3A (CYP3A) and P-glycoprotein (P-gp), some of the single nucleotide polymorphisms (SNPs) in these genes are associated with interindividual variations in CsA pharmacokinetics. Cyclosporine 27-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-73 23071109-8 2012 In contrast to CYP26A1, CYP3A4 formed the 4-OH-RA enantiomers in a 1:1 ratio and CYP3A5 preferentially formed (4R)-OH-RA. 4-oh-ra 42-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 23097240-2 2012 Ketoconazole was applied as a potent prototypic inhibitor of cytochrome CYP3A4, to determine the role of CYP3A4 in the metabolic clearance of safinamide. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 23097240-2 2012 Ketoconazole was applied as a potent prototypic inhibitor of cytochrome CYP3A4, to determine the role of CYP3A4 in the metabolic clearance of safinamide. safinamide 142-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 23097240-8 2012 Overall, the study shows that CYP3A4 plays a minor role in the metabolism of safinamide in vivo. safinamide 77-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 23097240-9 2012 Therefore, safinamide can be administered together with potent CYP3A4 inhibitors without any requirement for dose adjustment. safinamide 11-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 23085740-0 2012 Association of CYP3A polymorphisms with the pharmacokinetics of cyclosporine A in early post-renal transplant recipients in China. Cyclosporine 64-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-20 23085740-1 2012 AIM: To evaluate retrospectively the association of cytochrome P450 3A (CYP3A) and ATP-binding cassette sub-family B member 1 (ABCB1) gene polymorphisms with the pharmacokinetics of cyclosporine A (CsA) in Chinese renal transplant patients. Cyclosporine 182-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-70 23085740-1 2012 AIM: To evaluate retrospectively the association of cytochrome P450 3A (CYP3A) and ATP-binding cassette sub-family B member 1 (ABCB1) gene polymorphisms with the pharmacokinetics of cyclosporine A (CsA) in Chinese renal transplant patients. Cyclosporine 182-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-77 23053255-1 2012 PURPOSE: Dinaciclib, a selective inhibitor of cyclin-dependent kinase (CDK) 1, CDK2, CDK5, and CDK9, is metabolized via CYP3A4. dinaciclib 9-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 23217392-0 2012 CYP3A4 genetic polymorphisms predict cyclosporine-related clinical events in Chinese renal transplant recipients. Cyclosporine 37-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23217392-1 2012 BACKGROUND: Cyclosporin A (CsA) is a substrate of both cytochrome P450 3A (CYP3A) and P-glycoprotein (P-gp), some of the single nucleotide polymorphisms (SNPs) in these genes are associated with interindividual variations in CsA pharmacokinetics. Cyclosporine 27-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 23217392-1 2012 BACKGROUND: Cyclosporin A (CsA) is a substrate of both cytochrome P450 3A (CYP3A) and P-glycoprotein (P-gp), some of the single nucleotide polymorphisms (SNPs) in these genes are associated with interindividual variations in CsA pharmacokinetics. Cyclosporine 225-228 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-73 23217392-1 2012 BACKGROUND: Cyclosporin A (CsA) is a substrate of both cytochrome P450 3A (CYP3A) and P-glycoprotein (P-gp), some of the single nucleotide polymorphisms (SNPs) in these genes are associated with interindividual variations in CsA pharmacokinetics. Cyclosporine 225-228 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 23217392-4 2012 Retrospective case control study was utilized to identify the association between CYP3A4 1G, CYP3A5 3, ABCB1 genetic polymorphisms and CsA-related outcomes. Cyclosporine 135-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 22942318-6 2012 Use of this two-step statistical evaluation is illustrated with the examination of five drugs of varying capabilities to inactivate CYP3A4: ketoconazole, erythromycin, raloxifene, rosiglitazone, and pioglitazone. Ketoconazole 140-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 22942318-6 2012 Use of this two-step statistical evaluation is illustrated with the examination of five drugs of varying capabilities to inactivate CYP3A4: ketoconazole, erythromycin, raloxifene, rosiglitazone, and pioglitazone. Erythromycin 154-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 22930276-6 2012 In light of the in vitro findings, modeling and simulation approaches were used to examine the potential for ketoconazole (a CYP3A inhibitor) to inhibit the metabolism of AMG 853 as well as for AMG 853 to inhibit the metabolism of paclitaxel, rosiglitazone, and montelukast, commonly used substrates of CYP2C8. Ketoconazole 109-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-130 22942318-6 2012 Use of this two-step statistical evaluation is illustrated with the examination of five drugs of varying capabilities to inactivate CYP3A4: ketoconazole, erythromycin, raloxifene, rosiglitazone, and pioglitazone. Raloxifene Hydrochloride 168-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 22942318-6 2012 Use of this two-step statistical evaluation is illustrated with the examination of five drugs of varying capabilities to inactivate CYP3A4: ketoconazole, erythromycin, raloxifene, rosiglitazone, and pioglitazone. Rosiglitazone 180-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 22961682-9 2012 An in vitro phenotyping approach indicated that CYP3A4 was the largest contributor to LY2452473 depletion. LY2452473 86-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 22942318-6 2012 Use of this two-step statistical evaluation is illustrated with the examination of five drugs of varying capabilities to inactivate CYP3A4: ketoconazole, erythromycin, raloxifene, rosiglitazone, and pioglitazone. Pioglitazone 199-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 23126273-4 2012 EXPERT OPINION: Eszopiclone is metabolized mainly by Cytochrome P450-3A (CYP3A) isoforms. Eszopiclone 16-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-71 22434147-2 2012 Here, we show that modafinil, a well-known inducer of hepatic CYP enzymes, also increases CYP3A4 expression in human-derived neuron-like SH-SY5Y cells. Modafinil 19-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 22434147-3 2012 Upregulation of CYP3A4 by modafinil was associated with increased retinoic acid (RA) degradation, which could be blocked by specific CYP3A4 inhibitor erythromycin. Modafinil 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 22434147-3 2012 Upregulation of CYP3A4 by modafinil was associated with increased retinoic acid (RA) degradation, which could be blocked by specific CYP3A4 inhibitor erythromycin. Modafinil 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 22434147-3 2012 Upregulation of CYP3A4 by modafinil was associated with increased retinoic acid (RA) degradation, which could be blocked by specific CYP3A4 inhibitor erythromycin. Tretinoin 66-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 22434147-3 2012 Upregulation of CYP3A4 by modafinil was associated with increased retinoic acid (RA) degradation, which could be blocked by specific CYP3A4 inhibitor erythromycin. Tretinoin 66-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 22434147-3 2012 Upregulation of CYP3A4 by modafinil was associated with increased retinoic acid (RA) degradation, which could be blocked by specific CYP3A4 inhibitor erythromycin. Erythromycin 150-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 22434147-3 2012 Upregulation of CYP3A4 by modafinil was associated with increased retinoic acid (RA) degradation, which could be blocked by specific CYP3A4 inhibitor erythromycin. Erythromycin 150-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 23126273-4 2012 EXPERT OPINION: Eszopiclone is metabolized mainly by Cytochrome P450-3A (CYP3A) isoforms. Eszopiclone 16-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 23146034-0 2012 Inhibition of CYP3A4 by 6",7"-dihydroxybergamottin in human CYP3A4 over-expressed hepG2 cells. 6',7'-dihydroxybergamottin 24-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 22205719-2 2012 Bosentan, an endothelin (ET) receptor-type ET(A) and ET(B) antagonist, is metabolized to active metabolites by and an inducer of cytochrome P450 (CYP)2C9 and CYP3A. Bosentan 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-163 21635359-2 2012 This study investigated the effect of the herbal antidepressant St John"s wort, an inducer of cytochrome P450 3A4 (CYP3A4), on the pharmacokinetics and pharmacodynamics of oral S-ketamine. Ketamine 177-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-113 21635359-2 2012 This study investigated the effect of the herbal antidepressant St John"s wort, an inducer of cytochrome P450 3A4 (CYP3A4), on the pharmacokinetics and pharmacodynamics of oral S-ketamine. Ketamine 177-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 22642935-2 2012 Standard treatment regimens include vinblastine, which is known to cause neurotoxicity (NT) and is metabolized by cytochrome 3A4 (CYP3A4). Vinblastine 36-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 23146034-0 2012 Inhibition of CYP3A4 by 6",7"-dihydroxybergamottin in human CYP3A4 over-expressed hepG2 cells. 6',7'-dihydroxybergamottin 24-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 23146034-3 2012 The purpose of this study was to determine whether our CYP3A4-overexpresed cell could be applied to evaluate mechanisms of CYP3A4 inhibition by 6",7"-dihydroxybergamottin (DHB), which is one of the major furanocoumarins in grapefruit juice, by using these cells. 6',7'-dihydroxybergamottin 144-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 23146034-3 2012 The purpose of this study was to determine whether our CYP3A4-overexpresed cell could be applied to evaluate mechanisms of CYP3A4 inhibition by 6",7"-dihydroxybergamottin (DHB), which is one of the major furanocoumarins in grapefruit juice, by using these cells. 6',7'-dihydroxybergamottin 144-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 23146034-3 2012 The purpose of this study was to determine whether our CYP3A4-overexpresed cell could be applied to evaluate mechanisms of CYP3A4 inhibition by 6",7"-dihydroxybergamottin (DHB), which is one of the major furanocoumarins in grapefruit juice, by using these cells. 6',7'-dihydroxybergamottin 172-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 23146034-3 2012 The purpose of this study was to determine whether our CYP3A4-overexpresed cell could be applied to evaluate mechanisms of CYP3A4 inhibition by 6",7"-dihydroxybergamottin (DHB), which is one of the major furanocoumarins in grapefruit juice, by using these cells. 6',7'-dihydroxybergamottin 172-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 23146034-3 2012 The purpose of this study was to determine whether our CYP3A4-overexpresed cell could be applied to evaluate mechanisms of CYP3A4 inhibition by 6",7"-dihydroxybergamottin (DHB), which is one of the major furanocoumarins in grapefruit juice, by using these cells. Furocoumarins 204-219 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 23146034-3 2012 The purpose of this study was to determine whether our CYP3A4-overexpresed cell could be applied to evaluate mechanisms of CYP3A4 inhibition by 6",7"-dihydroxybergamottin (DHB), which is one of the major furanocoumarins in grapefruit juice, by using these cells. Furocoumarins 204-219 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 23146034-3 2012 The purpose of this study was to determine whether our CYP3A4-overexpresed cell could be applied to evaluate mechanisms of CYP3A4 inhibition by 6",7"-dihydroxybergamottin (DHB), which is one of the major furanocoumarins in grapefruit juice, by using these cells. juice 234-239 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 23146034-3 2012 The purpose of this study was to determine whether our CYP3A4-overexpresed cell could be applied to evaluate mechanisms of CYP3A4 inhibition by 6",7"-dihydroxybergamottin (DHB), which is one of the major furanocoumarins in grapefruit juice, by using these cells. juice 234-239 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 23146034-6 2012 KEY FINDINGS: DHB and ketoconazole, a well-known inhibitor of CYP3A4, inhibited nifedipine oxidation in a concentration-dependent manner. 6',7'-dihydroxybergamottin 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 23146034-6 2012 KEY FINDINGS: DHB and ketoconazole, a well-known inhibitor of CYP3A4, inhibited nifedipine oxidation in a concentration-dependent manner. Ketoconazole 22-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 23146034-6 2012 KEY FINDINGS: DHB and ketoconazole, a well-known inhibitor of CYP3A4, inhibited nifedipine oxidation in a concentration-dependent manner. Nifedipine 80-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 23146034-12 2012 CONCLUSIONS: We concluded that inhibition of CYP3A4 activity by DHB includes the inhibition of POR activity. 6',7'-dihydroxybergamottin 64-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 23215890-6 2012 The CYP450 enzymes CYP3A4, CYP3A5 and CYP2C8 are responsible for the conversion of taxanes into their metabolites. Taxoids 83-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 22903070-1 2012 Experimental studies on the molecular regulation of human drug metabolism have revealed that vitamin D up-regulates transcription of several key enzymes, such as CYP3A4, through the vitamin D receptor pathway in intestinal and hepatic cells. Vitamin D 93-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 22939842-1 2012 We investigated the capacity for vitamin D receptor (VDR) to modulate the expression of CYP3A4 and other genes that may facilitate the oxidative inactivation of androgens such as testosterone and androstanediol within prostate cells. Testosterone 179-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 23373092-11 2012 The potential for pharmacokinetic interactions is high: vemurafenib inhibits P-glycoprotein and CYP 1A2, and induces CYP 3A4. Vemurafenib 56-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-124 22939842-2 2012 We report that exposure to the active hormonal form of vitamin D markedly increased gene expression of CYP3A4 and CYP3A5 and ultimately achieved levels of intracellular CYP3A enzyme activity within LNCaP prostate cancer cells that were comparable to that observed for Caco2 cells, an established model of CYP3A induction, and resulted in the increased turnover of testosterone to its inactive 6beta-OH metabolite. Vitamin D 55-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 22939842-1 2012 We investigated the capacity for vitamin D receptor (VDR) to modulate the expression of CYP3A4 and other genes that may facilitate the oxidative inactivation of androgens such as testosterone and androstanediol within prostate cells. Androstane-3,17-diol 196-210 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 22939842-2 2012 We report that exposure to the active hormonal form of vitamin D markedly increased gene expression of CYP3A4 and CYP3A5 and ultimately achieved levels of intracellular CYP3A enzyme activity within LNCaP prostate cancer cells that were comparable to that observed for Caco2 cells, an established model of CYP3A induction, and resulted in the increased turnover of testosterone to its inactive 6beta-OH metabolite. Vitamin D 55-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 22939842-2 2012 We report that exposure to the active hormonal form of vitamin D markedly increased gene expression of CYP3A4 and CYP3A5 and ultimately achieved levels of intracellular CYP3A enzyme activity within LNCaP prostate cancer cells that were comparable to that observed for Caco2 cells, an established model of CYP3A induction, and resulted in the increased turnover of testosterone to its inactive 6beta-OH metabolite. Vitamin D 55-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 22369095-4 2012 We aimed to investigate the effect of methadone on the pathways of tramadol metabolism: O-demethylation (CYP2D6) to the opioid-active metabolite M1 and N-demethylation (CYP3A4) to M2 in subjects maintained on methadone or buprenorphine as a control. Methadone 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 22725721-8 2012 RESULTS: The p-PBPK model predicted the PK changes of three model compounds (namely caffeine, metoprolol and midazolam) for CYP1A2, CYP2D6 and CYP3A4 during pregnancy within twofold of observed values. Caffeine 84-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 22381043-5 2012 The potent CYP3A4 inhibitor ritonavir alters the sequential metabolism of tilidine, substantially reducing the partial metabolic clearances of tilidine to nortilidine and nortilidine to bisnortilidine, which increases the nortilidine exposure twofold. nortilidine 171-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 22369095-4 2012 We aimed to investigate the effect of methadone on the pathways of tramadol metabolism: O-demethylation (CYP2D6) to the opioid-active metabolite M1 and N-demethylation (CYP3A4) to M2 in subjects maintained on methadone or buprenorphine as a control. Tramadol 67-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 22381043-5 2012 The potent CYP3A4 inhibitor ritonavir alters the sequential metabolism of tilidine, substantially reducing the partial metabolic clearances of tilidine to nortilidine and nortilidine to bisnortilidine, which increases the nortilidine exposure twofold. bisnortilidine 186-200 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 22725721-8 2012 RESULTS: The p-PBPK model predicted the PK changes of three model compounds (namely caffeine, metoprolol and midazolam) for CYP1A2, CYP2D6 and CYP3A4 during pregnancy within twofold of observed values. Metoprolol 94-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 22725721-8 2012 RESULTS: The p-PBPK model predicted the PK changes of three model compounds (namely caffeine, metoprolol and midazolam) for CYP1A2, CYP2D6 and CYP3A4 during pregnancy within twofold of observed values. Midazolam 109-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 22381043-5 2012 The potent CYP3A4 inhibitor ritonavir alters the sequential metabolism of tilidine, substantially reducing the partial metabolic clearances of tilidine to nortilidine and nortilidine to bisnortilidine, which increases the nortilidine exposure twofold. nortilidine 171-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 22369095-8 2012 AIMS: To compare the O- (CYP2D6 mediated) and N- (CYP3A4 mediated) demethylation metabolism of tramadol between methadone and buprenorphine maintained CYP2D6 extensive metabolizer subjects. Tramadol 95-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 22381043-8 2012 AIMS: To investigate in vivo the effect of the CYP2C19 genotype on the pharmacokinetics of tilidine and the contribution of CYP3A4 and CYP2C19 to the formation of nortilidine using potent CYP3A4 inhibition by ritonavir. nortilidine 163-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 22381043-0 2012 Contribution of CYP2C19 and CYP3A4 to the formation of the active nortilidine from the prodrug tilidine. nortilidine 66-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 22381043-14 2012 CONCLUSIONS: The sequential metabolism of tilidine is inhibited by the potent CYP3A4 inhibitor, ritonavir, independent of the CYP2C19 genotype, with a twofold increase in the exposure of the active nortilidine. Tilidine 42-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 22381043-14 2012 CONCLUSIONS: The sequential metabolism of tilidine is inhibited by the potent CYP3A4 inhibitor, ritonavir, independent of the CYP2C19 genotype, with a twofold increase in the exposure of the active nortilidine. Ritonavir 96-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 22381043-0 2012 Contribution of CYP2C19 and CYP3A4 to the formation of the active nortilidine from the prodrug tilidine. Tilidine 69-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 22381043-14 2012 CONCLUSIONS: The sequential metabolism of tilidine is inhibited by the potent CYP3A4 inhibitor, ritonavir, independent of the CYP2C19 genotype, with a twofold increase in the exposure of the active nortilidine. nortilidine 198-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 22933344-4 2012 Among 11 recombinant P450 isozymes examined, CYP3A4 showed the highest formation rate of 1"-hydroxy BBR. 1'-hydroxybenzbromarone 89-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 22933344-13 2012 These results suggest that (i) the formation of 1"-hydroxy BBR and 6-hydroxy BBR is mainly catalysed by CYP3A4 and CYP2C9, respectively, and (ii) the formation of 5,6-dihydroxy BBR is catalysed by CYP2C9 and CYP1A2 in human liver microsomes. 1'-hydroxybenzbromarone 48-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 22381043-2 2012 Tilidine undergoes an extensive first-pass metabolism, which has been suggested to be mediated by CYP3A4 and CYP2C19; furthermore, strong inhibition of CYP3A4 and CYP2C19 by voriconazole increased exposure of nortilidine, probably by inhibition of further metabolism. Tilidine 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 22933344-13 2012 These results suggest that (i) the formation of 1"-hydroxy BBR and 6-hydroxy BBR is mainly catalysed by CYP3A4 and CYP2C9, respectively, and (ii) the formation of 5,6-dihydroxy BBR is catalysed by CYP2C9 and CYP1A2 in human liver microsomes. 6-hydroxybenzbromarone 67-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 22381043-2 2012 Tilidine undergoes an extensive first-pass metabolism, which has been suggested to be mediated by CYP3A4 and CYP2C19; furthermore, strong inhibition of CYP3A4 and CYP2C19 by voriconazole increased exposure of nortilidine, probably by inhibition of further metabolism. Tilidine 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 22933344-13 2012 These results suggest that (i) the formation of 1"-hydroxy BBR and 6-hydroxy BBR is mainly catalysed by CYP3A4 and CYP2C9, respectively, and (ii) the formation of 5,6-dihydroxy BBR is catalysed by CYP2C9 and CYP1A2 in human liver microsomes. 5,6-dihydroxy bbr 163-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 22381043-2 2012 Tilidine undergoes an extensive first-pass metabolism, which has been suggested to be mediated by CYP3A4 and CYP2C19; furthermore, strong inhibition of CYP3A4 and CYP2C19 by voriconazole increased exposure of nortilidine, probably by inhibition of further metabolism. Voriconazole 174-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 22381043-2 2012 Tilidine undergoes an extensive first-pass metabolism, which has been suggested to be mediated by CYP3A4 and CYP2C19; furthermore, strong inhibition of CYP3A4 and CYP2C19 by voriconazole increased exposure of nortilidine, probably by inhibition of further metabolism. nortilidine 209-220 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 22381043-5 2012 The potent CYP3A4 inhibitor ritonavir alters the sequential metabolism of tilidine, substantially reducing the partial metabolic clearances of tilidine to nortilidine and nortilidine to bisnortilidine, which increases the nortilidine exposure twofold. Ritonavir 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 22381043-5 2012 The potent CYP3A4 inhibitor ritonavir alters the sequential metabolism of tilidine, substantially reducing the partial metabolic clearances of tilidine to nortilidine and nortilidine to bisnortilidine, which increases the nortilidine exposure twofold. Tilidine 74-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 22381043-5 2012 The potent CYP3A4 inhibitor ritonavir alters the sequential metabolism of tilidine, substantially reducing the partial metabolic clearances of tilidine to nortilidine and nortilidine to bisnortilidine, which increases the nortilidine exposure twofold. Tilidine 143-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 22381043-5 2012 The potent CYP3A4 inhibitor ritonavir alters the sequential metabolism of tilidine, substantially reducing the partial metabolic clearances of tilidine to nortilidine and nortilidine to bisnortilidine, which increases the nortilidine exposure twofold. nortilidine 155-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 22682979-3 2012 As methadone is metabolized by CYP3A4 and lersivirine is a weak CYP3A4 inducer, it is possible that lersivirine may decrease methadone concentrations. Methadone 3-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 22990751-1 2012 Previous studies have demonstrated that the pharmacokinetic profile of erythromycin, a probe for CYP3A4 activity, is affected by inhibitors or inducers of hepatic solute carriers. Erythromycin 71-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 22851614-4 2012 Cytochrome P450 (P450) phenotyping studies revealed that the formation of M1 and M2 were NADPH-dependent and primarily catalyzed by CYP3A4 among the studied P450 isoforms. NADP 89-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 22851617-8 2012 In vitro studies demonstrated that remogliflozin etabonate and remogliflozin are Pgp substrates, and that CYP3A4 can form GSK279782 directly from remogliflozin. gsk279782 122-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 22851617-9 2012 A ketoconazole clinical drug interaction study, along with the human mass balance findings, confirmed that CYP3A4 contributes less than 50% to remogliflozin metabolism, demonstrating that other enzyme pathways (e.g., P450s, UDP-glucuronosyltransferases, and glucosidases) make significant contributions to the drug"s clearance. remogliflozin 143-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 22949220-0 2012 Electrophoretically mediated microanalysis for characterization of the enantioselective CYP3A4 catalyzed N-demethylation of ketamine. Nitrogen 105-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 22949220-0 2012 Electrophoretically mediated microanalysis for characterization of the enantioselective CYP3A4 catalyzed N-demethylation of ketamine. Ketamine 124-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 22949220-2 2012 An EMMA method was developed to investigate the stereoselectivity of the CYP3A4-mediated N-demethylation of ketamine. Nitrogen 89-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 22949220-2 2012 An EMMA method was developed to investigate the stereoselectivity of the CYP3A4-mediated N-demethylation of ketamine. Ketamine 108-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 22871069-5 2012 Based on the most recent findings the authors discuss the role of CYP2E1 in alcohol-mediated oxidative stress in monocytes/macrophages and astrocytes, as well as the role of CYP3A4 in alcohol-PI interactions leading to altered metabolism of PI in these cells. Alcohols 184-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 23461440-1 2012 INTRODUCTION: The new protease inhibitors (PIs), telaprevir and boceprevir, with peginterferon and ribavirin, have increased the response rate in patients with genotype 1 chronic hepatitis C. Both are metabolized by CYP3A and they are CYP3A inhibitors. telaprevir 49-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-221 23461440-1 2012 INTRODUCTION: The new protease inhibitors (PIs), telaprevir and boceprevir, with peginterferon and ribavirin, have increased the response rate in patients with genotype 1 chronic hepatitis C. Both are metabolized by CYP3A and they are CYP3A inhibitors. telaprevir 49-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 235-240 23461440-1 2012 INTRODUCTION: The new protease inhibitors (PIs), telaprevir and boceprevir, with peginterferon and ribavirin, have increased the response rate in patients with genotype 1 chronic hepatitis C. Both are metabolized by CYP3A and they are CYP3A inhibitors. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-221 23461440-1 2012 INTRODUCTION: The new protease inhibitors (PIs), telaprevir and boceprevir, with peginterferon and ribavirin, have increased the response rate in patients with genotype 1 chronic hepatitis C. Both are metabolized by CYP3A and they are CYP3A inhibitors. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 235-240 23461440-1 2012 INTRODUCTION: The new protease inhibitors (PIs), telaprevir and boceprevir, with peginterferon and ribavirin, have increased the response rate in patients with genotype 1 chronic hepatitis C. Both are metabolized by CYP3A and they are CYP3A inhibitors. peginterferon 81-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-221 23461440-1 2012 INTRODUCTION: The new protease inhibitors (PIs), telaprevir and boceprevir, with peginterferon and ribavirin, have increased the response rate in patients with genotype 1 chronic hepatitis C. Both are metabolized by CYP3A and they are CYP3A inhibitors. peginterferon 81-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 235-240 23084335-2 2012 As azoles, these antifungal agents are inhibitors of CYP3A4 and P-glycoprotein (P-gp); and thus therapeutic drug monitoring is important. Azoles 3-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 22896727-1 2012 (S)-Warfarin 7-hydroxylation and midazolam 1"-hydroxylation are among the preferred probe substrate reactions for CYP2C9 and CYP3A4/5, respectively. Warfarin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-133 22896727-1 2012 (S)-Warfarin 7-hydroxylation and midazolam 1"-hydroxylation are among the preferred probe substrate reactions for CYP2C9 and CYP3A4/5, respectively. Midazolam 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-133 22896728-8 2012 Molecular docking simulations showed that the 5" position of the pyrimidine moiety of PF-00734200 can access the heme iron-oxo of both CYP3A4 and CYP2D6 in an energetically favored orientation. pyrimidine 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 22896728-8 2012 Molecular docking simulations showed that the 5" position of the pyrimidine moiety of PF-00734200 can access the heme iron-oxo of both CYP3A4 and CYP2D6 in an energetically favored orientation. pyrazofurin 86-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 22896728-8 2012 Molecular docking simulations showed that the 5" position of the pyrimidine moiety of PF-00734200 can access the heme iron-oxo of both CYP3A4 and CYP2D6 in an energetically favored orientation. Heme 113-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 22896728-8 2012 Molecular docking simulations showed that the 5" position of the pyrimidine moiety of PF-00734200 can access the heme iron-oxo of both CYP3A4 and CYP2D6 in an energetically favored orientation. Iron 118-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 22913318-4 2012 However, PXR-mediated induction of CYP3A enhances APAP-induced acute liver injury by generating toxic metabolites. Acetaminophen 50-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-40 22576324-1 2012 UNLABELLED: The hepatitis C virus protease inhibitor boceprevir is a strong inhibitor of cytochrome P450 3A4 and 3A5 (CYP3A4/5). N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 53-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 22576324-2 2012 Cyclosporine and tacrolimus are calcineurin inhibitor immunosuppressants used to prevent organ rejection after liver transplantation; both are substrates of CYP3A4. Cyclosporine 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 22576324-2 2012 Cyclosporine and tacrolimus are calcineurin inhibitor immunosuppressants used to prevent organ rejection after liver transplantation; both are substrates of CYP3A4. Tacrolimus 17-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 22682979-3 2012 As methadone is metabolized by CYP3A4 and lersivirine is a weak CYP3A4 inducer, it is possible that lersivirine may decrease methadone concentrations. UK 453,061 42-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 22682979-3 2012 As methadone is metabolized by CYP3A4 and lersivirine is a weak CYP3A4 inducer, it is possible that lersivirine may decrease methadone concentrations. UK 453,061 100-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 22682979-3 2012 As methadone is metabolized by CYP3A4 and lersivirine is a weak CYP3A4 inducer, it is possible that lersivirine may decrease methadone concentrations. UK 453,061 100-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 22577882-7 2012 While arteether showed the highest activities in vitro, it was less active than artemisinin in inducing hepatic CYP3A4 gene expression in hepatocytes. artemisinin 80-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 22918158-2 2012 EFV is a known inducer of cytochrome P450 3A4, which converts artemether to dihydroartemisinin (DHA) that is also active and metabolizes longer acting lumefantrine (LR). efavirenz 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-45 22918158-2 2012 EFV is a known inducer of cytochrome P450 3A4, which converts artemether to dihydroartemisinin (DHA) that is also active and metabolizes longer acting lumefantrine (LR). Artemether 62-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-45 22918158-2 2012 EFV is a known inducer of cytochrome P450 3A4, which converts artemether to dihydroartemisinin (DHA) that is also active and metabolizes longer acting lumefantrine (LR). artenimol 76-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-45 22918158-2 2012 EFV is a known inducer of cytochrome P450 3A4, which converts artemether to dihydroartemisinin (DHA) that is also active and metabolizes longer acting lumefantrine (LR). artenimol 96-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-45 22918158-2 2012 EFV is a known inducer of cytochrome P450 3A4, which converts artemether to dihydroartemisinin (DHA) that is also active and metabolizes longer acting lumefantrine (LR). Lumefantrine 151-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-45 22918158-2 2012 EFV is a known inducer of cytochrome P450 3A4, which converts artemether to dihydroartemisinin (DHA) that is also active and metabolizes longer acting lumefantrine (LR). Lumefantrine 165-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-45 23210255-14 2012 Rilpivirine carries a risk of pharmacokinetic interactions with many other drugs, including inducers and inhibitors of cytochrome P450 isoenzyme CYP3A4, drugs that increase gastric pH, and drugs transported by P-glycoprotein. Rilpivirine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 22671777-8 2012 Using a mixture of recombinant P450 enzymes, turnover for PQ metabolism was estimated as 0.0099 min(-1); recombinant CYP3A4 had a higher metabolic rate (0.017 min(-1)) than recombinant CYP2C8 (p < .0001). piperaquine 58-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 22671777-9 2012 Inhibition of CYP3A4-mediated PQ loss was greatest using the selective inhibitor ketoconazole (9.1 +- 3.5% loss with ketoconazole vs 60.7 +- 5.9% with no inhibitor, p < .0001). piperaquine 30-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 22671777-9 2012 Inhibition of CYP3A4-mediated PQ loss was greatest using the selective inhibitor ketoconazole (9.1 +- 3.5% loss with ketoconazole vs 60.7 +- 5.9% with no inhibitor, p < .0001). Ketoconazole 81-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 22671777-9 2012 Inhibition of CYP3A4-mediated PQ loss was greatest using the selective inhibitor ketoconazole (9.1 +- 3.5% loss with ketoconazole vs 60.7 +- 5.9% with no inhibitor, p < .0001). Ketoconazole 117-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 22671777-10 2012 In summary, the extent of inhibition of in vitro metabolism with ketoconazole (83%) denotes that PQ appears to be primarily catalyzed by CYP3A4. Ketoconazole 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 22671777-10 2012 In summary, the extent of inhibition of in vitro metabolism with ketoconazole (83%) denotes that PQ appears to be primarily catalyzed by CYP3A4. piperaquine 97-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 22927483-9 2012 Of the CYPs evaluated, sorafenib was exclusively metabolized to sorafenib N-oxide by CYP3A4. Sorafenib 23-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 22927483-9 2012 Of the CYPs evaluated, sorafenib was exclusively metabolized to sorafenib N-oxide by CYP3A4. Sorafenib 64-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 22927483-10 2012 A trend for increased N-oxide formation in boys was observed in liver samples, which correlated with CYP3A4 mRNA expression. n-oxide 22-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 22927483-13 2012 This knowledge may provide important considerations for the clinical use of sorafenib in children and possibly other kinase inhibitors undergoing CYP3A4-mediated metabolism. Sorafenib 76-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 22809809-7 2012 The compounds 3-methylcholanthrene (a CYP1A2 inducer), phenobarbital (a CYP2B6 inducer), and rifampicin (a CYP3A4/5 inducer) served as positive controls. Rifampin 93-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 22809809-9 2012 Ritonavir resulted in a decrease in CYP3A/5 activity, yet a concomitant increase in mRNA and protein levels of CYP3A4. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 22859722-5 2012 However, raloxifene-mediated time-dependent inhibition only occurred in CYP2C8 and CYP3A4. Raloxifene Hydrochloride 9-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 22859722-8 2012 For each P450 enzyme, proposed substrate/metabolite access channels were mapped and active site cysteines were identified, which revealed that only CYP2C8 and CYP3A4 possess accessible cysteine residues near the active site cavities, a result consistent with the observed kinetics. Cysteine 96-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 22859722-8 2012 For each P450 enzyme, proposed substrate/metabolite access channels were mapped and active site cysteines were identified, which revealed that only CYP2C8 and CYP3A4 possess accessible cysteine residues near the active site cavities, a result consistent with the observed kinetics. Cysteine 96-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 22844081-7 2012 Treatment of Caco-2 cells with the CYP3A4 inhibitor, ketoconazole, inhibited the AFB1-induced cytotoxicity and micronucleus formation in TK6 cells, suggesting that intestinal metabolism is involved in the AFB1 genotoxic response in TK6 cells. Ketoconazole 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 22671777-0 2012 In vitro metabolism of piperaquine is primarily mediated by CYP3A4. piperaquine 23-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 22982774-4 2012 Treatment of HepG2 cells with glycyrrhizin resulted in marked increase in both CYP3A4 mRNA and protein levels. Glycyrrhizic Acid 30-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 22982774-6 2012 Glycyrrhizin activates the DNA-binding capacity of the PXR for the CYP3A4 element responding to xenobiotic signals, as measured by the electrophoretic-mobility shift assay (EMSA). Glycyrrhizic Acid 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 22982774-7 2012 These results indicate that the induction of the hepatic CYP3A4 by glycyrrhizin is mediated through the activation of PXR. Glycyrrhizic Acid 67-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 22982774-11 2012 Activation of the PXR by glycyrrhizin results in induction of CYP3A11 (CYP3A4 for human) expression and inhibition of CYP7A1 through an increase in small heterodimer partner (SHP) expression. Glycyrrhizic Acid 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 22326629-5 2012 Transport of CYP3A4 to the cell surface was monitored by SDS-PAGE and Western blot analysis of outer membrane proteins. Sodium Dodecyl Sulfate 57-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 22326629-7 2012 A HPLC assay confirmed the catalytic activity of displayed CYP3A4, using testosterone as a substrate. Testosterone 73-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 22677141-0 2012 Conformational dynamics of CYP3A4 demonstrate the important role of Arg212 coupled with the opening of ingress, egress and solvent channels to dehydrogenation of 4-hydroxy-tamoxifen. 4'-hydroxytamoxifen 162-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 22677141-4 2012 4-Hydroxy-tamoxifen (4OHT) is metabolized by CYP3A4 via competing hydroxylation and dehydrogenation reactions. 4'-hydroxytamoxifen 0-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 22677141-4 2012 4-Hydroxy-tamoxifen (4OHT) is metabolized by CYP3A4 via competing hydroxylation and dehydrogenation reactions. 4,17 beta-dihydroxy-4-androstene-3-one 21-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 22677141-6 2012 Conformational sampling of CYP3A4 with molecular dynamics simulations along multiple trajectories were used to generate representative structures for docking studies using recently published heme parameters. Heme 191-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 22677141-8 2012 RESULTS: Docking with MD-refined CYP3A4 structures incorporating hexa-coordinate heme parameters identifies a unique binding mode involving ARG212 and channel 4, unobserved in the starting PDB ID: 1TQN X-ray structure. Heme 81-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 23715232-0 2012 [Influence of CYP3A4/5 polymorphisms in the pharmacokinetics of levonorgestrel: a pilot study]. Levonorgestrel 64-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 23715232-2 2012 levonorgestrel is predominantly metabolised through hepatic routes that utilise the CYP3A system (CYP3A4 and CYP3A5). Levonorgestrel 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-89 23715232-2 2012 levonorgestrel is predominantly metabolised through hepatic routes that utilise the CYP3A system (CYP3A4 and CYP3A5). Levonorgestrel 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 23715232-3 2012 OBJECTIVE: This study aimed to evaluate the association between variant alleles of CYP3A4*1B and CYP3A5*3 polymorphisms and the pharmacokinetics of levonorgestrel. Levonorgestrel 148-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 22829543-9 2012 CYP3A4 was the predominant enzyme involved in the oxidative metabolism of Rh2, whereas alcohol dehydrogenase and aldehyde dehydrogenase mainly catalyzed the metabolic conversion of alcohol to the corresponding carboxylic acid. Carboxylic Acids 210-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22445438-14 2012 Coadministration of CYP3A4 modulators should be avoided where possible, and another type of contraception should be used when coadministration of CYP3A4 inducers like rifampicin is unavoidable. Rifampin 167-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 22752008-3 2012 Studies with recombinant human cytochromes P450 (P450s) indicate CYP2D6, CYP3A4, and CYP3A5 are the primary isoforms responsible for the oxidative metabolism of DM1, (S)-methyl-DM1, and DM4. N(2')-deacetyl-N(2')-(3-mercapto-1-oxopropyl)maytansine 161-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 22837187-17 2012 Sunitinib serum levels might have been profoundly reduced by mitotane induced cytochrome P450-3A4 activity attenuating its antitumor activity and adverse effects. Sunitinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-97 22752008-3 2012 Studies with recombinant human cytochromes P450 (P450s) indicate CYP2D6, CYP3A4, and CYP3A5 are the primary isoforms responsible for the oxidative metabolism of DM1, (S)-methyl-DM1, and DM4. (s)-methyl-dm1 166-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 22752008-3 2012 Studies with recombinant human cytochromes P450 (P450s) indicate CYP2D6, CYP3A4, and CYP3A5 are the primary isoforms responsible for the oxidative metabolism of DM1, (S)-methyl-DM1, and DM4. Maytansine 186-189 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 22752008-7 2012 DM1 and DM4 inactivated CYP3A from human liver microsomes with K(i)/k(inact) values of 4.8 +- 0.9 muM/0.035 +- 0.002 min(-1) and 3.3 +- 0.2 muM/0.114 +- 0.002 min(-1), respectively. N(2')-deacetyl-N(2')-(3-mercapto-1-oxopropyl)maytansine 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 22752008-7 2012 DM1 and DM4 inactivated CYP3A from human liver microsomes with K(i)/k(inact) values of 4.8 +- 0.9 muM/0.035 +- 0.002 min(-1) and 3.3 +- 0.2 muM/0.114 +- 0.002 min(-1), respectively. Maytansine 8-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 22752008-8 2012 DM1 and DM4 inactivated recombinant CYP3A4 with K(i)/k(inact) values of 3.4 +- 1.0 muM/0.058 +- 0.005 min(-1) and 1.4 +- 0.3 muM/0.117 +- 0.006 min(-1), respectively. N(2')-deacetyl-N(2')-(3-mercapto-1-oxopropyl)maytansine 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 22752008-8 2012 DM1 and DM4 inactivated recombinant CYP3A4 with K(i)/k(inact) values of 3.4 +- 1.0 muM/0.058 +- 0.005 min(-1) and 1.4 +- 0.3 muM/0.117 +- 0.006 min(-1), respectively. Maytansine 8-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 22789530-0 2012 The effects on metabolic clearance when administering a potent CYP3A autoinducer with the prototypic CYP3A inhibitor, ketoconazole. Ketoconazole 118-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 22789530-1 2012 Ketoconazole is recognized as the prototypical CYP3A inhibitor and is often used to determine the metabolic CYP3A liabilities of new chemical entities in preclinical and clinical studies. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 22789530-1 2012 Ketoconazole is recognized as the prototypical CYP3A inhibitor and is often used to determine the metabolic CYP3A liabilities of new chemical entities in preclinical and clinical studies. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 22789530-12 2012 More importantly, when administered with a potent CYP3A inducer at steady state, ketoconazole"s plasma exposure decreased, indicating that it may also be cleared by CYP3A, other inducible enzymes or transporters, or both. Ketoconazole 81-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 22789530-12 2012 More importantly, when administered with a potent CYP3A inducer at steady state, ketoconazole"s plasma exposure decreased, indicating that it may also be cleared by CYP3A, other inducible enzymes or transporters, or both. Ketoconazole 81-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-170 22162542-7 2012 Results show that telaprevir is an inhibitor of CYP3A and P-glycoprotein. telaprevir 18-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 23580932-4 2012 Tacrolimus has a large inter-/intra-patient variability in pharmacokinetics profile and a poor oral bioavailability because of its poor solubility, P-gp efflux, marked pre-systemic metabolism by CYP3A in the enterocytes and liver first pass effect. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-200 22926601-10 2012 Multiple regression analysis revealed that 33% of the overall variation in unbound (R)-methadone EC50 was explained by 3 variables, namely CYP3A activity (9%), age (16%), and sex (8%). Methadone 83-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-144 22926601-14 2012 Finally, it was established that CYP3A activity, years of dependent use, sex, and age are major determinants of methadone EC50 with respect to TMDS. Methadone 112-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 22837187-17 2012 Sunitinib serum levels might have been profoundly reduced by mitotane induced cytochrome P450-3A4 activity attenuating its antitumor activity and adverse effects. Mitotane 61-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-97 22943175-11 2012 CONCLUSIONS: The study indicated that CYP3A4 is likely to be the major enzyme responsible for glycyrrhetinic acid metabolism in HLM while CYP2C9 and CYP2C19 are considerably less active. Glycyrrhetinic Acid 94-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 22943175-12 2012 The results suggest that glycyrrhetinic acid has the potential to interact with a wide range of xenobiotics or endogenous chemicals that are CYP2C9, CYP2C19 and CYP3A4 substrates. Glycyrrhetinic Acid 25-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 22943175-6 2012 CYP3A4 is likely to be the major enzyme responsible for glycyrrhetinic acid metabolism in HLM while CYP2C9 and CYP2C19 are considerably less active. Glycyrrhetinic Acid 56-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22640941-12 2012 SFN has been shown to protect animals from AFB-induced tumors, to reduce AFB biomarkers in humans in vivo and to reduce efficiently AFB adduct formation in human hepatocytes, although it appears that this protective effect is the result of repression of human hepatic CYP3A4 expression, rather than induction of protective GSTs, at least in human hepatocytes. sulforaphane 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 268-274 22943175-9 2012 The inhibitory action of glycyrrhetinic acid was observed in CYP2C9 for 4-hydroxylation of diclofenac, CYP2C19 for 4"-hydroxylation of (S)-mephenytoin and CYP3A4 for 1"-hydroxylation of midazolam with half maximal inhibitory concentration (IC50) values of 4.3-fold, 3.8-fold and 9.6-fold higher than specific inhibitors in HLM, respectively. Glycyrrhetinic Acid 25-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 22509825-5 2012 Correlation analyses showed a significant correlation between mirabegron metabolism and testosterone 6beta-hydroxylation (CYP3A4/5 marker activity). testosterone 6beta 88-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 22524704-14 2012 The cytotoxicity of aflatoxin B(1), was decreased in upcyte( ) hepatocytes by co-incubation with the CYP3A4 inhibitor, ketoconazole. Aflatoxin B1 20-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 22524704-14 2012 The cytotoxicity of aflatoxin B(1), was decreased in upcyte( ) hepatocytes by co-incubation with the CYP3A4 inhibitor, ketoconazole. Ketoconazole 119-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 23835882-0 2012 A Semi-Mechanistic Metabolism Model of CYP3A Substrates in Pregnancy: Predicting Changes in Midazolam and Nifedipine Pharmacokinetics. Midazolam 92-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 23835882-0 2012 A Semi-Mechanistic Metabolism Model of CYP3A Substrates in Pregnancy: Predicting Changes in Midazolam and Nifedipine Pharmacokinetics. Nifedipine 106-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 23835882-2 2012 A semi-mechanistic metabolism model was developed to describe the pharmacokinetics of two cytochrome P450 3A (CYP3A) substrates, midazolam and nifedipine, in obstetrics patients. Midazolam 129-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-108 23835882-2 2012 A semi-mechanistic metabolism model was developed to describe the pharmacokinetics of two cytochrome P450 3A (CYP3A) substrates, midazolam and nifedipine, in obstetrics patients. Midazolam 129-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-115 23835882-2 2012 A semi-mechanistic metabolism model was developed to describe the pharmacokinetics of two cytochrome P450 3A (CYP3A) substrates, midazolam and nifedipine, in obstetrics patients. Nifedipine 143-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-108 23835882-2 2012 A semi-mechanistic metabolism model was developed to describe the pharmacokinetics of two cytochrome P450 3A (CYP3A) substrates, midazolam and nifedipine, in obstetrics patients. Nifedipine 143-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-115 23835882-3 2012 The model parameters were optimized to fit the data of oral midazolam pharmacokinetics in pregnant women, by increasing CYP3A-induced hepatic metabolism 1.6-fold in the model with no change in gut wall metabolism. Midazolam 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-125 23835882-7 2012 This model predicts the pharmacokinetics of two CYP3A substrates in pregnancy, and may be applicable to other CYP3A substrates as well.CPT: Pharmacometrics & Systems Pharmacology (2012) 1, e2; doi:10.1038/psp.2012.5; advance online publication 26 September 2012. Adenosine Monophosphate 157-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 23835883-8 2012 Our PBPK model is a useful tool to evaluate different dosing regimens during T3 for drugs cleared primarily via CYP3A metabolism.CPT: Pharmacometrics & Systems Pharmacology (2012) 1, e3; doi:10.1038/psp.2012.2; advance online publication 26 September 2012. Adenosine Monophosphate 151-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-117 23107701-5 2012 The extracts also inhibited the activity of CYP3A4, whose expression was induced by 1,25-dihydroxyvitamin D(3), and of CYP1A1, induced by benzo(a)pyrene. Calcitriol 84-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 23107701-5 2012 The extracts also inhibited the activity of CYP3A4, whose expression was induced by 1,25-dihydroxyvitamin D(3), and of CYP1A1, induced by benzo(a)pyrene. Benzo(a)pyrene 138-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 22651985-8 2012 Pre-incubation with recombinant human CYP3A4 not only caused degradation of clopidogrel and ticlopidine, but also increased cytotoxicity. Clopidogrel 76-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 22651985-8 2012 Pre-incubation with recombinant human CYP3A4 not only caused degradation of clopidogrel and ticlopidine, but also increased cytotoxicity. Ticlopidine 92-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 22828972-8 2012 Nevertheless, a phenotyping test to assess the activity of the cytochrome isoenzymes CYP3A4 and CYP2D6 (responsible for ranolazine metabolism) was performed, with dextromethorphan used as the probe drug. Ranolazine 120-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 22910411-3 2012 Using HepG2 cells expressing human CAR in the presence of tetracycline, we showed that knockdown of DP97 with small interfering RNAs suppressed tetracycline-inducible mRNA expression of CYP2B6 and UGT1A1 but not CYP3A4. Tetracycline 144-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 212-218 24900388-0 2012 Identification of the Significant Involvement and Mechanistic Role of CYP3A4/5 in Clopidogrel Bioactivation. Clopidogrel 82-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 24900388-5 2012 CYP3A4/5 was identified to be the enzyme metabolizing the piperidine motif. piperidine 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 24900388-7 2012 Identifying the significant involvement of CYP3A4/5 and characterizing its mechanistic role in clopidogrel bioactivation might assist future pharmacogenomic studies in exploring the full mechanism underlying clopidogrel efficacy. Clopidogrel 208-219 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 22828972-13 2012 Enzyme inhibition produced by diltiazem may have contributed to decreasing CYP3A4 activity. Diltiazem 30-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 22564264-3 2012 As posaconazole strongly inhibits CYP3A4, concurrent administration of sirolimus, a CYP3A4 substrate, and posaconazole has been reported to increase sirolimus drug exposure substantially. posaconazole 3-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 22564264-3 2012 As posaconazole strongly inhibits CYP3A4, concurrent administration of sirolimus, a CYP3A4 substrate, and posaconazole has been reported to increase sirolimus drug exposure substantially. posaconazole 3-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 22299599-7 2012 RESULTS: Midazolam clearance, a surrogate measure of CYP3A4/5 activity, was significantly decreased upon COC use (63.3 l h(-1) vs. 53.9 l h(-1), P < 0.05). Midazolam 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 22564264-3 2012 As posaconazole strongly inhibits CYP3A4, concurrent administration of sirolimus, a CYP3A4 substrate, and posaconazole has been reported to increase sirolimus drug exposure substantially. Sirolimus 71-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 22564264-3 2012 As posaconazole strongly inhibits CYP3A4, concurrent administration of sirolimus, a CYP3A4 substrate, and posaconazole has been reported to increase sirolimus drug exposure substantially. Sirolimus 71-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 22564264-3 2012 As posaconazole strongly inhibits CYP3A4, concurrent administration of sirolimus, a CYP3A4 substrate, and posaconazole has been reported to increase sirolimus drug exposure substantially. posaconazole 106-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 22564264-3 2012 As posaconazole strongly inhibits CYP3A4, concurrent administration of sirolimus, a CYP3A4 substrate, and posaconazole has been reported to increase sirolimus drug exposure substantially. Sirolimus 149-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 22489789-7 2012 Among the five CYPs evaluated, CYP3A4 and 2D6 are the most active in the oxidation of phospho-ibuprofen and phospho-sulindac respectively. 2-(4-isobutylphenyl)propionic acid 4-(diethoxyphosphoryloxy)butyl ester 86-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-45 22564264-3 2012 As posaconazole strongly inhibits CYP3A4, concurrent administration of sirolimus, a CYP3A4 substrate, and posaconazole has been reported to increase sirolimus drug exposure substantially. Sirolimus 149-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 22871995-0 2012 In vivo CYP3A4 activity, CYP3A5 genotype, and hematocrit predict tacrolimus dose requirements and clearance in renal transplant patients. Tacrolimus 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 22489789-7 2012 Among the five CYPs evaluated, CYP3A4 and 2D6 are the most active in the oxidation of phospho-ibuprofen and phospho-sulindac respectively. phospho-sulindac 108-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-45 22845044-2 2012 This study evaluated the effect of ketoconazole, a CYP3A4 inhibitor, on the metabolism of buprenorphine following the administration of a buprenorphine transdermal system 10 mug/hour (BTDS 10). Ketoconazole 35-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 22845044-2 2012 This study evaluated the effect of ketoconazole, a CYP3A4 inhibitor, on the metabolism of buprenorphine following the administration of a buprenorphine transdermal system 10 mug/hour (BTDS 10). Buprenorphine 90-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 22845044-3 2012 METHODS: This single-centre study enrolled 20 healthy subjects who had demonstrated ketoconazole-mediated CYP3A4 inhibition via an erythromycin breath test. Ketoconazole 84-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 22884766-2 2012 Bosutinib is metabolized primarily through the cytochrome P450 3A4 pathway. bosutinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-66 22775412-15 2012 In vitro studies, using recombinant enzymes, revealed that cytochrome P450 (CYP) 3A4 is the major CYP enzyme responsible for the biotransformation of atorvastatin lactone. Atorvastatin lactone 150-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-84 22871995-1 2012 Tacrolimus is metabolized by CYP3A4 and CYP3A5 and is characterized by a narrow therapeutic index and highly variable pharmacokinetics. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 22884766-3 2012 Inhibition of bosutinib metabolism by coadministration with the potent cytochrome P450 3A4 inhibitor ketoconazole could potentially increase plasma concentrations of bosutinib, allowing for the study of bosutinib tolerability at supratherapeutic concentrations in a healthy subject population. bosutinib 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-90 22884766-3 2012 Inhibition of bosutinib metabolism by coadministration with the potent cytochrome P450 3A4 inhibitor ketoconazole could potentially increase plasma concentrations of bosutinib, allowing for the study of bosutinib tolerability at supratherapeutic concentrations in a healthy subject population. Ketoconazole 101-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-90 22871995-2 2012 This cross-sectional study in 59 renal transplant patients investigated the relationship among in vivo CYP3A4 activity (assessed using midazolam as a drug probe), CYP3A5 genotype on the one hand, and tacrolimus pharmacokinetics on the other hand, taking into account other potential determinants of tacrolimus disposition. Midazolam 135-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 22884766-3 2012 Inhibition of bosutinib metabolism by coadministration with the potent cytochrome P450 3A4 inhibitor ketoconazole could potentially increase plasma concentrations of bosutinib, allowing for the study of bosutinib tolerability at supratherapeutic concentrations in a healthy subject population. bosutinib 166-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-90 22884766-3 2012 Inhibition of bosutinib metabolism by coadministration with the potent cytochrome P450 3A4 inhibitor ketoconazole could potentially increase plasma concentrations of bosutinib, allowing for the study of bosutinib tolerability at supratherapeutic concentrations in a healthy subject population. bosutinib 166-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-90 22871995-3 2012 In vivo CYP3A4 activity and CYP3A5 genotype explain 56-59% of variability in tacrolimus dose requirements and clearance, contributing ~25 and 30%, respectively. Tacrolimus 77-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 22871995-5 2012 These data indicate that CYP3A4- and CYP3A5-mediated tacrolimus metabolisms are major determinants of tacrolimus disposition in vivo and explain a substantial part of the clinically observed high interindividual variability in tacrolimus pharmacokinetics. Tacrolimus 53-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 22951253-15 2012 Telaprevir is a substrate/inhibitor of cytochrome P450 (CYP3A4) and a substrate/inhibitor of P-glycoprotein and poses an important risk for drug interactions. telaprevir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 22871995-5 2012 These data indicate that CYP3A4- and CYP3A5-mediated tacrolimus metabolisms are major determinants of tacrolimus disposition in vivo and explain a substantial part of the clinically observed high interindividual variability in tacrolimus pharmacokinetics. Tacrolimus 102-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 22871995-5 2012 These data indicate that CYP3A4- and CYP3A5-mediated tacrolimus metabolisms are major determinants of tacrolimus disposition in vivo and explain a substantial part of the clinically observed high interindividual variability in tacrolimus pharmacokinetics. Tacrolimus 102-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 22621802-10 2012 Use of human liver microsomes instead of recombinant CYP3A4 resulted in 5-fold lower k(inact)/K(I) for erythromycin. Erythromycin 103-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 22789987-8 2012 Dolutegravir drug interactions are similar to raltegravir, whereas boosted elvitegravir participates in additional CYP3A-mediated interactions. elvitegravir 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 22696420-3 2012 1-(4-Imidazopyridinyl-7phenyl)-3-(4"-cyanobiphenyl) urea (SR-9186) was optimized through several rounds of structural refinement from an initial screening hit to obtain greater than 1000-fold selectivity for the inhibition of CYP3A4 versus CYP3A5. 1-(4-imidazopyridinyl-7-phenyl)-3-(4'-cyanobiphenyl)urea 0-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 226-232 22679214-4 2012 To better understand the autoinduction and metabolic drug-drug interactions (DDIs), we evaluated the P450s (particularly CYP2B6 and CYP3A4) inhibited or induced by two artemisinin drugs, Qing-hao-su (QHS) and dihydroartemisinin (DHA) using human liver microsome, recombinant P450 enzymes, and primary human hepatocytes. artemisinin 168-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 22696420-8 2012 In addition, the long half-life (106 min) of SR-9186 in incubations containing 1 mg/ml human liver microsomes provided sustained CYP3A4 inhibition. Strontium 45-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 22507978-1 2012 AIMS: CYP3A4-metabolized statins can influence the pharmacodynamic effect of clopidogrel. Clopidogrel 77-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 22507978-12 2012 CONCLUSIONS: Among PCI-treated patients with HPR during co-administration of clopidogrel and atorvastatin, switching to a non-CYP3A4-metabolized statin can significantly decrease platelet reactivity and the prevalence of HPR. Clopidogrel 77-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 22507978-12 2012 CONCLUSIONS: Among PCI-treated patients with HPR during co-administration of clopidogrel and atorvastatin, switching to a non-CYP3A4-metabolized statin can significantly decrease platelet reactivity and the prevalence of HPR. Atorvastatin 93-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 22161476-1 2012 The present study investigated inhibitory effects of 1,4-dihydropyridines (1,4-DHPs) calcium channel antagonists (1,4-DHP-CCAs) on cytochromeP450 3A4 (CYP3A4) of human liver microsomes and further explored importance of 1,4-DHPs molecular structural descriptors. 1,4-dihydropyridine 53-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-149 22161476-1 2012 The present study investigated inhibitory effects of 1,4-dihydropyridines (1,4-DHPs) calcium channel antagonists (1,4-DHP-CCAs) on cytochromeP450 3A4 (CYP3A4) of human liver microsomes and further explored importance of 1,4-DHPs molecular structural descriptors. 1,4-dihydropyridine 53-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 22161476-1 2012 The present study investigated inhibitory effects of 1,4-dihydropyridines (1,4-DHPs) calcium channel antagonists (1,4-DHP-CCAs) on cytochromeP450 3A4 (CYP3A4) of human liver microsomes and further explored importance of 1,4-DHPs molecular structural descriptors. 1,4-dihydropyridine 75-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-149 22161476-1 2012 The present study investigated inhibitory effects of 1,4-dihydropyridines (1,4-DHPs) calcium channel antagonists (1,4-DHP-CCAs) on cytochromeP450 3A4 (CYP3A4) of human liver microsomes and further explored importance of 1,4-DHPs molecular structural descriptors. 1,4-dihydropyridine 75-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 22161476-1 2012 The present study investigated inhibitory effects of 1,4-dihydropyridines (1,4-DHPs) calcium channel antagonists (1,4-DHP-CCAs) on cytochromeP450 3A4 (CYP3A4) of human liver microsomes and further explored importance of 1,4-DHPs molecular structural descriptors. 1,4-dihydropyridine 75-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-149 22161476-1 2012 The present study investigated inhibitory effects of 1,4-dihydropyridines (1,4-DHPs) calcium channel antagonists (1,4-DHP-CCAs) on cytochromeP450 3A4 (CYP3A4) of human liver microsomes and further explored importance of 1,4-DHPs molecular structural descriptors. 1,4-dihydropyridine 75-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 22161476-1 2012 The present study investigated inhibitory effects of 1,4-dihydropyridines (1,4-DHPs) calcium channel antagonists (1,4-DHP-CCAs) on cytochromeP450 3A4 (CYP3A4) of human liver microsomes and further explored importance of 1,4-DHPs molecular structural descriptors. 1,4-dihydropyridine 220-228 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 22161476-2 2012 Partial Least Squares method was applied to probe the quantitative relationships between the 1,4-DHPs molecular structural descriptors and its inhibitory actions, which demonstrated that different 1,4-DHP-CCAs could inhibit CYP3A4 enzyme"s activity differently. 1,4-dihydropyridine 93-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 224-230 22161476-2 2012 Partial Least Squares method was applied to probe the quantitative relationships between the 1,4-DHPs molecular structural descriptors and its inhibitory actions, which demonstrated that different 1,4-DHP-CCAs could inhibit CYP3A4 enzyme"s activity differently. 1,4-dihydropyridine 93-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 224-230 22161476-6 2012 It is concluded that analysis of K (i) of 1,4-DHPs derivatives on the CYP3A4 activity may apply for the QSAR formula at the initial stage of clinical application of new drugs. 1,4-dihydropyridine 42-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 22451032-10 2012 Three clinical studies investigated the interaction showing simvastatin (CYP3A4 substrate) bioavailability reduced by TCZ and omeprazole bioavailability was decreased by TCZ-induced CYP2C19 activity. Simvastatin 60-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 22411763-5 2012 When CA-DADLE was incubated with hCYP3A4, similar oxidative metabolism of the peptide was observed. ca-dadle 5-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-40 22411763-6 2012 In contrast, incubation of the CA-DADLE analogs with hCYP3A4 showed that these amino-acid-modified analogs are not substrates for this CYP450 isozyme. DADLE 34-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-60 22411763-7 2012 These results suggest that the amino-acid-modified analogs of CA-DADLE prepared in this study could be stable to metabolic oxidation by CYP3A4 expressed in human intestinal mucosal cells. ca-dadle 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 22685215-3 2012 Initial in vitro data suggested that CYP3A4 is the major isoform responsible for the in vivo clearance of methadone in humans. Methadone 106-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 22688609-2 2012 The antidepressant activity is considered to be mediated by the active metabolite N-desalkylquetiapine, which is mainly formed by CYP3A4. norquetiapine 82-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 22688609-8 2012 Inhibition of CYP2D6 (by quinidine) reduced formation of 7-hydroxy-N-desalkylquetiapine by 81%, whereas the CYP3A4 inhibitor ketoconazole inhibited formation of N-desalkylquetiapine sulfoxide and M3 by 65 and 34%, respectively. Ketoconazole 125-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 22688609-8 2012 Inhibition of CYP2D6 (by quinidine) reduced formation of 7-hydroxy-N-desalkylquetiapine by 81%, whereas the CYP3A4 inhibitor ketoconazole inhibited formation of N-desalkylquetiapine sulfoxide and M3 by 65 and 34%, respectively. UNII-BIJ1Q409UA 161-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 22688609-10 2012 In recombinant systems, 7-hydroxy-N-desalkylquetiapine was exclusively formed by CYP2D6, whereas N-desalkylquetiapine sulfoxide and M3 were formed by both CYP3A4 and CYP2D6. UNII-BIJ1Q409UA 97-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 22688609-11 2012 Overall, intrinsic clearance of N-desalkylquetiapine was 12-fold higher by recombinant CYP2D6 relative to CYP3A4. norquetiapine 32-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 22688609-12 2012 In conclusion, N-desalkylquetiapine is metabolized by both CYP2D6 and CYP3A4 in vitro with preference for the former enzyme. norquetiapine 15-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 22735685-2 2012 Amlodipine is a well-known inhibitor of CYP 3A4, an isoenzyme of CYP3A that activates clopidogrel. Amlodipine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-47 22735685-2 2012 Amlodipine is a well-known inhibitor of CYP 3A4, an isoenzyme of CYP3A that activates clopidogrel. Clopidogrel 86-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-47 22735685-4 2012 In the presence of CYP3A4 inhibitors such as amlodipine, the genetic variation of CYP3A5, the isoenzyme responsible for the backup CYP3A activity, may play an important role in clopidogrel activation. Amlodipine 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 22735685-4 2012 In the presence of CYP3A4 inhibitors such as amlodipine, the genetic variation of CYP3A5, the isoenzyme responsible for the backup CYP3A activity, may play an important role in clopidogrel activation. Clopidogrel 177-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 21903893-2 2012 This open-label study in 37 adults with schizophrenia evaluated whether a drug-drug interaction occurs between armodafinil (a moderate CYP3A4 inducer) and the atypical antipsychotic quetiapine (primarily metabolized by CYP3A4). Modafinil 111-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 21903893-2 2012 This open-label study in 37 adults with schizophrenia evaluated whether a drug-drug interaction occurs between armodafinil (a moderate CYP3A4 inducer) and the atypical antipsychotic quetiapine (primarily metabolized by CYP3A4). Quetiapine Fumarate 182-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 23016247-6 2012 Apixaban is mainly metabolised by cytochrome P450 isoenzymes CYP 3A4 and 3A5 and also binds to P-glycoprotein, resulting in a high potential for pharmacokinetic interactions. apixaban 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-76 22525741-3 2012 Proposed mechanisms of effect for rifampicin include enhancement of multidrug-resistance protein 2 expression, activation of the enzymes of uridine diphosphate glucuronosyltransferase 1A1 and cytochrome P450 3A4, and stimulation of 6alpha-hydroxylation of bile acids. Rifampin 34-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-211 22428615-11 2012 Moreover, incubation with inhibitors of CYP3A, CYP2B6 and CYP2C19 significantly reduced clopidogrel bioactivation while a PON1 inhibitor, EDTA, had only a weak inhibitory effect. Clopidogrel 88-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 22809252-5 2012 In addition, the 1,2,3-TRZ fragment was incorporated into a well-established CYP3A4 substrate and mechanism-based inactivator, 17-alpha-ethynylestradiol (17EE), via click chemistry. Ethinyl Estradiol 127-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 22809252-5 2012 In addition, the 1,2,3-TRZ fragment was incorporated into a well-established CYP3A4 substrate and mechanism-based inactivator, 17-alpha-ethynylestradiol (17EE), via click chemistry. Ethinyl Estradiol 154-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 22809252-7 2012 Furthermore, the rate of CYP3A4-mediated metabolism of 17-click was comparable to that of 17EE, with a different regioselectivity. 17-click 55-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 22644026-2 2012 Lersivirine, a weak inducer of the cytochrome P450 (CYP) enzyme CYP3A4, is metabolized by CYP3A4 and UDP glucuronosyltransferase 2B7 (UGT2B7). UK 453,061 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 22644026-2 2012 Lersivirine, a weak inducer of the cytochrome P450 (CYP) enzyme CYP3A4, is metabolized by CYP3A4 and UDP glucuronosyltransferase 2B7 (UGT2B7). UK 453,061 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 22644026-10 2012 Lersivirine should not be coadministered with rifampin, which is a potent inducer of CYP3A4, UGT2B7, and P-glycoprotein activity and thus substantially lowers lersivirine exposure. UK 453,061 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 22644026-10 2012 Lersivirine should not be coadministered with rifampin, which is a potent inducer of CYP3A4, UGT2B7, and P-glycoprotein activity and thus substantially lowers lersivirine exposure. Rifampin 46-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 22480862-2 2012 The present study reports on the first electrochemically-driven drug-drug interactions of human cytochrome P450 3A4 probed with erythromycin, ketoconazole, cimetidine, diclofenac and quinidine. Erythromycin 128-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-115 22480862-2 2012 The present study reports on the first electrochemically-driven drug-drug interactions of human cytochrome P450 3A4 probed with erythromycin, ketoconazole, cimetidine, diclofenac and quinidine. Ketoconazole 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-115 22480862-2 2012 The present study reports on the first electrochemically-driven drug-drug interactions of human cytochrome P450 3A4 probed with erythromycin, ketoconazole, cimetidine, diclofenac and quinidine. Cimetidine 156-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-115 22480862-2 2012 The present study reports on the first electrochemically-driven drug-drug interactions of human cytochrome P450 3A4 probed with erythromycin, ketoconazole, cimetidine, diclofenac and quinidine. Diclofenac 168-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-115 22480862-2 2012 The present study reports on the first electrochemically-driven drug-drug interactions of human cytochrome P450 3A4 probed with erythromycin, ketoconazole, cimetidine, diclofenac and quinidine. Quinidine 183-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-115 22480862-3 2012 Cytochrome P450 3A4 was immobilized on glassy carbon electrodes in the presence of a cationic polyelectrolyte, PDDA (poly(diallyldimethylammonium chloride)). Carbon 46-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 22480862-3 2012 Cytochrome P450 3A4 was immobilized on glassy carbon electrodes in the presence of a cationic polyelectrolyte, PDDA (poly(diallyldimethylammonium chloride)). poly-N,N-dimethyl-N,N-diallylammonium chloride 117-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 22562045-0 2012 Human PXR-mediated induction of intestinal CYP3A4 attenuates 1alpha,25-dihydroxyvitamin D3 function in human colon adenocarcinoma LS180 cells. Calcitriol 61-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 22562045-1 2012 Oxidative catabolism of 1alpha,25-dihydroxyvitamin D(3) [1alpha,25(OH)(2)D(3)] is mediated by either CYP24A1 or CYP3A4. 1,25-dihydroxyvitamin D 24-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 22562045-3 2012 Treatment with the hPXR agonist rifampin significantly increased CYP3A4 mRNA content and catalytic activity, but had no effect on CYP24A1 or TRPV6 mRNA content. Rifampin 32-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 22562045-5 2012 Introduction of the CYP3A4 inhibitor, 6",7"-dihydroxybergamottin, an active inhibitor in grapefruit juice, reversed the effects of rifampin on 1alpha,25(OH)(2)D(3) clearance and TRPV6 expression. 6',7'-dihydroxybergamottin 38-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 22562045-5 2012 Introduction of the CYP3A4 inhibitor, 6",7"-dihydroxybergamottin, an active inhibitor in grapefruit juice, reversed the effects of rifampin on 1alpha,25(OH)(2)D(3) clearance and TRPV6 expression. Rifampin 131-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 22562045-6 2012 Over-expression of hPXR in LS180 cells greatly enhanced the CYP3A4 responsiveness to rifampin pretreatment, and elicited a greater relative suppression of TRPV6 expression and an increase in 1alpha,25(OH)(2)D(3) disappearance rate, compared to vector expressed cells, following hormone administration. Rifampin 85-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 22562045-7 2012 Together, these results suggest that induction of CYP3A4 in the intestinal epithelium by hPXR agonists can result in a greater metabolic clearance of 1alpha,25(OH)(2)D(3) and reduced effects of the hormone on the intestinal calcium absorption, which may contribute to an increased risk of drug-induced osteomalacia/osteoporosis in patients receiving chronic therapy with potent hPXR agonists. Calcium 224-231 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 22428615-13 2012 Moreover, CYP2C19, CYP2B6 and CYP3A play important roles in the bioactivation of clopidogrel. Clopidogrel 81-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-35 22673786-6 2012 Midazolam is primarily metabolized by the CYP3A4/CYP3A5 enzymes. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21730017-7 2012 Repeated administration of SB-649868 dose-dependently increased exposure to simvastatin (10 mg), suggesting CYP3A4 inhibition ranging from very mild (5 mg) to strong (30 mg). N-((1-((5-(4-fluorophenyl)-2-methyl-4-thiazolyl)carbonyl)-2-piperidinyl)methyl)-4-benzofurancarboxamide 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 21730017-7 2012 Repeated administration of SB-649868 dose-dependently increased exposure to simvastatin (10 mg), suggesting CYP3A4 inhibition ranging from very mild (5 mg) to strong (30 mg). Simvastatin 76-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 22529023-7 2012 The CYP3A4 statins (i.e., simvastatin, atorvastatin and lovastatin) accounted for 85% of all statins in 2004, increasing to 93% in 2008. Simvastatin 26-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 22529023-7 2012 The CYP3A4 statins (i.e., simvastatin, atorvastatin and lovastatin) accounted for 85% of all statins in 2004, increasing to 93% in 2008. Atorvastatin 39-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 22529023-7 2012 The CYP3A4 statins (i.e., simvastatin, atorvastatin and lovastatin) accounted for 85% of all statins in 2004, increasing to 93% in 2008. Lovastatin 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 22484315-8 2012 These data suggest VDR polymorphisms are predictors of intestinal CYP3A4, and that CYP3A4 intestinal expression varies seasonally--likely related to annual changes in UV sunlight and vitamin D levels. Vitamin D 183-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 22660604-1 2012 BACKGROUND: In children, a large variability in pharmacokinetics of midazolam, a cytochrome P450 3A4/5 (CYP3A4/5) enzyme substrate, has been described, which cannot be explained by age-related changes alone. Midazolam 68-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-102 22660604-1 2012 BACKGROUND: In children, a large variability in pharmacokinetics of midazolam, a cytochrome P450 3A4/5 (CYP3A4/5) enzyme substrate, has been described, which cannot be explained by age-related changes alone. Midazolam 68-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-112 22660604-7 2012 A reduction of 93% for CYP3A4/5 (midazolam to 1-hydroxymidazolam) and 86% for uridine diphosphate glucuronosyltransferase (1-hydroxymidazolam to 1-hydroxymidazolam glucuronide) mediated clearance was found in pediatric intensive care patients compared with the other 2 patient groups. Midazolam 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-31 22660604-10 2012 CONCLUSIONS: From infancy to adolescence, critical illness seems to be a major determinant of midazolam clearance, which may result from reduced CYP3A4/5 activity due to inflammation. Midazolam 94-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 23162896-0 2012 [Effects of isorhamnetin on CYP3A4 and herb-drug interaction]. 3-methylquercetin 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 23162896-1 2012 The study is to report the investigation of the effects of isorhamnetin on CYP3A4 and herb-drug interaction. 3-methylquercetin 59-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 23162896-2 2012 A reporter gene assay is used to test pregnane X receptor transactivation action, qRT-PCR and a luminescence-based assay were applied to determine mRNA induction and enzyme activity of CYP3A4 after isorhamnetin treatment. 3-methylquercetin 198-210 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 23162896-4 2012 Isorhamnetin at 1, 10 and 25 micromol x L(-1) transactivated the CYP3A4 reporter construct and upregulated CYP3A4 mRNA as well in a dose-dependent manner. 3-methylquercetin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 23162896-4 2012 Isorhamnetin at 1, 10 and 25 micromol x L(-1) transactivated the CYP3A4 reporter construct and upregulated CYP3A4 mRNA as well in a dose-dependent manner. 3-methylquercetin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 23162896-6 2012 In conclusion, activation of PXR by isorhamnetin played a role in the upregulation of CYP3A4 mRNA. 3-methylquercetin 36-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 22375838-1 2012 Raloxifene was metabolized predominantly by CYP3A4 in human liver microsomes to a pair of carbon-carbon (RD1-2) and ether (RD3-4) linked homodimers in an nicotinamide adenine dinucleotide phosphate-dependent manner. Raloxifene Hydrochloride 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 22375838-4 2012 The structures of the homodimers RD1, 3 and 4 provided evidence for free radical metabolism of raloxifene by predominantly CYP3A4 in human liver microsomes to oxygen-centered phenoxy radicals from 4-hydroxyphenyl and benzo[b]thiopen-6-ol moieties. Free Radicals 68-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 22375838-4 2012 The structures of the homodimers RD1, 3 and 4 provided evidence for free radical metabolism of raloxifene by predominantly CYP3A4 in human liver microsomes to oxygen-centered phenoxy radicals from 4-hydroxyphenyl and benzo[b]thiopen-6-ol moieties. Raloxifene Hydrochloride 95-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 22375838-4 2012 The structures of the homodimers RD1, 3 and 4 provided evidence for free radical metabolism of raloxifene by predominantly CYP3A4 in human liver microsomes to oxygen-centered phenoxy radicals from 4-hydroxyphenyl and benzo[b]thiopen-6-ol moieties. thiopen-6-ol 225-237 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 22513143-0 2012 Role of human CYP3A4 in the biotransformation of sorafenib to its major oxidized metabolites. Sorafenib 49-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 22513143-5 2012 cDNA-expressed CYP3A4 was the major catalyst in the formation of the principal N-oxide and N-hydroxymethyl metabolites of sorafenib, as well as the minor N-desmethyl metabolite. n-oxide 79-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 22513143-5 2012 cDNA-expressed CYP3A4 was the major catalyst in the formation of the principal N-oxide and N-hydroxymethyl metabolites of sorafenib, as well as the minor N-desmethyl metabolite. Sorafenib 122-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 22513143-7 2012 In human hepatic microsomes metabolite formation was correlated with CYP3A4-mediated midazolam 1"-hydroxylation, but not with other CYP-specific substrate oxidations. Midazolam 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 22513143-8 2012 In accord with these findings the CYP3A4 inhibitor ketoconazole selectively inhibited microsomal sorafenib oxidation pathways. Ketoconazole 51-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 22513143-8 2012 In accord with these findings the CYP3A4 inhibitor ketoconazole selectively inhibited microsomal sorafenib oxidation pathways. Sorafenib 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 22513143-9 2012 From computational modeling studies atoms in the structure of sorafenib that undergo biotransformation were within ~5.4 A of the CYP3A4 heme. Sorafenib 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 22513143-9 2012 From computational modeling studies atoms in the structure of sorafenib that undergo biotransformation were within ~5.4 A of the CYP3A4 heme. Heme 136-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 22513143-10 2012 Important hydrogen bonding interactions between sorafenib and amino acids Ser-119 and Glu-374 in the active center of CYP3A4 were identified. Hydrogen 10-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 22513143-10 2012 Important hydrogen bonding interactions between sorafenib and amino acids Ser-119 and Glu-374 in the active center of CYP3A4 were identified. Sorafenib 48-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 22513143-10 2012 Important hydrogen bonding interactions between sorafenib and amino acids Ser-119 and Glu-374 in the active center of CYP3A4 were identified. Serine 74-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 22513143-10 2012 Important hydrogen bonding interactions between sorafenib and amino acids Ser-119 and Glu-374 in the active center of CYP3A4 were identified. Glutamic Acid 86-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 22513143-11 2012 These findings indicate that sorafenib is oxidized selectively by human CYP3A4. Sorafenib 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 22543594-2 2012 It functions to boost the effectiveness of other PIs as a result of blocking their breakdown by the cytochrome P450 (3A4) pathway. Monothiopyrophosphoric acid 49-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-120 22484315-1 2012 Vitamin D, whose levels vary seasonally with sunlight, is activated to 1alpha,25-dihydroxyvitamin D(3) that binds the vitamin D receptor (VDR) and transcriptionally regulates intestinal CYP3A4 expression. Vitamin D 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 186-192 22484315-1 2012 Vitamin D, whose levels vary seasonally with sunlight, is activated to 1alpha,25-dihydroxyvitamin D(3) that binds the vitamin D receptor (VDR) and transcriptionally regulates intestinal CYP3A4 expression. 1,25-dihydroxyvitamin D 71-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 186-192 22233204-3 2012 This study was required to determine the effect of tofacitinib on the in vivo pharmacokinetics of a sensitive CYP3A4 substrate. tofacitinib 51-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 22122233-0 2012 A clinical study to assess CYP1A2 and CYP3A4 induction by AZD7325, a selective GABA(A) receptor modulator - an in vitro and in vivo comparison. 4-amino-8-(2-fluoro-6-methoxy-phenyl)-N-propylcinnoline-3-carboxamide 58-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 22233204-4 2012 WHAT THIS STUDY ADDS: The pharmacokinetics of midazolam, a sensitive CYP3A4 substrate, are not altered when co-administered with tofacitinib in healthy subjects. Midazolam 48-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 22122233-2 2012 The induction effects of AZD7325 on CYP1A2 and CYP3A4 have not been systematically studied. 4-amino-8-(2-fluoro-6-methoxy-phenyl)-N-propylcinnoline-3-carboxamide 25-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 22233204-7 2012 AIMS: To investigate inhibitive and inductive effects of tofacitinib (CP-690,550), a Janus kinase inhibitor, on CYP3A4 function via in vitro and in vivo studies. tofacitinib 57-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 22122233-3 2012 WHAT THIS STUDY ADDS: The in vitro studies showed that AZD7325 was a moderate CYP1A2 inducer and potent CYP3A4 inducer. 4-amino-8-(2-fluoro-6-methoxy-phenyl)-N-propylcinnoline-3-carboxamide 57-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 22122233-4 2012 The follow-up clinical studies in healthy volunteers demonstrated that the expected efficacious daily dose of AZD7325 only weakly induced the pharmacokinetics of the CYP3A4 sensitive substrate, midazolam, and had no effect on the pharmacokinetics of the CYP1A2 substrate, caffeine. 4-amino-8-(2-fluoro-6-methoxy-phenyl)-N-propylcinnoline-3-carboxamide 110-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-172 22122233-7 2012 AIM(S): To investigate the potential of AZD7325 to induce CYP1A2 and CYP3A4 enzyme activities. 4-amino-8-(2-fluoro-6-methoxy-phenyl)-N-propylcinnoline-3-carboxamide 40-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 22122233-8 2012 METHODS: Induction of CYP1A2 and CYP3A4 by AZD7325 was first evaluated using cultured human hepatocytes. 4-amino-8-(2-fluoro-6-methoxy-phenyl)-N-propylcinnoline-3-carboxamide 43-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 22122233-10 2012 RESULTS: The highest CYP1A2 and CYP3A4 induction responses were observed in human hepatocytes treated with 1 or 10 microm of AZD7325, in the range of 17.9%-54.9% and 76.9%-85.7% of the positive control responses, respectively. 4-amino-8-(2-fluoro-6-methoxy-phenyl)-N-propylcinnoline-3-carboxamide 125-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 22122233-16 2012 CONCLUSIONS: While AZD7325 appeared to be a potent CYP3A4 inducer and a moderate CYP1A2 inducer from in vitro studies, the expected efficacious dose of AZD7325 had no effect on CYP1A2 activity and only a weak inducing effect on CYP3A4 activity. 4-amino-8-(2-fluoro-6-methoxy-phenyl)-N-propylcinnoline-3-carboxamide 19-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 22233204-7 2012 AIMS: To investigate inhibitive and inductive effects of tofacitinib (CP-690,550), a Janus kinase inhibitor, on CYP3A4 function via in vitro and in vivo studies. tofacitinib 70-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 22233204-8 2012 METHODS: In vitro experiments were conducted to assess the inhibition and induction potential of tofacitinib for major drug metabolizing enzymes (CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 and CYP3A4). tofacitinib 97-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 198-204 22243420-1 2012 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: The CYP3A4 inhibition by lipophilic statins may attenuate the effectiveness of clopidogrel. Clopidogrel 123-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 22680343-7 2012 AIMS: To evaluate the use of rosiglitazone and the erythromycin breath test (ERMBT), as probes of CYP2C8 and CYP3A4, respectively, to explain inter-individual variability in paclitaxel exposure. Paclitaxel 174-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 23018254-0 2012 Impact of CYP3A4*1B and CYP3A5*3 polymorphisms on the pharmacokinetics of cyclosporine and sirolimus in renal transplant recipients. Cyclosporine 74-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 23018254-7 2012 The mean cyclosporine dose in CYP3A4*1/*1B subjects was 455.04+-128.68 mg/day vs. 261.68+-64.72 mg/day in CYP3A4*1/*1 subjects (p<0.001). Cyclosporine 9-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 23018254-8 2012 The mean cyclosporine dose-adjusted trough blood concentrations (ng/ml per mg/kg body weight) in CYP3A4*1/*1B subjects were lower than in the CYP3A4*1/*1 group (37.06+-10.38 vs. 44.63+-13.99; p<0.218). Cyclosporine 9-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 23018254-11 2012 CONCLUSIONS: Genetic polymorphisms in CYP3A4 and CYP3A5 may underlie inter-individual differences in cyclosporine pharmacokinetics after renal transplantation. Cyclosporine 101-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 23018254-12 2012 Patients with at least 1 functional CYP3A5*1 or CYP3A4*1B allele require significantly higher doses of cyclosporine to reach target drug levels compared to patients with the CYP3A4*1 or CYP3A5*3 alleles. Cyclosporine 103-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 23018254-12 2012 Patients with at least 1 functional CYP3A5*1 or CYP3A4*1B allele require significantly higher doses of cyclosporine to reach target drug levels compared to patients with the CYP3A4*1 or CYP3A5*3 alleles. Cyclosporine 103-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 22581509-6 2012 In experiments with human liver microsomes that examined the inhibition of nalfurafine metabolism by anti-human P450 antibodies, anti-CYP3A4 antibody predominantly, and anti-CYP2C8 and 2C19 antibodies moderately, inhibited de-CPM formation. TRK 820 75-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 22511346-9 2012 In silico docking studies supported the preferential formation of an O-dealkylated metabolite of lapatinib by CYP3A5 compared with an N-hydroxylation reaction that is predominantly catalyzed by CYP3A4. Lapatinib 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 22581509-7 2012 From these results, CYP3A4 appeared to be the major isoform involved in the metabolic decyclopropylmethylation of nalfurafine, while CYP2C8 and 2C19 most likely play a minor role in the formation of de-CPM. TRK 820 114-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 22568694-18 2012 Linagliptin plasma exposure is reduced by potent inducers of CYP3A4 or P-gp. Linagliptin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 22496391-9 2012 Cytochrome P450 (P450) enzymes CYP3A4 and CYP3A5 metabolized saxagliptin and formed M2. saxagliptin 61-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 22496396-4 2012 The formation of the 4-hydroxy-phenyl metabolite was catalyzed by CYP2D6 with some contribution from CYP2C9, whereas the formation of the sulfoxide was mediated by CYP3A4/5 and CYP2A6. sulfoxide 138-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 22451699-9 2012 This systematic analysis revealed a comparable in vitro contribution from CYP2C8 and CYP3A4 to the metabolism of repaglinide (<50%), whereas the contribution of glucuronidation ranged from 2 to 20%, depending on the in vitro system used. repaglinide 113-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 22517972-0 2012 Sequential metabolism of AMG 487, a novel CXCR3 antagonist, results in formation of quinone reactive metabolites that covalently modify CYP3A4 Cys239 and cause time-dependent inhibition of the enzyme. quinone 84-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 22531045-6 2012 In human liver microsomes, carnosic acid did not exhibit significant time-dependent inhibition for any of the cytochrome P450 enzymes investigated, although it did inhibit CYP2C9- and CYP3A4-catalyzed reactions with K(i) values of 9.2 and 4.3 muM, respectively. salvin 27-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 22531045-7 2012 Carnosic acid also induced CYP2B6 and CYP3A4 mRNA and enzyme activity in a dose-dependent manner. salvin 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 22531045-8 2012 At 10 muM, carnosic acid increased CYP2B6 enzyme activity 61.6 and 49.3% in two donors compared with phenobarbital, and it increased CYP3A enzyme activity 82.6 and 142% compared with rifampicin. salvin 11-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-138 22511346-2 2012 Recently, it has been found that lapatinib forms a metabolite-inhibitor complex (MIC) with CYP3A4 via the formation of an alkylnitroso intermediate. Lapatinib 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22511346-2 2012 Recently, it has been found that lapatinib forms a metabolite-inhibitor complex (MIC) with CYP3A4 via the formation of an alkylnitroso intermediate. alkylnitroso 122-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22517972-6 2012 CYP3A4-mediated biotransformation of [(3)H]M2 in the presence of GSH led to identification of two new metabolites, M4 and M5, which shifted focus away from M2 being directly responsible for TDI. Glutathione 65-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22517972-6 2012 CYP3A4-mediated biotransformation of [(3)H]M2 in the presence of GSH led to identification of two new metabolites, M4 and M5, which shifted focus away from M2 being directly responsible for TDI. Toluene 2,4-Diisocyanate 190-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22522748-3 2012 Using zaleplon as a probe substrate and simultaneously monitoring the AO-catalyzed formation of oxozaleplon and the CYP3A-catalyzed formation of desethyzaleplon in the presence of a range of hydralazine concentrations, it was determined that >90% inhibition of the AO activity with minimal effect on the CYP3A activity could be achieved with 25 to 50 muM hydralazine. desethyzaleplon 145-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 22522748-3 2012 Using zaleplon as a probe substrate and simultaneously monitoring the AO-catalyzed formation of oxozaleplon and the CYP3A-catalyzed formation of desethyzaleplon in the presence of a range of hydralazine concentrations, it was determined that >90% inhibition of the AO activity with minimal effect on the CYP3A activity could be achieved with 25 to 50 muM hydralazine. Hydralazine 191-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 22522748-3 2012 Using zaleplon as a probe substrate and simultaneously monitoring the AO-catalyzed formation of oxozaleplon and the CYP3A-catalyzed formation of desethyzaleplon in the presence of a range of hydralazine concentrations, it was determined that >90% inhibition of the AO activity with minimal effect on the CYP3A activity could be achieved with 25 to 50 muM hydralazine. Hydralazine 358-369 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 22993851-0 2012 [Effect of CYP3A4*18B, CYP3A5*3 gene polymorphism on dosage and concentration of tacrolimus in renal transplant patients]. Tacrolimus 81-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 22415140-12 2012 CONCLUSIONS: 13/26 oncology drugs investigated showed TDI potential towards CYP3A, formation of reactive metabolites was also observed. Toluene 2,4-Diisocyanate 54-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 22993851-6 2012 While after the effects of CYP3A4*18B genotype were eliminated, the C/D" ratio of tacrolimus in patients with CYP3A5*1/*1 and *1/*3 genotype group was significantly lower than those with CYP3A5*3/*3 genotype groups (P < 0.01). Tacrolimus 82-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 22313038-0 2012 Different effects of proton pump inhibitors and famotidine on the clopidogrel metabolic activation by recombinant CYP2B6, CYP2C19 and CYP3A4. Famotidine 48-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 22313038-0 2012 Different effects of proton pump inhibitors and famotidine on the clopidogrel metabolic activation by recombinant CYP2B6, CYP2C19 and CYP3A4. Clopidogrel 66-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 22313038-1 2012 Inhibitory potential of proton pump inhibitors (PPIs) and famotidine, an H(2) receptor antagonist, on the metabolic activation of clopidogrel was evaluated using recombinant CYP2B6, CYP2C19 and CYP3A4. Clopidogrel 130-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 22313038-3 2012 Omeprazole potently inhibited clopidogrel activation by CYP2C19 with an IC(50) of 12.8 mumol/L and more weakly inhibited that by CYP2B6 and CYP3A4. Omeprazole 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 22313038-4 2012 IC(50) of omeprazole for CYP2C19 and CYP3A4 was decreased about two- and three-fold, respectively, by 30-min preincubation with NADPH. Omeprazole 10-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 22313038-4 2012 IC(50) of omeprazole for CYP2C19 and CYP3A4 was decreased about two- and three-fold, respectively, by 30-min preincubation with NADPH. NADP 128-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 22652334-6 2012 To distinguish between quasi-irreversible and irreversible inhibition, diltiazem and mifepristone were used as quasi-irreversible and irreversible inhibitors of CYP3A4, respectively, and CYP3A4 activity was measured using midazolam and testosterone as substrates. Mifepristone 85-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 22652334-7 2012 After pre-incubation, CYP3A4 IC(50) shifts caused by diltiazem and mifepristone were greater than 2.5- and 3.7-fold, respectively. Diltiazem 53-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 22587011-0 2012 Cytochrome P450 3A4 inhibition by ketoconazole: tackling the problem of ligand cooperativity using molecular dynamics simulations and free-energy calculations. Ketoconazole 34-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 22652334-7 2012 After pre-incubation, CYP3A4 IC(50) shifts caused by diltiazem and mifepristone were greater than 2.5- and 3.7-fold, respectively. Mifepristone 67-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 22587011-4 2012 In the current study, a combination of molecular dynamics simulations and free-energy calculations was applied to elucidate the physicochemical origin of the observed positive homotropic cooperativity in ketoconazole binding to CYP3A4. Ketoconazole 204-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 22587011-5 2012 The binding of the first ketoconazole molecule was established to increase the affinity for the binding of the second ketoconazole molecule by 5 kJ mol(-1), which explains and quantifies the experimentally observed cooperative behavior of CYP3A4. Ketoconazole 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 239-245 22652334-8 2012 Incubation with 2mM potassium ferricyanide for 10min reversed the MDI of CYP3A4 by diltiazem, but not mifepristone. potassium ferricyanide 20-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 22587011-5 2012 The binding of the first ketoconazole molecule was established to increase the affinity for the binding of the second ketoconazole molecule by 5 kJ mol(-1), which explains and quantifies the experimentally observed cooperative behavior of CYP3A4. Ketoconazole 118-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 239-245 22652334-8 2012 Incubation with 2mM potassium ferricyanide for 10min reversed the MDI of CYP3A4 by diltiazem, but not mifepristone. Diltiazem 83-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 22652334-9 2012 Increases in potassium ferricyanide concentration and incubation time reduced the recovery of CYP3A4 activity. potassium ferricyanide 13-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 22652334-10 2012 The established methods were confirmed using three CYP3A4 inhibitors including diltiazem, mifepristone and amiodarone (a reversible metabolism-dependent inhibitor). Diltiazem 79-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 22652334-10 2012 The established methods were confirmed using three CYP3A4 inhibitors including diltiazem, mifepristone and amiodarone (a reversible metabolism-dependent inhibitor). Amiodarone 107-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 22559005-3 2012 Here we investigated the effects of exposure of carp (Cyprinus carpio) primary hepatocytes to the human PXR agonist rifampicin (RIF) on expression of target genes involved in phase I (cyp2k, cyp3a) and phase II (gstalpha, gstpi) drug metabolism and drug transporters mdr1 and mrp2. Rifampin 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-196 22644980-4 2012 While both dihydropyridine and nondihydropyridine CCBs are cytochrome P-450 isoenzyme 3A4 (CYP3A4) substrates, verapamil was the CCB implicated in three of the five case reports. 1,4-dihydropyridine 11-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-89 22644980-4 2012 While both dihydropyridine and nondihydropyridine CCBs are cytochrome P-450 isoenzyme 3A4 (CYP3A4) substrates, verapamil was the CCB implicated in three of the five case reports. 1,4-dihydropyridine 11-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22644980-4 2012 While both dihydropyridine and nondihydropyridine CCBs are cytochrome P-450 isoenzyme 3A4 (CYP3A4) substrates, verapamil was the CCB implicated in three of the five case reports. nondihydropyridine ccbs 31-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-89 22644980-4 2012 While both dihydropyridine and nondihydropyridine CCBs are cytochrome P-450 isoenzyme 3A4 (CYP3A4) substrates, verapamil was the CCB implicated in three of the five case reports. nondihydropyridine ccbs 31-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22644980-6 2012 Both erythromycin and clarithromycin have been shown to prolong the Q-T interval, an effect that appears to increase when these drugs are given with CYP3A4 inhibitors. Erythromycin 5-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 22644980-6 2012 Both erythromycin and clarithromycin have been shown to prolong the Q-T interval, an effect that appears to increase when these drugs are given with CYP3A4 inhibitors. Clarithromycin 22-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 22521607-0 2012 CYP3A-mediated apoptosis of dauricine in cultured human bronchial epithelial cells and in lungs of CD-1 mice. dauricine 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 22692316-6 2012 RESULTS: CYP1A2, CYP2C9, CYP2C19 and CYP3A4 in HLM were involved in bakuchiol metabolism, among which CYP2C19 showed the highest metabolic rate. bakuchiol 68-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 22692316-7 2012 Co-incubation with ABT (2.5 mmol/L) could inhibit more than 90% of the enzyme activities for CYP1A2, CYP2C9, CYP2C19 and CYP3A4. 1-aminobenzotriazole 19-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 22608922-1 2012 Four metabolites of okadaic acid were generated by incubation with human recombinant cytochrome P450 3A4. Okadaic Acid 20-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-104 22559005-3 2012 Here we investigated the effects of exposure of carp (Cyprinus carpio) primary hepatocytes to the human PXR agonist rifampicin (RIF) on expression of target genes involved in phase I (cyp2k, cyp3a) and phase II (gstalpha, gstpi) drug metabolism and drug transporters mdr1 and mrp2. Rifampin 128-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-196 22559005-4 2012 RIF induced expression of all target genes measured and the PXR antagonist ketoconazole (KET) inhibited responses of cyp2k and cyp3a. Ketoconazole 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 22559005-4 2012 RIF induced expression of all target genes measured and the PXR antagonist ketoconazole (KET) inhibited responses of cyp2k and cyp3a. Ketoconazole 89-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 22370628-0 2012 Effect of CYP3A4 inducer dexamethasone on hepatotoxicity of lapatinib: clinical and in vitro evidence. Lapatinib 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 21998445-4 2012 Haloperidol is extensively metabolized in the liver, with CYP3A4 the chief cytochrome oxidase responsible for metabolism. Haloperidol 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 22397757-6 2012 In present study, felotaxel has been identified as a potent inhibitor of metabolic activity of CYP3A4. felotaxel 18-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 22397757-7 2012 Therefore, clinically relevant pharmacokinetic drug-drug interactions are likely to occur between felotaxel and co-administered substrates of these CYP3A4 isozymes. felotaxel 98-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 22370628-1 2012 Concomitant usage of lapatinib, a cytochrome P450 (CYP) 3A4 substrate and dexamethasone, a CYP3A4 inducer, is a pharmacokinetic drug-drug interaction. Lapatinib 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22370628-1 2012 Concomitant usage of lapatinib, a cytochrome P450 (CYP) 3A4 substrate and dexamethasone, a CYP3A4 inducer, is a pharmacokinetic drug-drug interaction. Dexamethasone 74-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22292787-13 2012 ingestion of glycyrrhizin appears to be able to induce CYP3A in rodents and humans, while several deglycosylated products of ginsenosides can moderately inhibit CYP activities in vitro with IC50 values of 10-50 muM. Glycyrrhizic Acid 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 22415932-0 2012 Drug interaction of efavirenz and midazolam: efavirenz activates the CYP3A-mediated midazolam 1"-hydroxylation in vitro. efavirenz 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 22476221-6 2012 Both protease inhibitors can modify the levels of drugs metabolized by the CYP3A/4 pathway, and in posttransplant patients, the protease inhibitors increase the levels of cyclosporine and tacrolimus, with the magnitude of the drug-drug interactions varying with protease inhibitor and type of calcineurin inhibitor (CNI). Cyclosporine 171-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-82 22476221-6 2012 Both protease inhibitors can modify the levels of drugs metabolized by the CYP3A/4 pathway, and in posttransplant patients, the protease inhibitors increase the levels of cyclosporine and tacrolimus, with the magnitude of the drug-drug interactions varying with protease inhibitor and type of calcineurin inhibitor (CNI). Tacrolimus 188-198 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-82 22764771-5 2012 Important examples include ketoconazole inhibition of hepatic CYP3A4 in order to increase systemic exposure to docetaxel, irinotecan and etoposide, and cyclosporine inhibition of intestinal ATP-binding cassette transporters in order to decrease the toxicity of irinotecan and increase the bioavailability of oral docetaxel, paclitaxel and topotecan. Ketoconazole 27-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22764771-5 2012 Important examples include ketoconazole inhibition of hepatic CYP3A4 in order to increase systemic exposure to docetaxel, irinotecan and etoposide, and cyclosporine inhibition of intestinal ATP-binding cassette transporters in order to decrease the toxicity of irinotecan and increase the bioavailability of oral docetaxel, paclitaxel and topotecan. Docetaxel 111-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22764771-5 2012 Important examples include ketoconazole inhibition of hepatic CYP3A4 in order to increase systemic exposure to docetaxel, irinotecan and etoposide, and cyclosporine inhibition of intestinal ATP-binding cassette transporters in order to decrease the toxicity of irinotecan and increase the bioavailability of oral docetaxel, paclitaxel and topotecan. Irinotecan 122-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22764771-5 2012 Important examples include ketoconazole inhibition of hepatic CYP3A4 in order to increase systemic exposure to docetaxel, irinotecan and etoposide, and cyclosporine inhibition of intestinal ATP-binding cassette transporters in order to decrease the toxicity of irinotecan and increase the bioavailability of oral docetaxel, paclitaxel and topotecan. Etoposide 137-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22764771-5 2012 Important examples include ketoconazole inhibition of hepatic CYP3A4 in order to increase systemic exposure to docetaxel, irinotecan and etoposide, and cyclosporine inhibition of intestinal ATP-binding cassette transporters in order to decrease the toxicity of irinotecan and increase the bioavailability of oral docetaxel, paclitaxel and topotecan. Irinotecan 261-271 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22764771-5 2012 Important examples include ketoconazole inhibition of hepatic CYP3A4 in order to increase systemic exposure to docetaxel, irinotecan and etoposide, and cyclosporine inhibition of intestinal ATP-binding cassette transporters in order to decrease the toxicity of irinotecan and increase the bioavailability of oral docetaxel, paclitaxel and topotecan. Docetaxel 313-322 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22764771-5 2012 Important examples include ketoconazole inhibition of hepatic CYP3A4 in order to increase systemic exposure to docetaxel, irinotecan and etoposide, and cyclosporine inhibition of intestinal ATP-binding cassette transporters in order to decrease the toxicity of irinotecan and increase the bioavailability of oral docetaxel, paclitaxel and topotecan. Paclitaxel 324-334 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22764771-5 2012 Important examples include ketoconazole inhibition of hepatic CYP3A4 in order to increase systemic exposure to docetaxel, irinotecan and etoposide, and cyclosporine inhibition of intestinal ATP-binding cassette transporters in order to decrease the toxicity of irinotecan and increase the bioavailability of oral docetaxel, paclitaxel and topotecan. Topotecan 339-348 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22281720-1 2012 PURPOSE: Although CYP3A4/5 enzymes play the predominant role in the metabolism of simvastatin and lovastatin, polymorphisms in CYP2D6 were reported to be associated with the cholesterol-lowering effect and/or tolerability of simvastatin. Simvastatin 82-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 22281720-1 2012 PURPOSE: Although CYP3A4/5 enzymes play the predominant role in the metabolism of simvastatin and lovastatin, polymorphisms in CYP2D6 were reported to be associated with the cholesterol-lowering effect and/or tolerability of simvastatin. Lovastatin 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 22450566-3 2012 The objective of the present work was to evaluate the impact of vanillin and ethyl vanillin on the activities of CYP2C9, CYP2E1, CYP3A4, CYP2B6 and CYP1A2 in human liver microsomes (HLM) in vitro, and impact on the activities of CYP1A2, CYP2C, CYP3A and CYP2E1 in rat liver microsomes (RLM) in vivo. vanillin 64-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 22450566-3 2012 The objective of the present work was to evaluate the impact of vanillin and ethyl vanillin on the activities of CYP2C9, CYP2E1, CYP3A4, CYP2B6 and CYP1A2 in human liver microsomes (HLM) in vitro, and impact on the activities of CYP1A2, CYP2C, CYP3A and CYP2E1 in rat liver microsomes (RLM) in vivo. ethyl vanillin 77-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 22415932-0 2012 Drug interaction of efavirenz and midazolam: efavirenz activates the CYP3A-mediated midazolam 1"-hydroxylation in vitro. Midazolam 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 22415932-0 2012 Drug interaction of efavirenz and midazolam: efavirenz activates the CYP3A-mediated midazolam 1"-hydroxylation in vitro. efavirenz 45-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 22415932-0 2012 Drug interaction of efavirenz and midazolam: efavirenz activates the CYP3A-mediated midazolam 1"-hydroxylation in vitro. Midazolam 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 22415932-3 2012 In vivo data suggested a possible acute activation of CYP3A4-catalyzed midazolam metabolism by efavirenz. Midazolam 71-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 22415932-3 2012 In vivo data suggested a possible acute activation of CYP3A4-catalyzed midazolam metabolism by efavirenz. efavirenz 95-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 22415932-5 2012 The formation of 1"-hydroxymidazolam was studied in pooled human liver microsomes (HLM) and recombinant human CYP3A4 and CYP3A5 (rCYP3A4 and rCYP3A5) in the presence of efavirenz (0.5, 1, and 5 muM). 1-hydroxymethylmidazolam 17-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 22415932-8 2012 Concomitant inhibition of CYP3A activity with ketoconazole in HLM abolished the increase in the 1"-hydroxymidazolam formation rate, further confirming involvement of CYP3A. Ketoconazole 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-31 22415932-8 2012 Concomitant inhibition of CYP3A activity with ketoconazole in HLM abolished the increase in the 1"-hydroxymidazolam formation rate, further confirming involvement of CYP3A. Ketoconazole 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-171 22415932-8 2012 Concomitant inhibition of CYP3A activity with ketoconazole in HLM abolished the increase in the 1"-hydroxymidazolam formation rate, further confirming involvement of CYP3A. 1-hydroxymethylmidazolam 96-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-31 22415932-8 2012 Concomitant inhibition of CYP3A activity with ketoconazole in HLM abolished the increase in the 1"-hydroxymidazolam formation rate, further confirming involvement of CYP3A. 1-hydroxymethylmidazolam 96-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-171 22555080-3 2012 Rilpivirine is primarily metabolized by the cytochrome P-450 (CYP)3A isoenzyme system. Rilpivirine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-68 21646440-2 2012 The purpose of this study was to determine the influence of Panax ginseng on CYP3A and P-gp function using the probe substrates midazolam and fexofenadine, respectively. Midazolam 128-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 21646440-2 2012 The purpose of this study was to determine the influence of Panax ginseng on CYP3A and P-gp function using the probe substrates midazolam and fexofenadine, respectively. fexofenadine 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 21659627-2 2012 Brivanib alaninate inhibits CYP3A4 in vitro, and thus there is potential for drug-drug interaction with CYP3A4 substrates, such as midazolam. brivanib 0-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 21659627-2 2012 Brivanib alaninate inhibits CYP3A4 in vitro, and thus there is potential for drug-drug interaction with CYP3A4 substrates, such as midazolam. brivanib 0-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 21659627-2 2012 Brivanib alaninate inhibits CYP3A4 in vitro, and thus there is potential for drug-drug interaction with CYP3A4 substrates, such as midazolam. Midazolam 131-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 21680781-0 2012 Effect of quercetin on CYP3A activity in Chinese healthy participants. Quercetin 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-28 21680781-1 2012 The aims of this study were to investigate the effect of quercetin on CYP3A activity in vivo. Quercetin 57-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-75 21680781-9 2012 In conclusion, quercetin significantly induced CYP3A activity to substrate midazolam, and the induction was partly related to the CYP3A5 genotype, being more prominent in CYP3A5*1/*1 and CYP3A5*1/*3 individuals. Quercetin 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 21680781-9 2012 In conclusion, quercetin significantly induced CYP3A activity to substrate midazolam, and the induction was partly related to the CYP3A5 genotype, being more prominent in CYP3A5*1/*1 and CYP3A5*1/*3 individuals. Midazolam 75-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 21925256-0 2012 Andrographolide inhibits the expression and metabolic activity of cytochrome P450 3A4 in the modified Caco-2 cells. andrographolide 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-85 21925256-1 2012 AIM OF THE STUDY: The aim of this study is to examine the effects of andrographolide on intestinal enzyme cytochrome P450 3A4 (CYP3A4) and predict whether oral administration of andrographolide-containing remedy leads to herb-drug interaction. andrographolide 69-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-125 21925256-1 2012 AIM OF THE STUDY: The aim of this study is to examine the effects of andrographolide on intestinal enzyme cytochrome P450 3A4 (CYP3A4) and predict whether oral administration of andrographolide-containing remedy leads to herb-drug interaction. andrographolide 69-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 21925256-1 2012 AIM OF THE STUDY: The aim of this study is to examine the effects of andrographolide on intestinal enzyme cytochrome P450 3A4 (CYP3A4) and predict whether oral administration of andrographolide-containing remedy leads to herb-drug interaction. andrographolide 178-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-125 21925256-1 2012 AIM OF THE STUDY: The aim of this study is to examine the effects of andrographolide on intestinal enzyme cytochrome P450 3A4 (CYP3A4) and predict whether oral administration of andrographolide-containing remedy leads to herb-drug interaction. andrographolide 178-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 21925256-2 2012 MATERIALS AND METHODS: Caco-2 cells are treated with 1alpha, 25-dihydroxyvitamin D3 for 3 wks to induce the expression of CYP3A4, and then andrographolide (1, 10, 100 muM) is added and treated for 72 h. Upon the further 4-h testosterone (250 muM) or nifedipine (200 muM) treatment, the basolateral medium samples and the Caco-2 monolayers are collected for analyses. Calcitriol 53-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 21925256-3 2012 RESULTS: Andrographolide (1, 10, 100 muM) significantly down-regulates the mRNA level and protein level of CYP3A4, and inhibits nifedipine oxidation and testosterone 6beta-hydroxylation. andrographolide 9-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 21925256-4 2012 CONCLUSION: Oral administration of andrographolide likely leads to reduction of the metabolic activity of intestinal CYP3A4, therefore herb preparations containing andrographolide may result to herb-drug interactions in combination therapy. andrographolide 35-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 21925256-4 2012 CONCLUSION: Oral administration of andrographolide likely leads to reduction of the metabolic activity of intestinal CYP3A4, therefore herb preparations containing andrographolide may result to herb-drug interactions in combination therapy. andrographolide 164-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 22349139-4 2012 Cytochrome P450 isozymes (CYP) 3A4 and CYP2C19 were previously identified as isozymes mediating the formation of nortilidine. nortilidine 113-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-34 22083560-2 2012 Twenty-nine structurally related furanocoumarin compounds with known inhibitory interactions with cytochrome P450 3A (CYP3A), which is important for phase-I drug metabolism, were selected as a model system. Furocoumarins 33-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-116 22083560-2 2012 Twenty-nine structurally related furanocoumarin compounds with known inhibitory interactions with cytochrome P450 3A (CYP3A), which is important for phase-I drug metabolism, were selected as a model system. Furocoumarins 33-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-123 21602517-1 2012 Ruxolitinib, a selective Janus kinase (JAK) 1&2 inhibitor in development for the treatment of myeloproliferative neoplasms, is primarily metabolized by CYP3A4. ruxolitinib 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 21602517-1 2012 Ruxolitinib, a selective Janus kinase (JAK) 1&2 inhibitor in development for the treatment of myeloproliferative neoplasms, is primarily metabolized by CYP3A4. Adenosine Monophosphate 46-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 21602517-2 2012 The effects of inhibition or induction of CYP3A4 on single oral dose ruxolitinib pharmacokinetics (PK) and pharmacodynamics (PD) were evaluated in healthy volunteers. ruxolitinib 69-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21602517-3 2012 Coadministration of ketoconazole (a potent CYP3A4 inhibitor) and erythromycin (a moderate CYP3A4 inhibitor) increased total ruxolitinib plasma exposure (AUC(0- )) by 91% and 27%, respectively, and ruxolitinib PD, as measured by the inhibition of interleukin (IL)-6-stimulated STAT3 phosphorylation in whole blood, was generally consistent with the PK observed. Ketoconazole 20-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 21602517-3 2012 Coadministration of ketoconazole (a potent CYP3A4 inhibitor) and erythromycin (a moderate CYP3A4 inhibitor) increased total ruxolitinib plasma exposure (AUC(0- )) by 91% and 27%, respectively, and ruxolitinib PD, as measured by the inhibition of interleukin (IL)-6-stimulated STAT3 phosphorylation in whole blood, was generally consistent with the PK observed. Ketoconazole 20-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 21602517-3 2012 Coadministration of ketoconazole (a potent CYP3A4 inhibitor) and erythromycin (a moderate CYP3A4 inhibitor) increased total ruxolitinib plasma exposure (AUC(0- )) by 91% and 27%, respectively, and ruxolitinib PD, as measured by the inhibition of interleukin (IL)-6-stimulated STAT3 phosphorylation in whole blood, was generally consistent with the PK observed. Erythromycin 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 21602517-3 2012 Coadministration of ketoconazole (a potent CYP3A4 inhibitor) and erythromycin (a moderate CYP3A4 inhibitor) increased total ruxolitinib plasma exposure (AUC(0- )) by 91% and 27%, respectively, and ruxolitinib PD, as measured by the inhibition of interleukin (IL)-6-stimulated STAT3 phosphorylation in whole blood, was generally consistent with the PK observed. ruxolitinib 124-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 21602517-4 2012 Pretreatment with rifampin, a potent CYP3A4 inducer, decreased ruxolitinib AUC(0- ) by 71% while resulting in only a 10% decrease in the overall PD activity. Rifampin 18-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 21602517-4 2012 Pretreatment with rifampin, a potent CYP3A4 inducer, decreased ruxolitinib AUC(0- ) by 71% while resulting in only a 10% decrease in the overall PD activity. ruxolitinib 63-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 21602517-6 2012 The collective PK/PD data suggest that starting doses of ruxolitinib should be reduced by 50% if coadministered with a potent CYP3A4 inhibitor, whereas adjustments in ruxolitinib starting doses may not be needed when coadministered with inducers or mild/moderate inhibitors of CYP3A4. ruxolitinib 57-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 22764844-4 2012 Based upon this evaluation, Child-Pugh Score and use of a cytochrome P450 3A4 (CYP3A4) inducer were identified as the most significant factors in variations in serum fentanyl concentration and incorporated into the following Final Model formula: CL(fenta) (L/h) = 3.53 x (15 - Child-Pugh Score) x (1 + 1.38 x use or no use of CYP3A4 inducer). Fentanyl 166-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-77 22764844-4 2012 Based upon this evaluation, Child-Pugh Score and use of a cytochrome P450 3A4 (CYP3A4) inducer were identified as the most significant factors in variations in serum fentanyl concentration and incorporated into the following Final Model formula: CL(fenta) (L/h) = 3.53 x (15 - Child-Pugh Score) x (1 + 1.38 x use or no use of CYP3A4 inducer). Fentanyl 166-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 22764844-4 2012 Based upon this evaluation, Child-Pugh Score and use of a cytochrome P450 3A4 (CYP3A4) inducer were identified as the most significant factors in variations in serum fentanyl concentration and incorporated into the following Final Model formula: CL(fenta) (L/h) = 3.53 x (15 - Child-Pugh Score) x (1 + 1.38 x use or no use of CYP3A4 inducer). Fentanyl 166-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 326-332 22764844-4 2012 Based upon this evaluation, Child-Pugh Score and use of a cytochrome P450 3A4 (CYP3A4) inducer were identified as the most significant factors in variations in serum fentanyl concentration and incorporated into the following Final Model formula: CL(fenta) (L/h) = 3.53 x (15 - Child-Pugh Score) x (1 + 1.38 x use or no use of CYP3A4 inducer). ferric nitrilotriacetate 166-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-77 22764844-4 2012 Based upon this evaluation, Child-Pugh Score and use of a cytochrome P450 3A4 (CYP3A4) inducer were identified as the most significant factors in variations in serum fentanyl concentration and incorporated into the following Final Model formula: CL(fenta) (L/h) = 3.53 x (15 - Child-Pugh Score) x (1 + 1.38 x use or no use of CYP3A4 inducer). ferric nitrilotriacetate 166-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 22764844-4 2012 Based upon this evaluation, Child-Pugh Score and use of a cytochrome P450 3A4 (CYP3A4) inducer were identified as the most significant factors in variations in serum fentanyl concentration and incorporated into the following Final Model formula: CL(fenta) (L/h) = 3.53 x (15 - Child-Pugh Score) x (1 + 1.38 x use or no use of CYP3A4 inducer). ferric nitrilotriacetate 166-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 326-332 22822591-10 2012 Abiraterone is metabolised by cytochrome P450 isoenzyme CYP3A4 and inhibits isoenzyme CYP2D6, resulting in a high potential for drug interactions. abiraterone 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 22555080-6 2012 Coadministration with inducers of CYP3A isoenzymes or drugs that increase gastric pH may lead to decreased concentrations of rilpivirine, thus promoting virological failure or resistance to rilpivirine. Rilpivirine 125-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-39 22555080-6 2012 Coadministration with inducers of CYP3A isoenzymes or drugs that increase gastric pH may lead to decreased concentrations of rilpivirine, thus promoting virological failure or resistance to rilpivirine. Rilpivirine 190-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-39 22040521-10 2012 CONCLUSIONS: Inhibition of CYP3A4 and UGT2B7 by ketoconazole increased lersivirine exposure. Ketoconazole 48-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 22464029-7 2012 Some aliphatic pentacyclic acids also were predicted to exhibit androgenic activity and, uniquely amongst the compounds tested, act as substrates for the cytochrome P450 enzyme CYP3A4. aliphatic pentacyclic acids 5-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 22040521-10 2012 CONCLUSIONS: Inhibition of CYP3A4 and UGT2B7 by ketoconazole increased lersivirine exposure. UK 453,061 71-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 21814747-8 2012 Norendoxifen inhibited placental aromatase with an IC(50) of 90 nM, while it inhibited human liver CYP2C9 and CYP3A with IC(50) values of 990 and 908 nM, respectively. N,N-didesmethyl-4-hydroxytamoxifen 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-115 22497764-8 2012 In addition, LB42908 was a potent CYP3A4 inhibitor in human liver microsomes and induced the activities of several CYP isozymes, implying that it has the potential for drug-drug interactions. LB42908 13-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 22006179-2 2012 Everolimus and docetaxel are both metabolized by CYP3A4, which could result in a pharmacokinetic (PK) interaction. Everolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 22006179-2 2012 Everolimus and docetaxel are both metabolized by CYP3A4, which could result in a pharmacokinetic (PK) interaction. Docetaxel 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 22427354-9 2012 Human oral mucosal correlative studies showed substantial interdonor variations in levels of the enzyme (cytochrome P450 3A4-CYP3A4) responsible for conversion of fenretinide to its highly active metabolite, 4-oxo-4-HPR. Fenretinide 163-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-131 22245954-1 2012 PURPOSE: The prodrug cyclophosphamide is metabolized by cytochrome P450(CYP)2B6 to the active metabolite, 4-hydroxycyclophosphamide (4-OH), and by CYP3A4/5 to toxic chloracetaldehyde and 2-dechloroethylcyclophosphamide (DCE). Cyclophosphamide 21-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 22245954-1 2012 PURPOSE: The prodrug cyclophosphamide is metabolized by cytochrome P450(CYP)2B6 to the active metabolite, 4-hydroxycyclophosphamide (4-OH), and by CYP3A4/5 to toxic chloracetaldehyde and 2-dechloroethylcyclophosphamide (DCE). 4-hydroxycyclophosphamide 133-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 22245954-1 2012 PURPOSE: The prodrug cyclophosphamide is metabolized by cytochrome P450(CYP)2B6 to the active metabolite, 4-hydroxycyclophosphamide (4-OH), and by CYP3A4/5 to toxic chloracetaldehyde and 2-dechloroethylcyclophosphamide (DCE). chloroacetaldehyde 165-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 22245954-1 2012 PURPOSE: The prodrug cyclophosphamide is metabolized by cytochrome P450(CYP)2B6 to the active metabolite, 4-hydroxycyclophosphamide (4-OH), and by CYP3A4/5 to toxic chloracetaldehyde and 2-dechloroethylcyclophosphamide (DCE). 2-dechloroethylcyclophosphamide 187-218 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 22245954-1 2012 PURPOSE: The prodrug cyclophosphamide is metabolized by cytochrome P450(CYP)2B6 to the active metabolite, 4-hydroxycyclophosphamide (4-OH), and by CYP3A4/5 to toxic chloracetaldehyde and 2-dechloroethylcyclophosphamide (DCE). 2-dechloroethylcyclophosphamide 220-223 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 22108774-1 2012 PURPOSE: Zafirlukast is a substrate of cytochrome P450 2C9 (CYP2C9) and cytochrome P450 3A4 (CYP3A4) in vitro, but the role of these enzymes in its metabolism in vivo is unknown. zafirlukast 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-91 22440191-11 2012 Additionally, according to the currently approved prescribing information, the efficacy of linagliptin may be limited in patients receiving concurrent inducers of the cytochrome P450 3A4 isozyme or P-glycoprotein (eg, rifampin). Linagliptin 91-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 167-186 22344701-2 2012 Under catalysis of recombinant human CYP3A4 and CYP2D6 coexpressed with human cytochrome P450 reductase in Escherichia coli JM109, five metabolites of panobinostat were produced via whole-cell biotransformation. Panobinostat 151-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 22344702-0 2012 Identification of the residue in human CYP3A4 that is covalently modified by bergamottin and the reactive intermediate that contributes to the grapefruit juice effect. bergamottin 77-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 22344702-1 2012 Previous studies have demonstrated that bergamottin (BG), a component of grapefruit juice, is a mechanism-based inactivator of CYP3A4 and contributes, in part, to the grapefruit juice-drug interaction. bergamottin 40-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 22344702-1 2012 Previous studies have demonstrated that bergamottin (BG), a component of grapefruit juice, is a mechanism-based inactivator of CYP3A4 and contributes, in part, to the grapefruit juice-drug interaction. bergamottin 53-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 22344702-2 2012 Although the covalent binding of [(14)C]BG to the CYP3A4 apoprotein has been demonstrated by SDS-polyacrylamide gel electrophoresis, the identity of the modified amino acid residue and the reactive intermediate species of BG responsible for the inactivation have not been reported. Sodium Dodecyl Sulfate 93-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 22344702-2 2012 Although the covalent binding of [(14)C]BG to the CYP3A4 apoprotein has been demonstrated by SDS-polyacrylamide gel electrophoresis, the identity of the modified amino acid residue and the reactive intermediate species of BG responsible for the inactivation have not been reported. polyacrylamide 97-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 22344702-2 2012 Although the covalent binding of [(14)C]BG to the CYP3A4 apoprotein has been demonstrated by SDS-polyacrylamide gel electrophoresis, the identity of the modified amino acid residue and the reactive intermediate species of BG responsible for the inactivation have not been reported. bergamottin 40-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 22344702-3 2012 In the present study, we show that inactivation of CYP3A4 by BG results in formation of a modified apoprotein-3A4 and a GSH conjugate, both exhibiting mass increases of 388 Da, which corresponds to the mass of 6",7"-dihydroxybergamottin (DHBG), a metabolite of BG, plus one oxygen atom. bergamottin 61-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 22344702-3 2012 In the present study, we show that inactivation of CYP3A4 by BG results in formation of a modified apoprotein-3A4 and a GSH conjugate, both exhibiting mass increases of 388 Da, which corresponds to the mass of 6",7"-dihydroxybergamottin (DHBG), a metabolite of BG, plus one oxygen atom. Glutathione 120-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 22344702-3 2012 In the present study, we show that inactivation of CYP3A4 by BG results in formation of a modified apoprotein-3A4 and a GSH conjugate, both exhibiting mass increases of 388 Da, which corresponds to the mass of 6",7"-dihydroxybergamottin (DHBG), a metabolite of BG, plus one oxygen atom. 6',7'-dihydroxybergamottin 210-236 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 22344702-3 2012 In the present study, we show that inactivation of CYP3A4 by BG results in formation of a modified apoprotein-3A4 and a GSH conjugate, both exhibiting mass increases of 388 Da, which corresponds to the mass of 6",7"-dihydroxybergamottin (DHBG), a metabolite of BG, plus one oxygen atom. 6',7'-dihydroxybergamottin 238-242 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 22344702-3 2012 In the present study, we show that inactivation of CYP3A4 by BG results in formation of a modified apoprotein-3A4 and a GSH conjugate, both exhibiting mass increases of 388 Da, which corresponds to the mass of 6",7"-dihydroxybergamottin (DHBG), a metabolite of BG, plus one oxygen atom. bergamottin 240-242 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 22534255-3 2012 OBJECTIVE: The effects of multiple oral doses of ketoconazole (a potent CYP3A4 inhibitor) and multiple oral doses of rifampicin (a potent CYP3A4 inducer) on the pharmacokinetic properties of a single oral dose of gemigliptin were evaluated in fasting healthy male Korean volunteers. Rifampin 117-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 22534255-17 2012 These findings suggest that gemigliptin may require a dose adjustment when concurrently administered with drugs that alter CYP3A4 activity. LC15-0444 28-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 22159869-0 2012 Metabolism of alprazolam (a marker of CYP3A4) in hemodialysis patients with persistent inflammation. Alprazolam 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 22159869-1 2012 OBJECTIVE: To investigate the impact of persistent inflammation in hemodialysis (HD) patients on the pharmacokinetics of alprazolam, a cytochrome P450 (CYP) 3A4 substrate, and its metabolites and the role of HD in the impact of persistent inflammation in this clinical context. Alprazolam 121-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-160 22344702-3 2012 In the present study, we show that inactivation of CYP3A4 by BG results in formation of a modified apoprotein-3A4 and a GSH conjugate, both exhibiting mass increases of 388 Da, which corresponds to the mass of 6",7"-dihydroxybergamottin (DHBG), a metabolite of BG, plus one oxygen atom. Oxygen 274-280 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 22108774-1 2012 PURPOSE: Zafirlukast is a substrate of cytochrome P450 2C9 (CYP2C9) and cytochrome P450 3A4 (CYP3A4) in vitro, but the role of these enzymes in its metabolism in vivo is unknown. zafirlukast 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 22344702-7 2012 In conclusion, we have determined that the reactive intermediate, oxygenated DHBG, covalently binds to Gln273 and thereby contributes to the mechanism-based inactivation of CYP3A4 by BG. 6',7'-dihydroxybergamottin 77-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 22648626-12 2012 Our results suggest that capsaicin might induce CYP3A4 expression; thus, exposure to capsaicin may increase the metabolism of CYP3A4 substrate and potentially cause food-drug interactions. Capsaicin 25-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 22344702-7 2012 In conclusion, we have determined that the reactive intermediate, oxygenated DHBG, covalently binds to Gln273 and thereby contributes to the mechanism-based inactivation of CYP3A4 by BG. bergamottin 79-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 22159869-5 2012 CYP3A4 activity was estimated as the ratio of unconjugated alprazolam to 4-hydroxyalprazolam between 10 and 34 h following alprazolam intake. 4-hydroxyalprazolam 73-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22159869-5 2012 CYP3A4 activity was estimated as the ratio of unconjugated alprazolam to 4-hydroxyalprazolam between 10 and 34 h following alprazolam intake. Alprazolam 82-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22159869-11 2012 CONCLUSIONS: The correlation between CYP3A4 activity (assessed by alprazolam 4-hydroxylation) and CRP level suggests that inflammation may downregulate CYP3A4 activity. Alprazolam 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 22159869-11 2012 CONCLUSIONS: The correlation between CYP3A4 activity (assessed by alprazolam 4-hydroxylation) and CRP level suggests that inflammation may downregulate CYP3A4 activity. Alprazolam 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 22511698-2 2012 Methadone is primarily metabolized by N-demethylation to an inactive metabolite 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidene (EDDP) by CYP3A4 and CYP2B6. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 22511698-2 2012 Methadone is primarily metabolized by N-demethylation to an inactive metabolite 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidene (EDDP) by CYP3A4 and CYP2B6. 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidene 80-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 22511698-2 2012 Methadone is primarily metabolized by N-demethylation to an inactive metabolite 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidene (EDDP) by CYP3A4 and CYP2B6. 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine 131-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 21551317-1 2012 The muscarinic receptor antagonist propiverine is unique insofar as extended-release (ER) tablets are of higher bioavailability than immediate-release (IR) tablets; this is caused by lower "first-pass" elimination of propiverine via CYP3A4 and efflux transporters in the distal small intestine and colon. propiverine 35-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 233-239 21551317-1 2012 The muscarinic receptor antagonist propiverine is unique insofar as extended-release (ER) tablets are of higher bioavailability than immediate-release (IR) tablets; this is caused by lower "first-pass" elimination of propiverine via CYP3A4 and efflux transporters in the distal small intestine and colon. propiverine 217-228 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 233-239 22648626-12 2012 Our results suggest that capsaicin might induce CYP3A4 expression; thus, exposure to capsaicin may increase the metabolism of CYP3A4 substrate and potentially cause food-drug interactions. Capsaicin 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 22648626-12 2012 Our results suggest that capsaicin might induce CYP3A4 expression; thus, exposure to capsaicin may increase the metabolism of CYP3A4 substrate and potentially cause food-drug interactions. Capsaicin 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 22159869-5 2012 CYP3A4 activity was estimated as the ratio of unconjugated alprazolam to 4-hydroxyalprazolam between 10 and 34 h following alprazolam intake. Alprazolam 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22523293-5 2012 Cytochrome P-450 (CYP)3A4 activity was measured by beta-hydroxylation of testosterone in human recombinant CYP3A4. Testosterone 73-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-25 22523293-5 2012 Cytochrome P-450 (CYP)3A4 activity was measured by beta-hydroxylation of testosterone in human recombinant CYP3A4. Testosterone 73-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 22483397-2 2012 CYP isoform specific substrates and their metabolites of CYP1A2 (caffeine), CYP2C9 (losartan), CYP2C19 (omeprazole), CYP2D6 (dextromethorphan) and CYP3A (midazolam) were all simultaneously analyzed using LC-MS/MS after administration of a mixture of five drugs (i.e., a "cocktail approach") to healthy volunteers. Dextromethorphan 125-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-152 22648626-0 2012 Capsaicin induces CYP3A4 expression via pregnane X receptor and CCAAT/enhancer-binding protein beta activation. Capsaicin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 22648626-3 2012 However, the influence of capsaicin on CYP3A4, its involvement in drug metabolism, and the underlying mechanisms remain unclear. Capsaicin 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 22648626-4 2012 METHODS AND RESULTS: Here, we examined the effect of capsaicin on CYP3A4 expression and the metabolism of CYP3A1 substrate, nifedipine in male Sprague-Dawley rats. Capsaicin 53-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 22648626-5 2012 Capsaicin induced the enzymatic activity and expression of CYP3A4 in HepG2 cells. Capsaicin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 22648626-6 2012 Treatment with a human pregnane X receptor (hPXR) inhibitor reduced the inductive effects of capsaicin on CYP3A4 expression. Capsaicin 93-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 22648626-10 2012 CONCLUSION: From these data, we conclude that capsaicin induces CYP3A4 expression in vitro and in vivo. Capsaicin 46-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 22648626-12 2012 Our results suggest that capsaicin might induce CYP3A4 expression; thus, exposure to capsaicin may increase the metabolism of CYP3A4 substrate and potentially cause food-drug interactions. Capsaicin 25-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 22388796-0 2012 The new CYP3A4 intron 6 C>T polymorphism (CYP3A4*22) is associated with an increased risk of delayed graft function and worse renal function in cyclosporine-treated kidney transplant patients. Cyclosporine 147-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 22237927-1 2012 PURPOSE: The co-administration of cytochrome P450 3A4 (CYP3A4) inhibitors with simvastatin or atorvastatin (CYP3A4-metabolised statins) is associated with increased statin exposure and can increase the risk of adverse drug reactions. Simvastatin 79-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-53 22237927-1 2012 PURPOSE: The co-administration of cytochrome P450 3A4 (CYP3A4) inhibitors with simvastatin or atorvastatin (CYP3A4-metabolised statins) is associated with increased statin exposure and can increase the risk of adverse drug reactions. Simvastatin 79-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 22237927-1 2012 PURPOSE: The co-administration of cytochrome P450 3A4 (CYP3A4) inhibitors with simvastatin or atorvastatin (CYP3A4-metabolised statins) is associated with increased statin exposure and can increase the risk of adverse drug reactions. Atorvastatin 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-53 22237927-1 2012 PURPOSE: The co-administration of cytochrome P450 3A4 (CYP3A4) inhibitors with simvastatin or atorvastatin (CYP3A4-metabolised statins) is associated with increased statin exposure and can increase the risk of adverse drug reactions. Atorvastatin 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 22237927-1 2012 PURPOSE: The co-administration of cytochrome P450 3A4 (CYP3A4) inhibitors with simvastatin or atorvastatin (CYP3A4-metabolised statins) is associated with increased statin exposure and can increase the risk of adverse drug reactions. Atorvastatin 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 22237927-7 2012 Ninety-three percent of the patients were prescribed CYP3A4-metabolised statins, most whom received simvastatin (72%) and atorvastatin (24%). Simvastatin 100-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 22237927-7 2012 Ninety-three percent of the patients were prescribed CYP3A4-metabolised statins, most whom received simvastatin (72%) and atorvastatin (24%). Atorvastatin 122-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 22388796-0 2012 The new CYP3A4 intron 6 C>T polymorphism (CYP3A4*22) is associated with an increased risk of delayed graft function and worse renal function in cyclosporine-treated kidney transplant patients. Cyclosporine 147-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 22237927-8 2012 Approximately one third (30%) of the patients prescribed a CYP3A4-metabolised statin had also been prescribed a concomitant CYP3A4 inhibitor during the study period, including 11% prescribed a concomitant labelled inhibitor, with an annualised median days of concomitant use of 173 days, predominantly involving macrolide antibiotics and calcium channel blockers co-prescriptions. macrolide antibiotics 312-333 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 22388796-8 2012 Mixed-model analysis demonstrated that the overall creatinine clearance was 20% lower in CYP3A4*22 allele carriers compared with CYP3A4*1/*1 patients [CI(95%) (-33.1 to -7.2%), P=0.002]. Creatinine 51-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 22388796-10 2012 CONCLUSION: CYP3A4*22 constitutes a risk factor for DGF and worse creatinine clearance in patients receiving CsA-based immunosuppressive therapy. Creatinine 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 21796656-0 2012 Co-administration of piperine and docetaxel results in improved anti-tumor efficacy via inhibition of CYP3A4 activity. piperine 21-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 21796656-0 2012 Co-administration of piperine and docetaxel results in improved anti-tumor efficacy via inhibition of CYP3A4 activity. Docetaxel 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 21796656-2 2012 Docetaxel is metabolized in the liver by hepatic CYP3A4 activity. Docetaxel 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 21796656-3 2012 Piperine, a major plant alkaloid/amide, has been shown to inhibit the CYP3A4 enzymatic activity in a cell-free system. piperine 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 21796656-3 2012 Piperine, a major plant alkaloid/amide, has been shown to inhibit the CYP3A4 enzymatic activity in a cell-free system. Alkaloids 24-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 21796656-3 2012 Piperine, a major plant alkaloid/amide, has been shown to inhibit the CYP3A4 enzymatic activity in a cell-free system. Amides 33-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 21796656-8 2012 RESULTS: Inhibition of hepatic CYP3A4 activity resulted in an increased area under the curve, half-life and maximum plasma concentration of docetaxel when compared to docetaxel alone administration. Docetaxel 140-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 21796656-8 2012 RESULTS: Inhibition of hepatic CYP3A4 activity resulted in an increased area under the curve, half-life and maximum plasma concentration of docetaxel when compared to docetaxel alone administration. Docetaxel 167-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 22491658-2 2012 Continuous intravenous nicardipine (CIVN), prescribed for posttransplant hypertension, inhibits tacrolimus metabolism by cytochrome P450 (CYP) 3A4 and could lead to tacrolimus overexposure in patients genetically lacking the alternative pathway for tacrolimus metabolism, CYP3A5. Nicardipine 23-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-146 22106961-0 2012 Effect of voriconazole and other azole antifungal agents on CYP3A activity and metabolism of tacrolimus in human liver microsomes. Voriconazole 10-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 22106961-0 2012 Effect of voriconazole and other azole antifungal agents on CYP3A activity and metabolism of tacrolimus in human liver microsomes. Azoles 17-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 22106961-1 2012 Azole antifungal agents are known to inhibit cytochrome P450 3A (CYP3A) enzymes. Azoles 0-5 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-63 22106961-1 2012 Azole antifungal agents are known to inhibit cytochrome P450 3A (CYP3A) enzymes. Azoles 0-5 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 22106961-2 2012 Limited information is available regarding the effect of voriconazole on CYP3A activity. Voriconazole 57-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 22106961-3 2012 We examined the effect of voriconazole on CYP3A activity in human liver microsomes as measured by the formation of 6beta-hydroxytestosterone from testosterone. Voriconazole 26-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 22106961-5 2012 The effect of voriconazole on CYP3A activity and tacrolimus metabolism was compared to that of other azole antifungal agents. Voriconazole 14-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-35 22314385-7 2012 The activation of the canonical human PXR target gene CYP3A4 by walrycin A is dose and PXR dependent. walrycin A 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 23251772-4 2012 Boceprevir is given orally, rapidly absorbed, reaching plasma peak concentration within 1-2 h and is metabolized by aldo-ketoreductase and partly by the cytochrome P450 enzyme CYP3A4/5. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 22491658-2 2012 Continuous intravenous nicardipine (CIVN), prescribed for posttransplant hypertension, inhibits tacrolimus metabolism by cytochrome P450 (CYP) 3A4 and could lead to tacrolimus overexposure in patients genetically lacking the alternative pathway for tacrolimus metabolism, CYP3A5. civn 36-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-146 22491658-2 2012 Continuous intravenous nicardipine (CIVN), prescribed for posttransplant hypertension, inhibits tacrolimus metabolism by cytochrome P450 (CYP) 3A4 and could lead to tacrolimus overexposure in patients genetically lacking the alternative pathway for tacrolimus metabolism, CYP3A5. Tacrolimus 96-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-146 22433037-5 2012 Obtained via a partial cysteine-depletion approach, a functional triple mutant of CYP3A4 (C98S/C239S/C468G) is reported here which is singly modified at C64 by maleimide-containing groups. Cysteine 23-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 22433037-5 2012 Obtained via a partial cysteine-depletion approach, a functional triple mutant of CYP3A4 (C98S/C239S/C468G) is reported here which is singly modified at C64 by maleimide-containing groups. maleimide 160-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 22014153-7 2012 The time-dependent inhibition effect of imatinib was predicted to cause up to 90% inhibition of hepatic CYP3A4 activity with clinically relevant imatinib concentrations, whereas the direct inhibition was predicted to be negligible in vivo. Imatinib Mesylate 40-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 22252826-0 2012 PXR variants and artemisinin use in Vietnamese subjects: frequency distribution and impact on the interindividual variability of CYP3A induction by artemisinin. artemisinin 148-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-134 22252826-2 2012 Here, we report the resequencing and genotyping of PXR variants in 75 Vietnamese individuals previously characterized for CYP3A enzyme activity after artemisinin exposure. artemisinin 150-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-127 22252826-4 2012 A trend of significance was observed between the level of CYP3A4 induction by artemisinin and two PXR variants, the 8118C T (Y328Y) and 10719A G variants. artemisinin 78-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 22113809-8 2012 This indicates that the total binding free energies calculated for the inhibitor-heme model complexes can be a good descriptor in interpreting the inhibitor binding to CYP3A4 and the relative free energies in the gas phase are mainly responsible for the total binding free energies in water, although the desolvation can be a factor to affect the binding affinity of the inhibitors to CYP3A4. Water 285-290 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 385-391 22113809-9 2012 From the theozyme analysis of the X-ray structures for ketoconazole- and metyrapone-CYP3A4 complexes, the interaction free energy of the neighboring residues with each inhibitor in the active site is calculated to be about -3 kcal mol(-1) in water, whose the interaction energy and the desolvation free energy change are about -5 and 2 kcal mol(-1) , respectively. Ketoconazole 55-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 22113809-9 2012 From the theozyme analysis of the X-ray structures for ketoconazole- and metyrapone-CYP3A4 complexes, the interaction free energy of the neighboring residues with each inhibitor in the active site is calculated to be about -3 kcal mol(-1) in water, whose the interaction energy and the desolvation free energy change are about -5 and 2 kcal mol(-1) , respectively. Metyrapone 73-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 22113809-9 2012 From the theozyme analysis of the X-ray structures for ketoconazole- and metyrapone-CYP3A4 complexes, the interaction free energy of the neighboring residues with each inhibitor in the active site is calculated to be about -3 kcal mol(-1) in water, whose the interaction energy and the desolvation free energy change are about -5 and 2 kcal mol(-1) , respectively. Water 242-247 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 22014153-0 2012 Potent mechanism-based inhibition of CYP3A4 by imatinib explains its liability to interact with CYP3A4 substrates. Imatinib Mesylate 47-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 22014153-0 2012 Potent mechanism-based inhibition of CYP3A4 by imatinib explains its liability to interact with CYP3A4 substrates. Imatinib Mesylate 47-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 22014153-1 2012 BACKGROUND AND PURPOSE: Imatinib, a cytochrome P450 2C8 (CYP2C8) and CYP3A4 substrate, markedly increases plasma concentrations of the CYP3A4/5 substrate simvastatin and reduces hepatic CYP3A4/5 activity in humans. Imatinib Mesylate 24-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 22014153-1 2012 BACKGROUND AND PURPOSE: Imatinib, a cytochrome P450 2C8 (CYP2C8) and CYP3A4 substrate, markedly increases plasma concentrations of the CYP3A4/5 substrate simvastatin and reduces hepatic CYP3A4/5 activity in humans. Imatinib Mesylate 24-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 22014153-1 2012 BACKGROUND AND PURPOSE: Imatinib, a cytochrome P450 2C8 (CYP2C8) and CYP3A4 substrate, markedly increases plasma concentrations of the CYP3A4/5 substrate simvastatin and reduces hepatic CYP3A4/5 activity in humans. Imatinib Mesylate 24-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 22014153-1 2012 BACKGROUND AND PURPOSE: Imatinib, a cytochrome P450 2C8 (CYP2C8) and CYP3A4 substrate, markedly increases plasma concentrations of the CYP3A4/5 substrate simvastatin and reduces hepatic CYP3A4/5 activity in humans. Simvastatin 154-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 22014153-1 2012 BACKGROUND AND PURPOSE: Imatinib, a cytochrome P450 2C8 (CYP2C8) and CYP3A4 substrate, markedly increases plasma concentrations of the CYP3A4/5 substrate simvastatin and reduces hepatic CYP3A4/5 activity in humans. Simvastatin 154-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 22014153-1 2012 BACKGROUND AND PURPOSE: Imatinib, a cytochrome P450 2C8 (CYP2C8) and CYP3A4 substrate, markedly increases plasma concentrations of the CYP3A4/5 substrate simvastatin and reduces hepatic CYP3A4/5 activity in humans. Simvastatin 154-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 22410611-1 2012 Ritonavir is a HIV protease inhibitor that also potently inactivates cytochrome P450 3A4 (CYP3A4), a major human drug-metabolizing enzyme. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-88 22410611-1 2012 Ritonavir is a HIV protease inhibitor that also potently inactivates cytochrome P450 3A4 (CYP3A4), a major human drug-metabolizing enzyme. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 22410611-2 2012 To better understand the mechanism of ligand binding and to find strategies for improvement of the inhibitory potency of ritonavir, currently administered to enhance pharmacokinetics of other anti-HIV drugs that are quickly metabolized by CYP3A4, we compared the manner of CYP3A4 interaction with the drug and two analogs lacking either the heme-ligating thiazole nitrogen or the entire thiazole group. Ritonavir 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 239-245 22410611-2 2012 To better understand the mechanism of ligand binding and to find strategies for improvement of the inhibitory potency of ritonavir, currently administered to enhance pharmacokinetics of other anti-HIV drugs that are quickly metabolized by CYP3A4, we compared the manner of CYP3A4 interaction with the drug and two analogs lacking either the heme-ligating thiazole nitrogen or the entire thiazole group. Ritonavir 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 273-279 22113809-1 2012 The binding free energies of the inhibitor-heme model complexes are calculated using the density functional methods and the implicit solvation models in water, where the 16 structurally diverse compounds with a spectrum of IC(50) values from 0.05 (clotrimazole) to 1000 (piroxicam) muM are chosen as inhibitors for Cytochrome P450 3A4 (CYP3A4). Heme 43-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 315-334 22113809-1 2012 The binding free energies of the inhibitor-heme model complexes are calculated using the density functional methods and the implicit solvation models in water, where the 16 structurally diverse compounds with a spectrum of IC(50) values from 0.05 (clotrimazole) to 1000 (piroxicam) muM are chosen as inhibitors for Cytochrome P450 3A4 (CYP3A4). Heme 43-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 336-342 22113809-8 2012 This indicates that the total binding free energies calculated for the inhibitor-heme model complexes can be a good descriptor in interpreting the inhibitor binding to CYP3A4 and the relative free energies in the gas phase are mainly responsible for the total binding free energies in water, although the desolvation can be a factor to affect the binding affinity of the inhibitors to CYP3A4. Heme 81-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 22113809-8 2012 This indicates that the total binding free energies calculated for the inhibitor-heme model complexes can be a good descriptor in interpreting the inhibitor binding to CYP3A4 and the relative free energies in the gas phase are mainly responsible for the total binding free energies in water, although the desolvation can be a factor to affect the binding affinity of the inhibitors to CYP3A4. Heme 81-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 385-391 22113809-8 2012 This indicates that the total binding free energies calculated for the inhibitor-heme model complexes can be a good descriptor in interpreting the inhibitor binding to CYP3A4 and the relative free energies in the gas phase are mainly responsible for the total binding free energies in water, although the desolvation can be a factor to affect the binding affinity of the inhibitors to CYP3A4. Water 285-290 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 22398966-0 2012 Predicting drug interaction potential with a physiologically based pharmacokinetic model: a case study of telithromycin, a time-dependent CYP3A inhibitor. telithromycin 106-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-143 22398966-1 2012 Telithromycin is a substrate and an inhibitor of cytochrome P450 3A (CYP3A4), with dose- and time-dependent nonlinear pharmacokinetics (PK). telithromycin 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 22398966-4 2012 The model successfully predicted the clinical interaction with the CYP3A4 substrate midazolam, as verified by external data not used for the model-building (intravenous (i.v.) Midazolam 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 22398970-8 2012 Efavirenz induced hepatocyte CYP2B6 and CYP3A4 expression, activity, and methadone N-demethylation. efavirenz 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 22014153-2 2012 Because competitive inhibition of CYP3A4/5 does not explain these in vivo interactions, we investigated the reversible and time-dependent inhibitory effects of imatinib and its main metabolite N-desmethylimatinib on CYP2C8 and CYP3A4/5 in vitro. N-desmethylimatinib 193-212 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 227-233 22014153-3 2012 EXPERIMENTAL APPROACH: Amodiaquine N-deethylation and midazolam 1"-hydroxylation were used as marker reactions for CYP2C8 and CYP3A4/5 activity. Amodiaquine 23-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 22014153-5 2012 KEY RESULTS: Inhibition of CYP3A4 activity by imatinib was pre-incubation time-, concentration- and NADPH-dependent, and the time-dependent inactivation variables K(I) and k(inact) were 14.3 microM and 0.072 in(-1) respectively. Imatinib Mesylate 46-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 22014153-7 2012 The time-dependent inhibition effect of imatinib was predicted to cause up to 90% inhibition of hepatic CYP3A4 activity with clinically relevant imatinib concentrations, whereas the direct inhibition was predicted to be negligible in vivo. Imatinib Mesylate 145-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 22014153-5 2012 KEY RESULTS: Inhibition of CYP3A4 activity by imatinib was pre-incubation time-, concentration- and NADPH-dependent, and the time-dependent inactivation variables K(I) and k(inact) were 14.3 microM and 0.072 in(-1) respectively. NADP 100-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 22014153-8 2012 CONCLUSIONS AND IMPLICATIONS: Imatinib is a potent mechanism-based inhibitor of CYP3A4 in vitro and this finding explains the imatinib-simvastatin interaction and suggests that imatinib could markedly increase plasma concentrations of other CYP3A4 substrates. Imatinib Mesylate 30-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 22014153-8 2012 CONCLUSIONS AND IMPLICATIONS: Imatinib is a potent mechanism-based inhibitor of CYP3A4 in vitro and this finding explains the imatinib-simvastatin interaction and suggests that imatinib could markedly increase plasma concentrations of other CYP3A4 substrates. Imatinib Mesylate 30-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 241-247 22014153-8 2012 CONCLUSIONS AND IMPLICATIONS: Imatinib is a potent mechanism-based inhibitor of CYP3A4 in vitro and this finding explains the imatinib-simvastatin interaction and suggests that imatinib could markedly increase plasma concentrations of other CYP3A4 substrates. Imatinib Mesylate 126-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 22014153-8 2012 CONCLUSIONS AND IMPLICATIONS: Imatinib is a potent mechanism-based inhibitor of CYP3A4 in vitro and this finding explains the imatinib-simvastatin interaction and suggests that imatinib could markedly increase plasma concentrations of other CYP3A4 substrates. Simvastatin 135-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 22014153-9 2012 Our results also suggest a possibility of autoinhibition of CYP3A4-mediated imatinib metabolism leading to a less significant role for CYP3A4 in imatinib biotransformation in vivo than previously proposed. Imatinib Mesylate 76-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 22205779-0 2012 Cyclosporine A- and tacrolimus-mediated inhibition of CYP3A4 and CYP3A5 in vitro. Cyclosporine 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 22014153-9 2012 Our results also suggest a possibility of autoinhibition of CYP3A4-mediated imatinib metabolism leading to a less significant role for CYP3A4 in imatinib biotransformation in vivo than previously proposed. Imatinib Mesylate 145-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 22205779-0 2012 Cyclosporine A- and tacrolimus-mediated inhibition of CYP3A4 and CYP3A5 in vitro. Tacrolimus 20-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 22014153-9 2012 Our results also suggest a possibility of autoinhibition of CYP3A4-mediated imatinib metabolism leading to a less significant role for CYP3A4 in imatinib biotransformation in vivo than previously proposed. Imatinib Mesylate 145-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 22205779-3 2012 For CsA, in particular, inhibition of CYP3A has been suggested as the main mechanism of interactions seen clinically with various drugs. Cyclosporine 4-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 22205779-4 2012 The aim of this study was to investigate the inhibitory effect and inhibition characteristics of CsA and Tac on CYP3A4 and CYP3A5 in vitro and to evaluate its clinical relevance. Cyclosporine 97-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 22266842-7 2012 Furafylline, quinidine, and ketoconazole, selective inhibitors of CYP1A2, CYP2D6, and CYP3A4, respectively, inhibited 5-hydroxylorcaserin (IC(50) = 1.914 muM), 7-hydroxylorcaserin (IC(50) = 0.213 muM), and 1-hydroxylorcaserin formation (IC(50) = 0.281 muM), respectively. furafylline 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 22205779-5 2012 Inhibition by CsA and Tac was studied using midazolam as the probe substrate in coincubation and preincubation investigations using human liver microsomes (HLMs) as well as specific CYP3A4- and CYP3A5-expressing insect microsomes (Supersomes). Cyclosporine 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 182-188 22205779-8 2012 Experiments in Supersomes revealed that Tac inhibited both CYP3A4 and CYP3A5, whereas CsA only inhibited CYP3A4. Cyclosporine 86-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 22266842-4 2012 In 16 individual human liver microsomal preparations (HLM), formation of N-hydroxylorcaserin was correlated with CYP2B6, 7-hydroxylorcaserin was correlated with CYP2D6, 5-hydroxylorcaserin was correlated with CYP1A2 and CYP3A4, and 1-hydroxylorcaserin was correlated with CYP3A4 activity at 10.0 muM lorcaserin. N-Hydroxy Lorcaserin 73-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 22266842-4 2012 In 16 individual human liver microsomal preparations (HLM), formation of N-hydroxylorcaserin was correlated with CYP2B6, 7-hydroxylorcaserin was correlated with CYP2D6, 5-hydroxylorcaserin was correlated with CYP1A2 and CYP3A4, and 1-hydroxylorcaserin was correlated with CYP3A4 activity at 10.0 muM lorcaserin. N-Hydroxy Lorcaserin 73-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 272-278 22266842-7 2012 Furafylline, quinidine, and ketoconazole, selective inhibitors of CYP1A2, CYP2D6, and CYP3A4, respectively, inhibited 5-hydroxylorcaserin (IC(50) = 1.914 muM), 7-hydroxylorcaserin (IC(50) = 0.213 muM), and 1-hydroxylorcaserin formation (IC(50) = 0.281 muM), respectively. Quinidine 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 22266842-7 2012 Furafylline, quinidine, and ketoconazole, selective inhibitors of CYP1A2, CYP2D6, and CYP3A4, respectively, inhibited 5-hydroxylorcaserin (IC(50) = 1.914 muM), 7-hydroxylorcaserin (IC(50) = 0.213 muM), and 1-hydroxylorcaserin formation (IC(50) = 0.281 muM), respectively. Ketoconazole 28-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 22266842-7 2012 Furafylline, quinidine, and ketoconazole, selective inhibitors of CYP1A2, CYP2D6, and CYP3A4, respectively, inhibited 5-hydroxylorcaserin (IC(50) = 1.914 muM), 7-hydroxylorcaserin (IC(50) = 0.213 muM), and 1-hydroxylorcaserin formation (IC(50) = 0.281 muM), respectively. UNII-Q5ZY5ZLN9D 118-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 22266842-7 2012 Furafylline, quinidine, and ketoconazole, selective inhibitors of CYP1A2, CYP2D6, and CYP3A4, respectively, inhibited 5-hydroxylorcaserin (IC(50) = 1.914 muM), 7-hydroxylorcaserin (IC(50) = 0.213 muM), and 1-hydroxylorcaserin formation (IC(50) = 0.281 muM), respectively. UNII-NJZ27SG33S 160-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 22266842-7 2012 Furafylline, quinidine, and ketoconazole, selective inhibitors of CYP1A2, CYP2D6, and CYP3A4, respectively, inhibited 5-hydroxylorcaserin (IC(50) = 1.914 muM), 7-hydroxylorcaserin (IC(50) = 0.213 muM), and 1-hydroxylorcaserin formation (IC(50) = 0.281 muM), respectively. 1-Hydroxylorcaserin 206-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 22269145-6 2012 Two monohydroxylated metabolites of lower abundance were formed by CYP3A4, and interestingly, although CYP2C9 showed no activity toward the parent compound, this enzyme appeared to act in concert with CYP3A4 to form two minor dihydroxylated products of ETR. etravirine 253-256 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 22269145-6 2012 Two monohydroxylated metabolites of lower abundance were formed by CYP3A4, and interestingly, although CYP2C9 showed no activity toward the parent compound, this enzyme appeared to act in concert with CYP3A4 to form two minor dihydroxylated products of ETR. etravirine 253-256 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-207 22269145-9 2012 The presence of the pregnane X receptor antagonist sulforaphane blocked the ETR-mediated increase in CYP3A4 mRNA expression. sulforaphane 51-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 22269145-9 2012 The presence of the pregnane X receptor antagonist sulforaphane blocked the ETR-mediated increase in CYP3A4 mRNA expression. etravirine 76-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 22269145-10 2012 Taken together, these data suggest that ETR and ETR metabolites are substrates of CYP2C19, CYP3A4, CYP2C9, UGT1A3, and UGT1A8 and that ETR is a PXR-dependent modulator of CYP3A4 mRNA levels. etravirine 40-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22269145-10 2012 Taken together, these data suggest that ETR and ETR metabolites are substrates of CYP2C19, CYP3A4, CYP2C9, UGT1A3, and UGT1A8 and that ETR is a PXR-dependent modulator of CYP3A4 mRNA levels. etravirine 40-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 22269145-10 2012 Taken together, these data suggest that ETR and ETR metabolites are substrates of CYP2C19, CYP3A4, CYP2C9, UGT1A3, and UGT1A8 and that ETR is a PXR-dependent modulator of CYP3A4 mRNA levels. etravirine 48-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22269145-10 2012 Taken together, these data suggest that ETR and ETR metabolites are substrates of CYP2C19, CYP3A4, CYP2C9, UGT1A3, and UGT1A8 and that ETR is a PXR-dependent modulator of CYP3A4 mRNA levels. etravirine 48-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 22269145-10 2012 Taken together, these data suggest that ETR and ETR metabolites are substrates of CYP2C19, CYP3A4, CYP2C9, UGT1A3, and UGT1A8 and that ETR is a PXR-dependent modulator of CYP3A4 mRNA levels. etravirine 48-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22269145-10 2012 Taken together, these data suggest that ETR and ETR metabolites are substrates of CYP2C19, CYP3A4, CYP2C9, UGT1A3, and UGT1A8 and that ETR is a PXR-dependent modulator of CYP3A4 mRNA levels. etravirine 48-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 21644845-7 2012 Four women consumed CYP3A inhibitors and this affected the nifedipine concentrations (p < 0.001). Nifedipine 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-25 22310326-0 2012 Arsenic decreases RXRalpha-dependent transcription of CYP3A and suppresses immune regulators in hepatocytes. Arsenic 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-59 22310326-3 2012 Previous studies have shown that arsenic decreases expression of CYP3A, a critical drug metabolizing enzyme in human and rat liver. Arsenic 33-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 22310326-5 2012 Our work has shown that arsenite decreases nuclear levels of RXRalpha the nuclear receptor that, as a heterodimer partner with PXR, transactivates the CYP3A gene. arsenite 24-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-156 22310326-6 2012 These results suggest that arsenite decreases transcription of CYP3A by decreasing RXRalpha. arsenite 27-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 22310326-9 2012 Previous studies have shown that arsenic in the concentration range of 2-5 muM affects CYP3A mRNA. Arsenic 33-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 22310326-10 2012 When rifampicin-treated primary human hepatocyte cultures were exposed to arsenite concentrations as low as 50 nM, CYP3A mRNA was decreased. Rifampin 5-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 22310326-10 2012 When rifampicin-treated primary human hepatocyte cultures were exposed to arsenite concentrations as low as 50 nM, CYP3A mRNA was decreased. arsenite 74-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 21518375-0 2012 Effect of cytochrome P450 3A4 inhibitor ketoconazole on risperidone pharmacokinetics in healthy volunteers. Risperidone 56-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-29 21518375-2 2012 It is mainly metabolized by human cytochrome P450 CYP2D6 and partly by CYP3A4 to 9-hydroxyrisperidone. Paliperidone Palmitate 81-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 21518375-3 2012 Ketoconazole is used as a CYP3A4 inhibitor probe for studying drug-drug interactions. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 21518375-16 2012 Ketoconazole significantly inhibited the metabolism of risperidone through the inhibition of hepatic CYP3A4. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 21518375-16 2012 Ketoconazole significantly inhibited the metabolism of risperidone through the inhibition of hepatic CYP3A4. Risperidone 55-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 21518375-17 2012 our results suggest that besides CYP2D6, CYP3A4 contributes significantly to the metabolism of risperidone. Risperidone 95-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 21518375-19 2012 If a CYP3A4 inhibitor is used concomitantly with risperidone, it is necessary for the clinicians to monitor their patients for signs of adverse drug reactions. Risperidone 49-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 5-11 21535061-0 2012 Effect of CYP3A4*1G on the fentanyl consumption for intravenous patient-controlled analgesia after total abdominal hysterectomy in Chinese Han population. Fentanyl 27-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 21535061-2 2012 Cytochrome P450 3A4 (CYP3A4) is the main metabolism enzyme of fentanyl, and single nucleotide polymorphisms within the CYP3A4 gene may contribute to the variability of fentanyl analgesic efficacy. Fentanyl 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 21535061-2 2012 Cytochrome P450 3A4 (CYP3A4) is the main metabolism enzyme of fentanyl, and single nucleotide polymorphisms within the CYP3A4 gene may contribute to the variability of fentanyl analgesic efficacy. Fentanyl 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 21535061-2 2012 Cytochrome P450 3A4 (CYP3A4) is the main metabolism enzyme of fentanyl, and single nucleotide polymorphisms within the CYP3A4 gene may contribute to the variability of fentanyl analgesic efficacy. Fentanyl 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 21535061-2 2012 Cytochrome P450 3A4 (CYP3A4) is the main metabolism enzyme of fentanyl, and single nucleotide polymorphisms within the CYP3A4 gene may contribute to the variability of fentanyl analgesic efficacy. Fentanyl 168-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 21535061-2 2012 Cytochrome P450 3A4 (CYP3A4) is the main metabolism enzyme of fentanyl, and single nucleotide polymorphisms within the CYP3A4 gene may contribute to the variability of fentanyl analgesic efficacy. Fentanyl 168-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 21535061-2 2012 Cytochrome P450 3A4 (CYP3A4) is the main metabolism enzyme of fentanyl, and single nucleotide polymorphisms within the CYP3A4 gene may contribute to the variability of fentanyl analgesic efficacy. Fentanyl 168-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 21535061-3 2012 The aim of this study was to investigate whether the most common genetic variation in Chinese, CYP3A4*1G, has an impact on the fentanyl consumption for intravenous PCA in Chinese Han women undergone abdominal total hysterectomy. Fentanyl 127-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 21535061-14 2012 WHAT IS NEW AND CONCLUSIONS: CYP3A4*1G has an impact on the analgesic effect of fentanyl in Chinese Han subjects. Fentanyl 80-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 22515132-9 2012 Boceprevir is a potent inhibitor of cytochrome P450 isoenzyme CYP3A4; clinically relevant pharmacokinetic interactions can be thus anticipated when boceprevir is combined with drugs that have a narrow therapeutic margin. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22500483-5 2012 Ketamine is metabolized via cytochrome P450 3A4, although no significant interactions have been reported. Ketamine 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-47 22205755-0 2012 An inducible cytochrome P450 3A4-dependent vitamin D catabolic pathway. Vitamin D 43-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-32 22205755-3 2012 We now report a novel CYP3A4-dependent pathway, the 4-hydroxylation of 25-hydroxyvitamin D(3) (25OHD(3)), the induction of which may contribute to drug-induced vitamin D deficiency. Vitamin D 81-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 22205755-6 2012 4beta,25(OH)(2)D(3) was found in human plasma at concentrations comparable to that of 1alpha,25-dihydroxyvitamin D(3), and its formation rate in a panel of human liver microsomes was strongly correlated with CYP3A4 content and midazolam hydroxylation activity. 4beta 0-5 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 208-214 22205755-7 2012 Formation of 4beta,25(OH)(2)D(3) in primary human hepatocytes was induced by rifampin and inhibited by CYP3A4-specific inhibitors. 4beta 13-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 22205755-8 2012 Short-term treatment of healthy volunteers (n = 6) with rifampin selectively induced CYP3A4-dependent 4beta,25(OH)(2)D(3), but not CYP24A1-dependent 24R,25-dihydroxyvitamin D(3) formation, and altered systemic mineral homeostasis. Rifampin 56-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 21458012-0 2012 Cross-sectional study of hepatic CYP1A and CYP3A enzymes in hybrid striped bass, channel catfish and Nile tilapia following oxytetracycline treatment. Oxytetracycline 124-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-48 22422635-9 2012 MEASUREMENTS AND MAIN RESULTS: In the first DDI study, coadministration of ketoconazole (a CYP3A4 inhibitor) and clobazam increased clobazam"s area under the concentration time curve from time zero extrapolated to infinity (AUC(0- ) ) 54% and decreased clobazam"s maximum plasma concentration (C(max) ) by 15% versus administration of clobazam alone, but the combination affected these pharmacokinetic parameters for N-CLB to a lesser degree. Ketoconazole 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22422635-9 2012 MEASUREMENTS AND MAIN RESULTS: In the first DDI study, coadministration of ketoconazole (a CYP3A4 inhibitor) and clobazam increased clobazam"s area under the concentration time curve from time zero extrapolated to infinity (AUC(0- ) ) 54% and decreased clobazam"s maximum plasma concentration (C(max) ) by 15% versus administration of clobazam alone, but the combination affected these pharmacokinetic parameters for N-CLB to a lesser degree. Clobazam 132-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22422635-9 2012 MEASUREMENTS AND MAIN RESULTS: In the first DDI study, coadministration of ketoconazole (a CYP3A4 inhibitor) and clobazam increased clobazam"s area under the concentration time curve from time zero extrapolated to infinity (AUC(0- ) ) 54% and decreased clobazam"s maximum plasma concentration (C(max) ) by 15% versus administration of clobazam alone, but the combination affected these pharmacokinetic parameters for N-CLB to a lesser degree. Clobazam 132-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22422635-9 2012 MEASUREMENTS AND MAIN RESULTS: In the first DDI study, coadministration of ketoconazole (a CYP3A4 inhibitor) and clobazam increased clobazam"s area under the concentration time curve from time zero extrapolated to infinity (AUC(0- ) ) 54% and decreased clobazam"s maximum plasma concentration (C(max) ) by 15% versus administration of clobazam alone, but the combination affected these pharmacokinetic parameters for N-CLB to a lesser degree. Clobazam 132-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22515132-9 2012 Boceprevir is a potent inhibitor of cytochrome P450 isoenzyme CYP3A4; clinically relevant pharmacokinetic interactions can be thus anticipated when boceprevir is combined with drugs that have a narrow therapeutic margin. N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide 148-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22369694-6 2012 Our findings indicate that the CYP3A4*1B-CYP3A5*1 haplotype may have a more profound impact in tacrolimus PKs than the CYP3A5*1 allele. Tacrolimus 95-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 22310298-8 2012 CYP3A4 mRNA was induced most powerfully by pyrethroids; 50 muM cypermethrin increased CYP3A4 mRNA 35-fold. Pyrethrins 43-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22321050-1 2012 We recently designed the CIME cocktail consisting of 10 drugs to assess the activity of the major human CYPs (CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6 and CYP3A), a phase II enzyme (UGT1A1/6/9), two drug transporters (P-gp and OATP1B1) and a component of the renal function ( Videau et al. cime 25-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-159 22310298-8 2012 CYP3A4 mRNA was induced most powerfully by pyrethroids; 50 muM cypermethrin increased CYP3A4 mRNA 35-fold. cypermethrin 63-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22310298-8 2012 CYP3A4 mRNA was induced most powerfully by pyrethroids; 50 muM cypermethrin increased CYP3A4 mRNA 35-fold. cypermethrin 63-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 22342630-0 2012 Biotransformations of 6",7"-dihydroxybergamottin and 6",7"-epoxybergamottin by the citrus-pathogenic fungi diminish cytochrome P450 3A4 inhibitory activity. 6',7'-dihydroxybergamottin 22-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-135 22342630-0 2012 Biotransformations of 6",7"-dihydroxybergamottin and 6",7"-epoxybergamottin by the citrus-pathogenic fungi diminish cytochrome P450 3A4 inhibitory activity. 6",7"-epoxybergamottin 53-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-135 22421793-17 2012 Five compounds of the test set, including known strong inhibitors dalfopristin and tioconazole, were classified as probable potent inhibitors of CYP3A4. dalfopristin 66-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 22305191-4 2012 PSP (1.25-20muM) dose-dependently decreased CYP1A2-mediated metabolism of phenacetin to paracetamol (IC(50) 19.7muM) and CYP3A4-mediated metabolism of testosterone to 6beta-hydroxytestosterone (IC(20) 7.06muM). Testosterone 151-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 22421793-17 2012 Five compounds of the test set, including known strong inhibitors dalfopristin and tioconazole, were classified as probable potent inhibitors of CYP3A4. tioconazole 83-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 22421793-18 2012 Other known strong inhibitors, such as lopinavir, oltipraz, quercetin, raloxifene, and troglitazone, were among 18 compounds classified as plausible potent inhibitors of CYP3A4. Lopinavir 39-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 22421793-18 2012 Other known strong inhibitors, such as lopinavir, oltipraz, quercetin, raloxifene, and troglitazone, were among 18 compounds classified as plausible potent inhibitors of CYP3A4. oltipraz 50-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 22421793-18 2012 Other known strong inhibitors, such as lopinavir, oltipraz, quercetin, raloxifene, and troglitazone, were among 18 compounds classified as plausible potent inhibitors of CYP3A4. Quercetin 60-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 22421793-18 2012 Other known strong inhibitors, such as lopinavir, oltipraz, quercetin, raloxifene, and troglitazone, were among 18 compounds classified as plausible potent inhibitors of CYP3A4. Raloxifene Hydrochloride 71-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 22421793-18 2012 Other known strong inhibitors, such as lopinavir, oltipraz, quercetin, raloxifene, and troglitazone, were among 18 compounds classified as plausible potent inhibitors of CYP3A4. Troglitazone 87-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 22274748-5 2012 Covariate models have improved our understanding of the pharmacology of many anticancer drugs, including busulfan or melphalan that are part of high-dose pretransplant treatments, the antifolate methotrexate whose elimination is strongly dependent on GFR and comedication, the taxanes and tyrosine kinase inhibitors, the latter being subject of cytochrome p450 3A4 (CYP3A4) associated metabolism. Busulfan 105-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 345-364 22342832-10 2012 Consumption of berberine as an anti-hyperglycemic compound by diabetic patients might provide an extra benefit due to its potential to restore the expression of Cyp2e1, Cyp3a, and Cyp4a to normal levels. Berberine 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-174 22274748-5 2012 Covariate models have improved our understanding of the pharmacology of many anticancer drugs, including busulfan or melphalan that are part of high-dose pretransplant treatments, the antifolate methotrexate whose elimination is strongly dependent on GFR and comedication, the taxanes and tyrosine kinase inhibitors, the latter being subject of cytochrome p450 3A4 (CYP3A4) associated metabolism. Busulfan 105-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 366-372 22048224-0 2012 Evidence of CYP3A allosterism in vivo: analysis of interaction between fluconazole and midazolam. Fluconazole 71-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 22252655-0 2012 Quantification of femtomolar concentrations of the CYP3A substrate midazolam and its main metabolite 1"-hydroxymidazolam in human plasma using ultra performance liquid chromatography coupled to tandem mass spectrometry. Midazolam 67-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 22270945-2 2012 The primary objective of this communication was to quantitatively predict changes in rivaroxaban exposure when individuals with varying degrees of renal impairment are co-administered with another drug that is both a P-gp and a moderate CYP3A4 inhibitor. Rivaroxaban 85-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 237-243 21913896-7 2012 KEY RESULTS: All atorvastatin metabolites induced the assembly of PXR and activated CYP3A4 promoter activity. Atorvastatin 17-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 22048224-0 2012 Evidence of CYP3A allosterism in vivo: analysis of interaction between fluconazole and midazolam. Midazolam 87-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 22318618-7 2012 In conclusion, efavirenz enhances omeprazole metabolism in a nonstereoselective manner through induction of CYP3A and CYP2C19 activity. Omeprazole 34-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 22048224-1 2012 The allosteric effect of fluconazole (effector) on the formation of 1"-hydroxymidazolam (1"-OH-MDZ) and 4-hydroxymidazolam (4-OH-MDZ) from midazolam (MDZ), a substrate of CYP3A4/5--members of the cytochrome P450 superfamily of enzymes--was examined in healthy volunteers. Fluconazole 25-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 22048224-7 2012 The 1"-OH-MDZ/4-OH-MDZ ratio may serve as a biomarker of such interactions among MDZ, CYP3A4/5, and other putative effectors. 1"-oh-mdz 4-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 22048224-7 2012 The 1"-OH-MDZ/4-OH-MDZ ratio may serve as a biomarker of such interactions among MDZ, CYP3A4/5, and other putative effectors. 4-hydroxymidazolam 14-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 22112384-3 2012 Despite raloxifene"s in vitro bioactivation and TDI of CYP3A4, it is well tolerated in patients with no drug-drug interactions. Raloxifene Hydrochloride 8-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 22106171-0 2012 Stereospecific metabolism of itraconazole by CYP3A4: dioxolane ring scission of azole antifungals. Itraconazole 29-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 22112384-4 2012 This discordance is attributed to its presystemic glucuronidation, thereby decreasing the amount of unchanged raloxifene available for CYP3A inactivation. Raloxifene Hydrochloride 110-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-140 22106171-0 2012 Stereospecific metabolism of itraconazole by CYP3A4: dioxolane ring scission of azole antifungals. formal glycol 53-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 22106171-0 2012 Stereospecific metabolism of itraconazole by CYP3A4: dioxolane ring scission of azole antifungals. Azoles 36-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 22106171-1 2012 Itraconazole (ITZ) is a mixture of four cis-stereoisomers that inhibit CYP3A4 potently and coordinate CYP3A4 heme via the triazole nitrogen. Itraconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 22106171-1 2012 Itraconazole (ITZ) is a mixture of four cis-stereoisomers that inhibit CYP3A4 potently and coordinate CYP3A4 heme via the triazole nitrogen. Itraconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 22106171-1 2012 Itraconazole (ITZ) is a mixture of four cis-stereoisomers that inhibit CYP3A4 potently and coordinate CYP3A4 heme via the triazole nitrogen. Itraconazole 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 22112384-5 2012 The current study used raloxifene as a model to assess the effect of hepatic and intestinal glucuronidation on the kinetic parameters of CYP3A4 inactivation. Raloxifene Hydrochloride 23-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 22106171-1 2012 Itraconazole (ITZ) is a mixture of four cis-stereoisomers that inhibit CYP3A4 potently and coordinate CYP3A4 heme via the triazole nitrogen. Itraconazole 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 22112384-9 2012 In contrast, the absence of glucuronidation resulted in a 4.1-fold increase in the area under the curve (AUC) of midazolam, when in the presence of raloxifene, hence providing an understanding of the impact of intestinal glucuronidation on raloxifene"s time-dependent inhibition of CYP3A4 and also providing a validation of a simple in vitro experiment to assess the influence of gut metabolism on time-dependent inhibitors at the discovery phase. Midazolam 113-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 282-288 22106171-1 2012 Itraconazole (ITZ) is a mixture of four cis-stereoisomers that inhibit CYP3A4 potently and coordinate CYP3A4 heme via the triazole nitrogen. Heme 109-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 22106171-1 2012 Itraconazole (ITZ) is a mixture of four cis-stereoisomers that inhibit CYP3A4 potently and coordinate CYP3A4 heme via the triazole nitrogen. Heme 109-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 22112384-9 2012 In contrast, the absence of glucuronidation resulted in a 4.1-fold increase in the area under the curve (AUC) of midazolam, when in the presence of raloxifene, hence providing an understanding of the impact of intestinal glucuronidation on raloxifene"s time-dependent inhibition of CYP3A4 and also providing a validation of a simple in vitro experiment to assess the influence of gut metabolism on time-dependent inhibitors at the discovery phase. Raloxifene Hydrochloride 148-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 282-288 22106171-1 2012 Itraconazole (ITZ) is a mixture of four cis-stereoisomers that inhibit CYP3A4 potently and coordinate CYP3A4 heme via the triazole nitrogen. Triazoles 122-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 22170330-1 2012 Pulmonary penetration of clarithromycin (CLR) in epithelial lining fluid (ELF) and bronchoalveolar lavage cells (BALCs) can be influenced by CYP3A4, by P-glycoprotein, and, according to our hypothesis, by a member of the organic anion-transporting protein (OATP) family, for which rifampicin (RIF) is inhibiting in single doses but inducing after long-term coadministration. Clarithromycin 25-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 22106171-1 2012 Itraconazole (ITZ) is a mixture of four cis-stereoisomers that inhibit CYP3A4 potently and coordinate CYP3A4 heme via the triazole nitrogen. Triazoles 122-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 22106171-1 2012 Itraconazole (ITZ) is a mixture of four cis-stereoisomers that inhibit CYP3A4 potently and coordinate CYP3A4 heme via the triazole nitrogen. Nitrogen 131-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 22106171-1 2012 Itraconazole (ITZ) is a mixture of four cis-stereoisomers that inhibit CYP3A4 potently and coordinate CYP3A4 heme via the triazole nitrogen. Nitrogen 131-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 22106171-2 2012 However, (2R,4S,2"R)-ITZ and (2R,4S,2"S)-ITZ also undergo stereoselective sequential metabolism by CYP3A4 at a site distant from the triazole ring to 3"-OH-ITZ, keto-ITZ, and N-desalkyl-ITZ. (2r,4s,2"r)-itz 9-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 22106171-2 2012 However, (2R,4S,2"R)-ITZ and (2R,4S,2"S)-ITZ also undergo stereoselective sequential metabolism by CYP3A4 at a site distant from the triazole ring to 3"-OH-ITZ, keto-ITZ, and N-desalkyl-ITZ. (2r,4s,2"s)-itz 29-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 22106171-2 2012 However, (2R,4S,2"R)-ITZ and (2R,4S,2"S)-ITZ also undergo stereoselective sequential metabolism by CYP3A4 at a site distant from the triazole ring to 3"-OH-ITZ, keto-ITZ, and N-desalkyl-ITZ. Triazoles 133-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 22106171-2 2012 However, (2R,4S,2"R)-ITZ and (2R,4S,2"S)-ITZ also undergo stereoselective sequential metabolism by CYP3A4 at a site distant from the triazole ring to 3"-OH-ITZ, keto-ITZ, and N-desalkyl-ITZ. 3"-oh-itz 150-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 22170330-1 2012 Pulmonary penetration of clarithromycin (CLR) in epithelial lining fluid (ELF) and bronchoalveolar lavage cells (BALCs) can be influenced by CYP3A4, by P-glycoprotein, and, according to our hypothesis, by a member of the organic anion-transporting protein (OATP) family, for which rifampicin (RIF) is inhibiting in single doses but inducing after long-term coadministration. Clarithromycin 41-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 22106171-2 2012 However, (2R,4S,2"R)-ITZ and (2R,4S,2"S)-ITZ also undergo stereoselective sequential metabolism by CYP3A4 at a site distant from the triazole ring to 3"-OH-ITZ, keto-ITZ, and N-desalkyl-ITZ. keto-itz 161-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 22106171-2 2012 However, (2R,4S,2"R)-ITZ and (2R,4S,2"S)-ITZ also undergo stereoselective sequential metabolism by CYP3A4 at a site distant from the triazole ring to 3"-OH-ITZ, keto-ITZ, and N-desalkyl-ITZ. n-desalkyl-itz 175-189 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 22187487-9 2012 The results from in vitro experiments with recombinant isoforms suggested that the oxidative metabolism of CP-945,598 to M1 is catalyzed primarily by CYP3A4/3A5. cp-945 107-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 22106171-5 2012 All four trans-ITZ stereoisomers were tight binding inhibitors of CYP3A4-mediated midazolam hydroxylation (IC(50) 16-26 nM), and each gave a type II spectrum upon binding to CYP3A4. Midazolam 82-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 22106171-8 2012 The catalytic rates of dioxolane ring scission were similar to the dissociation rates of ITZ stereoisomers from CYP3A4, suggesting that the heme iron is reduced while the triazole moiety coordinates to it and no dissociation of ITZ is necessary before catalysis. Heme 140-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 22106171-9 2012 The triazole containing metabolite [1-(2,4-dichlorophenyl)-2-(1H-1,2,4-triazol-1-yl)ethanone] also inhibited CYP3A4 (IC(50) >15 muM) and showed type II binding with CYP3A4. Triazoles 4-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 22106171-9 2012 The triazole containing metabolite [1-(2,4-dichlorophenyl)-2-(1H-1,2,4-triazol-1-yl)ethanone] also inhibited CYP3A4 (IC(50) >15 muM) and showed type II binding with CYP3A4. Triazoles 4-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 22106171-9 2012 The triazole containing metabolite [1-(2,4-dichlorophenyl)-2-(1H-1,2,4-triazol-1-yl)ethanone] also inhibited CYP3A4 (IC(50) >15 muM) and showed type II binding with CYP3A4. 1-(2,4-dichlorophenyl)-2-(1h-1,2,4-triazol-1-yl)ethanone 36-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 22106171-9 2012 The triazole containing metabolite [1-(2,4-dichlorophenyl)-2-(1H-1,2,4-triazol-1-yl)ethanone] also inhibited CYP3A4 (IC(50) >15 muM) and showed type II binding with CYP3A4. 1-(2,4-dichlorophenyl)-2-(1h-1,2,4-triazol-1-yl)ethanone 36-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 22187487-10 2012 The molecular docking study showed that the N-ethyl moiety of CP-945,598 can access to the heme iron-oxo of CYP3A4 in an energetically favored orientation. Nitrogen 44-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 22187487-10 2012 The molecular docking study showed that the N-ethyl moiety of CP-945,598 can access to the heme iron-oxo of CYP3A4 in an energetically favored orientation. Heme 91-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 22187487-10 2012 The molecular docking study showed that the N-ethyl moiety of CP-945,598 can access to the heme iron-oxo of CYP3A4 in an energetically favored orientation. Iron 96-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 21834799-1 2012 BACKGROUND: The CYP3A4 inhibition by calcium channel blockers (CCBs) may attenuate the effectiveness of clopidogrel. Clopidogrel 104-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 22372550-5 2012 SB1317 was mainly metabolized by CYP3A4 and CY1A2 in vitro. 14-methyl-20-oxa-5,7,14,26-tetraazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8(27),9,11,16,21,23-decaene 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 22372724-2 2012 Donepezil is metabolized by the cytochrome P450 isozyme 3A4 (CYP3A4). Donepezil 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-59 22372724-2 2012 Donepezil is metabolized by the cytochrome P450 isozyme 3A4 (CYP3A4). Donepezil 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 22372724-3 2012 Clarithromycin is a potent inhibitor of CYP3A4, and patients taking both of these drugs may be at increased risk of cardiac adverse events. Clarithromycin 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 22253426-8 2012 Glucocorticoids, including dexamethasone, cortisol, corticosterone, and cortisone all induced the expression of CYP3A7 mRNA, whereas rifampicin, an activator of PXR and an inducer of CYP3A4 in adult liver, had no effect on CYP3A7 expression. Dexamethasone 27-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 183-189 22253426-8 2012 Glucocorticoids, including dexamethasone, cortisol, corticosterone, and cortisone all induced the expression of CYP3A7 mRNA, whereas rifampicin, an activator of PXR and an inducer of CYP3A4 in adult liver, had no effect on CYP3A7 expression. Hydrocortisone 42-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 183-189 22253426-8 2012 Glucocorticoids, including dexamethasone, cortisol, corticosterone, and cortisone all induced the expression of CYP3A7 mRNA, whereas rifampicin, an activator of PXR and an inducer of CYP3A4 in adult liver, had no effect on CYP3A7 expression. Corticosterone 52-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 183-189 22253426-8 2012 Glucocorticoids, including dexamethasone, cortisol, corticosterone, and cortisone all induced the expression of CYP3A7 mRNA, whereas rifampicin, an activator of PXR and an inducer of CYP3A4 in adult liver, had no effect on CYP3A7 expression. Cortisone 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 183-189 22253426-8 2012 Glucocorticoids, including dexamethasone, cortisol, corticosterone, and cortisone all induced the expression of CYP3A7 mRNA, whereas rifampicin, an activator of PXR and an inducer of CYP3A4 in adult liver, had no effect on CYP3A7 expression. Rifampin 133-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 183-189 21820929-6 2012 RESULTS: CYP3A4 was responsible for the metabolism of lovastatin, simvastatin and atorvastatin; fluvastatin depends on CYP2C9; P-glycoprotein is responsible for decreased atorvastatin, pravastatin, simvastatin and lovastatin concentrations. Lovastatin 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 21820929-6 2012 RESULTS: CYP3A4 was responsible for the metabolism of lovastatin, simvastatin and atorvastatin; fluvastatin depends on CYP2C9; P-glycoprotein is responsible for decreased atorvastatin, pravastatin, simvastatin and lovastatin concentrations. Simvastatin 66-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 21820929-6 2012 RESULTS: CYP3A4 was responsible for the metabolism of lovastatin, simvastatin and atorvastatin; fluvastatin depends on CYP2C9; P-glycoprotein is responsible for decreased atorvastatin, pravastatin, simvastatin and lovastatin concentrations. Atorvastatin 82-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 21820929-6 2012 RESULTS: CYP3A4 was responsible for the metabolism of lovastatin, simvastatin and atorvastatin; fluvastatin depends on CYP2C9; P-glycoprotein is responsible for decreased atorvastatin, pravastatin, simvastatin and lovastatin concentrations. Atorvastatin 171-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 21820929-6 2012 RESULTS: CYP3A4 was responsible for the metabolism of lovastatin, simvastatin and atorvastatin; fluvastatin depends on CYP2C9; P-glycoprotein is responsible for decreased atorvastatin, pravastatin, simvastatin and lovastatin concentrations. Pravastatin 185-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 21820929-6 2012 RESULTS: CYP3A4 was responsible for the metabolism of lovastatin, simvastatin and atorvastatin; fluvastatin depends on CYP2C9; P-glycoprotein is responsible for decreased atorvastatin, pravastatin, simvastatin and lovastatin concentrations. Simvastatin 198-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 21820929-6 2012 RESULTS: CYP3A4 was responsible for the metabolism of lovastatin, simvastatin and atorvastatin; fluvastatin depends on CYP2C9; P-glycoprotein is responsible for decreased atorvastatin, pravastatin, simvastatin and lovastatin concentrations. Lovastatin 214-224 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 22328106-0 2012 Hypercortisolism caused by ritonavir associated inhibition of CYP 3A4 under inhalative glucocorticoid therapy. Ritonavir 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-69 22328106-3 2012 The PI ritonavir is described as the most potent compound within these CYP3A4 inhibitors. Ritonavir 7-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 22155270-0 2012 Major furocoumarins in grapefruit juice II: phototoxicity, photogenotoxicity, and inhibitory potency vs. cytochrome P450 3A4 activity. Furocoumarins 6-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-124 22113252-2 2012 Especially, it induces CYP1A2 and CYP3A4, enzymes that are closely involved in the metabolism of clozapine. Clozapine 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 22351667-5 2012 Cytochrome P-450 (CYP)3A4 activity was measured by beta-hydroxylation of testosterone in human recombinant CYP3A4. Testosterone 73-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-25 22351667-5 2012 Cytochrome P-450 (CYP)3A4 activity was measured by beta-hydroxylation of testosterone in human recombinant CYP3A4. Testosterone 73-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 22246918-8 2012 Z-Guggulsterone underwent metabolism by CYP3A4, and the metabolites greatly increased the induction potency on BSEP but not on CES1. pregna-4,17-diene-3,16-dione 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 21505085-3 2012 The pharmacokinetics of docetaxel are determined by the activity of the metabolizing enzyme cytochrome P450 3A (CYP3A) and the drug efflux transporter P-glycoprotein (P-gp). Docetaxel 24-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-110 21505085-3 2012 The pharmacokinetics of docetaxel are determined by the activity of the metabolizing enzyme cytochrome P450 3A (CYP3A) and the drug efflux transporter P-glycoprotein (P-gp). Docetaxel 24-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-117 21842479-1 2012 The aim of this study was to evaluate the inhibitory potency (IC50 values) of ethanol extracts of two commercially available aloe vera juice (AVJ) products, on CYP3A4 and CYP2D6 activities in vitro and to determine if such inhibitions could be mechanism-based. Ethanol 78-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 21842479-2 2012 Recombinant human CYP3A4 and CYP2D6 enzymes were used and the activities were expressed by the metabolism of testosterone and dextromethorphan with ketoconazole and quinidine as positive inhibitor controls, respectively. Testosterone 109-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 21842479-2 2012 Recombinant human CYP3A4 and CYP2D6 enzymes were used and the activities were expressed by the metabolism of testosterone and dextromethorphan with ketoconazole and quinidine as positive inhibitor controls, respectively. Dextromethorphan 126-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 21842479-2 2012 Recombinant human CYP3A4 and CYP2D6 enzymes were used and the activities were expressed by the metabolism of testosterone and dextromethorphan with ketoconazole and quinidine as positive inhibitor controls, respectively. Ketoconazole 148-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 21842479-2 2012 Recombinant human CYP3A4 and CYP2D6 enzymes were used and the activities were expressed by the metabolism of testosterone and dextromethorphan with ketoconazole and quinidine as positive inhibitor controls, respectively. Quinidine 165-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 22186153-6 2012 Additionally, human CYP3A4 and rat CYP3A2 were the primary enzymes for PA production via heteroatom dealkylation of MEHP. phthalic acid 71-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 22186153-6 2012 Additionally, human CYP3A4 and rat CYP3A2 were the primary enzymes for PA production via heteroatom dealkylation of MEHP. mono-(2-ethylhexyl)phthalate 116-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 22613391-3 2012 A total of 1021 patients were enrolled, with 178 of them prescribed clopidogrel and 843 patients were administrated clopidogrel combined with statins (CYP3A4-metabolized statins 636 and non CYP3A4-metabolized statins 207). Clopidogrel 116-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 22022918-0 2012 Ilaprazole, a new proton pump inhibitor, is primarily metabolized to ilaprazole sulfone by CYP3A4 and 3A5. ilaprazole 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22022918-0 2012 Ilaprazole, a new proton pump inhibitor, is primarily metabolized to ilaprazole sulfone by CYP3A4 and 3A5. ilaprazole sulfone 69-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 22022918-5 2012 Incubation of ilaprazole with cDNA-expressed recombinant CYPs indicated that CYP3A was the major enzyme that catalyses ilaprozole to ilaprazole sulfone. ilaprazole 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 22194603-1 2012 The mechanisms of ligand binding and allostery in the major human drug-metabolizing enzyme cytochrome P450 3A4 (CYP3A4) were explored with fluorescence resonance energy transfer (FRET) using a laser dye, fluorol-7GA (F7GA), as a model substrate. Sodium Fluoride 204-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-110 22022918-5 2012 Incubation of ilaprazole with cDNA-expressed recombinant CYPs indicated that CYP3A was the major enzyme that catalyses ilaprozole to ilaprazole sulfone. ilaprozole 119-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 22022918-5 2012 Incubation of ilaprazole with cDNA-expressed recombinant CYPs indicated that CYP3A was the major enzyme that catalyses ilaprozole to ilaprazole sulfone. ilaprazole sulfone 133-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 22022918-6 2012 This reaction was inhibited significantly by ketoconazole, a CYP3A inhibitor, and azamulin, a mechanism-based inhibitor of CYP3A, while no substantial effect was observed using selective inhibitors for eight other P450s (CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, and CYP2E1). Ketoconazole 45-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-66 22022918-6 2012 This reaction was inhibited significantly by ketoconazole, a CYP3A inhibitor, and azamulin, a mechanism-based inhibitor of CYP3A, while no substantial effect was observed using selective inhibitors for eight other P450s (CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, and CYP2E1). Ketoconazole 45-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-128 22022918-6 2012 This reaction was inhibited significantly by ketoconazole, a CYP3A inhibitor, and azamulin, a mechanism-based inhibitor of CYP3A, while no substantial effect was observed using selective inhibitors for eight other P450s (CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, and CYP2E1). azamulin 82-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-128 22022918-7 2012 In addition, the formation of ilaprazole sulfone correlated well with CYP3A-catalysed testosterone 6beta-hydroxylation and midazolam 1"-hydroxylation in 20 different human liver microsome panels. ilaprazole sulfone 30-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-75 22022918-7 2012 In addition, the formation of ilaprazole sulfone correlated well with CYP3A-catalysed testosterone 6beta-hydroxylation and midazolam 1"-hydroxylation in 20 different human liver microsome panels. testosterone 6beta 86-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-75 22022918-8 2012 The intrinsic clearance of the formation of ilaprazole sulfone by CYP3A4 was 16-fold higher than that by CYP3A5. ilaprazole sulfone 44-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 22022918-9 2012 Collectively, these results indicate that the formation of the major metabolite of ilaprazole, ilaprazole sulfone, is predominantly catalysed by CYP3A4/5. ilaprazole 83-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 22022918-9 2012 Collectively, these results indicate that the formation of the major metabolite of ilaprazole, ilaprazole sulfone, is predominantly catalysed by CYP3A4/5. ilaprazole sulfone 95-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 22022919-1 2012 Midazolam, a potent benzodiazepine derivative and a typical substrate of CYP3A4/3A5, is essentially metabolized in human into 1"-hydroxymidazolam, then eliminated as the corresponding phase II metabolite, the 1"-O-beta-D-glucuronide derivative. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 22022919-1 2012 Midazolam, a potent benzodiazepine derivative and a typical substrate of CYP3A4/3A5, is essentially metabolized in human into 1"-hydroxymidazolam, then eliminated as the corresponding phase II metabolite, the 1"-O-beta-D-glucuronide derivative. 1-hydroxymethylmidazolam 126-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 22194603-1 2012 The mechanisms of ligand binding and allostery in the major human drug-metabolizing enzyme cytochrome P450 3A4 (CYP3A4) were explored with fluorescence resonance energy transfer (FRET) using a laser dye, fluorol-7GA (F7GA), as a model substrate. Sodium Fluoride 204-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 22194603-7 2012 It is located in the vicinity of residues 217-220, similar to the position of the progesterone molecule bound at the distal surface of the CYP3A4 in a prior x-ray crystal structure. Progesterone 82-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 22120734-2 2012 We investigated the effect of four polymorphisms in CYP3A4, CYP3A5 and ABCB1 genes on response to atorvastatin and CYP3A4 activity in Chilean subjects with HC. Atorvastatin 98-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 22120734-6 2012 CYP3A4 enzyme activity in urine samples was assessed through determination of 6beta-hydroxycortisol/cortisol free ratio (6betaOHC/FC). 6 beta-hydroxycortisol 78-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22120734-6 2012 CYP3A4 enzyme activity in urine samples was assessed through determination of 6beta-hydroxycortisol/cortisol free ratio (6betaOHC/FC). Hydrocortisone 91-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22120734-6 2012 CYP3A4 enzyme activity in urine samples was assessed through determination of 6beta-hydroxycortisol/cortisol free ratio (6betaOHC/FC). 6betaohc 121-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22120734-6 2012 CYP3A4 enzyme activity in urine samples was assessed through determination of 6beta-hydroxycortisol/cortisol free ratio (6betaOHC/FC). Fc(alpha) receptor 130-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22120734-12 2012 CONCLUSION: Our results suggest that presence of G allele for -290A>G polymorphism determines a better response to atorvastatin, being also associated with lower CYP3A4 activity in vivo, causing an increased atorvastatin activity. Atorvastatin 118-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 22120734-12 2012 CONCLUSION: Our results suggest that presence of G allele for -290A>G polymorphism determines a better response to atorvastatin, being also associated with lower CYP3A4 activity in vivo, causing an increased atorvastatin activity. Atorvastatin 211-223 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 22273859-2 2012 Methadone clearance and drug interactions have been attributed to cytochrome P4503A4 (CYP3A4), but actual mechanisms are unknown. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-84 22264486-0 2012 Imidazopyridines as selective CYP3A4 inhibitors. imidazopyridine 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 22273859-2 2012 Methadone clearance and drug interactions have been attributed to cytochrome P4503A4 (CYP3A4), but actual mechanisms are unknown. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 22273859-10 2012 RESULTS: Indinavir significantly inhibited hepatic and first-pass CYP3A activity. Indinavir 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 22123705-3 2012 Previous studies have demonstrated that lersivirine is metabolized by glucuronidation via UGT2B7 and by cytochrome P450 3A4 (CYP3A4). UK 453,061 40-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-123 22123705-3 2012 Previous studies have demonstrated that lersivirine is metabolized by glucuronidation via UGT2B7 and by cytochrome P450 3A4 (CYP3A4). UK 453,061 40-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 22123705-4 2012 Lersivirine is also a weak inducer of the CYP3A4 enzyme. UK 453,061 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 22123705-5 2012 Therefore, coadministered lersivirine could potentially affect the pharmacokinetics of maraviroc, a CCR5 antagonist metabolized by CYP3A4, and raltegravir, an integrase inhibitor metabolized by glucuronidation. UK 453,061 26-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 22057855-10 2012 The likely mechanism for this interaction is through induction of CYP3A4 by bexarotene given the role of this enzyme in the metabolism of atorvastatin. Atorvastatin 138-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 21838784-1 2012 AIM: According to product information, montelukast is extensively metabolized by CYP3A4 and CYP2C9. montelukast 39-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 21838784-3 2012 Our aim was to study the effects of selective CYP2C8 and CYP3A4 inhibitors on the pharmacokinetics of montelukast. montelukast 102-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 21838784-7 2012 The CYP3A4 inhibitor itraconazole had no significant effect on the pharmacokinetic variables of montelukast or its M6 and M4 metabolites, but markedly reduced the AUC and C(max) of M5a and M5b (P < 0.05). Itraconazole 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 22057855-1 2012 PURPOSE: Bexarotene (Targretin( ) capsules) is a retinoid-X-receptor agonist and an inducer of CYP3A4-mediated metabolism. Bexarotene 9-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 22096084-0 2012 Assessment of the impact of CYP3A polymorphisms on the formation of alpha-hydroxytamoxifen and N-desmethyltamoxifen in human liver microsomes. alpha-hydroxytamoxifen 68-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 22057855-1 2012 PURPOSE: Bexarotene (Targretin( ) capsules) is a retinoid-X-receptor agonist and an inducer of CYP3A4-mediated metabolism. Bexarotene 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 22057855-10 2012 The likely mechanism for this interaction is through induction of CYP3A4 by bexarotene given the role of this enzyme in the metabolism of atorvastatin. Bexarotene 76-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 22319066-2 2012 BACKGROUND: Clopidogrel is an inactive prodrug; it is converted to its active metabolite through the cytochrome P450 (CYP3A4) pathway, which also metabolizes calcium channel blockers (CCBs). Clopidogrel 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 22096084-0 2012 Assessment of the impact of CYP3A polymorphisms on the formation of alpha-hydroxytamoxifen and N-desmethyltamoxifen in human liver microsomes. N-desmethyltamoxifen 95-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 22096084-2 2012 Its biotransformation to alpha-hydroxytamoxifen (alpha-OHT), which may be genotoxic, and to N-desmethyltamoxifen (N-DMT), which is partially hydroxylated to 4-hydroxy-N-DMT (endoxifen), a potent antiestrogen, is mediated by CYP3A enzymes. N-desmethyltamoxifen 92-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 224-229 22096084-2 2012 Its biotransformation to alpha-hydroxytamoxifen (alpha-OHT), which may be genotoxic, and to N-desmethyltamoxifen (N-DMT), which is partially hydroxylated to 4-hydroxy-N-DMT (endoxifen), a potent antiestrogen, is mediated by CYP3A enzymes. N-desmethyltamoxifen 114-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 224-229 22096084-2 2012 Its biotransformation to alpha-hydroxytamoxifen (alpha-OHT), which may be genotoxic, and to N-desmethyltamoxifen (N-DMT), which is partially hydroxylated to 4-hydroxy-N-DMT (endoxifen), a potent antiestrogen, is mediated by CYP3A enzymes. 4-hydroxy-N-desmethyltamoxifen 157-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 224-229 22096084-5 2012 We observed that the catalytic efficiency [intrinsic clearance (CL(int))] for alpha-OHT formation with recombinant CYP3A4 was 5-fold higher than that with recombinant CYP3A5 (0.81 versus 0.16 nl min-1 pmol cytochrome P450-1). cl(int)) 64-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 21870106-8 2012 CYP3A4 activity was also inhibited, as the C(max), AUC(0- ), and AUC(0-12) of midazolam were increased 38% (P < 0.05), 40% (P < 0.01), and 37% (P < 0.05) after BBR treatment, respectively. Midazolam 78-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22096084-7 2012 For N-DMT formation, the CL(int) with recombinant CYP3A4 was only 1.7-fold higher, relative to that with recombinant CYP3A5. N-desmethyltamoxifen 4-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 21870106-8 2012 CYP3A4 activity was also inhibited, as the C(max), AUC(0- ), and AUC(0-12) of midazolam were increased 38% (P < 0.05), 40% (P < 0.01), and 37% (P < 0.05) after BBR treatment, respectively. bbr 169-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21848931-6 2012 Rivaroxaban is a substrate of CYP3A4 and P-glycoprotein and therefore not recommended for concomitant use with strong inhibitors of both pathways, e.g. most azole antimycotics and protease inhibitors. Rivaroxaban 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 21128989-2 2012 In this study, we investigated the association between cytochrome P450 3A4 (CYP3A4) genetic polymorphisms and post-operative fentanyl requirements. Fentanyl 125-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-74 20740300-3 2012 This study evaluated changes in axitinib plasma pharmacokinetic parameters and assessed safety and tolerability in healthy subjects, following axitinib co-administration with the potent CYP3A inhibitor ketoconazole. Ketoconazole 202-214 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 186-191 21128989-2 2012 In this study, we investigated the association between cytochrome P450 3A4 (CYP3A4) genetic polymorphisms and post-operative fentanyl requirements. Fentanyl 125-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 22101235-6 2012 We document herein that of these, Ser-478 plays a pivotal role in UBC7/gp78-mediated CYP3A4 ubiquitination, which is accelerated and enhanced on its mutation to the phosphomimetic Asp residue but attenuated on its Ala mutation. Alanine 214-217 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 22101235-7 2012 Intriguingly, CYP3A5, a polymorphically expressed human liver CYP3A4 isoform (containing Asp-478) is ubiquitinated but not degraded to a greater extent than CYP3A4 in HepG2 cells. Aspartic Acid 89-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22101235-0 2012 Multisite phosphorylation of human liver cytochrome P450 3A4 enhances Its gp78- and CHIP-mediated ubiquitination: a pivotal role of its Ser-478 residue in the gp78-catalyzed reaction. Serine 136-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-60 22101235-5 2012 We have documented that UBC7/gp78-mediated CYP3A4 ubiquitination requires protein phosphorylation by protein kinase (PK) A and PKC and identified three residues (Ser-478, Thr-264, and Ser-420) whose phosphorylation is required for intracellular CYP3A4 ERAD. Serine 162-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 22101235-8 2012 This suggests that although Ser-478 phosphorylation is essential for UBC7/gp78-mediated CYP3A4 ubiquitination, it is not sufficient for its ERAD. Serine 28-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 22101235-5 2012 We have documented that UBC7/gp78-mediated CYP3A4 ubiquitination requires protein phosphorylation by protein kinase (PK) A and PKC and identified three residues (Ser-478, Thr-264, and Ser-420) whose phosphorylation is required for intracellular CYP3A4 ERAD. Threonine 171-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 22101235-9 2012 Additionally, we now report that CYP3A4 protein phosphorylation by PKA and/or PKC at sites other than Ser-478, Thr-264, and Ser-420 also enhances UbcH5a/CHIP-mediated ubiquitination. Serine 102-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 22101235-5 2012 We have documented that UBC7/gp78-mediated CYP3A4 ubiquitination requires protein phosphorylation by protein kinase (PK) A and PKC and identified three residues (Ser-478, Thr-264, and Ser-420) whose phosphorylation is required for intracellular CYP3A4 ERAD. Serine 184-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 22101235-9 2012 Additionally, we now report that CYP3A4 protein phosphorylation by PKA and/or PKC at sites other than Ser-478, Thr-264, and Ser-420 also enhances UbcH5a/CHIP-mediated ubiquitination. Threonine 111-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 22101235-6 2012 We document herein that of these, Ser-478 plays a pivotal role in UBC7/gp78-mediated CYP3A4 ubiquitination, which is accelerated and enhanced on its mutation to the phosphomimetic Asp residue but attenuated on its Ala mutation. Serine 34-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 22101235-6 2012 We document herein that of these, Ser-478 plays a pivotal role in UBC7/gp78-mediated CYP3A4 ubiquitination, which is accelerated and enhanced on its mutation to the phosphomimetic Asp residue but attenuated on its Ala mutation. Aspartic Acid 180-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 22101235-9 2012 Additionally, we now report that CYP3A4 protein phosphorylation by PKA and/or PKC at sites other than Ser-478, Thr-264, and Ser-420 also enhances UbcH5a/CHIP-mediated ubiquitination. Serine 124-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 22101235-10 2012 Through proteomic analyses, we identify (i) 12 additional phosphorylation sites that may be involved in CHIP-CYP3A4 interactions and (ii) 8 previously unidentified CYP3A4 ubiquitination sites within spatially associated clusters of Asp/Glu and phosphorylatable Ser/Thr residues that may serve to engage each E2-E3 complex. Aspartic Acid 232-235 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 22101235-10 2012 Through proteomic analyses, we identify (i) 12 additional phosphorylation sites that may be involved in CHIP-CYP3A4 interactions and (ii) 8 previously unidentified CYP3A4 ubiquitination sites within spatially associated clusters of Asp/Glu and phosphorylatable Ser/Thr residues that may serve to engage each E2-E3 complex. Threonine 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 22101235-10 2012 Through proteomic analyses, we identify (i) 12 additional phosphorylation sites that may be involved in CHIP-CYP3A4 interactions and (ii) 8 previously unidentified CYP3A4 ubiquitination sites within spatially associated clusters of Asp/Glu and phosphorylatable Ser/Thr residues that may serve to engage each E2-E3 complex. Threonine 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 21678521-0 2012 The in vitro inhibition of human CYP1A2, CYP2D6 and CYP3A4 by tetrahydropalmatine, neferine and berberine. Berberine 96-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 21678521-1 2012 The purpose of this study was to investigate the in vitro inhibition potential of the three purified herbal constituents tetrahydropalmatine (Tet), neferine (Nef) and berberine (Ber) towards recombinant human CYP1A2, CYP2D6 and CYP3A4 metabolic activities. Berberine 167-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 21678521-0 2012 The in vitro inhibition of human CYP1A2, CYP2D6 and CYP3A4 by tetrahydropalmatine, neferine and berberine. tetrahydropalmatine 62-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 21678521-1 2012 The purpose of this study was to investigate the in vitro inhibition potential of the three purified herbal constituents tetrahydropalmatine (Tet), neferine (Nef) and berberine (Ber) towards recombinant human CYP1A2, CYP2D6 and CYP3A4 metabolic activities. Berberine 178-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 21678521-0 2012 The in vitro inhibition of human CYP1A2, CYP2D6 and CYP3A4 by tetrahydropalmatine, neferine and berberine. neferine 83-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 21943317-0 2012 Effect of genistein on the activities of cytochrome P450 3A and P-glycoprotein in Chinese healthy participants. Genistein 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-59 21943317-1 2012 To determine the effect of genistein on cytochrome P450 3A (CYP3A) and P-glycoprotein (P-gp) function using the probe substrates midazolam and talinolol, respectively. Genistein 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-58 21943317-9 2012 Administration of genistein can result in a modest induction of CYP3A and possibly P-gp activity in healthy volunteers. Genistein 18-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 21943317-1 2012 To determine the effect of genistein on cytochrome P450 3A (CYP3A) and P-glycoprotein (P-gp) function using the probe substrates midazolam and talinolol, respectively. Genistein 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 22178124-8 2012 It was found that bufalin, cinobufagin, and resibufogenin were novel CYP3A4 inducers. bufalin 18-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 22157006-0 2012 Structural and mechanistic insights into the interaction of cytochrome P4503A4 with bromoergocryptine, a type I ligand. Bromocriptine 84-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-78 22157006-2 2012 One of the CYP3A4 substrates is bromoergocryptine (BEC), a dopamine receptor agonist prescribed for the inhibition of prolactin secretion and treatment of Parkinson disease, type 2 diabetes, and several other pathological conditions. Bromocriptine 32-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 22157006-2 2012 One of the CYP3A4 substrates is bromoergocryptine (BEC), a dopamine receptor agonist prescribed for the inhibition of prolactin secretion and treatment of Parkinson disease, type 2 diabetes, and several other pathological conditions. Bromocriptine 51-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 22178124-8 2012 It was found that bufalin, cinobufagin, and resibufogenin were novel CYP3A4 inducers. cinobufagin 27-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 22157006-3 2012 Here we present a 2.15 A crystal structure of the CYP3A4-BEC complex in which the drug, a type I heme ligand, is bound in a productive mode. Heme 97-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 22178124-8 2012 It was found that bufalin, cinobufagin, and resibufogenin were novel CYP3A4 inducers. bufogenin 44-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 22178124-9 2012 Among them, bufalin and cinobufagin significantly promoted the CYP3A4 enzyme activity, mRNA and protein levels, with the maximal induction challenging or exceeding that of the induction by rifampicin, indicating that they might play a critical role in CYP3A4 enzyme-inducing effects of SBP. bufalin 12-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 22178124-9 2012 Among them, bufalin and cinobufagin significantly promoted the CYP3A4 enzyme activity, mRNA and protein levels, with the maximal induction challenging or exceeding that of the induction by rifampicin, indicating that they might play a critical role in CYP3A4 enzyme-inducing effects of SBP. bufalin 12-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 252-258 22178124-9 2012 Among them, bufalin and cinobufagin significantly promoted the CYP3A4 enzyme activity, mRNA and protein levels, with the maximal induction challenging or exceeding that of the induction by rifampicin, indicating that they might play a critical role in CYP3A4 enzyme-inducing effects of SBP. cinobufagin 24-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 22178124-9 2012 Among them, bufalin and cinobufagin significantly promoted the CYP3A4 enzyme activity, mRNA and protein levels, with the maximal induction challenging or exceeding that of the induction by rifampicin, indicating that they might play a critical role in CYP3A4 enzyme-inducing effects of SBP. cinobufagin 24-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 252-258 22178124-9 2012 Among them, bufalin and cinobufagin significantly promoted the CYP3A4 enzyme activity, mRNA and protein levels, with the maximal induction challenging or exceeding that of the induction by rifampicin, indicating that they might play a critical role in CYP3A4 enzyme-inducing effects of SBP. Rifampin 189-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 21996064-7 2012 In addition, both dominant negative form and siRNA of HDAC1 could repress the CBZ-induced CYP3A4 expression. Carbamazepine 78-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 21993197-1 2012 The metabolic conversion of midazolam (MDZ) to its main metabolite 1"-hydroxy-midazolam (1-OH-MDZ) can be used as a probe drug for cytochrome P450 3A (CYP3A) activity. Midazolam 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-149 21993197-1 2012 The metabolic conversion of midazolam (MDZ) to its main metabolite 1"-hydroxy-midazolam (1-OH-MDZ) can be used as a probe drug for cytochrome P450 3A (CYP3A) activity. Midazolam 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-156 21996064-8 2012 These data, for the first time indicate that HDAC1, is required for the CBZ-induced CYP3A4 expression. Carbamazepine 72-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 21993197-1 2012 The metabolic conversion of midazolam (MDZ) to its main metabolite 1"-hydroxy-midazolam (1-OH-MDZ) can be used as a probe drug for cytochrome P450 3A (CYP3A) activity. Midazolam 39-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-149 22087535-0 2012 Comparative study of the affinity and metabolism of type I and type II binding quinoline carboxamide analogues by cytochrome P450 3A4. 2-quinolinecarboxamide 79-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-133 21993197-1 2012 The metabolic conversion of midazolam (MDZ) to its main metabolite 1"-hydroxy-midazolam (1-OH-MDZ) can be used as a probe drug for cytochrome P450 3A (CYP3A) activity. Midazolam 39-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-156 21993197-1 2012 The metabolic conversion of midazolam (MDZ) to its main metabolite 1"-hydroxy-midazolam (1-OH-MDZ) can be used as a probe drug for cytochrome P450 3A (CYP3A) activity. 1-hydroxymethylmidazolam 67-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-149 21993197-1 2012 The metabolic conversion of midazolam (MDZ) to its main metabolite 1"-hydroxy-midazolam (1-OH-MDZ) can be used as a probe drug for cytochrome P450 3A (CYP3A) activity. 1-hydroxymethylmidazolam 67-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-156 21993197-1 2012 The metabolic conversion of midazolam (MDZ) to its main metabolite 1"-hydroxy-midazolam (1-OH-MDZ) can be used as a probe drug for cytochrome P450 3A (CYP3A) activity. 1-hydroxymethylmidazolam 89-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-149 21993197-1 2012 The metabolic conversion of midazolam (MDZ) to its main metabolite 1"-hydroxy-midazolam (1-OH-MDZ) can be used as a probe drug for cytochrome P450 3A (CYP3A) activity. 1-hydroxymethylmidazolam 89-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-156 21996064-0 2012 Histone deacetylase 1 is required for Carbamazepine-induced CYP3A4 expression. Carbamazepine 38-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 21996064-3 2012 CBZ is mainly metabolized by cytochrome P450 (CYP) 3A4, a strong inducer of CYP3A4 as well, which in turn influences the pharmaceutical profiles of the co-administrated drugs. Carbamazepine 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-54 21996064-3 2012 CBZ is mainly metabolized by cytochrome P450 (CYP) 3A4, a strong inducer of CYP3A4 as well, which in turn influences the pharmaceutical profiles of the co-administrated drugs. Carbamazepine 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 21996064-4 2012 To date, little is known about the mechanisms underlying CBZ-induced CYP3A4 expression. Carbamazepine 57-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 21996064-5 2012 In this study, we explored the possible roles of Pregnane X receptor (PXR) and the histone deacetylase 1 (HDAC1) on the CBZ-induced CYP3A4 expression. Carbamazepine 120-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 21997754-5 2012 Our previous work with preliminary gas-phase quantum mechanics (QM)-derived atomic partial charges greatly improved the accuracy of docking studies of raloxifene to CYP3A4. Raloxifene Hydrochloride 151-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 21997754-7 2012 Our results indicate that the use of the atomic partial charges from the F-HM further improves the accuracy of docked predictions for raloxifene to CYP3A4. Raloxifene Hydrochloride 134-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 21997754-9 2012 Newly parameterized heme models are tested in implicit and explicitly solvated MD simulations in the absence and presence of enzyme structures, for CYP3A4, and appear to be stable on the nanosecond simulation timescale. Heme 20-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 22197672-0 2012 Prediction of sites of metabolism in a substrate molecule, instanced by carbamazepine oxidation by CYP3A4. Carbamazepine 72-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 22197672-10 2012 The experimentally known epoxidized sites of CBZ by CYP3A4 were successfully predicted as the most accessible sites to the heme iron that was judged from a numerical analysis of calculated DeltaG(binding) and the frequency of appearance. Carbamazepine 45-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 22197672-10 2012 The experimentally known epoxidized sites of CBZ by CYP3A4 were successfully predicted as the most accessible sites to the heme iron that was judged from a numerical analysis of calculated DeltaG(binding) and the frequency of appearance. Heme 123-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 22197672-10 2012 The experimentally known epoxidized sites of CBZ by CYP3A4 were successfully predicted as the most accessible sites to the heme iron that was judged from a numerical analysis of calculated DeltaG(binding) and the frequency of appearance. Iron 128-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 22291644-4 2011 Oxycodone (0.1, 1, and 10 muM) was incubated with hepatocytes for 4 h, and 1 muM oxycodone also with CYP3A inhibitor ketoconazole (1 muM). Oxycodone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 21840145-2 2012 VEN is also metabolized to N-desmetylvenlafaxine (NDV) via CYP3A4. n-desmetylvenlafaxine 27-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 21840145-2 2012 VEN is also metabolized to N-desmetylvenlafaxine (NDV) via CYP3A4. (2s,4s)-2-[(1r)-1-{[(2r)-2-Amino-2-Phenylacetyl]amino}-2-Oxoethyl]-5,5-Dimethyl-1,3-Thiazolidine-4-Carboxylic Acid 50-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 22291644-8 2011 A clear correlation between in vitro oxycodone clearance and CYP3A4 activity was observed. Oxycodone 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 22291644-11 2011 Moreover, CYP3A activity seems to be the major determinant in metabolic clearance of oxycodone regardless of age group or individual variability in hepatocyte batches. Oxycodone 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 22190251-9 2012 Drugs such as atorvastatin, which undergo presystemic intestinal metabolism via CYP3A, may show increased bioavailability, whereas those such as amoxicillin, which rely on transport mediators, may be decreased. Atorvastatin 14-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-85 23631285-6 2012 The mutations in other enzyme systems also play role in the etiopathogenesis of the irinotecan toxicity: CYP3A (cytochrome P-450), ABC family of transmembrane transporters (adenosine-triphosphate binding cassette). Irinotecan 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-110 22293086-1 2012 BACKGROUND: Rilpivirine and efavirenz share metabolic pathways (CYP3A), potentially leading to drug-drug interactions. Rilpivirine 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 22180548-8 2012 Drugs that induce or inhibit CYP3A4 may affect concentrations of telaprevir, resulting in reduced efficacy or increased concentrations of telaprevir (and an increased risk for adverse reactions). telaprevir 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 22180548-8 2012 Drugs that induce or inhibit CYP3A4 may affect concentrations of telaprevir, resulting in reduced efficacy or increased concentrations of telaprevir (and an increased risk for adverse reactions). telaprevir 138-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 22298448-3 2012 The enzymatic activity of CYP3A4 was estimated by determing the 6beta-hydroxytestosterone metabolized from testosterone performed on a liquid chromatography-tandem mass spectrometry (LC-MS/MS). 6 beta-hydroxytestosterone 64-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 22298448-3 2012 The enzymatic activity of CYP3A4 was estimated by determing the 6beta-hydroxytestosterone metabolized from testosterone performed on a liquid chromatography-tandem mass spectrometry (LC-MS/MS). Testosterone 77-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 22741198-2 2012 The activity of cytochrome P450 isoenzyme CYP3A4 was estimated by the ratio of 6-beta-hydroxycortisol and cortisol. 6 beta-hydroxycortisol 79-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 22293514-1 2012 The cytochrome P450 isoforms primarily involved in clobazam metabolism are CYP3A4 and 2C19. Clobazam 51-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 22293514-3 2012 Etravirine, a second-generation non-nucleoside reverse transcriptase inhibitor has been shown to induce CYP3A4, while inhibiting CYP2C9 and CYP2C19. etravirine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 22741198-2 2012 The activity of cytochrome P450 isoenzyme CYP3A4 was estimated by the ratio of 6-beta-hydroxycortisol and cortisol. Hydrocortisone 93-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 22687401-8 2012 Consequently, VDR ligand (1,25-dihydroxyvitamin D(3))-mediated inductions of CALUX and CYP3A4 mRNA were observed in the cells. Calcitriol 26-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 22382318-4 2012 Ethyl acetate extracts of the tomato juices moderately reduced residual activity of CYP3A4 testosterone 6beta-hydroxylation activity by 19.3-26.2% with 0-min preincubation. ethyl acetate 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 22382318-4 2012 Ethyl acetate extracts of the tomato juices moderately reduced residual activity of CYP3A4 testosterone 6beta-hydroxylation activity by 19.3-26.2% with 0-min preincubation. testosterone 6beta 91-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 22382318-6 2012 One juice extract (tomato juice C) showed irreversible dose- and preincubation time-dependent and partial nicotinamide adenine dinucleotide phosphate (NADPH)-dependent inhibition of CYP3A4 activity. juice 4-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 182-188 22382318-6 2012 One juice extract (tomato juice C) showed irreversible dose- and preincubation time-dependent and partial nicotinamide adenine dinucleotide phosphate (NADPH)-dependent inhibition of CYP3A4 activity. NADP 106-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 182-188 22382318-6 2012 One juice extract (tomato juice C) showed irreversible dose- and preincubation time-dependent and partial nicotinamide adenine dinucleotide phosphate (NADPH)-dependent inhibition of CYP3A4 activity. NADP 151-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 182-188 22053102-5 2012 As a cytochrome P450, 3A4 inducer, rifampin is thought to favourably alter the metabolism of endogenous steroids, thereby leading to an improvement in CSR manifestations. Steroids 104-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 5-25 22094027-0 2012 Dirlotapide as a model substrate to refine structure-based drug design strategies on CYP3A4-catalyzed metabolism. dirlotapide 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 22094027-2 2012 Herein, modeling studies with dirlotapide, a CYP3A4 substrate, indicated that a substantial conformational change of CYP3A4 was necessary to accommodate it within the active site cavity, which is in good agreement with a new published CYP3A4 ritonavir co-crystal structure. dirlotapide 30-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 22094027-2 2012 Herein, modeling studies with dirlotapide, a CYP3A4 substrate, indicated that a substantial conformational change of CYP3A4 was necessary to accommodate it within the active site cavity, which is in good agreement with a new published CYP3A4 ritonavir co-crystal structure. dirlotapide 30-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 22094027-2 2012 Herein, modeling studies with dirlotapide, a CYP3A4 substrate, indicated that a substantial conformational change of CYP3A4 was necessary to accommodate it within the active site cavity, which is in good agreement with a new published CYP3A4 ritonavir co-crystal structure. dirlotapide 30-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 22094027-2 2012 Herein, modeling studies with dirlotapide, a CYP3A4 substrate, indicated that a substantial conformational change of CYP3A4 was necessary to accommodate it within the active site cavity, which is in good agreement with a new published CYP3A4 ritonavir co-crystal structure. Ritonavir 242-251 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 22094027-2 2012 Herein, modeling studies with dirlotapide, a CYP3A4 substrate, indicated that a substantial conformational change of CYP3A4 was necessary to accommodate it within the active site cavity, which is in good agreement with a new published CYP3A4 ritonavir co-crystal structure. Ritonavir 242-251 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 22094027-2 2012 Herein, modeling studies with dirlotapide, a CYP3A4 substrate, indicated that a substantial conformational change of CYP3A4 was necessary to accommodate it within the active site cavity, which is in good agreement with a new published CYP3A4 ritonavir co-crystal structure. Ritonavir 242-251 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 21692828-12 2012 Bodyweight and age, along with the SNPs rs3814637 (in CYP2C19) and rs2242480 (in CYP3A4), significantly influenced R-warfarin clearance. Warfarin 117-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 21692828-13 2012 The R-warfarin clearance was estimated to be 0.125 l h-1 (95% confidence interval 0.115, 0.135) in a 70 kg individual aged 69.8 years with the wild-type CYP2C19 and CYP3A4 genotypes, and the volume of distribution was 10.9 l (95% confidence interval 8.63, 13.2). Warfarin 4-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 21594721-3 2012 The inductive effects of tanespimycin and 17-AG on CYP1A2, CYP2B6, and CYP3A4/5 were determined in cultured primary human hepatocytes. tanespimycin 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 21594721-4 2012 RESULTS: Tanespimycin did not inhibit the activities of CYP1A2, 2A6, 2B6, and 2E1 up to a concentration of 60 muM, while it moderately inhibited CYP3A4/5 and 2C19, and weakly inhibited CYP2C8, 2C9, and 2D6. tanespimycin 9-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 21594721-6 2012 17-AG moderately inhibited the activities of CYP3A4/5 and CYP2C19, but did not inhibit other CYPs up to a concentration of 30 muM. 17-AG 0-5 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 21594721-7 2012 The inhibition of CYP3A4/5 by 17-AG was not time-dependent. 17-AG 30-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 21594721-9 2012 CONCLUSIONS: Tanespimycin together with its active metabolite, 17-AG are moderate inhibitors of CYP3A4/5 and CYP2C19, but not inducers of CYPs. tanespimycin 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 21594721-9 2012 CONCLUSIONS: Tanespimycin together with its active metabolite, 17-AG are moderate inhibitors of CYP3A4/5 and CYP2C19, but not inducers of CYPs. 17-AG 63-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 21594721-10 2012 Therefore, co-administration of tanespimycin has the potential to increase the exposure of substrates of CYP2C19 and CYP3A4/5. tanespimycin 32-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 21890570-9 2012 It is hypothesized that warfarin and dapsone compete for binding on the CYP2C9 and CYP3A4 isoenzymes and therefore serum concentration of warfarin was elevated. Warfarin 24-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 22174351-0 2012 Lack of drug interaction between the migraine drug MAP0004 (orally inhaled dihydroergotamine) and a CYP3A4 inhibitor in humans. Dihydroergotamine 51-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 22174351-1 2012 BACKGROUND: Dihydroergotamine (DHE), a proven migraine treatment, currently has product labeling warning against concomitant use of CYP3A4 inhibitors because of potential drug interactions. Dihydroergotamine 12-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 22174351-1 2012 BACKGROUND: Dihydroergotamine (DHE), a proven migraine treatment, currently has product labeling warning against concomitant use of CYP3A4 inhibitors because of potential drug interactions. Dihydroergotamine 31-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 22174351-8 2012 CYP3A4 inhibition slowed elimination of the metabolite 8"-OH-DHE, but concentrations were too low to be pharmacologically relevant. 8"-oh-dhe 55-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22793052-5 2012 A three-dimensional aggregate culture of THLE-5b showed a higher expression level of liver-specific genes such as albumin, alpha1-antitrypsin, and CYP3A4, thus suggesting that THLE-5b possess the capability to differentiate into hepatocytes. thle 41-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 22793052-5 2012 A three-dimensional aggregate culture of THLE-5b showed a higher expression level of liver-specific genes such as albumin, alpha1-antitrypsin, and CYP3A4, thus suggesting that THLE-5b possess the capability to differentiate into hepatocytes. thle-5b 41-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 21890570-9 2012 It is hypothesized that warfarin and dapsone compete for binding on the CYP2C9 and CYP3A4 isoenzymes and therefore serum concentration of warfarin was elevated. Dapsone 37-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 21890570-9 2012 It is hypothesized that warfarin and dapsone compete for binding on the CYP2C9 and CYP3A4 isoenzymes and therefore serum concentration of warfarin was elevated. Warfarin 138-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 21834667-0 2012 Ochratoxin A induces CYP3A4, 2B6, 3A5, 2C9, 1A1, and CYP1A2 gene expression in primary cultured human hepatocytes: a possible activation of nuclear receptors. ochratoxin A 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 22148986-7 2012 CYP3A4 inactivates methadone, meperidine, and buprenorphine. Methadone 19-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22148986-7 2012 CYP3A4 inactivates methadone, meperidine, and buprenorphine. Meperidine 30-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22148986-7 2012 CYP3A4 inactivates methadone, meperidine, and buprenorphine. Buprenorphine 46-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21953914-0 2012 CYP3A4-mediated lopinavir bioactivation and its inhibition by ritonavir. Lopinavir 16-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21989950-8 2012 Incubation of brivanib with human cDNA-expressed P450 enzymes and with HLM in the presence of selective chemical inhibitors and monoclonal P450 antibodies demonstrated that CYP1A2 and CYP3A4 were the major contributors for the formation of M7. brivanib 14-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 22076448-0 2012 Polycyclic aromatic hydrocarbons activate CYP3A4 gene transcription through human pregnane X receptor. Polycyclic Aromatic Hydrocarbons 0-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21953914-0 2012 CYP3A4-mediated lopinavir bioactivation and its inhibition by ritonavir. Ritonavir 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22076448-3 2012 AhR activators, polycyclic aromatic hydrocarbons (PAHs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased CYP3A4 reporter activity and CYP3A4 mRNA expression in HepG2 cells. Polycyclic Aromatic Hydrocarbons 16-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 22076448-3 2012 AhR activators, polycyclic aromatic hydrocarbons (PAHs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased CYP3A4 reporter activity and CYP3A4 mRNA expression in HepG2 cells. Polycyclic Aromatic Hydrocarbons 16-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 22076448-6 2012 The CYP3A4 reporter activity enhanced by overexpression of human PXR was further increased by treatment with PAHs and TCDD as well as by treatment with rifampicin. Polychlorinated Dibenzodioxins 118-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 22076448-3 2012 AhR activators, polycyclic aromatic hydrocarbons (PAHs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased CYP3A4 reporter activity and CYP3A4 mRNA expression in HepG2 cells. Polycyclic Aromatic Hydrocarbons 50-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 22076448-3 2012 AhR activators, polycyclic aromatic hydrocarbons (PAHs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased CYP3A4 reporter activity and CYP3A4 mRNA expression in HepG2 cells. Polycyclic Aromatic Hydrocarbons 50-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 22076448-3 2012 AhR activators, polycyclic aromatic hydrocarbons (PAHs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased CYP3A4 reporter activity and CYP3A4 mRNA expression in HepG2 cells. Polychlorinated Dibenzodioxins 60-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 22076448-6 2012 The CYP3A4 reporter activity enhanced by overexpression of human PXR was further increased by treatment with PAHs and TCDD as well as by treatment with rifampicin. Rifampin 152-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 22076448-3 2012 AhR activators, polycyclic aromatic hydrocarbons (PAHs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased CYP3A4 reporter activity and CYP3A4 mRNA expression in HepG2 cells. Polychlorinated Dibenzodioxins 60-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 22076448-7 2012 These results suggest that PAHs contained in cigarette smoke induce CYP3A4 in human liver. Polycyclic Aromatic Hydrocarbons 27-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 22076448-3 2012 AhR activators, polycyclic aromatic hydrocarbons (PAHs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased CYP3A4 reporter activity and CYP3A4 mRNA expression in HepG2 cells. Polychlorinated Dibenzodioxins 97-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 22076448-3 2012 AhR activators, polycyclic aromatic hydrocarbons (PAHs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased CYP3A4 reporter activity and CYP3A4 mRNA expression in HepG2 cells. Polychlorinated Dibenzodioxins 97-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 22333269-0 2012 Lower expression of HNF4alpha and PGC1alpha might impair rifampicin-mediated CYP3A4 induction under conditions where PXR is overexpressed in human fetal liver cells. Rifampin 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 22076448-6 2012 The CYP3A4 reporter activity enhanced by overexpression of human PXR was further increased by treatment with PAHs and TCDD as well as by treatment with rifampicin. Polycyclic Aromatic Hydrocarbons 109-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 22277676-1 2012 Distinctive response patterns of CYP3A4 and CYP3A7 to cobalt chloride (CoCl(2)) in human fetal liver (HFL) cells were observed and compared with those under hypoxic conditions. cobaltous chloride 54-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 22277676-1 2012 Distinctive response patterns of CYP3A4 and CYP3A7 to cobalt chloride (CoCl(2)) in human fetal liver (HFL) cells were observed and compared with those under hypoxic conditions. cobaltous chloride 71-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 22333269-2 2012 CYP3A4 was induced by rifampicin (RIF), mifepristone (RU486), clotrimazole (CTZ), and dexamethasone (DEX) in HepG2 cells, while these PXR ligands with the exception of DEX did not induce CYP3A4 mRNA expression in HFL cells. Rifampin 22-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22277676-2 2012 The expression levels of CYP3A4 and CYP3A7 mRNAs were decreased by CoCl(2) and hypoxia, although significance could not be determined in HFL cells cultured under 3% O(2). cobaltous chloride 67-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 22333269-2 2012 CYP3A4 was induced by rifampicin (RIF), mifepristone (RU486), clotrimazole (CTZ), and dexamethasone (DEX) in HepG2 cells, while these PXR ligands with the exception of DEX did not induce CYP3A4 mRNA expression in HFL cells. Rifampin 34-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22333269-2 2012 CYP3A4 was induced by rifampicin (RIF), mifepristone (RU486), clotrimazole (CTZ), and dexamethasone (DEX) in HepG2 cells, while these PXR ligands with the exception of DEX did not induce CYP3A4 mRNA expression in HFL cells. Mifepristone 40-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22277676-2 2012 The expression levels of CYP3A4 and CYP3A7 mRNAs were decreased by CoCl(2) and hypoxia, although significance could not be determined in HFL cells cultured under 3% O(2). o(2) 165-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 22277676-4 2012 Transcriptional activities of CYP3A4 and CYP3A7 were not altered by 3% O(2) when reporter plasmids containing the promoter region ranging up to about 10 kb and 12 kb upstream, respectively, were transfected into HFL cells, although the activity was significantly suppressed by CoCl(2). cobaltous chloride 277-284 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 22333269-2 2012 CYP3A4 was induced by rifampicin (RIF), mifepristone (RU486), clotrimazole (CTZ), and dexamethasone (DEX) in HepG2 cells, while these PXR ligands with the exception of DEX did not induce CYP3A4 mRNA expression in HFL cells. Mifepristone 54-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22333269-2 2012 CYP3A4 was induced by rifampicin (RIF), mifepristone (RU486), clotrimazole (CTZ), and dexamethasone (DEX) in HepG2 cells, while these PXR ligands with the exception of DEX did not induce CYP3A4 mRNA expression in HFL cells. Clotrimazole 62-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22333269-2 2012 CYP3A4 was induced by rifampicin (RIF), mifepristone (RU486), clotrimazole (CTZ), and dexamethasone (DEX) in HepG2 cells, while these PXR ligands with the exception of DEX did not induce CYP3A4 mRNA expression in HFL cells. Clotrimazole 76-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22333269-2 2012 CYP3A4 was induced by rifampicin (RIF), mifepristone (RU486), clotrimazole (CTZ), and dexamethasone (DEX) in HepG2 cells, while these PXR ligands with the exception of DEX did not induce CYP3A4 mRNA expression in HFL cells. Dexamethasone 86-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22333269-2 2012 CYP3A4 was induced by rifampicin (RIF), mifepristone (RU486), clotrimazole (CTZ), and dexamethasone (DEX) in HepG2 cells, while these PXR ligands with the exception of DEX did not induce CYP3A4 mRNA expression in HFL cells. Dexamethasone 101-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22333269-2 2012 CYP3A4 was induced by rifampicin (RIF), mifepristone (RU486), clotrimazole (CTZ), and dexamethasone (DEX) in HepG2 cells, while these PXR ligands with the exception of DEX did not induce CYP3A4 mRNA expression in HFL cells. Dexamethasone 101-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 22333269-2 2012 CYP3A4 was induced by rifampicin (RIF), mifepristone (RU486), clotrimazole (CTZ), and dexamethasone (DEX) in HepG2 cells, while these PXR ligands with the exception of DEX did not induce CYP3A4 mRNA expression in HFL cells. Dexamethasone 168-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22333269-10 2012 These results suggested that lower expression of HNF4alpha and PGC1alpha may impair RIF-mediated CYP3A4 induction under conditions of PXR overexpression in HFL cells. Rifampin 84-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 22673009-2 2012 In the fetal hepatocytes, betamethasone and dexamethasone (DEX) markedly enhanced the expression levels of CYP3A4 and CYP3A7 mRNAs and slightly increased the expression level of CYP3A5 mRNA. Betamethasone 26-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 22673009-2 2012 In the fetal hepatocytes, betamethasone and dexamethasone (DEX) markedly enhanced the expression levels of CYP3A4 and CYP3A7 mRNAs and slightly increased the expression level of CYP3A5 mRNA. Dexamethasone 44-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 22785256-5 2012 Cluster of differentiation (CD) 86 and CD54 expression levels on THP-1 cells were upregulated by treatment with albendazole and amiodarone (AMD), respectively, in the presence of CYP3A4. Albendazole 112-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 22673009-2 2012 In the fetal hepatocytes, betamethasone and dexamethasone (DEX) markedly enhanced the expression levels of CYP3A4 and CYP3A7 mRNAs and slightly increased the expression level of CYP3A5 mRNA. Dexamethasone 59-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 22673009-4 2012 Human glucocorticoid receptor (GR)-small interfering RNA clearly attenuated the expression level of GR mRNA, and diminished the DEX-stimulated CYP3A4, CYP3A5 and CYP3A7 expression in HFL cells. Dexamethasone 128-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 22785256-5 2012 Cluster of differentiation (CD) 86 and CD54 expression levels on THP-1 cells were upregulated by treatment with albendazole and amiodarone (AMD), respectively, in the presence of CYP3A4. Amiodarone 128-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 22785256-6 2012 Additionally, N-desethylamiodarone (DEA), a major metabolite of AMD, upregulated the CD54 expression of THP-1 cells with CYP3A4. desethylamiodarone 14-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 22785256-6 2012 Additionally, N-desethylamiodarone (DEA), a major metabolite of AMD, upregulated the CD54 expression of THP-1 cells with CYP3A4. desethylamiodarone 36-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 22785256-7 2012 The release of interleukin (IL)-8 and tumor necrosis factor (TNF) alpha from THP-1 cells was significantly increased by the treatment of AMD or DEA with CYP3A4. desethylamiodarone 144-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 21739267-5 2012 Coadministration of fluvoxamine, a less potent CYP3A4 inhibitor, decreased the CL/F of aripiprazole by 39% in CYP2D6 EMs and 40% in IMs, indicating the same inhibitory effect on CYP enzymes, regardless of the CYP2D6 genotype. Fluvoxamine 20-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 21739267-5 2012 Coadministration of fluvoxamine, a less potent CYP3A4 inhibitor, decreased the CL/F of aripiprazole by 39% in CYP2D6 EMs and 40% in IMs, indicating the same inhibitory effect on CYP enzymes, regardless of the CYP2D6 genotype. Aripiprazole 87-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 21739267-6 2012 Percent contribution of CYP2D6 to total CL/F (CYP2D6 plus CYP3A4) of aripiprazole estimated as a reduced percentage of CL/F by CYP enzyme inhibition was 62% for CYP2D6 EMs and 24% for IMs in paroxetine coadministration, and 40% for CYP2D6 EMs and 18% for IMs in fluvoxamine coadministration. Aripiprazole 69-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 21906676-1 2012 Saquinavir is an anti-retroviral drug with very low oral bioavailability (e.g. 0.7-4.0%) due to its affinity toward efflux transporters (P-gp) and metabolic enzymes (CYP3A4). Saquinavir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-172 22005822-2 2012 We have previously shown that AKI decreases midazolam metabolism, a substrate of the cytochrome P450 3A (CYP3A) enzymes and our primary aim was to determine if this effect is dependent on the severity of AKI. Midazolam 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-103 22176629-7 2012 significantly inhibited CYP3A4-mediated metabolism of midazolam (three to sixfold increase in AUC). Midazolam 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 22176629-8 2012 CONCLUSION: These findings support the classification of posaconazole as a strong CYP3A4 inhibitor. posaconazole 57-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 22176629-9 2012 Simvastatin, or other statins predominantly metabolized by CYP3A4, should not be co-administered with posaconazole. Simvastatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 22005822-2 2012 We have previously shown that AKI decreases midazolam metabolism, a substrate of the cytochrome P450 3A (CYP3A) enzymes and our primary aim was to determine if this effect is dependent on the severity of AKI. Midazolam 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-110 22375877-2 2012 In this study, we examined the inhibitory potentials of capsaicin and dihydrocapsaicin against CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4/5 activities in human liver microsomes. Capsaicin 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 22365086-3 2012 The interaction of thioxanthones with cytochrome P450 3A4 (CYP3A4) together with the prediction of their binding conformations and metabolism sites was also investigated. thioxanthone 19-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-57 22375877-2 2012 In this study, we examined the inhibitory potentials of capsaicin and dihydrocapsaicin against CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4/5 activities in human liver microsomes. dihydrocapsaicin 70-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 22375877-6 2012 Time-dependent inhibition of CYP3A4/5 by capsaicin was found. Capsaicin 41-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 22188805-4 2012 The identities of (+)-terpinen-4-ol metabolites were determined through the relative abundance of mass fragments and retention times on GC-MS. Of 11 recombinant human P450 enzymes tested, CYP1A2, CYP2A6, and CYP3A4 were found to catalyze the oxidation of (+)-terpinen-4-ol. terpinenol-4 18-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 208-214 22188805-5 2012 Based on several lines of evidence, CYP2A6 and CYP3A4 were determined to be major enzymes involved in the oxidation of (+)-terpinen-4-ol by human liver microsomes. terpinenol-4 119-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 22188805-6 2012 First, of the 11 recombinant human P450 enzymes tested, CYP1A2, CYP2A6 and CYP3A4 catalyzed oxidation of (+)-terpinen-4-ol. terpinenol-4 105-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 22579001-9 2012 CYP3A4 and CYP2C19 were involved in indapamide metabolism in human live microsomes. Indapamide 36-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22365086-3 2012 The interaction of thioxanthones with cytochrome P450 3A4 (CYP3A4) together with the prediction of their binding conformations and metabolism sites was also investigated. thioxanthone 19-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 22365086-7 2012 Finally, the in silico prediction of the most probable metabolism sites and docking studies of thioxanthones on CYP3A4 binding site were investigated. thioxanthone 95-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 23106957-9 2012 This seems to indicate important contributions of CYP1A1 and CYP3A7 as compared to CYP1A2 and CYP3A4, respectively, because furafylline and ketokonazole are stronger inhibitors of CYP1A2 and CYP3A4 than CYP1A1 and CYP3A7, respectively. ketokonazole 140-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 23106957-9 2012 This seems to indicate important contributions of CYP1A1 and CYP3A7 as compared to CYP1A2 and CYP3A4, respectively, because furafylline and ketokonazole are stronger inhibitors of CYP1A2 and CYP3A4 than CYP1A1 and CYP3A7, respectively. furafylline 124-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 23106957-9 2012 This seems to indicate important contributions of CYP1A1 and CYP3A7 as compared to CYP1A2 and CYP3A4, respectively, because furafylline and ketokonazole are stronger inhibitors of CYP1A2 and CYP3A4 than CYP1A1 and CYP3A7, respectively. furafylline 124-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-197 23106957-9 2012 This seems to indicate important contributions of CYP1A1 and CYP3A7 as compared to CYP1A2 and CYP3A4, respectively, because furafylline and ketokonazole are stronger inhibitors of CYP1A2 and CYP3A4 than CYP1A1 and CYP3A7, respectively. ketokonazole 140-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-197 23106957-10 2012 Interestingly, alpha-naphathoflavone enhanced the metabolic activity in liver microsomes due to its activator effect on CYP3A4. alpha-naphathoflavone 15-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 22363234-3 2012 In this study, we determined whether fucoxanthin could overcome drug resistance through attenuation of rifampin-induced CYP3A4 and MDR1 gene expression by PXR-mediated pathways in HepG2 hepatoma cells. fucoxanthin 37-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 22363234-0 2012 Fucoxanthin attenuates rifampin-induced cytochrome P450 3A4 (CYP3A4) and multiple drug resistance 1 (MDR1) gene expression through pregnane X receptor (PXR)-mediated pathways in human hepatoma HepG2 and colon adenocarcinoma LS174T cells. fucoxanthin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-59 22363234-3 2012 In this study, we determined whether fucoxanthin could overcome drug resistance through attenuation of rifampin-induced CYP3A4 and MDR1 gene expression by PXR-mediated pathways in HepG2 hepatoma cells. Rifampin 103-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 22363234-0 2012 Fucoxanthin attenuates rifampin-induced cytochrome P450 3A4 (CYP3A4) and multiple drug resistance 1 (MDR1) gene expression through pregnane X receptor (PXR)-mediated pathways in human hepatoma HepG2 and colon adenocarcinoma LS174T cells. fucoxanthin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 22363234-0 2012 Fucoxanthin attenuates rifampin-induced cytochrome P450 3A4 (CYP3A4) and multiple drug resistance 1 (MDR1) gene expression through pregnane X receptor (PXR)-mediated pathways in human hepatoma HepG2 and colon adenocarcinoma LS174T cells. Rifampin 23-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-59 22363234-4 2012 We found that fucoxanthin (1-10 muM) significantly attenuated rifampin (20 muM)-induced CYP3A4, MDR1 mRNA and CYP3A4 protein expression at 24 h of incubation. fucoxanthin 14-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 22363234-0 2012 Fucoxanthin attenuates rifampin-induced cytochrome P450 3A4 (CYP3A4) and multiple drug resistance 1 (MDR1) gene expression through pregnane X receptor (PXR)-mediated pathways in human hepatoma HepG2 and colon adenocarcinoma LS174T cells. Rifampin 23-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 22363234-4 2012 We found that fucoxanthin (1-10 muM) significantly attenuated rifampin (20 muM)-induced CYP3A4, MDR1 mRNA and CYP3A4 protein expression at 24 h of incubation. fucoxanthin 14-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 22363234-4 2012 We found that fucoxanthin (1-10 muM) significantly attenuated rifampin (20 muM)-induced CYP3A4, MDR1 mRNA and CYP3A4 protein expression at 24 h of incubation. Rifampin 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 22363234-4 2012 We found that fucoxanthin (1-10 muM) significantly attenuated rifampin (20 muM)-induced CYP3A4, MDR1 mRNA and CYP3A4 protein expression at 24 h of incubation. Rifampin 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 22363234-5 2012 Mechanistically, fucoxanthin strongly attenuated the PXR-mediated CYP3A4 promoter activity in HepG2 cells. fucoxanthin 17-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 22363234-6 2012 In addition, fucoxanthin attenuated constitutive androstane receptor (CAR)- and rPXR-mediated CYP3A4 promoter activity in this cell line. fucoxanthin 13-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 22363234-8 2012 Thus, fucoxanthin can decrease rifampin-induced CYP3A4 and MDR1 expression through attenuation of PXR-mediated CYP3A4 promoter activation and interaction between PXR and co-activator. fucoxanthin 6-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 22363234-8 2012 Thus, fucoxanthin can decrease rifampin-induced CYP3A4 and MDR1 expression through attenuation of PXR-mediated CYP3A4 promoter activation and interaction between PXR and co-activator. fucoxanthin 6-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 22363234-8 2012 Thus, fucoxanthin can decrease rifampin-induced CYP3A4 and MDR1 expression through attenuation of PXR-mediated CYP3A4 promoter activation and interaction between PXR and co-activator. Rifampin 31-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 22363234-8 2012 Thus, fucoxanthin can decrease rifampin-induced CYP3A4 and MDR1 expression through attenuation of PXR-mediated CYP3A4 promoter activation and interaction between PXR and co-activator. Rifampin 31-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 23032911-7 2012 Simvastatin is a substrate of CYP3A4 enzyme. Simvastatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 23032911-8 2012 Clinical and pharmacological data, available in the published literature, allow the assumption that simvastatin may induce CYP3A4 and result in increased hepatoxicity of paracetamol. Simvastatin 100-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 21998292-9 2012 Quantification of the transcripts by RNA-Seq and real time quantitative PCR revealed that the CYP3A4 transcript with shorter 3"-UTR was preferentially expressed in developed livers, differentiated hepatocytes, and in rifampicin- and phenobarbital-induced hepatocytes. Rifampin 217-227 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 21998292-9 2012 Quantification of the transcripts by RNA-Seq and real time quantitative PCR revealed that the CYP3A4 transcript with shorter 3"-UTR was preferentially expressed in developed livers, differentiated hepatocytes, and in rifampicin- and phenobarbital-induced hepatocytes. Phenobarbital 233-246 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 23226064-4 2012 Overall, the level of evidence linking genetic variability (CYP2D6 and CYP3A4) to oxycodone response and phenotype (altered biotransformation of oxycodone into oxymorphone and overall clearance of oxycodone and oxymorphone) is strong; however, there has been no randomized clinical trial on the benefits of genetic testing prior to oxycodone therapy. Oxycodone 145-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 22108237-9 2012 RESULTS: In analyses, which adjusted for race and other clinical factors, we replicated the association of tacrolimus blood concentration to dose ratio with CYP3A5 rs776746 (P=7.15x10), and identified associations with nine variants in linkage disequilibrium with rs776746, including eight CYP3A4 variants. Tacrolimus 107-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 290-296 22912565-8 2012 Based on additional literature data on in vitro drug metabolism and inhibition potency, loratadine and simvastatin and tegaserod and promethazine were predicted to have a strong DDI through the CYP3A4 and CYP2D6 enzymes, respectively. Loratadine 88-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 23226064-4 2012 Overall, the level of evidence linking genetic variability (CYP2D6 and CYP3A4) to oxycodone response and phenotype (altered biotransformation of oxycodone into oxymorphone and overall clearance of oxycodone and oxymorphone) is strong; however, there has been no randomized clinical trial on the benefits of genetic testing prior to oxycodone therapy. Oxycodone 82-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 23226064-4 2012 Overall, the level of evidence linking genetic variability (CYP2D6 and CYP3A4) to oxycodone response and phenotype (altered biotransformation of oxycodone into oxymorphone and overall clearance of oxycodone and oxymorphone) is strong; however, there has been no randomized clinical trial on the benefits of genetic testing prior to oxycodone therapy. Oxycodone 145-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 23226064-4 2012 Overall, the level of evidence linking genetic variability (CYP2D6 and CYP3A4) to oxycodone response and phenotype (altered biotransformation of oxycodone into oxymorphone and overall clearance of oxycodone and oxymorphone) is strong; however, there has been no randomized clinical trial on the benefits of genetic testing prior to oxycodone therapy. Oxycodone 145-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 23406770-6 2012 CONCLUSION: The obtained results suggest that the tested phenothiazines may stimulate their own metabolism by inducing CYP1A2, CYP3A4 and CYP2C19 isoforms. Phenothiazines 57-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 22912565-8 2012 Based on additional literature data on in vitro drug metabolism and inhibition potency, loratadine and simvastatin and tegaserod and promethazine were predicted to have a strong DDI through the CYP3A4 and CYP2D6 enzymes, respectively. Simvastatin 103-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 22912565-8 2012 Based on additional literature data on in vitro drug metabolism and inhibition potency, loratadine and simvastatin and tegaserod and promethazine were predicted to have a strong DDI through the CYP3A4 and CYP2D6 enzymes, respectively. tegaserod 119-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 22912565-8 2012 Based on additional literature data on in vitro drug metabolism and inhibition potency, loratadine and simvastatin and tegaserod and promethazine were predicted to have a strong DDI through the CYP3A4 and CYP2D6 enzymes, respectively. Promethazine 133-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 23272261-10 2012 In this condition, the effect of BZL on P-gp, MRP2, CYP3A4, and GSTpi protein up-regulation was completely abolished. benzonidazole 33-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 23272261-6 2012 CYP3A4 and GST activities were evaluated through their abilities to convert proluciferin into luciferin and 1-chloro-2,4-dinitrobenzene into DNP-SG, respectively. proluciferin 76-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22984610-10 2012 Astemizole inhibited basal and calcitriol-induced CYP24A1 and CYP3A4 mRNA expression (cytochromes involved in calcitriol and astemizole degradation) in breast and hepatoma cancer cells, respectively, while upregulated vitamin D receptor (VDR) expression. Astemizole 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 23272261-6 2012 CYP3A4 and GST activities were evaluated through their abilities to convert proluciferin into luciferin and 1-chloro-2,4-dinitrobenzene into DNP-SG, respectively. D-luciferin 79-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23272261-6 2012 CYP3A4 and GST activities were evaluated through their abilities to convert proluciferin into luciferin and 1-chloro-2,4-dinitrobenzene into DNP-SG, respectively. Dinitrochlorobenzene 108-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23272261-6 2012 CYP3A4 and GST activities were evaluated through their abilities to convert proluciferin into luciferin and 1-chloro-2,4-dinitrobenzene into DNP-SG, respectively. 2,4-Dinitrophenol 141-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 23272261-7 2012 BZL (200 microM) increased the expression (protein and mRNA) of P-gp, MRP2, CYP3A4, and GSTpi class. benzonidazole 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 23077486-7 2012 Rs2242480 located in the CYP3A4 was associated with a different distribution of the UKU neurologic scores through time (permutated p = 0.047) along with a trend for a different haloperidol plasma levels (lower in CC subjects). Haloperidol 177-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 22984610-10 2012 Astemizole inhibited basal and calcitriol-induced CYP24A1 and CYP3A4 mRNA expression (cytochromes involved in calcitriol and astemizole degradation) in breast and hepatoma cancer cells, respectively, while upregulated vitamin D receptor (VDR) expression. Calcitriol 31-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22984610-10 2012 Astemizole inhibited basal and calcitriol-induced CYP24A1 and CYP3A4 mRNA expression (cytochromes involved in calcitriol and astemizole degradation) in breast and hepatoma cancer cells, respectively, while upregulated vitamin D receptor (VDR) expression. Calcitriol 110-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22984610-10 2012 Astemizole inhibited basal and calcitriol-induced CYP24A1 and CYP3A4 mRNA expression (cytochromes involved in calcitriol and astemizole degradation) in breast and hepatoma cancer cells, respectively, while upregulated vitamin D receptor (VDR) expression. Astemizole 125-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 22719896-4 2012 Surprisingly, both mutants, Y181D and A287P in POR completely inhibited the CYP3A4 activity with testosterone, while the catalytic activity of CYP2B6 with bupropion was reduced to approximately ~70% of wild-type activity by Y181D and A287P mutations. Testosterone 97-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 22778656-2 2012 Multi-walled carbon nanotubes were functionalized with three different cytochrome P450 isoforms (CYP1A2, CYP2B6, and CYP3A4). Carbon 13-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 22864345-1 2012 Vitamin K2 is a ligand for a nuclear receptor, steroid and xenobiotic receptor (SXR), that induces the gene expressions of CYP3A4. Vitamin K 2 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 22310591-1 2012 BACKGROUND: Tacrolimus is a substrate of cytochrome P450 3A (CYP3A) and P-glycoprotein (P-gp), encoded by the CYP3A and ATP-binding cassette subfamily B member 1 (ABCB1) genes, respectively. Tacrolimus 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-59 22310591-1 2012 BACKGROUND: Tacrolimus is a substrate of cytochrome P450 3A (CYP3A) and P-glycoprotein (P-gp), encoded by the CYP3A and ATP-binding cassette subfamily B member 1 (ABCB1) genes, respectively. Tacrolimus 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-66 22310591-1 2012 BACKGROUND: Tacrolimus is a substrate of cytochrome P450 3A (CYP3A) and P-glycoprotein (P-gp), encoded by the CYP3A and ATP-binding cassette subfamily B member 1 (ABCB1) genes, respectively. Tacrolimus 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-115 22310591-2 2012 This study was aimed to investigate the impact of CYP3A and ABCB1 polymorphisms on the tacrolimus pharmacokinetics and clinical outcomes in Korean renal transplant recipients. Tacrolimus 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 22094953-1 2011 BACKGROUNDS: Sirolimus (SRL) absorption and metabolism are affected by p-glycoprotein-mediated transport and CYP3A enzyme activity, which are further under the influences of cytokine concentrations. Sirolimus 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-114 22741471-6 2012 CONCLUSION: The effects of alpha-GL and beta-GL on the expression of MDR1 mRNA and CYP3A mRNA showed the same trend. alpha-gl 27-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 22741471-6 2012 CONCLUSION: The effects of alpha-GL and beta-GL on the expression of MDR1 mRNA and CYP3A mRNA showed the same trend. beta-gl 40-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 21992114-0 2011 The structural basis for homotropic and heterotropic cooperativity of midazolam metabolism by human cytochrome P450 3A4. Midazolam 70-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-119 21992114-4 2011 To unravel the structural basis of MDZ cooperativity, we probed MDZ and CBZ bound to CYP3A4 using longitudinal T(1) nuclear magnetic resonance (NMR) relaxation and molecular docking with AutoDock 4.2. Carbamazepine 72-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 21992114-6 2011 These simulations revealed that either two MDZ molecules or an MDZ molecule and a CBZ molecule assume a stacked configuration within the CYP3A4 active site. Midazolam 43-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 21992114-6 2011 These simulations revealed that either two MDZ molecules or an MDZ molecule and a CBZ molecule assume a stacked configuration within the CYP3A4 active site. Midazolam 63-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 21992114-6 2011 These simulations revealed that either two MDZ molecules or an MDZ molecule and a CBZ molecule assume a stacked configuration within the CYP3A4 active site. Carbamazepine 82-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 21682753-0 2011 Differential effects of ethanol on spectral binding and inhibition of cytochrome P450 3A4 with eight protease inhibitors antiretroviral drugs. Ethanol 24-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-89 22178823-6 2011 CONCLUSION: It is of important clinical significance in individualized warfarin therapy to systematically study distribution of mutation frequencies at 12 polymorphisms loci in 4 genes including CYP2C9, CYP3A4 , VKORC1 and GGCX related to warfarin pharmacodynamics and pharmacokinetics in the Chinese Han population receiving valve replacement. Warfarin 71-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 205-211 22178823-6 2011 CONCLUSION: It is of important clinical significance in individualized warfarin therapy to systematically study distribution of mutation frequencies at 12 polymorphisms loci in 4 genes including CYP2C9, CYP3A4 , VKORC1 and GGCX related to warfarin pharmacodynamics and pharmacokinetics in the Chinese Han population receiving valve replacement. Warfarin 242-250 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 205-211 21682753-12 2011 CONCLUSIONS: Overall, our results suggest that ethanol differentially alters the binding and inhibition of CYP3A4 with the PIs that have different physicochemical properties. Ethanol 47-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 21682753-2 2011 CYP3A4 induction by ethanol and its impact on drug metabolism and toxicity is known. Ethanol 20-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21682753-12 2011 CONCLUSIONS: Overall, our results suggest that ethanol differentially alters the binding and inhibition of CYP3A4 with the PIs that have different physicochemical properties. Monothiopyrophosphoric acid 123-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 21682753-3 2011 However, CYP3A4-ethanol physical interaction and its impact on drug binding, inhibition, or metabolism is not known, except that we have recently shown that ethanol facilitates the binding of a protease inhibitor (PI), nelfinavir, with CYP3A4. Ethanol 16-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 21682753-3 2011 However, CYP3A4-ethanol physical interaction and its impact on drug binding, inhibition, or metabolism is not known, except that we have recently shown that ethanol facilitates the binding of a protease inhibitor (PI), nelfinavir, with CYP3A4. Ethanol 157-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 21682753-3 2011 However, CYP3A4-ethanol physical interaction and its impact on drug binding, inhibition, or metabolism is not known, except that we have recently shown that ethanol facilitates the binding of a protease inhibitor (PI), nelfinavir, with CYP3A4. Ethanol 157-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 236-242 21682753-3 2011 However, CYP3A4-ethanol physical interaction and its impact on drug binding, inhibition, or metabolism is not known, except that we have recently shown that ethanol facilitates the binding of a protease inhibitor (PI), nelfinavir, with CYP3A4. Nelfinavir 219-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 21682753-3 2011 However, CYP3A4-ethanol physical interaction and its impact on drug binding, inhibition, or metabolism is not known, except that we have recently shown that ethanol facilitates the binding of a protease inhibitor (PI), nelfinavir, with CYP3A4. Nelfinavir 219-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 236-242 21682753-4 2011 The current study was designed to examine the effect of ethanol on spectral binding and inhibition of CYP3A4 with all currently used PIs that differ in physicochemical properties. Ethanol 56-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 21682753-4 2011 The current study was designed to examine the effect of ethanol on spectral binding and inhibition of CYP3A4 with all currently used PIs that differ in physicochemical properties. Monothiopyrophosphoric acid 133-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 21682753-6 2011 We also performed CYP3A4 inhibition using 7-benzyloxy-4-trifluoromethylcoumarin substrate and NADPH at varying concentrations of PIs and ethanol. 7-benzyloxy-4-trifluoromethylcoumarin 42-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 21682753-6 2011 We also performed CYP3A4 inhibition using 7-benzyloxy-4-trifluoromethylcoumarin substrate and NADPH at varying concentrations of PIs and ethanol. Monothiopyrophosphoric acid 129-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 21856291-6 2011 Luciferase assay using a reporter plasmid containing CYP3A4 direct repeat 3 and everted repeat 6 motifs revealed that 25-deacetylrifamycins have lesser potency to transactivate CYP3A4 compared with the parent drugs. 25-deacetylrifamycins 118-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 22128044-6 2011 Saquinavir, therapeutically boosted with the potent CYP3A4 inhibitor ritonavir, was the only PI shown to be associated with significant QT interval prolongation in studies with healthy volunteers. Saquinavir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 22128044-6 2011 Saquinavir, therapeutically boosted with the potent CYP3A4 inhibitor ritonavir, was the only PI shown to be associated with significant QT interval prolongation in studies with healthy volunteers. Ritonavir 69-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 21856291-6 2011 Luciferase assay using a reporter plasmid containing CYP3A4 direct repeat 3 and everted repeat 6 motifs revealed that 25-deacetylrifamycins have lesser potency to transactivate CYP3A4 compared with the parent drugs. 25-deacetylrifamycins 118-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 21856291-7 2011 Supporting these results, HepG2 cells infected with a recombinant adenovirus expressing human AADAC showed low cytotoxicity and induction potency of CYP3A4 by rifamycins. Rifamycins 159-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 21856291-8 2011 In addition, CYP3A4 induction in human hepatocytes by rifamycins was increased by transfecting siRNA for human AADAC. Rifamycins 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 21920351-0 2011 Metformin suppresses pregnane X receptor (PXR)-regulated transactivation of CYP3A4 gene. Metformin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 21968951-0 2011 Impact of plasma and intracellular exposure and CYP3A4, CYP3A5, and ABCB1 genetic polymorphisms on vincristine-induced neurotoxicity. Vincristine 99-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 21920351-4 2011 In this study, we hypothesize that metformin suppresses the expression of CYP3A4, a main detoxification enzyme and a target gene of PXR, due to SHP up-regulation. Metformin 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 21920351-6 2011 We show that metformin dramatically suppresses PXR-mediated expression of CYP3A4 in hepatocytes. Metformin 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 21920351-11 2011 Metformin also inhibited vitamin D receptor-, glucocorticoid receptor- and constitutive androstane receptor (CAR)-mediated induction of CYP3A4 mRNA in human hepatocytes. Metformin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 21920351-12 2011 We show, therefore, a suppressive effect of metformin on PXR and other ligand-activated nuclear receptors in transactivation of the main detoxification enzyme CYP3A4 in human hepatocytes. Metformin 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 21499896-1 2011 PURPOSE: Patupilone is a novel microtubule-targeting cytotoxic agent with potential interaction with CYP3A4/CYP2C19 enzymes. epothilone B 9-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 21499896-2 2011 Midazolam and omeprazole are primarily metabolized by CYP3A4 and CYP2C19, respectively. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 21499896-2 2011 Midazolam and omeprazole are primarily metabolized by CYP3A4 and CYP2C19, respectively. Omeprazole 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 21499896-3 2011 We evaluated the inhibitory effects of patupilone on the CYP3A4/CYP2C19 pathways. epothilone B 39-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 21968951-1 2011 PURPOSE: The aim of this study was to investigate the impact of plasma and intracellular exposure and CYP3A4, CYP3A5, and ABCB1 polymorphisms on vincristine neurotoxicity. Vincristine 145-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 22177374-4 2011 OBJECTIVE: This study was designed to assess the influence of the POR*28 polymorphism on the CYP3A activity in vivo in healthy Chinese men using midazolam (MID) as a probe drug. Midazolam 156-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 22087865-0 2011 Effect of cytochrome P450 3A4 inducers on the pharmacokinetic, pharmacodynamic and safety profiles of bortezomib in patients with multiple myeloma or non-Hodgkin"s lymphoma. Bortezomib 102-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-29 22177374-17 2011 CONCLUSION: These findings suggest that individuals with the POR*28 C > T polymorphism underwent an increase in 1-hydroxylation of MID after intravenous MID administration, and that the polymorphism was associated with increased hepatic, but not intestinal, CYP3A activity in these healthy Chinese volunteers. Midazolam 134-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 261-266 22087865-1 2011 BACKGROUND AND OBJECTIVE: Bortezomib, an antineoplastic agent with proteasome inhibitory activity, is extensively metabolized by the hepatic microsomal cytochrome P450 (CYP) enzymes CYP3A4 and CYP2C19. Bortezomib 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 182-188 22177374-17 2011 CONCLUSION: These findings suggest that individuals with the POR*28 C > T polymorphism underwent an increase in 1-hydroxylation of MID after intravenous MID administration, and that the polymorphism was associated with increased hepatic, but not intestinal, CYP3A activity in these healthy Chinese volunteers. Midazolam 156-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 261-266 22087865-13 2011 Concomitant administration of bortezomib with strong CYP3A4 inducers such as rifampicin is not recommended, as it may result in a reduction of the clinical effect, whereas concomitant administration of weak CYP3A4 inducers such as dexamethasone does not affect the pharmacological profile of bortezomib. Rifampin 77-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 21890735-4 2011 In particular, one proluciferin acetal has demonstrated sensitive and selective CYP3A4-catalyzed oxidation to a luciferin ester-K(m) and k(cat) are 2.88 muM and 5.87 pmol metabolite min(-1) pmol enzyme(-1), respectively. proluciferin acetal 19-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 21873472-5 2011 Human cytochrome P450 (P450) phenotyping showed that SB939 was primarily metabolized by CYP3A4 and CYP1A2. SB939 compound 53-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 21890735-4 2011 In particular, one proluciferin acetal has demonstrated sensitive and selective CYP3A4-catalyzed oxidation to a luciferin ester-K(m) and k(cat) are 2.88 muM and 5.87 pmol metabolite min(-1) pmol enzyme(-1), respectively. luciferin ester 112-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 21890735-7 2011 Luciferin acetals are rapidly oxidized to unstable hemi-orthoesters by CYP3A resulting in luciferin esters and, therefore, are conducive to simple rapid CYP3A bioluminescent assays. luciferin acetals 0-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-76 21890735-7 2011 Luciferin acetals are rapidly oxidized to unstable hemi-orthoesters by CYP3A resulting in luciferin esters and, therefore, are conducive to simple rapid CYP3A bioluminescent assays. luciferin acetals 0-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-158 21890735-7 2011 Luciferin acetals are rapidly oxidized to unstable hemi-orthoesters by CYP3A resulting in luciferin esters and, therefore, are conducive to simple rapid CYP3A bioluminescent assays. luciferin esters 90-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-76 21890735-7 2011 Luciferin acetals are rapidly oxidized to unstable hemi-orthoesters by CYP3A resulting in luciferin esters and, therefore, are conducive to simple rapid CYP3A bioluminescent assays. luciferin esters 90-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-158 21952236-4 2011 Using primary hepatocyte cultures derived from men and women exposed to physiologic-like levels of continuous GH (the feminine circulating profile) alone, dexamethasone alone, and the combined regimen, we observed a dramatic inherent CYP3A4 sexual dimorphism (women more than men) with all treatments. Dexamethasone 155-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 234-240 21713461-5 2011 Wogonin was a potent, competitive inhibitor of CYP1A2 (K (i) = 0.24 muM), and a weak inhibitor of CYP2C19 (IC(50) = 101.10 muM), but was not able to inhibit CYP2C9, CYP2D6, CYP2E1 and CYP3A4 (IC(50) > 200 muM). wogonin 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 21963990-4 2011 Using the redox-sensitive dye RedoxSensor red, we demonstrate that CYP3A4 expression increases levels of ROS in viable cells. Reactive Oxygen Species 105-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 20706860-1 2011 Sorafenib, an orally active multi-kinase inhibitor approved for the treatment of hepatocellular carcinoma (HCC), is primarily metabolized both via cytochrome P450 3A4 isoform (CYP3A4) and UGT1A9. Sorafenib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-166 20706860-1 2011 Sorafenib, an orally active multi-kinase inhibitor approved for the treatment of hepatocellular carcinoma (HCC), is primarily metabolized both via cytochrome P450 3A4 isoform (CYP3A4) and UGT1A9. Sorafenib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 20706860-2 2011 Due to the contribution of these two biotransformation pathways, sorafenib is considered to be less susceptible than other agents to CYP3A4 drug-drug interactions. Sorafenib 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 20623161-4 2011 The patient received anti-tuberculosis therapy including rifampicin, a potent CYP3A4/5 inducer. Rifampin 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 20706860-3 2011 This report discusses a clinically relevant pharmacokinetic CYP3A4 drug-drug interaction between sorafenib and felodipine in an 80-year-old Caucasian patient with HCC. Sorafenib 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 20623161-5 2011 After introduction of rifampicin-based treatment, the patient experienced tumour progression, leaving questionable the potential pharmacokinetic interaction between rifampicin and temsirolimus, a substrate for CYP3A4. Rifampin 22-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 210-216 20706860-3 2011 This report discusses a clinically relevant pharmacokinetic CYP3A4 drug-drug interaction between sorafenib and felodipine in an 80-year-old Caucasian patient with HCC. Felodipine 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 20623161-5 2011 After introduction of rifampicin-based treatment, the patient experienced tumour progression, leaving questionable the potential pharmacokinetic interaction between rifampicin and temsirolimus, a substrate for CYP3A4. Rifampin 165-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 210-216 20706860-5 2011 Felodipine (5 mg bid), an anti-hypertensive agent that is exclusively CYP3A4 substrate, was then introduced due to grade 2 sorafenib-related hypertension. Felodipine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 20623161-5 2011 After introduction of rifampicin-based treatment, the patient experienced tumour progression, leaving questionable the potential pharmacokinetic interaction between rifampicin and temsirolimus, a substrate for CYP3A4. temsirolimus 180-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 210-216 20706860-10 2011 This observation suggests a pharmacokinetic interaction involving CYP3A4 inhibition by felodipine. Felodipine 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 20706860-13 2011 The clinical relevance of pharmacokinetic interactions involving CYP3A4 inhibition in HCC patients receiving sorafenib is analyzed in this case report. Sorafenib 109-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 22116286-0 2011 Inhibition of CYP3A4 and CYP2C9 by podophyllotoxin: implication for clinical drug-drug interactions. Podophyllotoxin 35-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 22116286-3 2011 Inhibition of CYP3A4, CYP2C9, CYP2C8, CYP2D6, CYP2E1 and CYP2A6 by PPT was investigated in the human liver microsomal system. Podophyllotoxin 67-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 21058968-11 2011 Repeated administration of SJW decreases the plasma concentration of zolpidem, probably by enhancing CYP3A4 activity. Zolpidem 69-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 22116286-4 2011 Time-dependent inhibition of CYP3A4 by PPT was also evaluated. Podophyllotoxin 39-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 22116286-5 2011 The results showed that PPT strongly exhibited inhibitory effects on CYP3A4 and CYP2C9 in a concentration-dependent manner. Podophyllotoxin 24-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 22116286-7 2011 Inhibition kinetic analysis showed that PPT exhibited competitive inhibition towards CYP3A4 and CYP2C9 with Ki of 1.6 and 2.0 meu M, respectively. Podophyllotoxin 40-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 22116286-8 2011 Additionally, PPT exerted time-dependent inhibition towards CYP3A4 and the kinetic parameters were 4.4+/- 2.1 meu M and 0.06 +/- 0.01 min-1 for KI and kinact, respectively. Podophyllotoxin 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 22116286-9 2011 Our experimental data indicate that potential drug-drug interaction (DDI) might exist when PPT is co-administered with the substrates which mainly undergo CYP3A4- or CYP2C9-mediated metabolism. Podophyllotoxin 91-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 20716581-12 2011 Cimetidine has a shorter duration of action, but should be used with caution because of its effects on cytochrome P450 3A4, a pathway also utilized by erlotinib. Cimetidine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-122 20716581-12 2011 Cimetidine has a shorter duration of action, but should be used with caution because of its effects on cytochrome P450 3A4, a pathway also utilized by erlotinib. Erlotinib Hydrochloride 151-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-122 22001938-5 2011 Enzyme activities were examined using high performance liquid chromatography (HPLC) assays with probe substrates dextromethorphan and testosterone for CYP2D6 and CYP3A4, respectively. Dextromethorphan 113-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 21946898-0 2011 Novel CYP3A4 intron 6 single nucleotide polymorphism is associated with simvastatin-mediated cholesterol reduction in the Rotterdam Study. Simvastatin 72-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 21946898-0 2011 Novel CYP3A4 intron 6 single nucleotide polymorphism is associated with simvastatin-mediated cholesterol reduction in the Rotterdam Study. Cholesterol 93-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 21946898-1 2011 OBJECTIVES: CYP3A4 is involved in the oxidative metabolism of many drugs and xenobiotics including the HMG-CoA reductase inhibitor simvastatin. Simvastatin 131-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 21946898-2 2011 The objective of this study was to investigate whether a new CYP3A4 functional single nucleotide polymorphism (SNP) in intron 6 (CYP3A4*22) modifies the effect of simvastatin on total cholesterol (TOTc) or LDL cholesterol (LDLc) reduction in a population-based cohort study. Simvastatin 163-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 21946898-2 2011 The objective of this study was to investigate whether a new CYP3A4 functional single nucleotide polymorphism (SNP) in intron 6 (CYP3A4*22) modifies the effect of simvastatin on total cholesterol (TOTc) or LDL cholesterol (LDLc) reduction in a population-based cohort study. Simvastatin 163-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 21946898-2 2011 The objective of this study was to investigate whether a new CYP3A4 functional single nucleotide polymorphism (SNP) in intron 6 (CYP3A4*22) modifies the effect of simvastatin on total cholesterol (TOTc) or LDL cholesterol (LDLc) reduction in a population-based cohort study. Cholesterol 184-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 21946898-2 2011 The objective of this study was to investigate whether a new CYP3A4 functional single nucleotide polymorphism (SNP) in intron 6 (CYP3A4*22) modifies the effect of simvastatin on total cholesterol (TOTc) or LDL cholesterol (LDLc) reduction in a population-based cohort study. Cholesterol 184-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 21946898-2 2011 The objective of this study was to investigate whether a new CYP3A4 functional single nucleotide polymorphism (SNP) in intron 6 (CYP3A4*22) modifies the effect of simvastatin on total cholesterol (TOTc) or LDL cholesterol (LDLc) reduction in a population-based cohort study. totc 197-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 21946898-2 2011 The objective of this study was to investigate whether a new CYP3A4 functional single nucleotide polymorphism (SNP) in intron 6 (CYP3A4*22) modifies the effect of simvastatin on total cholesterol (TOTc) or LDL cholesterol (LDLc) reduction in a population-based cohort study. totc 197-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 21946898-3 2011 METHODS: In a total of 80 incident simvastatin users, the association between the CYP3A4 intron 6 C>T SNP (rs35599367) and reduction in cholesterol levels was analyzed using linear regression analysis and adjusting for potential confounding factors. Simvastatin 35-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 21946898-3 2011 METHODS: In a total of 80 incident simvastatin users, the association between the CYP3A4 intron 6 C>T SNP (rs35599367) and reduction in cholesterol levels was analyzed using linear regression analysis and adjusting for potential confounding factors. Cholesterol 139-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 21946898-4 2011 RESULTS: The CYP3A4*22 allele was associated with a trend towards a stronger simvastatin lipid-lowering response, as reflected by the greater reduction in both TOTc and LDLc levels when compared with homozygous wild type. Simvastatin 77-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 21946898-5 2011 We observed that the CYP3A4*22 allele carriers had an increased reduction in TOTc and LDLc: -0.25 mmol/l (95% confidence interval [CI(95%)]=[-0.52; 0.01], P=0.058) and -0.29 mmol/l (CI(95%)=[-0.58; 0.01], P=0.054) when compared with homozygous CC. totc 77-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 21946898-7 2011 CONCLUSION: The CYP3A4*22 intron 6 SNP T-variant allele was associated with reduced CYP3A4 activity, resulting in a better lipid lowering response to simvastatin, when data were adjusted for confounding factors. Simvastatin 150-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 21946898-7 2011 CONCLUSION: The CYP3A4*22 intron 6 SNP T-variant allele was associated with reduced CYP3A4 activity, resulting in a better lipid lowering response to simvastatin, when data were adjusted for confounding factors. Simvastatin 150-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 22001938-5 2011 Enzyme activities were examined using high performance liquid chromatography (HPLC) assays with probe substrates dextromethorphan and testosterone for CYP2D6 and CYP3A4, respectively. Testosterone 134-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 21964476-0 2011 Cytotoxicity of 3-(3,5-dichlorophenyl)-2,4-thiazolidinedione (DCPT) and analogues in wild type and CYP3A4 stably transfected HepG2 cells. 3-(3,5-dichlorophenyl)-2,4-thiazolidinedione 16-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 22001672-6 2011 However, potent inhibition of CYP3A4 by limonin is observed with IC50 values of 6.20 muM (CYP3A4/testosterone) and 19.10 muM (CYP3A4/midazolam). Testosterone 97-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 21964476-6 2011 CYP3A4 activity was confirmed by measuring testosterone 6beta-hydroxylation. testosterone 6beta 43-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 22001672-6 2011 However, potent inhibition of CYP3A4 by limonin is observed with IC50 values of 6.20 muM (CYP3A4/testosterone) and 19.10 muM (CYP3A4/midazolam). Midazolam 133-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 21964476-10 2011 Treatment with a CYP3A4 inhibitor or inducer attenuated or potentiated DCPT cytotoxicity, respectively. 3-(3,5-dichlorophenyl)-2,4-thiazolidinedione 71-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 21964476-11 2011 These results suggest that DCPT-induced cytotoxicity in the transfected HepG2 cells is partially dependent on CYP3A4. 3-(3,5-dichlorophenyl)-2,4-thiazolidinedione 27-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 21859392-6 2011 It was identified as an N-oxide derivative and, under hypoxia, it underwent retroreduction back to C-1305, what was extremely effective with participation of CYP3A4. n-oxide 24-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 21859392-6 2011 It was identified as an N-oxide derivative and, under hypoxia, it underwent retroreduction back to C-1305, what was extremely effective with participation of CYP3A4. Carbon 99-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 22004098-0 2011 Allosteric activation of cytochrome P450 3A4 by alpha-naphthoflavone: branch point regulation revealed by isotope dilution analysis. alpha-naphthoflavone 48-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-44 21964418-5 2011 The substrate oxidation reactions catalyzed by CYP2A6, CYP2B6, CYP2C19 and CYP3A4 were moderately (K(i) values of 35 to 45 muM), and those by CYP1A2, CYP2D6 and CYP2E1 were weakly inhibited by PFOS (K(i) values of 190-300 muM). perfluorooctane sulfonic acid 193-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 22023129-7 2011 For all 3 species, inhibitors of CYP3A4, CYP2A6, CYP2C19, CYP2B6, and CYP2C9 diminished N-demethylation of ketamine. Nitrogen 88-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 27366135-6 2012 Aliquots of the extract were tested for their ability to inhibit the metabolism of the human CYP3A4 substrate quinine, using an in vitro liver microsomal technique. Quinine 110-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 27366135-8 2012 Formation of quinine"s metabolite 3-hydroxyquinine, generated by the CYP3A4-mediated reaction was measured by a HPLC method. Quinine 13-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 27366135-8 2012 Formation of quinine"s metabolite 3-hydroxyquinine, generated by the CYP3A4-mediated reaction was measured by a HPLC method. 3-hydroxyquinidine 34-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 22023129-8 2011 Anti-CYP3A4, anti-CYP2C9, and anti-CYP2B6 antibodies also inhibited ketamine N-demethylation. Ketamine 68-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 5-11 22023129-12 2011 Ketamine N-demethylation was stereoselective in single human CYP3A4 and canine CYP2C21 enzymes. Ketamine 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 22023129-7 2011 For all 3 species, inhibitors of CYP3A4, CYP2A6, CYP2C19, CYP2B6, and CYP2C9 diminished N-demethylation of ketamine. Ketamine 107-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 21698408-1 2011 Steroids and H(2) blockers are commonly used as supportive care for taxane-containing chemotherapy, but they also affect docetaxel"s primary metabolizer, cytochrome P(450) 3A4. Steroids 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-175 22023129-13 2011 CONCLUSIONS AND CLINICAL RELEVANCE: Human-specific inhibitors of CYP2A6, CYP2C19, CYP3A4, CYP2B6, and CYP2C9 diminished ketamine N-demethylation in dogs and horses. ketamine n 120-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 21698408-1 2011 Steroids and H(2) blockers are commonly used as supportive care for taxane-containing chemotherapy, but they also affect docetaxel"s primary metabolizer, cytochrome P(450) 3A4. Docetaxel 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-175 21883349-0 2011 Drug interactions with mitotane by induction of CYP3A4 metabolism in the clinical management of adrenocortical carcinoma. Mitotane 23-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 21903774-0 2011 A new functional CYP3A4 intron 6 polymorphism significantly affects tacrolimus pharmacokinetics in kidney transplant recipients. Tacrolimus 68-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 21937987-5 2011 Recovery of CYP3A activity occurred with a half-life of 24 h after voriconazole, whereas ritonavir inhibition was still strong 3 days after discontinuation. Voriconazole 67-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 21975350-3 2011 CYP2A6 and CYP3A showed effects on letrozole metabolism in vitro. Letrozole 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-16 21605066-0 2011 Comparison of metabolic soft spot predictions of CYP3A4, CYP2C9 and CYP2D6 substrates using MetaSite and StarDrop. stardrop 105-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 21953762-1 2011 Interactions between naringenin and the cytochrome P450 (CYP) system have been of interest since the first demonstration that grapefruit juice reduced CYP3A activity. naringenin 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-156 21953762-7 2011 Whereas (S)-naringenin was 2-fold more potent as an inhibitor of CYP19 and CYP2C19 than (R)-naringenin, (R)-naringenin was 2-fold more potent for CYP2C9 and CYP3A. (R)-naringenin 104-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-162 21883349-4 2011 Recently, sunitinib, a multityrosine kinase inhibitor (TKI), has been found to be rapidly metabolized by CYP3A4 during mitotane treatment, indicating clinically relevant drug interactions with mitotane. Sunitinib 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 21883349-4 2011 Recently, sunitinib, a multityrosine kinase inhibitor (TKI), has been found to be rapidly metabolized by CYP3A4 during mitotane treatment, indicating clinically relevant drug interactions with mitotane. Mitotane 119-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 21883349-4 2011 Recently, sunitinib, a multityrosine kinase inhibitor (TKI), has been found to be rapidly metabolized by CYP3A4 during mitotane treatment, indicating clinically relevant drug interactions with mitotane. Mitotane 193-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 21883349-5 2011 We here summarize the current evidence concerning mitotane-induced changes in hepatic monooxygenase expression, list drugs potentially affected by mitotane-related CYP3A4 induction and suggest alternatives. Mitotane 50-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 21883349-5 2011 We here summarize the current evidence concerning mitotane-induced changes in hepatic monooxygenase expression, list drugs potentially affected by mitotane-related CYP3A4 induction and suggest alternatives. Mitotane 147-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 21883349-7 2011 Similarly, statins such as simvastatin are metabolized by CYP3A4, whereas others like pravastatin are not. Simvastatin 27-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 21883349-10 2011 Thus, induction of CYP3A4 by mitotane needs to be considered in the design of future clinical trials in ACC. Mitotane 29-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 21515002-4 2011 Buprenorphine N-dealkylation to norbuprenorphine is primarily performed by CYP3A. Buprenorphine 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 21515002-4 2011 Buprenorphine N-dealkylation to norbuprenorphine is primarily performed by CYP3A. norbuprenorphine 32-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 21871880-8 2011 Induction of CYP3A4 mRNA by rifampicin was about 1.5-2.5 fold (clones 2, 4, 6, 7) and it was not significantly different from CYP3A4 mRNA induction in parent HepG2. Rifampin 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 21835977-5 2011 Using two of the optimized methods, the time-dependent inhibition kinetic parameters (K(I) and k(inact)) for four known CYP3A4 TDI (diltiazem, erythromycin, verapamil, and troleandomycin) were determined. Diltiazem 132-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 21871880-9 2011 The basal expression of CYP3A4 protein was increased in all clones, but rifampicin-induced expression of CYP3A4 protein was in all clones lower than in parent HepG2. Rifampin 72-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 21209240-2 2011 Diltiazem interaction studies assess a given compound"s sensitivity to moderate CYP3A inhibition. Diltiazem 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-85 21839818-3 2011 It has been reported that duloxetine causes time-dependent inhibition (TDI) of CYP1A2, CYP2B6, CYP2C19 and CYP3A4/5; but the nature of these TDI (whether reversible or irreversible) is not known. Duloxetine Hydrochloride 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 21849623-11 2011 CYP2D and CYP3A4 contents were significantly correlated with typical reactions of human CYP2D (bufuralol 1"-hydroxylation and dextromethorphan O-deethylation) and CYP3A (midazolam 1"-hydroxylation and 4-hydroxylation). bufuralol 95-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 21849623-11 2011 CYP2D and CYP3A4 contents were significantly correlated with typical reactions of human CYP2D (bufuralol 1"-hydroxylation and dextromethorphan O-deethylation) and CYP3A (midazolam 1"-hydroxylation and 4-hydroxylation). bufuralol 95-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 21849623-11 2011 CYP2D and CYP3A4 contents were significantly correlated with typical reactions of human CYP2D (bufuralol 1"-hydroxylation and dextromethorphan O-deethylation) and CYP3A (midazolam 1"-hydroxylation and 4-hydroxylation). Dextromethorphan 126-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 21849623-11 2011 CYP2D and CYP3A4 contents were significantly correlated with typical reactions of human CYP2D (bufuralol 1"-hydroxylation and dextromethorphan O-deethylation) and CYP3A (midazolam 1"-hydroxylation and 4-hydroxylation). Dextromethorphan 126-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 21849623-11 2011 CYP2D and CYP3A4 contents were significantly correlated with typical reactions of human CYP2D (bufuralol 1"-hydroxylation and dextromethorphan O-deethylation) and CYP3A (midazolam 1"-hydroxylation and 4-hydroxylation). Midazolam 170-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 21849623-11 2011 CYP2D and CYP3A4 contents were significantly correlated with typical reactions of human CYP2D (bufuralol 1"-hydroxylation and dextromethorphan O-deethylation) and CYP3A (midazolam 1"-hydroxylation and 4-hydroxylation). Midazolam 170-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 22066308-19 2011 Quetiapine is metabolised by cytochrome P450 isoenzyme CYP3A4, creating a high risk of pharmacokinetic interactions. Quetiapine Fumarate 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 21828263-6 2011 These studies show that, in vitro, CYP3A4/5, 2C19, and 2B6 are individually capable of converting clopidogrel and prasugrel to the AM and that the cytochrome P450 preference for these two thienopyridines is very similar. Clopidogrel 98-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-49 21828263-6 2011 These studies show that, in vitro, CYP3A4/5, 2C19, and 2B6 are individually capable of converting clopidogrel and prasugrel to the AM and that the cytochrome P450 preference for these two thienopyridines is very similar. Prasugrel Hydrochloride 114-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-49 21828263-6 2011 These studies show that, in vitro, CYP3A4/5, 2C19, and 2B6 are individually capable of converting clopidogrel and prasugrel to the AM and that the cytochrome P450 preference for these two thienopyridines is very similar. Thienopyridines 188-203 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-49 21550074-9 2011 Using recombinant microsomes, prasugrel biotransformation was mainly performed by CYP2B6, CYP2D6, CYP2C19, CYP3A4, and CYP3A5. Prasugrel Hydrochloride 30-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 21550074-10 2011 With specific inhibitors of CYP3A, CYP2B6, CYP2D6, CYP2C9, and CYP2C19, active metabolite production was decreased by 38% +- 15% with 4-(4-chlorobenzyl)pyridine (CYP2B6 inhibitor) and by 45 +- 16% with ketoconazole (CYP3A inhibitor). 4-(4-Chlorobenzyl)pyridine 134-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 21550074-10 2011 With specific inhibitors of CYP3A, CYP2B6, CYP2D6, CYP2C9, and CYP2C19, active metabolite production was decreased by 38% +- 15% with 4-(4-chlorobenzyl)pyridine (CYP2B6 inhibitor) and by 45 +- 16% with ketoconazole (CYP3A inhibitor). 4-(4-Chlorobenzyl)pyridine 134-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-221 21550074-10 2011 With specific inhibitors of CYP3A, CYP2B6, CYP2D6, CYP2C9, and CYP2C19, active metabolite production was decreased by 38% +- 15% with 4-(4-chlorobenzyl)pyridine (CYP2B6 inhibitor) and by 45 +- 16% with ketoconazole (CYP3A inhibitor). Ketoconazole 202-214 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 21550074-13 2011 In this in-vitro study, we found a potent inhibition of prasugrel bioactivation by ritonavir compared to the specific inhibitors of CYP3A and CYP2B6 due to the simultaneous inhibition of CYP2B6 and CYP3A by ritonavir. Prasugrel Hydrochloride 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 198-203 21550074-13 2011 In this in-vitro study, we found a potent inhibition of prasugrel bioactivation by ritonavir compared to the specific inhibitors of CYP3A and CYP2B6 due to the simultaneous inhibition of CYP2B6 and CYP3A by ritonavir. Ritonavir 83-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 198-203 21550074-13 2011 In this in-vitro study, we found a potent inhibition of prasugrel bioactivation by ritonavir compared to the specific inhibitors of CYP3A and CYP2B6 due to the simultaneous inhibition of CYP2B6 and CYP3A by ritonavir. Ritonavir 207-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-137 21550074-13 2011 In this in-vitro study, we found a potent inhibition of prasugrel bioactivation by ritonavir compared to the specific inhibitors of CYP3A and CYP2B6 due to the simultaneous inhibition of CYP2B6 and CYP3A by ritonavir. Ritonavir 207-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 198-203 21726170-6 2011 CYP3A4 catalyzed the formation of 7-OH-NBL with the highest activity and of 6-OH-NBL with lower activity. 7-oh-nbl 34-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21726170-6 2011 CYP3A4 catalyzed the formation of 7-OH-NBL with the highest activity and of 6-OH-NBL with lower activity. 6-oh-nbl 76-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21771587-1 2011 BACKGROUND: Itraconazole is a potent inhibitor of CYP3A4 and P-glycoprotein, but not CYP2C9. Itraconazole 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 22016125-8 2011 Calcineurin inhibitors (cyclosporine, tacrolimus) and mTOR inhibitors (sirolimus, everolimus) are particularly susceptible to the effects of substances that inhibit or induce cytochrome P450 (CYP) 3A4 and P-glycoprotein. Cyclosporine 24-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-200 22016125-8 2011 Calcineurin inhibitors (cyclosporine, tacrolimus) and mTOR inhibitors (sirolimus, everolimus) are particularly susceptible to the effects of substances that inhibit or induce cytochrome P450 (CYP) 3A4 and P-glycoprotein. Tacrolimus 38-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-200 22016125-8 2011 Calcineurin inhibitors (cyclosporine, tacrolimus) and mTOR inhibitors (sirolimus, everolimus) are particularly susceptible to the effects of substances that inhibit or induce cytochrome P450 (CYP) 3A4 and P-glycoprotein. Sirolimus 71-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-200 22016125-8 2011 Calcineurin inhibitors (cyclosporine, tacrolimus) and mTOR inhibitors (sirolimus, everolimus) are particularly susceptible to the effects of substances that inhibit or induce cytochrome P450 (CYP) 3A4 and P-glycoprotein. Everolimus 82-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-200 22016125-10 2011 Methylprednisolone and prednisolone may also be affected by substances that modulate CYP3A4 and P-glycoprotein. Methylprednisolone 0-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 22016125-10 2011 Methylprednisolone and prednisolone may also be affected by substances that modulate CYP3A4 and P-glycoprotein. Prednisolone 6-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 21854846-10 2011 The results point towards the combination of low CYP3A4 activity and CYP2D6 PM status of major importance for attaining possibly toxic nortriptyline concentrations. Nortriptyline 135-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 21204116-12 2011 The validated method was successfully applied in a pharmacokinetic study investigating in vivo CYP3A-activity in a large cohort of renal allograft recipients using sub-therapeutic doses of midazolam as a drug-probe. Midazolam 189-198 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-100 21854846-12 2011 In a clinical context, the simulations suggest that precise individual dose adjustment of nortriptyline requires information regarding the activity of both CYP3A4 and CYP2D6. Nortriptyline 90-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 21825288-2 2011 Amlodipine and atorvastatin are both substrates of CYP3A and are among the drugs most frequently used by patients with hepatitis C. This study was conducted to examine the effect of telaprevir on atorvastatin and amlodipine pharmacokinetics (PK). Amlodipine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 21825288-2 2011 Amlodipine and atorvastatin are both substrates of CYP3A and are among the drugs most frequently used by patients with hepatitis C. This study was conducted to examine the effect of telaprevir on atorvastatin and amlodipine pharmacokinetics (PK). Atorvastatin 15-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 21825288-8 2011 Telaprevir significantly increased exposure to amlodipine and atorvastatin, consistent with the inhibitory effect of telaprevir on the CYP3A-mediated metabolism of these agents. telaprevir 117-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-140 21287583-2 2011 Midazolam (MDZ) was used as a substrate for phenotyping CYP3A4 activity; the concentrations of MDZ and its main metabolite 1"-hydroxymidazolam (1-OH MDZ) were compared between the DBS method from finger punctures, plasma and whole blood (WB), drawn by venipuncture, whereby several methodological parameters were studied (i.e. punch width, amount of dots analyzed and storage time stability). Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 21287583-2 2011 Midazolam (MDZ) was used as a substrate for phenotyping CYP3A4 activity; the concentrations of MDZ and its main metabolite 1"-hydroxymidazolam (1-OH MDZ) were compared between the DBS method from finger punctures, plasma and whole blood (WB), drawn by venipuncture, whereby several methodological parameters were studied (i.e. punch width, amount of dots analyzed and storage time stability). Midazolam 11-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 21825288-1 2011 Telaprevir is a hepatitis C virus protease inhibitor that is both a substrate and an inhibitor of CYP3A. telaprevir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 21826477-6 2011 Several other drugs (metabolized through CYP3A4 such as statins or antifungals) similarly impact the pharmacologic response to clopidogrel. Clopidogrel 127-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 21826677-3 2011 The resultant data indicated that loxapine was mainly metabolized by human liver microsomes to (i) 8-hydroxyloxapine by CYP1A2, (ii) 7-hydroxyloxapine by CYP2D6, (iii) N-desmethyloxapine by CYP3A4 and (iv) loxapine N-oxide by CYP3A4. Loxapine 34-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-196 21826677-3 2011 The resultant data indicated that loxapine was mainly metabolized by human liver microsomes to (i) 8-hydroxyloxapine by CYP1A2, (ii) 7-hydroxyloxapine by CYP2D6, (iii) N-desmethyloxapine by CYP3A4 and (iv) loxapine N-oxide by CYP3A4. Loxapine 34-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 226-232 21290248-5 2011 The in vivo activity of CYP3A was evaluated using midazolam as a marker drug. Midazolam 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 21832990-1 2011 Clearance of atorvastatin occurs through hepatic uptake by organic anion transporting polypeptides (OATPs) and subsequent metabolism by cytochrome P450 (CYP) 3A4. Atorvastatin 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-161 21832990-2 2011 To demonstrate the relative importance of OATPs and CYP3A4 in the hepatic elimination of atorvastatin in vivo, a clinical cassette microdose study was performed. Atorvastatin 89-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 21832990-4 2011 The pharmacokinetics of this cocktail was observed at baseline, after an oral dose of 600 mg rifampicin (an inhibitor of OATPs), and after an intravenous dose of 200 mg itraconazole (a CYP3A4 inhibitor). Itraconazole 169-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 21746968-4 2011 Of 14 recombinant P450s examined in this study, CYP2B6 and CYP3A4 were primarily responsible for production of the desmethyl metabolite dihydroartemisinin. artenimol 136-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 21771933-1 2011 Rifampin is a potent inducer of CYP3A4 in vitro and precipitates numerous drug-drug interactions (DDIs) when coadministered with CYP3A4 substrates. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 21771933-1 2011 Rifampin is a potent inducer of CYP3A4 in vitro and precipitates numerous drug-drug interactions (DDIs) when coadministered with CYP3A4 substrates. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 21983822-0 2011 Enantioselective capillary electrophoresis for the assessment of CYP3A4-mediated ketamine demethylation and inhibition in vitro. Ketamine 81-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 21959260-2 2011 OBJECTIVE: This study was designed to evaluate the dronedarone prescribers" adherence to PI regarding the following contraindications: (1) patients with heart failure (HF) with a recent decompensation requiring hospitalization or referral to a specialist, (2) concomitant use of potent CYP3A4 inhibitors, and (3) concomitant use of QT-prolonging drugs. Dronedarone 51-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 286-292 21959260-8 2011 Potent CYP3A4 inhibitors were prescribed to 10 (0.6%) patients within a month following dronedarone initiation, 6 of whom received them for topical use only. Dronedarone 88-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 21959260-11 2011 In the LabRx database, dronedarone was commonly dispensed to patients with cardiovascular risk factors and rarely dispensed to patients with contraindications such as worsening HF or hospitalization for HF or with concomitant prescriptions of potent CYP3A4 inhibitors, QT-prolonging drugs, or both. Dronedarone 23-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 250-256 21983822-1 2011 Enantioselective CE with sulfated cyclodextrins as chiral selectors was used to determine the CYP3A4-catalyzed N-demethylation kinetics of ketamine to norketamine and its inhibition in the presence of ketoconazole in vitro. Cyclodextrins 34-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 21983822-1 2011 Enantioselective CE with sulfated cyclodextrins as chiral selectors was used to determine the CYP3A4-catalyzed N-demethylation kinetics of ketamine to norketamine and its inhibition in the presence of ketoconazole in vitro. Nitrogen 111-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 21983822-1 2011 Enantioselective CE with sulfated cyclodextrins as chiral selectors was used to determine the CYP3A4-catalyzed N-demethylation kinetics of ketamine to norketamine and its inhibition in the presence of ketoconazole in vitro. Ketamine 139-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 21983822-1 2011 Enantioselective CE with sulfated cyclodextrins as chiral selectors was used to determine the CYP3A4-catalyzed N-demethylation kinetics of ketamine to norketamine and its inhibition in the presence of ketoconazole in vitro. norketamine 151-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 21983822-1 2011 Enantioselective CE with sulfated cyclodextrins as chiral selectors was used to determine the CYP3A4-catalyzed N-demethylation kinetics of ketamine to norketamine and its inhibition in the presence of ketoconazole in vitro. Ketoconazole 201-213 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 21983822-2 2011 Ketamine, a chiral phencyclidine derivative, was incubated with recombinant human CYP3A4 from a baculovirus expression system as racemic mixture and as single enantiomer. Ketamine 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 21947724-5 2011 This study was designed to investigate the effects of salvianolic acid B (Sal B), a pure compound extracted from Radix Salviae Miltiorrhizae, a Chinese herb, on cell proliferation and CYP1A2 and CYP3A4 mRNA expression in the presence or absence of rifampicin, a potent inducer of CYPs and GST protein expression in HepG2 cells. salvianolic acid B 54-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 22009620-11 2011 CYP3A is probably one of the most important isoenzymes since it contributes to at least the partial transformation of 60% of drugs that undergo oxidation: erythromycin and clarithromycin are CYP3A4 substrates. Erythromycin 155-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 21947724-5 2011 This study was designed to investigate the effects of salvianolic acid B (Sal B), a pure compound extracted from Radix Salviae Miltiorrhizae, a Chinese herb, on cell proliferation and CYP1A2 and CYP3A4 mRNA expression in the presence or absence of rifampicin, a potent inducer of CYPs and GST protein expression in HepG2 cells. salvianolic acid B 74-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 21947724-11 2011 Ten mumol/L Sal B, but not 1 mumol/L, down-regulated CYP3A4 and CYP1A2 mRNA expression after 24 hours of incubation, whereas both 1 and 10 mumol/L Sal B down-regulated CYP3A4 mRNA expression after 96 hours of incubation; moreover, 1 and 10 mumol/L Sal B inhibited CYP3A4 mRNA expression induced by rifampicin. salvianolic acid B 12-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 21947724-11 2011 Ten mumol/L Sal B, but not 1 mumol/L, down-regulated CYP3A4 and CYP1A2 mRNA expression after 24 hours of incubation, whereas both 1 and 10 mumol/L Sal B down-regulated CYP3A4 mRNA expression after 96 hours of incubation; moreover, 1 and 10 mumol/L Sal B inhibited CYP3A4 mRNA expression induced by rifampicin. salvianolic acid B 12-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 21947724-11 2011 Ten mumol/L Sal B, but not 1 mumol/L, down-regulated CYP3A4 and CYP1A2 mRNA expression after 24 hours of incubation, whereas both 1 and 10 mumol/L Sal B down-regulated CYP3A4 mRNA expression after 96 hours of incubation; moreover, 1 and 10 mumol/L Sal B inhibited CYP3A4 mRNA expression induced by rifampicin. salvianolic acid B 12-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 21947724-11 2011 Ten mumol/L Sal B, but not 1 mumol/L, down-regulated CYP3A4 and CYP1A2 mRNA expression after 24 hours of incubation, whereas both 1 and 10 mumol/L Sal B down-regulated CYP3A4 mRNA expression after 96 hours of incubation; moreover, 1 and 10 mumol/L Sal B inhibited CYP3A4 mRNA expression induced by rifampicin. salvianolic acid B 147-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 21947724-11 2011 Ten mumol/L Sal B, but not 1 mumol/L, down-regulated CYP3A4 and CYP1A2 mRNA expression after 24 hours of incubation, whereas both 1 and 10 mumol/L Sal B down-regulated CYP3A4 mRNA expression after 96 hours of incubation; moreover, 1 and 10 mumol/L Sal B inhibited CYP3A4 mRNA expression induced by rifampicin. salvianolic acid B 147-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 21947724-11 2011 Ten mumol/L Sal B, but not 1 mumol/L, down-regulated CYP3A4 and CYP1A2 mRNA expression after 24 hours of incubation, whereas both 1 and 10 mumol/L Sal B down-regulated CYP3A4 mRNA expression after 96 hours of incubation; moreover, 1 and 10 mumol/L Sal B inhibited CYP3A4 mRNA expression induced by rifampicin. salvianolic acid B 147-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 21947724-11 2011 Ten mumol/L Sal B, but not 1 mumol/L, down-regulated CYP3A4 and CYP1A2 mRNA expression after 24 hours of incubation, whereas both 1 and 10 mumol/L Sal B down-regulated CYP3A4 mRNA expression after 96 hours of incubation; moreover, 1 and 10 mumol/L Sal B inhibited CYP3A4 mRNA expression induced by rifampicin. salvianolic acid B 147-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 21947724-13 2011 CONCLUSION: Sal B inhibits CYP3A4 and CYP1A2 mRNA expression and induces GST expression in HepG2 cells. salvianolic acid B 12-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 21726661-7 2011 DMSO treatment increased cytochrome P450 (CYP) transcript levels and CYP3A4 activity, but also cell damage and repressed hepatic functionality in cluster-neighbouring regions. Dimethyl Sulfoxide 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 21996963-2 2011 Furthermore, azole anti-fungal agents are known to enhance VA toxicity because they delay the metabolism and excretion of VA by inhibiting CYP3A4. Azoles 13-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 22009620-11 2011 CYP3A is probably one of the most important isoenzymes since it contributes to at least the partial transformation of 60% of drugs that undergo oxidation: erythromycin and clarithromycin are CYP3A4 substrates. Erythromycin 155-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-197 21854345-5 2011 Inhaled steroids do not usually lead to systemic adverse events, since their plasma concentrations are quite low due to extensive first-pass metabolism and clearance by CYP3A4. Steroids 8-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 21854345-6 2011 However, the coadministration of Ritonavir with inhaled (or intranasal) corticosteroids may result in an increase in the plasma corticosteroid levels due to the potent CYP3A4 inhibition by Ritonavir. Ritonavir 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 21854345-6 2011 However, the coadministration of Ritonavir with inhaled (or intranasal) corticosteroids may result in an increase in the plasma corticosteroid levels due to the potent CYP3A4 inhibition by Ritonavir. Ritonavir 189-198 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 22009620-11 2011 CYP3A is probably one of the most important isoenzymes since it contributes to at least the partial transformation of 60% of drugs that undergo oxidation: erythromycin and clarithromycin are CYP3A4 substrates. Clarithromycin 172-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 22009620-11 2011 CYP3A is probably one of the most important isoenzymes since it contributes to at least the partial transformation of 60% of drugs that undergo oxidation: erythromycin and clarithromycin are CYP3A4 substrates. Clarithromycin 172-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-197 21916909-0 2011 Association of ABCB1, CYP3A4*18B and CYP3A5*3 genotypes with the pharmacokinetics of tacrolimus in healthy Chinese subjects: a population pharmacokinetic analysis. Tacrolimus 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 21916909-10 2011 The combined genotypes of CYP3A4*18B and CYP3A5*3 had a greater impact than either genotype alone, and they were estimated to account for 28 4% of the inter-subject variability of apparent clearance (CL/F) by NONMEM. Fluorine 203-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 21916909-11 2011 The CL/F in subjects with CYP3A4*1/*1-CYP3A5*3/*3 was 10 3 L/h and was 48 5% in those not carrying CYP3A4*1/*1-CYP3A5*3/*3. Fluorine 7-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 21726172-5 2011 However, toremifene is a competitive inhibitor of CYP3A4, non-competitive inhibitor of CYP2A6, 2C8, 2C9, 2C19 and 2E1 and mixed-type inhibitor of CYP2B6. Toremifene 9-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 21742782-2 2011 SXR is highly expressed in the liver and intestine, where it regulates cytochrome P450 3A4 (CYP3A4), which in turn controls xenobiotic and endogenous steroid hormone metabolism. Steroids 150-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-90 21742782-2 2011 SXR is highly expressed in the liver and intestine, where it regulates cytochrome P450 3A4 (CYP3A4), which in turn controls xenobiotic and endogenous steroid hormone metabolism. Steroids 150-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 21750466-3 2011 Cytochrome P450 3A4 is highly involved in the metabolism of steroids. Steroids 60-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 21902501-0 2011 Genetic polymorphisms in CYP3A4 are associated with withdrawal symptoms and adverse reactions in methadone maintenance patients. Methadone 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 21902501-2 2011 The isozyme CYP3A4 of the CYP system is one of the metabolic enzymes, as well as CYP2B6, responsible for the metabolism of methadone. Methadone 123-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 21902501-3 2011 The aim of the present study is to evaluate the potential use of genetic polymorphisms in CYP3A4 as biomarkers for the prediction of methadone treatment responses. Methadone 133-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 21726172-7 2011 Toremifene did not induce CYP1A2 but increased CYP3A4 monooxygenase activity and gene expression in drug-exposed human primary hepatocytes. Toremifene 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 21726172-8 2011 Although clinical doses of toremifene produce steady state exposures to toremifene and NDMT that may be sufficient to cause pharmacokinetic drug-drug interactions with other drugs metabolised by CYP2B6, CYP2C8, CYP3A4, CYP2C9 and CYP2C19, these data indicate that toremifene is unlikely to play a role in clinical drug-drug interactions with substrate drugs of CYP1A2 and CYP2D6. Toremifene 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-217 21726172-8 2011 Although clinical doses of toremifene produce steady state exposures to toremifene and NDMT that may be sufficient to cause pharmacokinetic drug-drug interactions with other drugs metabolised by CYP2B6, CYP2C8, CYP3A4, CYP2C9 and CYP2C19, these data indicate that toremifene is unlikely to play a role in clinical drug-drug interactions with substrate drugs of CYP1A2 and CYP2D6. N-desmethyltoremifene 87-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-217 21728364-1 2011 It has recently been proposed that plasma levels of 4beta-hydroxycholesterol (4betaHC) may be indicative of cytochrome P450 3A4 (P450 3A) activity and therefore could be used to probe for P450 3A-mediated drug-drug interactions. cholest-5-ene-3,4-diol 52-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-127 21728364-1 2011 It has recently been proposed that plasma levels of 4beta-hydroxycholesterol (4betaHC) may be indicative of cytochrome P450 3A4 (P450 3A) activity and therefore could be used to probe for P450 3A-mediated drug-drug interactions. cholest-5-ene-3,4-diol 78-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-127 21798277-7 2011 Based on our results, we suggest that hCYP3A4 is involved in the metabolism of DBC and its tissue-specific derivatives. 7H-dibenzo(c,g)carbazole 79-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-45 21902501-10 2011 CONCLUSION: These results suggested that genetic variants in the CYP3A4 gene may be useful indicators for the severity of side effects and withdrawal symptoms for methadone treatment. Methadone 163-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 21902502-1 2011 AIMS: CYP3A4 is involved in the oxidative metabolism of many drugs and xenobiotics including the immunosuppressants tacrolimus (Tac) and cyclosporine (CsA). Tacrolimus 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 21902502-1 2011 AIMS: CYP3A4 is involved in the oxidative metabolism of many drugs and xenobiotics including the immunosuppressants tacrolimus (Tac) and cyclosporine (CsA). Tacrolimus 128-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 21902502-1 2011 AIMS: CYP3A4 is involved in the oxidative metabolism of many drugs and xenobiotics including the immunosuppressants tacrolimus (Tac) and cyclosporine (CsA). Cyclosporine 137-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 21902502-1 2011 AIMS: CYP3A4 is involved in the oxidative metabolism of many drugs and xenobiotics including the immunosuppressants tacrolimus (Tac) and cyclosporine (CsA). Cyclosporine 151-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 21902502-8 2011 CONCLUSION: The CYP3A4 intron 6 C>T polymorphism is associated with altered Tac and CsA metabolism. Cyclosporine 87-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 21798277-3 2011 A slight but significant level of gene mutations and DNA adducts detected in V79MZh3A4 cells treated with N-MeDBC, only at the highest concentration (30muM), revealed that this sarcomagenic carcinogen was also metabolized by hCYP3A4. n-medbc 106-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 225-232 21673127-0 2011 A novel biotransformation of alkyl aminopyrrolidine to aminopiperidine ring by human CYP3A. alkyl aminopyrrolidine 29-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-90 21706316-0 2011 Effect of ketoconazole-mediated CYP3A4 inhibition on clinical pharmacokinetics of panobinostat (LBH589), an orally active histone deacetylase inhibitor. Ketoconazole 10-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 21706316-0 2011 Effect of ketoconazole-mediated CYP3A4 inhibition on clinical pharmacokinetics of panobinostat (LBH589), an orally active histone deacetylase inhibitor. Panobinostat 82-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 21753749-1 2011 In vitro studies have identified cyclosporine and tacrolimus as CYP3A inhibitors. Tacrolimus 50-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 21753749-5 2011 This implies that in vivo hepatic and first-pass CYP3A activities are significantly lower in patients receiving cyclosporine than in those receiving tacrolimus, indicating that, at the doses generally used in clinical practice, cyclosporine is the stronger of the two with respect to CYP3A inhibition. Cyclosporine 112-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 21753749-5 2011 This implies that in vivo hepatic and first-pass CYP3A activities are significantly lower in patients receiving cyclosporine than in those receiving tacrolimus, indicating that, at the doses generally used in clinical practice, cyclosporine is the stronger of the two with respect to CYP3A inhibition. Cyclosporine 112-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 284-289 21753749-5 2011 This implies that in vivo hepatic and first-pass CYP3A activities are significantly lower in patients receiving cyclosporine than in those receiving tacrolimus, indicating that, at the doses generally used in clinical practice, cyclosporine is the stronger of the two with respect to CYP3A inhibition. Tacrolimus 149-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 21753749-5 2011 This implies that in vivo hepatic and first-pass CYP3A activities are significantly lower in patients receiving cyclosporine than in those receiving tacrolimus, indicating that, at the doses generally used in clinical practice, cyclosporine is the stronger of the two with respect to CYP3A inhibition. Cyclosporine 228-240 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 21753749-5 2011 This implies that in vivo hepatic and first-pass CYP3A activities are significantly lower in patients receiving cyclosporine than in those receiving tacrolimus, indicating that, at the doses generally used in clinical practice, cyclosporine is the stronger of the two with respect to CYP3A inhibition. Cyclosporine 228-240 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 284-289 21673127-11 2011 A chemical inhibition study in NADPH-fortified S9 fraction indicated that the oxidation of AMG657417 was catalyzed almost exclusively by CYP3A. 5-(4-chlorophenyl)-3-methyl-2-(2-(((1-methylethyl)amino)methyl)-1-pyrrolidinyl)-6-(4-pyridinyl)-4(3H)-pyrimidinone 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-142 21753749-0 2011 In vivo CYP3A activity is significantly lower in cyclosporine-treated as compared with tacrolimus-treated renal allograft recipients. Cyclosporine 49-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-13 21753749-0 2011 In vivo CYP3A activity is significantly lower in cyclosporine-treated as compared with tacrolimus-treated renal allograft recipients. Tacrolimus 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-13 21753749-1 2011 In vitro studies have identified cyclosporine and tacrolimus as CYP3A inhibitors. Cyclosporine 33-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 21622627-11 2011 CYP3A4 was important for enniatin B metabolism in human microsomes as shown by 80% inhibition and impaired metabolite formation in the presence of troleandomycin. enniatins 25-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21622627-11 2011 CYP3A4 was important for enniatin B metabolism in human microsomes as shown by 80% inhibition and impaired metabolite formation in the presence of troleandomycin. Troleandomycin 147-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21673127-0 2011 A novel biotransformation of alkyl aminopyrrolidine to aminopiperidine ring by human CYP3A. N-aminopiperidine 55-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-90 21673127-8 2011 The presence of the aldehyde intermediate was verified by the formation of semicarbazide conjugates in human liver microsomal, S9, and recombinant CYP3A4 incubations of AMG657417. Aldehydes 20-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 21673127-8 2011 The presence of the aldehyde intermediate was verified by the formation of semicarbazide conjugates in human liver microsomal, S9, and recombinant CYP3A4 incubations of AMG657417. carbamylhydrazine 75-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 21673127-11 2011 A chemical inhibition study in NADPH-fortified S9 fraction indicated that the oxidation of AMG657417 was catalyzed almost exclusively by CYP3A. NADP 31-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-142 21832258-5 2011 In the 96-well plate induction assay, the CYP3A4 inducers rifampin, phenobarbital, carbamazepine, phenytoin, troglitazone, rosiglitazone, and pioglitazone yielded dose-dependent induction of LIPA metabolism, whereas the CYP1A2 inducers omeprazole and 3-methylcholanthrene did not display any induction in the CYP3A4 activity. Rosiglitazone 123-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21832258-5 2011 In the 96-well plate induction assay, the CYP3A4 inducers rifampin, phenobarbital, carbamazepine, phenytoin, troglitazone, rosiglitazone, and pioglitazone yielded dose-dependent induction of LIPA metabolism, whereas the CYP1A2 inducers omeprazole and 3-methylcholanthrene did not display any induction in the CYP3A4 activity. lipa 191-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21832258-2 2011 Using human recombinant CYP450 isoforms, LIPA was found to be metabolized extensively by CYP3A4 but not by CYP1A2, CYP2C9, CYP2C19, CYP2D6, or CYP2E1. lipa 41-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 21832258-5 2011 In the 96-well plate induction assay, the CYP3A4 inducers rifampin, phenobarbital, carbamazepine, phenytoin, troglitazone, rosiglitazone, and pioglitazone yielded dose-dependent induction of LIPA metabolism, whereas the CYP1A2 inducers omeprazole and 3-methylcholanthrene did not display any induction in the CYP3A4 activity. Omeprazole 236-246 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21832258-3 2011 In the 384-well plate CYP3A4 inhibition assay, the known inhibitors 1-aminobenzotriazole, erythromycin, ketoconazole, and verapamil were found to cause extensive (maximum inhibition of >80%), dose-dependent, statistically significant inhibition of LIPA metabolism. 1-aminobenzotriazole 68-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 21832258-5 2011 In the 96-well plate induction assay, the CYP3A4 inducers rifampin, phenobarbital, carbamazepine, phenytoin, troglitazone, rosiglitazone, and pioglitazone yielded dose-dependent induction of LIPA metabolism, whereas the CYP1A2 inducers omeprazole and 3-methylcholanthrene did not display any induction in the CYP3A4 activity. Methylcholanthrene 251-271 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21832258-3 2011 In the 384-well plate CYP3A4 inhibition assay, the known inhibitors 1-aminobenzotriazole, erythromycin, ketoconazole, and verapamil were found to cause extensive (maximum inhibition of >80%), dose-dependent, statistically significant inhibition of LIPA metabolism. Erythromycin 90-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 21832258-3 2011 In the 384-well plate CYP3A4 inhibition assay, the known inhibitors 1-aminobenzotriazole, erythromycin, ketoconazole, and verapamil were found to cause extensive (maximum inhibition of >80%), dose-dependent, statistically significant inhibition of LIPA metabolism. Ketoconazole 104-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 22687664-3 2011 Etoposide is metabolised by cytochrome P450 3A4. Etoposide 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-47 21832258-3 2011 In the 384-well plate CYP3A4 inhibition assay, the known inhibitors 1-aminobenzotriazole, erythromycin, ketoconazole, and verapamil were found to cause extensive (maximum inhibition of >80%), dose-dependent, statistically significant inhibition of LIPA metabolism. Verapamil 122-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 21832258-4 2011 The non-CYP3A4 inhibitors diethyldithiocarbamate, quercetin, quinidine, sulfaphenazole, ticlopidine, and tranylcypromine were found to have substantially lower (maximum inhibition of <50%) or no apparent inhibitory effects in the HTS assay. Ditiocarb 26-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 21832258-4 2011 The non-CYP3A4 inhibitors diethyldithiocarbamate, quercetin, quinidine, sulfaphenazole, ticlopidine, and tranylcypromine were found to have substantially lower (maximum inhibition of <50%) or no apparent inhibitory effects in the HTS assay. Quercetin 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 21832258-4 2011 The non-CYP3A4 inhibitors diethyldithiocarbamate, quercetin, quinidine, sulfaphenazole, ticlopidine, and tranylcypromine were found to have substantially lower (maximum inhibition of <50%) or no apparent inhibitory effects in the HTS assay. Quinidine 61-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 21832258-4 2011 The non-CYP3A4 inhibitors diethyldithiocarbamate, quercetin, quinidine, sulfaphenazole, ticlopidine, and tranylcypromine were found to have substantially lower (maximum inhibition of <50%) or no apparent inhibitory effects in the HTS assay. Sulfaphenazole 72-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 21832258-4 2011 The non-CYP3A4 inhibitors diethyldithiocarbamate, quercetin, quinidine, sulfaphenazole, ticlopidine, and tranylcypromine were found to have substantially lower (maximum inhibition of <50%) or no apparent inhibitory effects in the HTS assay. Ticlopidine 88-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 21832258-4 2011 The non-CYP3A4 inhibitors diethyldithiocarbamate, quercetin, quinidine, sulfaphenazole, ticlopidine, and tranylcypromine were found to have substantially lower (maximum inhibition of <50%) or no apparent inhibitory effects in the HTS assay. Tranylcypromine 105-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 21832258-5 2011 In the 96-well plate induction assay, the CYP3A4 inducers rifampin, phenobarbital, carbamazepine, phenytoin, troglitazone, rosiglitazone, and pioglitazone yielded dose-dependent induction of LIPA metabolism, whereas the CYP1A2 inducers omeprazole and 3-methylcholanthrene did not display any induction in the CYP3A4 activity. Rifampin 58-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21832258-5 2011 In the 96-well plate induction assay, the CYP3A4 inducers rifampin, phenobarbital, carbamazepine, phenytoin, troglitazone, rosiglitazone, and pioglitazone yielded dose-dependent induction of LIPA metabolism, whereas the CYP1A2 inducers omeprazole and 3-methylcholanthrene did not display any induction in the CYP3A4 activity. Phenobarbital 68-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21832258-5 2011 In the 96-well plate induction assay, the CYP3A4 inducers rifampin, phenobarbital, carbamazepine, phenytoin, troglitazone, rosiglitazone, and pioglitazone yielded dose-dependent induction of LIPA metabolism, whereas the CYP1A2 inducers omeprazole and 3-methylcholanthrene did not display any induction in the CYP3A4 activity. Carbamazepine 83-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21832258-5 2011 In the 96-well plate induction assay, the CYP3A4 inducers rifampin, phenobarbital, carbamazepine, phenytoin, troglitazone, rosiglitazone, and pioglitazone yielded dose-dependent induction of LIPA metabolism, whereas the CYP1A2 inducers omeprazole and 3-methylcholanthrene did not display any induction in the CYP3A4 activity. Phenytoin 98-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21832258-5 2011 In the 96-well plate induction assay, the CYP3A4 inducers rifampin, phenobarbital, carbamazepine, phenytoin, troglitazone, rosiglitazone, and pioglitazone yielded dose-dependent induction of LIPA metabolism, whereas the CYP1A2 inducers omeprazole and 3-methylcholanthrene did not display any induction in the CYP3A4 activity. Troglitazone 109-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21911167-4 2011 In vitro experiments have shown sorafenib to be metabolized by the drug-metabolizing enzyme cytochrome P450 3A4 (CYP3A4) and glucuronosyltransferase (UGT1A9). Sorafenib 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-111 21911167-4 2011 In vitro experiments have shown sorafenib to be metabolized by the drug-metabolizing enzyme cytochrome P450 3A4 (CYP3A4) and glucuronosyltransferase (UGT1A9). Sorafenib 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 21641981-0 2011 Aflatoxins upregulate CYP3A4 mRNA expression in a process that involves the PXR transcription factor. Aflatoxins 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 21641981-9 2011 The results of this study indicate that aflatoxin B1 is able to activate PXR, a known regulator of liver xenobiotic metabolism, in human hepatocytes, and it can upregulate the expression of PXR-dependent genes responsible for aflatoxin B1 biotransformation, including CYP3A4. Aflatoxin B1 40-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 268-274 21766881-3 2011 When recombinant cytochrome P450 3A4 was incubated with 4-hydroxynonenal, O(2), and NADPH, several products were produced, including 1,4-dihydroxynonene (DHN), 4-hydroxy-2-nonenoic acid (HNA), and an unknown metabolite. 4-hydroxy-2-nonenal 56-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-36 21766881-3 2011 When recombinant cytochrome P450 3A4 was incubated with 4-hydroxynonenal, O(2), and NADPH, several products were produced, including 1,4-dihydroxynonene (DHN), 4-hydroxy-2-nonenoic acid (HNA), and an unknown metabolite. o(2) 74-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-36 21766881-3 2011 When recombinant cytochrome P450 3A4 was incubated with 4-hydroxynonenal, O(2), and NADPH, several products were produced, including 1,4-dihydroxynonene (DHN), 4-hydroxy-2-nonenoic acid (HNA), and an unknown metabolite. NADP 84-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-36 21766881-3 2011 When recombinant cytochrome P450 3A4 was incubated with 4-hydroxynonenal, O(2), and NADPH, several products were produced, including 1,4-dihydroxynonene (DHN), 4-hydroxy-2-nonenoic acid (HNA), and an unknown metabolite. 1,4-dihydroxynonene 133-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-36 21766881-3 2011 When recombinant cytochrome P450 3A4 was incubated with 4-hydroxynonenal, O(2), and NADPH, several products were produced, including 1,4-dihydroxynonene (DHN), 4-hydroxy-2-nonenoic acid (HNA), and an unknown metabolite. dhn 154-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-36 21766881-3 2011 When recombinant cytochrome P450 3A4 was incubated with 4-hydroxynonenal, O(2), and NADPH, several products were produced, including 1,4-dihydroxynonene (DHN), 4-hydroxy-2-nonenoic acid (HNA), and an unknown metabolite. 4-hydroxy-2-nonenoic acid 160-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-36 21766881-3 2011 When recombinant cytochrome P450 3A4 was incubated with 4-hydroxynonenal, O(2), and NADPH, several products were produced, including 1,4-dihydroxynonene (DHN), 4-hydroxy-2-nonenoic acid (HNA), and an unknown metabolite. 4-hydroxy-2-nonenoic acid 187-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-36 21841964-1 2011 4-Aminopiperidines are a variety of therapeutic agents that are extensively metabolized by cytochrome P450s with CYP3A4 as a major isoform catalyzing their N-dealkylation reaction. 4-aminopiperidine 0-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 21841964-5 2011 Our results herein suggested that the molecular interactions between substrates and CYP3A4 active site residues are essential for the N-dealkylation of 4-aminopiperidines. 4-aminopiperidine 152-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 21841964-6 2011 We also found that the serine 119 residue of CYP3A4 may serve as a key hydrogen-bonding partner to interact with the 4-amino groups of the studied drugs. Serine 23-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 21841964-6 2011 We also found that the serine 119 residue of CYP3A4 may serve as a key hydrogen-bonding partner to interact with the 4-amino groups of the studied drugs. Hydrogen 71-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 21826053-4 2011 In the presence of corydaline, CYP3A-mediated midazolam hydroxylation showed a decrease with increasing preincubation time in a dose-dependent manner with K(i) values of 30.0 mM. corydaline 19-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-36 21826053-4 2011 In the presence of corydaline, CYP3A-mediated midazolam hydroxylation showed a decrease with increasing preincubation time in a dose-dependent manner with K(i) values of 30.0 mM. Midazolam 46-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-36 22687664-5 2011 There is an additional increased risk of toxicity due to a potential interaction between etoposide and ketoconazole, which is a strong inhibitor of cytochrome P450 3A4, and theoretically can lead to greater myelosuppression. Etoposide 89-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-167 22687664-5 2011 There is an additional increased risk of toxicity due to a potential interaction between etoposide and ketoconazole, which is a strong inhibitor of cytochrome P450 3A4, and theoretically can lead to greater myelosuppression. Ketoconazole 103-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-167 21480191-0 2011 Novel evidence-based colchicine dose-reduction algorithm to predict and prevent colchicine toxicity in the presence of cytochrome P450 3A4/P-glycoprotein inhibitors. Colchicine 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-138 21768449-1 2011 PURPOSE: Tamoxifen, a widely used agent for the prevention and treatment of breast cancer, is mainly metabolized by CYP2D6 and CYP3A to form its most abundant active metabolite, endoxifen. Tamoxifen 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 21768449-1 2011 PURPOSE: Tamoxifen, a widely used agent for the prevention and treatment of breast cancer, is mainly metabolized by CYP2D6 and CYP3A to form its most abundant active metabolite, endoxifen. 4-hydroxy-N-desmethyltamoxifen 178-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 21768449-4 2011 In this pharmacokinetic study, we investigated the value of dextromethorphan, a known probe drug for both CYP2D6 and CYP3A enzymatic activity, as a potential phenotyping probe for tamoxifen pharmacokinetics. Dextromethorphan 60-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-122 21480191-0 2011 Novel evidence-based colchicine dose-reduction algorithm to predict and prevent colchicine toxicity in the presence of cytochrome P450 3A4/P-glycoprotein inhibitors. Colchicine 80-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-138 21480191-2 2011 Seven separate drug-drug interaction (DDI) studies were performed to elucidate the in vivo effects of concomitant treatment with colchicine and known inhibitors of cytochrome P450 3A4 (CYP3A4)/P-glycoprotein (cyclosporine, ketoconazole, ritonavir, clarithromycin, azithromycin, verapamil ER [extended release]), and diltiazem ER) on the pharmacokinetics of colchicine. Colchicine 129-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 21480191-2 2011 Seven separate drug-drug interaction (DDI) studies were performed to elucidate the in vivo effects of concomitant treatment with colchicine and known inhibitors of cytochrome P450 3A4 (CYP3A4)/P-glycoprotein (cyclosporine, ketoconazole, ritonavir, clarithromycin, azithromycin, verapamil ER [extended release]), and diltiazem ER) on the pharmacokinetics of colchicine. Cyclosporine 209-221 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 21480191-2 2011 Seven separate drug-drug interaction (DDI) studies were performed to elucidate the in vivo effects of concomitant treatment with colchicine and known inhibitors of cytochrome P450 3A4 (CYP3A4)/P-glycoprotein (cyclosporine, ketoconazole, ritonavir, clarithromycin, azithromycin, verapamil ER [extended release]), and diltiazem ER) on the pharmacokinetics of colchicine. Ketoconazole 223-235 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 21480191-2 2011 Seven separate drug-drug interaction (DDI) studies were performed to elucidate the in vivo effects of concomitant treatment with colchicine and known inhibitors of cytochrome P450 3A4 (CYP3A4)/P-glycoprotein (cyclosporine, ketoconazole, ritonavir, clarithromycin, azithromycin, verapamil ER [extended release]), and diltiazem ER) on the pharmacokinetics of colchicine. Ritonavir 237-246 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 21480191-2 2011 Seven separate drug-drug interaction (DDI) studies were performed to elucidate the in vivo effects of concomitant treatment with colchicine and known inhibitors of cytochrome P450 3A4 (CYP3A4)/P-glycoprotein (cyclosporine, ketoconazole, ritonavir, clarithromycin, azithromycin, verapamil ER [extended release]), and diltiazem ER) on the pharmacokinetics of colchicine. Clarithromycin 248-262 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 21480191-2 2011 Seven separate drug-drug interaction (DDI) studies were performed to elucidate the in vivo effects of concomitant treatment with colchicine and known inhibitors of cytochrome P450 3A4 (CYP3A4)/P-glycoprotein (cyclosporine, ketoconazole, ritonavir, clarithromycin, azithromycin, verapamil ER [extended release]), and diltiazem ER) on the pharmacokinetics of colchicine. Azithromycin 264-276 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 21480191-2 2011 Seven separate drug-drug interaction (DDI) studies were performed to elucidate the in vivo effects of concomitant treatment with colchicine and known inhibitors of cytochrome P450 3A4 (CYP3A4)/P-glycoprotein (cyclosporine, ketoconazole, ritonavir, clarithromycin, azithromycin, verapamil ER [extended release]), and diltiazem ER) on the pharmacokinetics of colchicine. verapamil er 278-290 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 21480191-2 2011 Seven separate drug-drug interaction (DDI) studies were performed to elucidate the in vivo effects of concomitant treatment with colchicine and known inhibitors of cytochrome P450 3A4 (CYP3A4)/P-glycoprotein (cyclosporine, ketoconazole, ritonavir, clarithromycin, azithromycin, verapamil ER [extended release]), and diltiazem ER) on the pharmacokinetics of colchicine. Diltiazem 316-325 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 21480191-2 2011 Seven separate drug-drug interaction (DDI) studies were performed to elucidate the in vivo effects of concomitant treatment with colchicine and known inhibitors of cytochrome P450 3A4 (CYP3A4)/P-glycoprotein (cyclosporine, ketoconazole, ritonavir, clarithromycin, azithromycin, verapamil ER [extended release]), and diltiazem ER) on the pharmacokinetics of colchicine. Colchicine 357-367 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 21480191-7 2011 Significant DDIs were present when single doses of colchicine were coadministered with most of the selected CYP3A4/P-glycoprotein inhibitors. Colchicine 51-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 21480191-9 2011 CONCLUSION: These studies provide quantitative evidence regarding drug interactions and necessary adjustments in the dose of colchicine if colchicine treatment is continued during therapy with multiple CYP3A4/P-glycoprotein inhibitors. Colchicine 125-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 202-208 21722087-8 2011 The use of luciferin-IPA allows CYP3A4 activity to be quantified rapidly using a plate reader, thereby avoiding the need for LC/MS that is required for traditional substrates such as testosterone and midazolam. Midazolam 200-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 21496064-3 2011 WHAT THIS STUDY ADDS: This study provides information on the drug-drug interactions of tamsulosin with strong CYP2D6 and strong CYP3A4 inhibitors after single dose administration in healthy subjects. Tamsulosin 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 21496064-4 2011 AIM: To determine the effect of the strong CYP2D6 inhibitor paroxetine and strong CYP3A4 inhibitor ketoconazole on the pharmacokinetics and safety (orthostatic challenge) of tamsulosin. Tamsulosin 174-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 21716267-1 2011 This study examined drug-drug interactions of oral S-ketamine with the cytochrome P450 (CYP) 2B6 inhibitor ticlopidine and the CYP3A inhibitor itraconazole. Itraconazole 143-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 21716273-3 2011 Verapamil and quinidine are good substrates of both the multidrug resistance 1 transporter (MDR1) and the cytochrome P450 (CYP) 3A4 enzyme (CYP3A4). Verapamil 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 21716273-3 2011 Verapamil and quinidine are good substrates of both the multidrug resistance 1 transporter (MDR1) and the cytochrome P450 (CYP) 3A4 enzyme (CYP3A4). Quinidine 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 21555507-6 2011 IL-6 suppressed induction of CYP1A2 enzyme activity by omeprazole and CYP3A4 enzyme activity by rifampicin but only at supraphysiological concentrations of IL-6. Rifampin 96-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 21545485-0 2011 Effects of the moderate CYP3A4 inhibitor, fluconazole, on the pharmacokinetics of fesoterodine in healthy subjects. Fluconazole 42-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 21545485-0 2011 Effects of the moderate CYP3A4 inhibitor, fluconazole, on the pharmacokinetics of fesoterodine in healthy subjects. fesoterodine 82-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 21545485-1 2011 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: Available data suggest that fesoterodine dosage should not exceed 4 mg once daily when taken concomitantly with potent CYP3A4 inhibitors, such as ketoconazole. fesoterodine 70-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 21545485-2 2011 Currently, no information is available on whether dose adjustment is necessary when fesoterodine is administered with a moderate CYP3A4 inhibitor. fesoterodine 84-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 21545485-4 2011 AIMS: To assess the effects of fluconazole, a moderate CYP3A4 inhibitor, on the pharmacokinetics (PK) and safety/tolerability of fesoterodine. Fluconazole 31-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 21722087-8 2011 The use of luciferin-IPA allows CYP3A4 activity to be quantified rapidly using a plate reader, thereby avoiding the need for LC/MS that is required for traditional substrates such as testosterone and midazolam. Testosterone 183-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 21722087-17 2011 With this assay, time and concentration dependent inhibition of CYP3A4 were observed for 1-aminobenzotriazole and erythromycin. 1-aminobenzotriazole 89-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 21722087-17 2011 With this assay, time and concentration dependent inhibition of CYP3A4 were observed for 1-aminobenzotriazole and erythromycin. Erythromycin 114-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 21080015-2 2011 We used the docking method to explore possible binding modes of an entry inhibitor (maraviroc) and non-nucleoside reverse transcriptase inhibitors (delavirdine, efavirenz and etravirine) to cytochrome P450 3A4 (CYP3A4). Delavirdine 148-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-209 21362475-4 2011 7-Benzyloxy-4-(trifluoromethyl)-coumarin (BFC) and 7-hydroxycoumarin (7-HC) were used as fluorescent substrates in order to determine CYP3A4 and CYP2A6 catalytic activity, respectively. 7-benzyloxy-4-trifluoromethylcoumarin 0-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 21362475-4 2011 7-Benzyloxy-4-(trifluoromethyl)-coumarin (BFC) and 7-hydroxycoumarin (7-HC) were used as fluorescent substrates in order to determine CYP3A4 and CYP2A6 catalytic activity, respectively. 7-benzyloxy-4-trifluoromethylcoumarin 42-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 21362475-6 2011 All tested (thiolated) polymers were found to be more potent inhibitors of CYP3A4 than of CYP2A6 catalytic activity. Polymers 23-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 21576599-0 2011 Cholesterol 25-hydroxylation activity of CYP3A. Cholesterol 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 21576599-5 2011 We now report that CYP3A synthesizes a significant amount of 25-hydroxycholesterol and may participate in the regulation of lipid metabolism. 25-hydroxycholesterol 61-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-24 21576599-7 2011 Furthermore, treatment of the cells with troleandomycin, a specific inhibitor of CYP3A, significantly reduced cellular 25-hydroxycholesterol concentrations. Troleandomycin 41-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 21576599-7 2011 Furthermore, treatment of the cells with troleandomycin, a specific inhibitor of CYP3A, significantly reduced cellular 25-hydroxycholesterol concentrations. 25-hydroxycholesterol 119-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 21576599-8 2011 In cells that overexpressed human recombinant CYP3A4, the activity of cholesterol 25-hydroxylation was found to be higher than that of cholesterol 4beta-hydroxylation, a known marker activity of CYP3A4. Cholesterol 70-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 21576599-8 2011 In cells that overexpressed human recombinant CYP3A4, the activity of cholesterol 25-hydroxylation was found to be higher than that of cholesterol 4beta-hydroxylation, a known marker activity of CYP3A4. Cholesterol 135-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 21576599-10 2011 These results demonstrate the significance of CYP3A on the production of 25-hydroxycholesterol. 25-hydroxycholesterol 73-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-51 21652732-0 2011 Still another activity by the highly promiscuous enzyme CYP3A4: 25-hydroxylation of cholesterol. Cholesterol 84-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 21080015-2 2011 We used the docking method to explore possible binding modes of an entry inhibitor (maraviroc) and non-nucleoside reverse transcriptase inhibitors (delavirdine, efavirenz and etravirine) to cytochrome P450 3A4 (CYP3A4). Delavirdine 148-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-217 21080015-2 2011 We used the docking method to explore possible binding modes of an entry inhibitor (maraviroc) and non-nucleoside reverse transcriptase inhibitors (delavirdine, efavirenz and etravirine) to cytochrome P450 3A4 (CYP3A4). efavirenz 161-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-209 21080015-2 2011 We used the docking method to explore possible binding modes of an entry inhibitor (maraviroc) and non-nucleoside reverse transcriptase inhibitors (delavirdine, efavirenz and etravirine) to cytochrome P450 3A4 (CYP3A4). efavirenz 161-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-217 21080015-2 2011 We used the docking method to explore possible binding modes of an entry inhibitor (maraviroc) and non-nucleoside reverse transcriptase inhibitors (delavirdine, efavirenz and etravirine) to cytochrome P450 3A4 (CYP3A4). etravirine 175-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-209 21080015-2 2011 We used the docking method to explore possible binding modes of an entry inhibitor (maraviroc) and non-nucleoside reverse transcriptase inhibitors (delavirdine, efavirenz and etravirine) to cytochrome P450 3A4 (CYP3A4). etravirine 175-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-217 21080015-4 2011 We observed that efavirenz and etravirine induce metabolism of co-administered drugs by binding to a unique position in the active site of CYP3A4. efavirenz 17-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 21080015-4 2011 We observed that efavirenz and etravirine induce metabolism of co-administered drugs by binding to a unique position in the active site of CYP3A4. etravirine 31-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 21487929-5 2011 Real-time RT-PCR and Western blotting analysis in HPHs showed that both CPA and IFO induced the expressions of CYP2B6 and CYP3A4. Cyclophosphamide 72-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 21704641-7 2011 Seven of 14 recombinant human CYP enzymes examined (CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) were capable of metabolizing CBD. Cannabidiol 142-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 21704641-8 2011 The correlations between CYP isoform-specific activities and CBD oxidative activities in 16 individual HLMs indicated that 6beta-OH- and 4""-OH-CBDs were mainly formed by CYP3A4, which was supported by inhibition studies using ketoconazole and an anti-CYP3A4 antibody. 6beta-oh- and 4""-oh-cbds 123-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 21704641-8 2011 The correlations between CYP isoform-specific activities and CBD oxidative activities in 16 individual HLMs indicated that 6beta-OH- and 4""-OH-CBDs were mainly formed by CYP3A4, which was supported by inhibition studies using ketoconazole and an anti-CYP3A4 antibody. 6beta-oh- and 4""-oh-cbds 123-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 252-258 21704641-8 2011 The correlations between CYP isoform-specific activities and CBD oxidative activities in 16 individual HLMs indicated that 6beta-OH- and 4""-OH-CBDs were mainly formed by CYP3A4, which was supported by inhibition studies using ketoconazole and an anti-CYP3A4 antibody. Ketoconazole 227-239 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 21507593-1 2011 A novel liquid chromatography-tandem mass spectrometry method is described for the quantitative determination of the endogenous CYP 3A4/5 marker 4beta-hydroxycholesterol in human K(2)-EDTA plasma. cholest-5-ene-3,4-diol 145-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-135 21466844-8 2011 At concentration of 1 ng/ml, trantinterol was about 3.6 +- 3.1% as effective as rifampin (CYP3A4/5 inducer). Rifampin 80-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 21507593-1 2011 A novel liquid chromatography-tandem mass spectrometry method is described for the quantitative determination of the endogenous CYP 3A4/5 marker 4beta-hydroxycholesterol in human K(2)-EDTA plasma. Edetic Acid 184-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-135 21651615-2 2011 Saxagliptin is metabolized by CYP3A4/3A5 to 5-hydroxy saxagliptin, its major pharmacologically active metabolite. saxagliptin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 21712512-4 2011 Seven weeks after the initiation of inhaled fluticasone, she developed vaginal candidiasis and was prescribed fluconazole 100 mg/day, a CYP3A4 inhibitor. Fluconazole 110-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 21391977-3 2011 This study characterized metabolism of 4-HPR in humans and mice, and to explore the effects of ketoconazole, an inhibitor of CYP3A4, as a modulator to increase 4-HPR plasma levels in mice and to increase the low bioavailability of 4-HPR. Ketoconazole 95-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 21391977-8 2011 4-HPR was oxidized to 4-oxo-4-HPR, at least in part via human CYP3A4. Fenretinide 0-5 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 21391977-8 2011 4-HPR was oxidized to 4-oxo-4-HPR, at least in part via human CYP3A4. 4-oxofenretinide 22-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 21391977-9 2011 The CYP3A4 inhibitor ketoconazole significantly reduced 4-oxo-4-HPR formation in both human and mouse liver microsomes. Ketoconazole 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 21438849-15 2011 The current evaluation of glucuronide metabolites of BUP and norBUP are suggestive of combined inhibition of Uridine diphosphate (UDP)-glucuronosyltransferase of the 1A family and cytochrome P450 3A4 that spares UGT2B7 leading to a shunting of BUP away from production of norBUP and toward BUP-3G as seen by a statistically significant increase in the AUC of BUP-3G. Glucuronides 26-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-199 21391977-9 2011 The CYP3A4 inhibitor ketoconazole significantly reduced 4-oxo-4-HPR formation in both human and mouse liver microsomes. 4-oxofenretinide 56-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 21651615-2 2011 Saxagliptin is metabolized by CYP3A4/3A5 to 5-hydroxy saxagliptin, its major pharmacologically active metabolite. 5-hydroxysaxagliptin 44-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 22035341-3 2011 Methadone is extensively metabolized by cytochrome P450 (CYP) 3A4 and to a lesser extent by CYP 1A2, 2D6, 2D8, 2C9/2C8, 2C19, and 2B6. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-65 21596874-0 2011 CYP2D6- and CYP3A-dependent enantioselective plasma concentrations of ondansetron in postanesthesia care. Ondansetron 70-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 21596874-3 2011 In this study, we evaluated the hypothesis that genotype-dependent CYP2D6 and CYP3A activity selectively influences plasma concentrations of ondansetron enantiomers. Ondansetron 141-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 21596874-12 2011 Doubling the ondansetron dose increased plasma concentrations only in individuals with low CYP3A activity, but not in individuals with high enzyme activity (P < 0.001). Ondansetron 13-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-96 21562488-1 2011 Systemic and oral clearances of alfentanil (ALF) are in vivo probes for hepatic and first-pass cytochrome P450 (CYP) 3A. Alfentanil 32-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-119 21562488-1 2011 Systemic and oral clearances of alfentanil (ALF) are in vivo probes for hepatic and first-pass cytochrome P450 (CYP) 3A. Alfentanil 44-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-119 21562488-3 2011 This investigation determined ALF sensitivity for detecting graded CYP3A induction and compared it with that of midazolam (MDZ). Alfentanil 30-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-72 21511944-4 2011 Despite addition of GSH, CBLs of troglitazone and rosiglitazone in human liver microsomes were correlated with CYP3A (or CYP2C8) and CYP2C8 activities, respectively. Troglitazone 33-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-116 21436404-6 2011 Ketoconazole treatment decreased the CYP3A4 activity by 69%, and rifampicin induced the CYP3A4- and CYP2B6-dependent activity 6-fold, which predicts well the magnitude of changes observed in vivo. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 21436404-6 2011 Ketoconazole treatment decreased the CYP3A4 activity by 69%, and rifampicin induced the CYP3A4- and CYP2B6-dependent activity 6-fold, which predicts well the magnitude of changes observed in vivo. Rifampin 65-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 21441468-1 2011 Rifampin and carbamazepine have been recommended in the U.S. Food and Drug Administration draft drug interaction guidance as CYP3A4 inducers for clinical drug-drug interaction (DDI) studies. Rifampin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 21447734-0 2011 Mechanism-based inactivation of cytochrome P450 3A4 by mibefradil through heme destruction. Heme 74-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-51 21447734-3 2011 Mibefradil has previously been shown to be a potent reversible (IC(50) = 0.3-2 muM) and mechanism-based (K(i) = 2.3 muM; k(inact) = 0.4 min(-1)) inhibitor of CYP3A4-catalyzed statin metabolism. Mibefradil 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 21447734-5 2011 Mechanism-based inactivation experiments and spectral studies were used to examine the mechanism of CYP3A4 inactivation by mibefradil and its major metabolite, des-methoxyacetyl mibefradil (Ro 40-5966), in vitro. Mibefradil 123-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 21441468-1 2011 Rifampin and carbamazepine have been recommended in the U.S. Food and Drug Administration draft drug interaction guidance as CYP3A4 inducers for clinical drug-drug interaction (DDI) studies. Carbamazepine 13-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 21511944-4 2011 Despite addition of GSH, CBLs of troglitazone and rosiglitazone in human liver microsomes were correlated with CYP3A (or CYP2C8) and CYP2C8 activities, respectively. Rosiglitazone 50-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-116 21441468-8 2011 Comparison of the maximal CYP3A4 induction potential among the three inducers indicated that rifampin is the most potent inducer and is the best choice for clinical CYP3A4 induction DDI studies. Rifampin 93-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 21447734-5 2011 Mechanism-based inactivation experiments and spectral studies were used to examine the mechanism of CYP3A4 inactivation by mibefradil and its major metabolite, des-methoxyacetyl mibefradil (Ro 40-5966), in vitro. des-methoxyacetyl mibefradil 160-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 21441468-8 2011 Comparison of the maximal CYP3A4 induction potential among the three inducers indicated that rifampin is the most potent inducer and is the best choice for clinical CYP3A4 induction DDI studies. Rifampin 93-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 21246351-9 2011 CONCLUSION: Pregnancy leads to increased CYP3A enzyme activity as determined by the 4beta-hydroxycholesterol/cholesterol ratio. 4beta 84-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 21441468-9 2011 Moreover, a near-maximal CYP3A4 DDI was predicted to result from administration of rifampin for approximately 7 days at 450 to 600 mg q.d. Rifampin 83-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 21447734-5 2011 Mechanism-based inactivation experiments and spectral studies were used to examine the mechanism of CYP3A4 inactivation by mibefradil and its major metabolite, des-methoxyacetyl mibefradil (Ro 40-5966), in vitro. ro 40 190-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 21447734-7 2011 Complete K(i)/k(inact) experiments were performed, revealing a rapid and irreversible decrease in CYP3A4-catalyzed 1"-hydroxymidazolam formation. 1-hydroxymethylmidazolam 115-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 21447734-8 2011 Approximately 70% of CYP3A4 activity was lost in the first minute of incubation with mibefradil, and inactivation was nonlinear after 2 min. Mibefradil 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 21447734-9 2011 Ro 40-5966 also resulted in time-dependent inhibition of CYP3A4, albeit to a lesser extent than mibefradil. ro 40-5966 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 21447734-10 2011 The decrease in CYP3A4 activity in the presence of mibefradil and NADPH was subsequently shown to have a good correlation with the time-dependent loss of CO binding, which, coupled with the lack of stable heme and/or apoprotein adducts, suggests heme destruction as the mechanism of inactivation of CYP3A4 by mibefradil. Mibefradil 51-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 21447734-10 2011 The decrease in CYP3A4 activity in the presence of mibefradil and NADPH was subsequently shown to have a good correlation with the time-dependent loss of CO binding, which, coupled with the lack of stable heme and/or apoprotein adducts, suggests heme destruction as the mechanism of inactivation of CYP3A4 by mibefradil. Mibefradil 51-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 299-305 21447734-10 2011 The decrease in CYP3A4 activity in the presence of mibefradil and NADPH was subsequently shown to have a good correlation with the time-dependent loss of CO binding, which, coupled with the lack of stable heme and/or apoprotein adducts, suggests heme destruction as the mechanism of inactivation of CYP3A4 by mibefradil. NADP 66-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 21447734-10 2011 The decrease in CYP3A4 activity in the presence of mibefradil and NADPH was subsequently shown to have a good correlation with the time-dependent loss of CO binding, which, coupled with the lack of stable heme and/or apoprotein adducts, suggests heme destruction as the mechanism of inactivation of CYP3A4 by mibefradil. NADP 66-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 299-305 21447734-10 2011 The decrease in CYP3A4 activity in the presence of mibefradil and NADPH was subsequently shown to have a good correlation with the time-dependent loss of CO binding, which, coupled with the lack of stable heme and/or apoprotein adducts, suggests heme destruction as the mechanism of inactivation of CYP3A4 by mibefradil. Heme 205-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 21447734-10 2011 The decrease in CYP3A4 activity in the presence of mibefradil and NADPH was subsequently shown to have a good correlation with the time-dependent loss of CO binding, which, coupled with the lack of stable heme and/or apoprotein adducts, suggests heme destruction as the mechanism of inactivation of CYP3A4 by mibefradil. Heme 246-250 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 21447734-10 2011 The decrease in CYP3A4 activity in the presence of mibefradil and NADPH was subsequently shown to have a good correlation with the time-dependent loss of CO binding, which, coupled with the lack of stable heme and/or apoprotein adducts, suggests heme destruction as the mechanism of inactivation of CYP3A4 by mibefradil. Mibefradil 309-319 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 21327421-2 2011 Paclitaxel is metabolized in the liver by CYP2C8 and CYP3A4 and transported by P-glycoprotein. Paclitaxel 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 21246351-9 2011 CONCLUSION: Pregnancy leads to increased CYP3A enzyme activity as determined by the 4beta-hydroxycholesterol/cholesterol ratio. Hydroxycholesterols 90-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 21246351-9 2011 CONCLUSION: Pregnancy leads to increased CYP3A enzyme activity as determined by the 4beta-hydroxycholesterol/cholesterol ratio. Cholesterol 97-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 21844990-13 2011 No significant clinical interaction or effect was observed, even with the use of atorvastatin or simvastatin, which are metabolized by CYP3A4 such as tacrolimus. Atorvastatin 81-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 21844990-13 2011 No significant clinical interaction or effect was observed, even with the use of atorvastatin or simvastatin, which are metabolized by CYP3A4 such as tacrolimus. Simvastatin 97-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 21844990-13 2011 No significant clinical interaction or effect was observed, even with the use of atorvastatin or simvastatin, which are metabolized by CYP3A4 such as tacrolimus. Tacrolimus 150-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 21501604-8 2011 50 muM bosentan up-regulated e.g. CYP3A4 8.5-fold, ABCB1 5.1-fold, and ABCB11 1.9-fold at the mRNA level in LS180 cells. Bosentan 7-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 21635144-0 2011 Impact of the CYP3A4*1G polymorphism and its combination with CYP3A5 genotypes on tacrolimus pharmacokinetics in renal transplant patients. Tacrolimus 82-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 21635144-1 2011 AIM: Tacrolimus is a substrate of CYP3A4 and CYP3A5. Tacrolimus 5-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 21635144-2 2011 The present study investigated the impact of the CYP3A4*1/*1G polymorphism compared with CYP3A5 genotypes on the dose-adjusted pharmacokinetics of tacrolimus. Tacrolimus 147-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 21635144-5 2011 RESULTS: The dose-adjusted AUC0-12 and C0 of tacrolimus were significantly lower in patients with the CYP3A4*1G allele and CYP3A5 expressers than those with the CYP3A4*1/*1 genotype and nonexpressers, respectively. Tacrolimus 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 21635144-5 2011 RESULTS: The dose-adjusted AUC0-12 and C0 of tacrolimus were significantly lower in patients with the CYP3A4*1G allele and CYP3A5 expressers than those with the CYP3A4*1/*1 genotype and nonexpressers, respectively. Tacrolimus 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 21635144-7 2011 The standardized regression coefficient for the AUC0-12 of tacrolimus was approximately twofold less for CYP3A4*1/*1 than CYP3A5*3/*3. Tacrolimus 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 21635144-9 2011 CONCLUSION: The CYP3A4*1/*1G polymorphism was associated with the pharmacokinetics of tacrolimus, however, its contribution to dose-adjusted pharmacokinetics was approximately twofold less than that of the CYP3A5*1/*3 polymorphism. Tacrolimus 86-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 21635144-10 2011 Although its effect on CYP3A4 activity is not clear, CYP3A4*1/*1G may be a candidate for a polymorphism affecting the interindividual variability in tacrolimus pharmacokinetics among CYP3A5 expressers. Tacrolimus 149-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 21635144-10 2011 Although its effect on CYP3A4 activity is not clear, CYP3A4*1/*1G may be a candidate for a polymorphism affecting the interindividual variability in tacrolimus pharmacokinetics among CYP3A5 expressers. Tacrolimus 149-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 21595477-4 2011 Etoposide is metabolized by CYP3A4 to etoposide catechol, which can be further oxidized to etoposide quinone. Etoposide 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 21595477-4 2011 Etoposide is metabolized by CYP3A4 to etoposide catechol, which can be further oxidized to etoposide quinone. 3',4'-Dihydroxyetoposide 38-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 21595477-4 2011 Etoposide is metabolized by CYP3A4 to etoposide catechol, which can be further oxidized to etoposide quinone. Etoposide quinone 91-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 21595477-5 2011 A CYP3A4 variant is associated with a lower risk of etoposide-related leukemias, suggesting that etoposide metabolites may be involved in leukemogenesis. Etoposide 52-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 2-8 21635243-4 2011 In this study, the effects of two commonly prescribed AEDs, lamotrigine and phenytoin, with different routes of metabolism (CYP3A4 versus glucuronic acid conjugation) on atorvastatin pharmacokinetics were evaluated. Lamotrigine 60-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 21635243-4 2011 In this study, the effects of two commonly prescribed AEDs, lamotrigine and phenytoin, with different routes of metabolism (CYP3A4 versus glucuronic acid conjugation) on atorvastatin pharmacokinetics were evaluated. Phenytoin 76-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 21635243-4 2011 In this study, the effects of two commonly prescribed AEDs, lamotrigine and phenytoin, with different routes of metabolism (CYP3A4 versus glucuronic acid conjugation) on atorvastatin pharmacokinetics were evaluated. Atorvastatin 170-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 21365364-5 2011 Andrographolide was found to exclusively but weakly inhibit CYP3A4 activity. andrographolide 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 21595477-5 2011 A CYP3A4 variant is associated with a lower risk of etoposide-related leukemias, suggesting that etoposide metabolites may be involved in leukemogenesis. Etoposide 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 2-8 21501604-9 2011 In HuH-7 cells induction was much less pronounced (e.g. CYP3A4 1.9-fold for bosentan). Bosentan 76-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 21666091-8 2011 Methadone is a synthetic opioid primarily metabolized by CYP3A4 and, to a lesser degree, by other isoenzymes, including CYP1A2. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 21524698-2 2011 MATERIALS AND METHODS: We screened ethanol extracts of 28 commonly used TCMs for their capability to induce cytochrome P450 3A4 (CYP3A4) via PXR signalling pathway using a cell-based reporter gene assay combined with RT-PCR analysis. Ethanol 35-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 21524698-4 2011 RESULTS: Our observations showed that 22 ethanol extracts and 8 compounds could activate human PXR and induce CYP3A4 reporter construct in HepG2 cells. Ethanol 41-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 21524698-7 2011 CONCLUSIONS: Twenty-two TCM ethanol extracts and eight bioactive compounds could activate PXR signalling pathway and induce CYP3A4 reporter gene. Ethanol 28-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 21561094-1 2011 Vitamin K(2) is a ligand for a nuclear receptor, steroid and xenobiotic receptor (SXR), that induces the gene expressions of CYP3A4. Vitamin K 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 21447389-4 2011 This was done by using human substrates of CYP3A4 (verapamil and testosterone), CYP2C9 (diclofenac) and CYP2D6 (dextromethorphan). Verapamil 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 21447389-7 2011 Verapamil showed similar metabolism pattern as in humans and the CYP3A4 inhibitor ketoconazole was able to inhibit the depletion of both R- and S-verapamil. Ketoconazole 82-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 21447389-7 2011 Verapamil showed similar metabolism pattern as in humans and the CYP3A4 inhibitor ketoconazole was able to inhibit the depletion of both R- and S-verapamil. r- and s-verapamil 137-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 21508826-10 2011 CONCLUSIONS: : A novel observation is the large effect of rifampicin on S-norketamine concentrations and indicates that rifampicin induces the elimination of S-ketamine"s metabolite, S-norketamine, probably via induction of the CYP3A4 and/or CYP2B6 enzymes. Rifampin 120-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 21508826-10 2011 CONCLUSIONS: : A novel observation is the large effect of rifampicin on S-norketamine concentrations and indicates that rifampicin induces the elimination of S-ketamine"s metabolite, S-norketamine, probably via induction of the CYP3A4 and/or CYP2B6 enzymes. Ketamine 158-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 21508826-10 2011 CONCLUSIONS: : A novel observation is the large effect of rifampicin on S-norketamine concentrations and indicates that rifampicin induces the elimination of S-ketamine"s metabolite, S-norketamine, probably via induction of the CYP3A4 and/or CYP2B6 enzymes. norketamine 183-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 21468756-1 2011 PURPOSE: This exploratory study aimed to explain the interindividual variabilities of docetaxel pharmacokinetics and pharmacodynamics in Asian nasopharyngeal carcinoma patients (n = 54) through the genotyping of CYP3A4, CYP3A5, ABCB1, ABCC2, ABCG2 and SLCO1B3 genes. Docetaxel 86-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 212-218 20798939-4 2011 CYP3A activity was assessed a day before and a day after docetaxel by 7.5 mg oral midazolam. Midazolam 82-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 20798939-7 2011 RESULTS: CYP3A activity was clearly induced when assessed a day after docetaxel administration as shown by lower midazolam AUC (P < 0.0001) and higher AUC ratio (1-OH-midazolam/midazolam, P = 0.018). Docetaxel 70-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-14 20798939-7 2011 RESULTS: CYP3A activity was clearly induced when assessed a day after docetaxel administration as shown by lower midazolam AUC (P < 0.0001) and higher AUC ratio (1-OH-midazolam/midazolam, P = 0.018). Midazolam 113-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-14 20798939-7 2011 RESULTS: CYP3A activity was clearly induced when assessed a day after docetaxel administration as shown by lower midazolam AUC (P < 0.0001) and higher AUC ratio (1-OH-midazolam/midazolam, P = 0.018). 1-oh-midazolam 165-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-14 20798939-7 2011 RESULTS: CYP3A activity was clearly induced when assessed a day after docetaxel administration as shown by lower midazolam AUC (P < 0.0001) and higher AUC ratio (1-OH-midazolam/midazolam, P = 0.018). Midazolam 170-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-14 20798939-11 2011 CONCLUSIONS: We show here a markedly reduced docetaxel exposure followed by CYP3A induction by, most likely, dexamethasone. Dexamethasone 109-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 20798939-13 2011 Slow CYP3A-mediated metabolism might predispose patients to adverse events of docetaxel. Docetaxel 78-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 5-10 21490593-2 2011 The aim of this study was to determine whether formation clearance (CL(f)) of the sum of 6beta-hydroxycortisol and 6beta-hydroxycortisone is a useful probe of CYP3A4 inhibition in vivo. 6 beta-hydroxycortisol 89-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 21490593-2 2011 The aim of this study was to determine whether formation clearance (CL(f)) of the sum of 6beta-hydroxycortisol and 6beta-hydroxycortisone is a useful probe of CYP3A4 inhibition in vivo. 6 beta-hydroxycortisone 115-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 21553932-7 2011 Gefitinib, erlotinib and the absorbed fraction of lapatinib undergo extensive metabolism - mainly via hepatic and intestinal cytochrome P450 (CYP) 3A4 and also via CYP2D6 (gefitinib) and CYP1A2 (erlotinib) - and are primarily eliminated by biotransformation. Gefitinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-150 21553932-10 2011 Limited available data indicate that genetic polymorphisms in enzymes and transporters involved in the pharmacokinetics of gefitinib (CYP2D6) and erlotinib (CYP3A4, CYP3A5 and ABCG2 [breast cancer resistance protein]) alter the exposure to these drugs. Gefitinib 123-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 21490593-3 2011 In human liver microsomes (HLMs), the formation of 6beta-hydroxycortisol and 6beta-hydroxycortisone was catalyzed by CYP3A4, and itraconazole inhibited these reactions with half maximal inhibitory concentration (IC(50))(,u) values of 3.1 nmol/l and 3.4 nmol/l, respectively. 6 beta-hydroxycortisol 51-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 21553932-10 2011 Limited available data indicate that genetic polymorphisms in enzymes and transporters involved in the pharmacokinetics of gefitinib (CYP2D6) and erlotinib (CYP3A4, CYP3A5 and ABCG2 [breast cancer resistance protein]) alter the exposure to these drugs. Erlotinib Hydrochloride 146-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-163 21553932-7 2011 Gefitinib, erlotinib and the absorbed fraction of lapatinib undergo extensive metabolism - mainly via hepatic and intestinal cytochrome P450 (CYP) 3A4 and also via CYP2D6 (gefitinib) and CYP1A2 (erlotinib) - and are primarily eliminated by biotransformation. Erlotinib Hydrochloride 11-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-150 21490593-3 2011 In human liver microsomes (HLMs), the formation of 6beta-hydroxycortisol and 6beta-hydroxycortisone was catalyzed by CYP3A4, and itraconazole inhibited these reactions with half maximal inhibitory concentration (IC(50))(,u) values of 3.1 nmol/l and 3.4 nmol/l, respectively. 6 beta-hydroxycortisone 77-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 21553932-7 2011 Gefitinib, erlotinib and the absorbed fraction of lapatinib undergo extensive metabolism - mainly via hepatic and intestinal cytochrome P450 (CYP) 3A4 and also via CYP2D6 (gefitinib) and CYP1A2 (erlotinib) - and are primarily eliminated by biotransformation. Lapatinib 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-150 21490593-6 2011 The maximum in vivo inhibition was 59%, suggesting that f(m,CYP3A4) for cortisol and cortisone 6beta-hydroxylation is ~60%. Hydrocortisone 72-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 21490593-6 2011 The maximum in vivo inhibition was 59%, suggesting that f(m,CYP3A4) for cortisol and cortisone 6beta-hydroxylation is ~60%. Cortisone 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 21490593-7 2011 Given the significant decrease in CL(f) of 6beta-hydroxycortisone and 6beta-hydroxycortisol after 200-mg and 400-mg single doses of itraconazole, this endogenous probe can be used to detect moderate and potent CYP3A4 inhibition in vivo. 6 beta-hydroxycortisol 70-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 210-216 21490593-7 2011 Given the significant decrease in CL(f) of 6beta-hydroxycortisone and 6beta-hydroxycortisol after 200-mg and 400-mg single doses of itraconazole, this endogenous probe can be used to detect moderate and potent CYP3A4 inhibition in vivo. Itraconazole 132-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 210-216 21273732-6 2011 This includes midazolam 1"-hydroxylation and testosterone 6beta-hydroxylation, which are catalyzed by cynomolgus monkey cytochrome P450 (CYP) 3A4/5, orthologs of human CYP3A4/5, which are important drug-metabolizing enzymes. Midazolam 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 21273732-6 2011 This includes midazolam 1"-hydroxylation and testosterone 6beta-hydroxylation, which are catalyzed by cynomolgus monkey cytochrome P450 (CYP) 3A4/5, orthologs of human CYP3A4/5, which are important drug-metabolizing enzymes. testosterone 6beta 45-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 21363997-0 2011 Metabolic intermediate complex formation of human cytochrome P450 3A4 by lapatinib. Lapatinib 73-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-69 21297316-8 2011 Rifampicin is also an inducer of metabolic enzymes, and although its single coadministration produces an increase in the plasma concentration of the affected drugs, multiple coadministrations may result in reductions in the plasma concentrations of OATP1B1 and CYP3A4 bisubstrates. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 261-267 21491455-4 2011 Using nonlinear mixed-effects modeling, we could separately quantify the effects of intestinal CYP3A4 expression, hepatic CYP3A4 expression, and the presence of ritonavir on both the absorption and elimination of lopinavir, which was previously not possible using noncompartmental methods. Lopinavir 213-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 21491455-0 2011 An integrated pharmacokinetic model for the influence of CYP3A4 expression on the in vivo disposition of lopinavir and its modulation by ritonavir. Lopinavir 105-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 21491455-0 2011 An integrated pharmacokinetic model for the influence of CYP3A4 expression on the in vivo disposition of lopinavir and its modulation by ritonavir. Ritonavir 137-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 21491455-2 2011 Our aim was to separately quantify the role of intestinal and hepatic cytochrome P450 3A (CYP3A4) expression on lopinavir disposition in a novel mouse model. Lopinavir 112-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 21491455-3 2011 Lopinavir and ritonavir were administered to mice selectively expressing human CYP3A4 in the intestine and/or liver. Lopinavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 21491455-4 2011 Using nonlinear mixed-effects modeling, we could separately quantify the effects of intestinal CYP3A4 expression, hepatic CYP3A4 expression, and the presence of ritonavir on both the absorption and elimination of lopinavir, which was previously not possible using noncompartmental methods. Lopinavir 213-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 21491455-5 2011 Intestinal, but not hepatic, CYP3A4-related first-pass metabolism was the major barrier for systemic entry of lopinavir. Lopinavir 110-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 21491455-6 2011 Relative oral bioavailability of lopinavir in mice expressing both hepatic and intestinal CYP3A4 was only 1.3% when compared with mice that were CYP3A deficient. Lopinavir 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 21491455-8 2011 Hepatic CYP3A4 related systemic clearance was inversely related to ritonavir exposure and not only hepatic but also intestinal CYP3A4 expression contributed to systemic clearance of lopinavir. Ritonavir 67-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 21491455-8 2011 Hepatic CYP3A4 related systemic clearance was inversely related to ritonavir exposure and not only hepatic but also intestinal CYP3A4 expression contributed to systemic clearance of lopinavir. Lopinavir 182-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 21491455-8 2011 Hepatic CYP3A4 related systemic clearance was inversely related to ritonavir exposure and not only hepatic but also intestinal CYP3A4 expression contributed to systemic clearance of lopinavir. Lopinavir 182-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 21349323-2 2011 The median inhibitory concentrations (IC50) of asiaticoside and madecassoside were determined for CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1 and CYP3A4. asiaticoside 47-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 21349323-3 2011 Asiaticoside inhibited CYP2C19 (IC50 = 412.68 +- 15.44 muM) and CYP3A4 (IC50=343.35 +- 29.35 muM). asiaticoside 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 21402137-2 2011 In the present study, we investigated interactions between MDMA and several therapeutic and recreational drugs on CYP3A and its regulator pregnane X receptor (PXR), using a human PXR-mediated CYP3A4-reporter gene assay, rat primary hepatocytes and microsomes. N-Methyl-3,4-methylenedioxyamphetamine 59-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 21349323-4 2011 Madecassoside also inhibited CYP2C19 (IC50 = 539.04 +- 14.18 muM) and CYP3A4 (IC50 = 453.32 +- 39.33 muM). madecassoside 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 21349323-6 2011 Assessment of mechanism-based inhibition and the type of inhibition were performed for asiaticoside and madecassoside with CYP2C19 and CYP3A4. asiaticoside 87-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 21349323-6 2011 Assessment of mechanism-based inhibition and the type of inhibition were performed for asiaticoside and madecassoside with CYP2C19 and CYP3A4. madecassoside 104-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 21349323-7 2011 These results suggested that madecassoside is a mechanism-based inhibitor of CYP2C19 and CYP3A4. madecassoside 29-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 21349323-9 2011 Asiaticoside exhibited non-competitive inhibition of CYP2C19 (Ki=385.24 +- 8.75 muM) and CYP3A4 (Ki = 535.93 +- 18.99 muM). asiaticoside 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 21349323-10 2011 Madecassoside also showed non-competitive inhibition of CYP2C19 (Ki = 109.62 +- 6.14 muM) and CYP3A4 (Ki = 456.84 +- 16.43 muM). madecassoside 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 21349323-11 2011 These results suggest that asiaticoside and madecassoside could cause drug-drug interactions via inhibition of CYP2C19 and CYP3A4. asiaticoside 27-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 21349323-11 2011 These results suggest that asiaticoside and madecassoside could cause drug-drug interactions via inhibition of CYP2C19 and CYP3A4. madecassoside 44-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 21341986-3 2011 The formation of KR66223 via an esterase and the formation of KR68334 via CYP3A5 and CYP3A4 seem to be major factors in the in vitro metabolism of KR66222 using HLMs. kr68334 62-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 21341986-3 2011 The formation of KR66223 via an esterase and the formation of KR68334 via CYP3A5 and CYP3A4 seem to be major factors in the in vitro metabolism of KR66222 using HLMs. KR 66222 147-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 21341986-9 2011 In conclusion, considering pharmacokinetic variability and the intestinal first-pass effect caused by the involvement of CYP3A and P-gp, KR66223 seems to have better in vitro metabolism and permeability characteristics than KR66222. KR 66223 137-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-126 20932495-6 2011 Morphine and nicotine enhance CYP3A4 and MDR1 expression in vitro. Morphine 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 21471209-0 2011 Inhibition of human cytochrome P450 3A4 by cholesterol. Cholesterol 43-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-39 20932495-6 2011 Morphine and nicotine enhance CYP3A4 and MDR1 expression in vitro. Nicotine 13-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 21466223-0 2011 Quercetin and rutin reduced the bioavailability of cyclosporine from Neoral, an immunosuppressant, through activating P-glycoprotein and CYP 3A4. Quercetin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-144 21402692-0 2011 CYP3A4 mediates growth of estrogen receptor-positive breast cancer cells in part by inducing nuclear translocation of phospho-Stat3 through biosynthesis of (+-)-14,15-epoxyeicosatrienoic acid (EET). 14,15-epoxy-5,8,11-eicosatrienoic acid 156-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21402692-0 2011 CYP3A4 mediates growth of estrogen receptor-positive breast cancer cells in part by inducing nuclear translocation of phospho-Stat3 through biosynthesis of (+-)-14,15-epoxyeicosatrienoic acid (EET). 14,15-epoxy-5,8,11-eicosatrienoic acid 193-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21402692-4 2011 CYP3A4 was profiled for NADPH-dependent arachidonic acid (AA) metabolism and synthesized AA epoxygenase products (+-)-8,9-, (+-)-11,12-, and (+-)-14,15-epoxyeicosatrienoic acid (EET) (total turnover of ~2 pmol/pmol CYP3A4/min) but not hydroxylase products (+-)-15-, (+-)-19-, or 20-hydroxyeicosatetraenoic acid. NADP 24-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21402692-4 2011 CYP3A4 was profiled for NADPH-dependent arachidonic acid (AA) metabolism and synthesized AA epoxygenase products (+-)-8,9-, (+-)-11,12-, and (+-)-14,15-epoxyeicosatrienoic acid (EET) (total turnover of ~2 pmol/pmol CYP3A4/min) but not hydroxylase products (+-)-15-, (+-)-19-, or 20-hydroxyeicosatetraenoic acid. Arachidonic Acid 40-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21402692-4 2011 CYP3A4 was profiled for NADPH-dependent arachidonic acid (AA) metabolism and synthesized AA epoxygenase products (+-)-8,9-, (+-)-11,12-, and (+-)-14,15-epoxyeicosatrienoic acid (EET) (total turnover of ~2 pmol/pmol CYP3A4/min) but not hydroxylase products (+-)-15-, (+-)-19-, or 20-hydroxyeicosatetraenoic acid. 14,15-epoxy-5,8,11-eicosatrienoic acid 141-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21402692-4 2011 CYP3A4 was profiled for NADPH-dependent arachidonic acid (AA) metabolism and synthesized AA epoxygenase products (+-)-8,9-, (+-)-11,12-, and (+-)-14,15-epoxyeicosatrienoic acid (EET) (total turnover of ~2 pmol/pmol CYP3A4/min) but not hydroxylase products (+-)-15-, (+-)-19-, or 20-hydroxyeicosatetraenoic acid. Hydroxyeicosatetraenoic Acids 281-310 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21402692-5 2011 Furthermore, eicosanoid profiling revealed that MCF7 cells synthesize EETs in a CYP3A4-dependent manner. Eicosanoids 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 21402692-7 2011 Stat3 (Tyr-705) phosphorylation was inhibited by CYP3A4 silencing, providing a potential mechanism for CYP3A4 involvement in breast cancer cell growth. Tyrosine 7-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 21402692-7 2011 Stat3 (Tyr-705) phosphorylation was inhibited by CYP3A4 silencing, providing a potential mechanism for CYP3A4 involvement in breast cancer cell growth. Tyrosine 7-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 21402692-9 2011 Although silencing of CYP3A4 reduces nuclear Tyr(P)-705-Stat3, (+-)-14,15-EET restores this signaling process and promotes Tyr(P)-705-Stat3 translocation to the nucleus, suggesting that (+-)-14,15-EET may be involved in an autocrine/paracrine pathway driving cell growth. Tyrosine 45-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 21466223-8 2011 In conclusion, quercetin and rutin decreased the bioavailability of CSP through activating P-gp and CYP3A. Quercetin 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 21466223-8 2011 In conclusion, quercetin and rutin decreased the bioavailability of CSP through activating P-gp and CYP3A. Rutin 29-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 21466223-0 2011 Quercetin and rutin reduced the bioavailability of cyclosporine from Neoral, an immunosuppressant, through activating P-glycoprotein and CYP 3A4. Rutin 14-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-144 21466223-0 2011 Quercetin and rutin reduced the bioavailability of cyclosporine from Neoral, an immunosuppressant, through activating P-glycoprotein and CYP 3A4. Cyclosporine 51-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-144 21466223-2 2011 Cyclosporine (CSP), an immunosuppressant with a narrow therapeutic window, is a substrate of P-glycoprotein (P-gp) and cytochrome P-450 3A4 (CYP3A4). Cyclosporine 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-139 21466223-2 2011 Cyclosporine (CSP), an immunosuppressant with a narrow therapeutic window, is a substrate of P-glycoprotein (P-gp) and cytochrome P-450 3A4 (CYP3A4). Cyclosporine 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 21466223-2 2011 Cyclosporine (CSP), an immunosuppressant with a narrow therapeutic window, is a substrate of P-glycoprotein (P-gp) and cytochrome P-450 3A4 (CYP3A4). Cyclosporine 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-139 21466223-2 2011 Cyclosporine (CSP), an immunosuppressant with a narrow therapeutic window, is a substrate of P-glycoprotein (P-gp) and cytochrome P-450 3A4 (CYP3A4). Cyclosporine 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 21466223-7 2011 The in vitro studies indicated that the quercetin and rutin induced the functions of P-gp and CYP3A4. Quercetin 40-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 21466223-7 2011 The in vitro studies indicated that the quercetin and rutin induced the functions of P-gp and CYP3A4. Rutin 54-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 21350820-1 2011 Docetaxel is primarily metabolized by CYP3A4 and susceptible to alterations in clearance by CYP3A4 inhibition and induction. Docetaxel 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 21548957-6 2011 Dynamic simulations of atorvastatin biotransformation considering the inter-individual variability of the two major involved enzymes CYP3A4 and UGT1A3 based on quantitative protein expression data in a large human liver bank (n = 150) highlighted the variability in the individual biotransformation profiles and therefore also points to the individuality of pharmacokinetics. Atorvastatin 23-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 21497079-3 2011 The MWCNT structuring improves the sensitivity from 5.1 to 20.5 nA/mM mm(2) in case of CYP2B4-mediated Benzphetamine detection, from 0.26 to 0.63 nA/muM mm(2) in case of CYP3A4-mediated Cyclophosphamide detection, and from 0.11 to 0.25 nA/muM mm(2) in case of CYP2C9-mediated Naproxen detection. Benzphetamine 103-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 21505109-1 2011 OBJECTIVE: To report a case in which the anticoagulant effects of warfarin were attenuated during concomitant administration of rifaximin, possibly through induction of CYP3A4 following increased absorption of rifaximin in a patient with small intestine bacterial overgrowth (SIBO). Warfarin 66-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 21505109-1 2011 OBJECTIVE: To report a case in which the anticoagulant effects of warfarin were attenuated during concomitant administration of rifaximin, possibly through induction of CYP3A4 following increased absorption of rifaximin in a patient with small intestine bacterial overgrowth (SIBO). Rifaximin 128-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 21505109-1 2011 OBJECTIVE: To report a case in which the anticoagulant effects of warfarin were attenuated during concomitant administration of rifaximin, possibly through induction of CYP3A4 following increased absorption of rifaximin in a patient with small intestine bacterial overgrowth (SIBO). Rifaximin 210-219 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 21505109-6 2011 DISCUSSION: Rifaximin has been shown in vitro to induce the CYP3A4 enzyme for which the R-isomer of warfarin is a known substrate. Rifaximin 12-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 21505109-6 2011 DISCUSSION: Rifaximin has been shown in vitro to induce the CYP3A4 enzyme for which the R-isomer of warfarin is a known substrate. Warfarin 100-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 21505109-8 2011 In this patient population it is plausible that rifaximin bioavailability increases enough to induce CYP3A4, leading to clinically significant reductions in the bioavailability of CYP3A4 substrates, including R-warfarin. Rifaximin 48-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 21505109-8 2011 In this patient population it is plausible that rifaximin bioavailability increases enough to induce CYP3A4, leading to clinically significant reductions in the bioavailability of CYP3A4 substrates, including R-warfarin. Rifaximin 48-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 21505109-8 2011 In this patient population it is plausible that rifaximin bioavailability increases enough to induce CYP3A4, leading to clinically significant reductions in the bioavailability of CYP3A4 substrates, including R-warfarin. Warfarin 209-219 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 21505109-8 2011 In this patient population it is plausible that rifaximin bioavailability increases enough to induce CYP3A4, leading to clinically significant reductions in the bioavailability of CYP3A4 substrates, including R-warfarin. Warfarin 209-219 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 21350820-1 2011 Docetaxel is primarily metabolized by CYP3A4 and susceptible to alterations in clearance by CYP3A4 inhibition and induction. Docetaxel 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 21350820-2 2011 Imatinib is a CYP3A4 inhibitor. Imatinib Mesylate 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 21350820-11 2011 Despite a 42% decrease in CYP3A4 activity after 3 weeks of imatinib co-administration, docetaxel clearance was unchanged. Imatinib Mesylate 59-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 21350820-13 2011 In conclusion, imatinib inhibited CYP3A4 but did not affect docetaxel clearance. Imatinib Mesylate 15-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 21456632-3 2011 This study assessed the inhibition and recovery half-life of CYP2D6 and CYP3A4 activity in female subjects by administering the probe drug dextromethorphan before and repeatedly after MDMA administration. Dextromethorphan 139-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 21456632-21 2011 Regarding CYP3A4 activity, there is an apparent decrease in its activity after MDMA use. N-Methyl-3,4-methylenedioxyamphetamine 79-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 21266595-8 2011 Sorafenib N-oxidation and sunitinib N-deethylation, the primary routes of metabolism, were predominantly catalyzed by CYP3A4 but not by CYP3A5. Sorafenib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 21266595-0 2011 Sorafenib and sunitinib, two anticancer drugs, inhibit CYP3A4-mediated and activate CY3A5-mediated midazolam 1"-hydroxylation. Sorafenib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 21863748-0 2011 [The influence of vitamin B group on monooxygenase activity of cytochrome P450 3A4: pharmacokinetics and electro analysis of catalytic properties]. Riboflavin 18-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-82 21863748-7 2011 Electrochemical analysis reviled the influence of vitamin B group on metabolism of non steroid anti inflammation drug diclofenac catalyzed by cytochrome P450 3A4. Riboflavin 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-161 21863748-7 2011 Electrochemical analysis reviled the influence of vitamin B group on metabolism of non steroid anti inflammation drug diclofenac catalyzed by cytochrome P450 3A4. Steroids 87-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-161 21863748-7 2011 Electrochemical analysis reviled the influence of vitamin B group on metabolism of non steroid anti inflammation drug diclofenac catalyzed by cytochrome P450 3A4. Diclofenac 118-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-161 21863748-8 2011 Riboflavin was the most effective inhibitor of diclofenac hydroxylation by cytochrome P450 3A4 as was compared at 300 M concentration of vitamin B group (B1, B2, B6). Riboflavin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-94 21863748-8 2011 Riboflavin was the most effective inhibitor of diclofenac hydroxylation by cytochrome P450 3A4 as was compared at 300 M concentration of vitamin B group (B1, B2, B6). Diclofenac 47-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-94 21863748-9 2011 These data confirmed the opportunity of pharmacokinetic parameters regulation and the level of pharmacodynamic effects by the influence of vitamin B group on the catalytic activity of cytochrome P450 3A4. Riboflavin 139-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-203 21266595-0 2011 Sorafenib and sunitinib, two anticancer drugs, inhibit CYP3A4-mediated and activate CY3A5-mediated midazolam 1"-hydroxylation. Sunitinib 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 21266595-3 2011 The effects of sorafenib and sunitinib on midazolam 1"-hydroxylation catalyzed by human CYP3A4 or CYP3A5 were investigated. Sorafenib 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 21266595-3 2011 The effects of sorafenib and sunitinib on midazolam 1"-hydroxylation catalyzed by human CYP3A4 or CYP3A5 were investigated. Sunitinib 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 21266595-3 2011 The effects of sorafenib and sunitinib on midazolam 1"-hydroxylation catalyzed by human CYP3A4 or CYP3A5 were investigated. Midazolam 42-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 21266595-4 2011 Sorafenib and sunitinib inhibited metabolic reactions catalyzed by recombinant CYP3A4. Sorafenib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 21266595-8 2011 Sorafenib N-oxidation and sunitinib N-deethylation, the primary routes of metabolism, were predominantly catalyzed by CYP3A4 but not by CYP3A5. Sunitinib 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 21266595-4 2011 Sorafenib and sunitinib inhibited metabolic reactions catalyzed by recombinant CYP3A4. Sunitinib 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 21266595-10 2011 Docking studies with a CYP3A5 homology model based on the structure of CYP3A4 revealed that midazolam closely docked to the heme of CYP3A5 compared with sorafenib or sunitinib, suggesting that these anticancer drugs act as enhancers, not as substrates. Midazolam 92-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 21266595-10 2011 Docking studies with a CYP3A5 homology model based on the structure of CYP3A4 revealed that midazolam closely docked to the heme of CYP3A5 compared with sorafenib or sunitinib, suggesting that these anticancer drugs act as enhancers, not as substrates. Heme 124-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 21266595-11 2011 Our results thus showed that sorafenib and sunitinib activated midazolam 1"-hydroxylation by CYP3A5 but inhibited that by CYP3A4. Sorafenib 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 21289076-1 2011 According to published in vitro studies, cytochrome P450 3A4 catalyzes montelukast 21-hydroxylation (M5 formation), whereas CYP2C9 catalyzes 36-hydroxylation (M6), the primary step in the main metabolic pathway of montelukast. montelukast 71-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-60 21266595-11 2011 Our results thus showed that sorafenib and sunitinib activated midazolam 1"-hydroxylation by CYP3A5 but inhibited that by CYP3A4. Sunitinib 43-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 21289076-1 2011 According to published in vitro studies, cytochrome P450 3A4 catalyzes montelukast 21-hydroxylation (M5 formation), whereas CYP2C9 catalyzes 36-hydroxylation (M6), the primary step in the main metabolic pathway of montelukast. montelukast 214-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-60 21140139-5 2011 RESULTS: Sex, CYP3A4 inducers/inhibitors, total daily dose, and "time from last oxycodone dose" predicted oxycodone concentrations. Oxycodone 106-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 21140139-6 2011 CYP3A4 inducers, total daily dose, and "number of medications taken in the last 24 h" predicted the oxymorphone/oxycodone ratio. Oxymorphone 100-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21140139-6 2011 CYP3A4 inducers, total daily dose, and "number of medications taken in the last 24 h" predicted the oxymorphone/oxycodone ratio. Oxycodone 112-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21140139-7 2011 Total daily dose, "time from last dose to blood sample", albumin, sex, CYP3A4 inducers/inhibitors, steroids, BMI and GFR predicted the noroxycodone/oxycodone ratio. noroxycodone 135-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 21140139-9 2011 CYP3A4 inducers/inhibitors should be used with caution as these are predicted to have a significant impact on oxycodone pharmacokinetics. Oxycodone 110-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21111054-4 2011 METHODS: To evaluate the xenobiotic-mediated induction of hepatocellular gene expression, the prototypical inducers rifampicin (10 muM) and phenobarbital (1 mM) were used for CYP3A4, CITCO (1 muM) and artemisinin (50 muM) were used for CYP2B6, and 3-methylcholanthrene (1 muM) and omeprazole (50 muM) were utilized for induction of CYP1A2. Rifampin 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 21349923-2 2011 Published in vitro data indicate that vitamin D may up-regulate the expression of the CYP3A4 gene. Vitamin D 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 21349923-4 2011 The aim of the present study was to investigate whether plasma concentrations of CYP3A4 drug substrates exhibit seasonal changes compatible with a stimulatory effect of vitamin D on drug metabolism. Vitamin D 169-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 21349923-5 2011 Three immunosuppressants (tacrolimus, sirolimus, and cyclosporine) were analyzed, because these CYP3A4 drug substrates are subject to long-term use and repeated concentration determinations. Cyclosporine 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 21111054-6 2011 The assessment of CYP activity was performed with a rapid, sensitive liquid chromatography-tandem mass spectrometry method which simultaneously assessed activity of CYP3A4, CYP2B6, and CYP1A2 in a single 3-min method by examining the formation of the probe substrate metabolites, 1"-hydroxymidazolam, hydroxybupropion, and acetaminophen, respectively. 1-hydroxymethylmidazolam 280-299 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 21111054-4 2011 METHODS: To evaluate the xenobiotic-mediated induction of hepatocellular gene expression, the prototypical inducers rifampicin (10 muM) and phenobarbital (1 mM) were used for CYP3A4, CITCO (1 muM) and artemisinin (50 muM) were used for CYP2B6, and 3-methylcholanthrene (1 muM) and omeprazole (50 muM) were utilized for induction of CYP1A2. Phenobarbital 140-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 21111054-6 2011 The assessment of CYP activity was performed with a rapid, sensitive liquid chromatography-tandem mass spectrometry method which simultaneously assessed activity of CYP3A4, CYP2B6, and CYP1A2 in a single 3-min method by examining the formation of the probe substrate metabolites, 1"-hydroxymidazolam, hydroxybupropion, and acetaminophen, respectively. hydroxybupropion 301-317 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 21111054-6 2011 The assessment of CYP activity was performed with a rapid, sensitive liquid chromatography-tandem mass spectrometry method which simultaneously assessed activity of CYP3A4, CYP2B6, and CYP1A2 in a single 3-min method by examining the formation of the probe substrate metabolites, 1"-hydroxymidazolam, hydroxybupropion, and acetaminophen, respectively. Acetaminophen 323-336 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 21533940-0 2011 CYP3A4 expression to predict treatment response to docetaxel for metastasis and recurrence of primary breast cancer. Docetaxel 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21292004-6 2011 NCOA6 enhances the synergistic activation of CYP2C9 and CYP3A4 promoter activity by PXR and HNF4alpha in the presence of rifampicin. Rifampin 121-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 20868352-12 2011 Since tolvaptan is metabolized by the cytochrome CYP3A4 in the liver physicians should be aware of possible drug to drug interactions. Tolvaptan 6-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 21533940-1 2011 PURPOSE: Tumors expressing high levels of CYP3A4 are likely to have a poor treatment response to docetaxel (DOC), which is metabolized by CYP3A4. Docetaxel 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21819807-1 2011 The HIV protease inhibitor lopinavir presents a wide inter-individual variability related to liver and intestinal metabolism involving CYP3A. Lopinavir 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-140 21533940-1 2011 PURPOSE: Tumors expressing high levels of CYP3A4 are likely to have a poor treatment response to docetaxel (DOC), which is metabolized by CYP3A4. Docetaxel 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 21533940-1 2011 PURPOSE: Tumors expressing high levels of CYP3A4 are likely to have a poor treatment response to docetaxel (DOC), which is metabolized by CYP3A4. Docetaxel 108-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21533940-1 2011 PURPOSE: Tumors expressing high levels of CYP3A4 are likely to have a poor treatment response to docetaxel (DOC), which is metabolized by CYP3A4. Docetaxel 108-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 27393203-1 2011 The HIV protease inhibitor lopinavir presents a wide inter-individual variability related to liver and intestinal metabolism involving CYP3A. Lopinavir 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-140 21533940-6 2011 RESULTS: Patients with CYP3A4-negative tumors (n = 19) showed a significantly higher response rate (63.2%) to DOC treatment than did those with CYP3A4-positive tumors (n = 23) (26.1%). Docetaxel 110-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 21533940-7 2011 The predictive value, negative predictive value, and diagnostic accuracy of CYP3A4 expression in the prediction response to DOC were 63.2%, 73.9%, and 68.6%, respectively. Docetaxel 124-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 21294626-4 2011 CYP2C8, CYP2C9, CYP2C19, and CYP3A4 were identified as the major enzymes responsible for the formation of the two O-desmethyl magnolins (M1 and M2), on the basis of a combination of correlation analysis and experiments, including immunoinhibition of magnolin in human liver microsomes and metabolism of magnolin by human cDNA-expressed CYP enzymes. magnolin 126-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 21294626-4 2011 CYP2C8, CYP2C9, CYP2C19, and CYP3A4 were identified as the major enzymes responsible for the formation of the two O-desmethyl magnolins (M1 and M2), on the basis of a combination of correlation analysis and experiments, including immunoinhibition of magnolin in human liver microsomes and metabolism of magnolin by human cDNA-expressed CYP enzymes. magnolin 250-258 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 21333639-10 2011 The results suggested that PA-1-mediated enhancement in the oral bioavailability of etoposide could possibly be due to its ability to modify P-gp/CYP 3A4 mediated drug disposition mechanisms. Etoposide 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-153 21333771-0 2011 Drug-drug interactions by azole antifungals: Beyond a dogma of CYP3A4 enzyme activity inhibition. Azoles 26-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 21333639-0 2011 Involvement of P-glycoprotein and CYP 3A4 in the enhancement of etoposide bioavailability by a piperine analogue. Etoposide 64-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-41 21333771-3 2011 In the current communication a complex view on the molecular interactions between azoles antimycotics and CYP3A4 is presented. Azoles 82-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 21333639-0 2011 Involvement of P-glycoprotein and CYP 3A4 in the enhancement of etoposide bioavailability by a piperine analogue. piperine 95-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-41 21333771-4 2011 Beside inhibition of CYP3A4 catalytic activity, azoles influence transcriptional activity of pregnane X receptor (PXR) and consequently expression of drug-metabolizing enzymes, including CYP3A4. Azoles 48-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 21333771-4 2011 Beside inhibition of CYP3A4 catalytic activity, azoles influence transcriptional activity of pregnane X receptor (PXR) and consequently expression of drug-metabolizing enzymes, including CYP3A4. Azoles 48-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 21333771-8 2011 In conclusion, while inhibition of CYP3A4 enzymatic activity by azoles is considered as primary cause of azoles drug-drug interactions, the effects of azoles on PXR and GR should be taken in account. Azoles 64-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 21333771-8 2011 In conclusion, while inhibition of CYP3A4 enzymatic activity by azoles is considered as primary cause of azoles drug-drug interactions, the effects of azoles on PXR and GR should be taken in account. Azoles 105-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 21333771-8 2011 In conclusion, while inhibition of CYP3A4 enzymatic activity by azoles is considered as primary cause of azoles drug-drug interactions, the effects of azoles on PXR and GR should be taken in account. Azoles 105-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 21429746-1 2011 The incorporation of a carboxylic acid within in a series of 3-amido-4-aryl substituted piperidines (represented by general structure 32) led to the discovery of potent, zwitterionic, renin inhibitors with improved off-target profiles (CYP3A4 time-dependent inhibition and hERG affinity) relative to analogous non-zwitterionic inhibitors of the past (i.e., 3). Carboxylic Acids 23-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 236-242 21376070-8 2011 NP-mediated Cyp3a induction from three human hepatocyte donors was not significant, confirming that hPXR is not very sensitive to NP-mediated CYP induction. nonylphenol 0-2 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 21429746-1 2011 The incorporation of a carboxylic acid within in a series of 3-amido-4-aryl substituted piperidines (represented by general structure 32) led to the discovery of potent, zwitterionic, renin inhibitors with improved off-target profiles (CYP3A4 time-dependent inhibition and hERG affinity) relative to analogous non-zwitterionic inhibitors of the past (i.e., 3). 3-amido-4-aryl substituted piperidines 61-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 236-242 21277363-0 2011 Involvement of CYP3A4/5 and CYP2D6 in the metabolism of aconitine using human liver microsomes and recombinant CYP450 enzymes. Aconitine 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 20851588-7 2011 Many of these alkaloids inhibited the CYP3A4 form, with 30/36 alkaloids inhibiting CYP3A4 with at least moderate potency (IC50 < 10 muM) and 15/36 inhibiting CYP3A4 potently (IC50 < 1 muM). Alkaloids 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 20851588-7 2011 Many of these alkaloids inhibited the CYP3A4 form, with 30/36 alkaloids inhibiting CYP3A4 with at least moderate potency (IC50 < 10 muM) and 15/36 inhibiting CYP3A4 potently (IC50 < 1 muM). Alkaloids 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 20851588-8 2011 Among them corydine, parfumine and 8-methyl-2,3,10,11-tetraethoxyberbine were potent and selective inhibitors for CYP3A4. corydine 11-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 20851588-8 2011 Among them corydine, parfumine and 8-methyl-2,3,10,11-tetraethoxyberbine were potent and selective inhibitors for CYP3A4. Parfumine 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 20851588-8 2011 Among them corydine, parfumine and 8-methyl-2,3,10,11-tetraethoxyberbine were potent and selective inhibitors for CYP3A4. 8-methyl-2,3,10,11-tetraethoxyberbine 35-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 21277363-4 2011 Fluvoxamine maleate, gemfibrozil, amiodarone hydrochloride, omeprazole, quinidine, diethyldithiocarbamic acid and ketoconazole were successfully applied as test inhibitors for CYP1A2, CYP2C8, CYP2C9, CYP2C19*1, CYP2D6*1, CYP2E1 and CYP3A4/5 in HLMs, respectively. Ketoconazole 114-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 232-238 20851588-7 2011 Many of these alkaloids inhibited the CYP3A4 form, with 30/36 alkaloids inhibiting CYP3A4 with at least moderate potency (IC50 < 10 muM) and 15/36 inhibiting CYP3A4 potently (IC50 < 1 muM). Alkaloids 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 21223952-0 2011 Impact of CYP3A4*1G polymorphism on metabolism of fentanyl in Chinese patients undergoing lower abdominal surgery. Fentanyl 50-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 21223952-1 2011 PURPOSE: This study aimed to investigate the impact of CYP3A4*1G genetic polymorphism on metabolism of fentanyl in Chinese patients undergoing lower abdominal surgery. Fentanyl 103-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 21223952-8 2011 After grouping according to the genotype of CYP3A4*1G, plasma fentanyl concentration in the *1/*1 variant (wild-type) group (12.8+-6.5 ng/ml) was significantly lower than that in the *1/*1G group (16.8+-9.0 ng/ml, P<0.01) and the *1G/*1G group (28.1+-9.5 ng/ml, P<0.01). Fentanyl 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 21223952-11 2011 CONCLUSIONS: CYP3A4*1G polymorphism is related to the pharmacokinetics of fentanyl, and patients with CYP3A4*1G variant A allele have a lower metabolic rate of fentanyl. Fentanyl 74-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 21223952-11 2011 CONCLUSIONS: CYP3A4*1G polymorphism is related to the pharmacokinetics of fentanyl, and patients with CYP3A4*1G variant A allele have a lower metabolic rate of fentanyl. Fentanyl 74-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 21223952-11 2011 CONCLUSIONS: CYP3A4*1G polymorphism is related to the pharmacokinetics of fentanyl, and patients with CYP3A4*1G variant A allele have a lower metabolic rate of fentanyl. Fentanyl 160-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 21223952-11 2011 CONCLUSIONS: CYP3A4*1G polymorphism is related to the pharmacokinetics of fentanyl, and patients with CYP3A4*1G variant A allele have a lower metabolic rate of fentanyl. Fentanyl 160-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 21223952-12 2011 The specific CYP3A4*1G polymorphism may predict the individual requirement of fentanyl. Fentanyl 78-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 21277363-7 2011 Hydroxylation and di-demethylation of aconitine were conducted by human recombinant CYP 3A5 and 2D6, dehydrogenation was only processed by CYP3A4/5, and the main CYP isoforms metabolizing aconitine to demethyl-aconitine and N-deethyl-aconitine were CYP3A4/5 and CYP2D6. Aconitine 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 21277363-7 2011 Hydroxylation and di-demethylation of aconitine were conducted by human recombinant CYP 3A5 and 2D6, dehydrogenation was only processed by CYP3A4/5, and the main CYP isoforms metabolizing aconitine to demethyl-aconitine and N-deethyl-aconitine were CYP3A4/5 and CYP2D6. Aconitine 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 249-255 21277363-8 2011 In conclusion, aconitine can be transformed into at least six CYP-mediated metabolites in HLMs, CYP 3A4/5 and 2D6 were the most important CYP isoforms responsible for the de-methylation, N-deethylation, dehydrogenation, and hydroxylation of aconitine. Aconitine 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-103 21277363-4 2011 Fluvoxamine maleate, gemfibrozil, amiodarone hydrochloride, omeprazole, quinidine, diethyldithiocarbamic acid and ketoconazole were successfully applied as test inhibitors for CYP1A2, CYP2C8, CYP2C9, CYP2C19*1, CYP2D6*1, CYP2E1 and CYP3A4/5 in HLMs, respectively. Fluvoxamine 0-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 232-238 21360715-10 2011 CONCLUSION: Ciprofloxacin decreases the metabolism of itraconazole, most likely through inhibition of CYP3A4. Ciprofloxacin 12-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 21356216-3 2011 MAIN METHODS: Diltiazem N-demethylase activity of recombinant CYP3A4, CYP3A5, CYP3A7, and human liver microsomes (HLMs) in the presence of cannabinoids was determined. Diltiazem 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 21356216-5 2011 The IC(50) values of Delta(9)-THC and CBN for CYP3A4 and CYP3A5 were higher than 35 muM. Dronabinol 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 21356216-7 2011 CBD competitively inhibited the activity of CYP3A4, CYP3A5, and HLMs (K(i)=1.00, 0.195, and 6.14 muM, respectively). Cannabidiol 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 21356216-9 2011 Olivetol partially inhibited all the CYP3A isoforms tested, whereas d-limonene showed lack of inhibition. olivetol 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-42 21356216-10 2011 The lesser inhibitory effects of monomethyl and dimethyl ethers of CBD indicated that the ability of CYP3A inhibition by the cannabinoid attenuated with the number of methylation on the phenolic hydroxyl groups in the resorcinol moiety. monomethyl and dimethyl ethers 33-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 21356216-10 2011 The lesser inhibitory effects of monomethyl and dimethyl ethers of CBD indicated that the ability of CYP3A inhibition by the cannabinoid attenuated with the number of methylation on the phenolic hydroxyl groups in the resorcinol moiety. Cannabidiol 67-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 21356216-10 2011 The lesser inhibitory effects of monomethyl and dimethyl ethers of CBD indicated that the ability of CYP3A inhibition by the cannabinoid attenuated with the number of methylation on the phenolic hydroxyl groups in the resorcinol moiety. Cannabinoids 125-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 21356216-10 2011 The lesser inhibitory effects of monomethyl and dimethyl ethers of CBD indicated that the ability of CYP3A inhibition by the cannabinoid attenuated with the number of methylation on the phenolic hydroxyl groups in the resorcinol moiety. resorcinol 218-228 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 21356216-11 2011 SIGNIFICANCE: This study indicated that CBD most potently inhibited catalytic activity of human CYP3A enzymes, especially CYP3A4 and CYP3A5. Cannabidiol 40-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-101 21356216-11 2011 SIGNIFICANCE: This study indicated that CBD most potently inhibited catalytic activity of human CYP3A enzymes, especially CYP3A4 and CYP3A5. Cannabidiol 40-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 21356216-12 2011 These results suggest that two phenolic hydroxyl groups in the resorcinol moiety of CBD may play an important role in the CYP3A inhibition. resorcinol 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-127 21356216-12 2011 These results suggest that two phenolic hydroxyl groups in the resorcinol moiety of CBD may play an important role in the CYP3A inhibition. Cannabidiol 84-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-127 21360715-10 2011 CONCLUSION: Ciprofloxacin decreases the metabolism of itraconazole, most likely through inhibition of CYP3A4. Itraconazole 54-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 21185724-3 2011 Tamoxifen is a pro-drug that is metabolised to its active metabolites by the cytochrome P450 (CYP) enzymes including CYP2D6, CYP3A, CYP2B6, and CYP2C19. Tamoxifen 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-130 21185724-10 2011 The genetic variations in other enzymes involved in tamoxifen metabolism (CYP3A, CYP2B6, CYP2C19) do not appear to cause any meaningful difference in the efficacy of tamoxifen. Tamoxifen 52-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-79 21395644-11 2011 CONCLUSION: Co-administration of neratinib with ketoconazole, a potent CYP3A inhibitor, increased neratinib C(max) by 3.2-fold and AUC by 4.8-fold compared with administration of neratinib alone. neratinib 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-76 21395644-11 2011 CONCLUSION: Co-administration of neratinib with ketoconazole, a potent CYP3A inhibitor, increased neratinib C(max) by 3.2-fold and AUC by 4.8-fold compared with administration of neratinib alone. Ketoconazole 48-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-76 21395644-12 2011 These results indicate that neratinib is a substrate of CYP3A and is susceptible to interaction with potent CYP3A inhibitors and, thus, dose adjustments may be needed if neratinib is administered with such compounds. neratinib 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 21395644-12 2011 These results indicate that neratinib is a substrate of CYP3A and is susceptible to interaction with potent CYP3A inhibitors and, thus, dose adjustments may be needed if neratinib is administered with such compounds. neratinib 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 21395644-12 2011 These results indicate that neratinib is a substrate of CYP3A and is susceptible to interaction with potent CYP3A inhibitors and, thus, dose adjustments may be needed if neratinib is administered with such compounds. neratinib 170-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 21395644-12 2011 These results indicate that neratinib is a substrate of CYP3A and is susceptible to interaction with potent CYP3A inhibitors and, thus, dose adjustments may be needed if neratinib is administered with such compounds. neratinib 170-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 21185724-11 2011 This review article will summarize the available published breast cancer data on the interaction between the relevant SNPs for CYP2D6, CYP3A, CYP2B6, and CYP2C19 and the efficacy of tamoxifen, their role in individualisation of hormonal therapy and the role of the commercially available genotyping kits. Tamoxifen 182-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-140 21348537-2 2011 Because elvitegravir is metabolized primarily by cytochrome P450 (CYP) 3A enzymes, coadministration with a strong CYP3A inhibitor such as ritonavir or cobicistat (also known as GS-9350), an investigational pharmacoenhancer, substantially increases (boosts) elvitegravir plasma exposures and prolongs its elimination half-life to ~9.5 hours, allowing once-daily administration of a low 150 mg dose. elvitegravir 8-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 21189330-5 2011 AR-67 was metabolized by CYP3A5, CYP3A4, CYP1A1, and CYP1A2, in order of activity. Argon 0-2 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 21205911-7 2011 Furthermore, ketoconazole, a specific inhibitor of CYP3A, strongly inhibited CB hydroxylation in MLM, DLM, PLM, and CyLM, indicating that CYP3A was responsible for CB hydroxylation in these animal species. Ketoconazole 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 21205911-7 2011 Furthermore, ketoconazole, a specific inhibitor of CYP3A, strongly inhibited CB hydroxylation in MLM, DLM, PLM, and CyLM, indicating that CYP3A was responsible for CB hydroxylation in these animal species. Ketoconazole 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-143 21220434-0 2011 Mitotane has a strong and a durable inducing effect on CYP3A4 activity. Mitotane 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 21220434-5 2011 The sunitinib PK study was designed to determine the relationship between CYP3A4 activity and sunitinib exposure using 7.5 mg midazolam orally as a phenotypic probe. Sunitinib 4-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 21220434-5 2011 The sunitinib PK study was designed to determine the relationship between CYP3A4 activity and sunitinib exposure using 7.5 mg midazolam orally as a phenotypic probe. Sunitinib 94-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 21220434-10 2011 CONCLUSION: Mitotane has a strong and long-lasting inducing effect on CYP3A4 activity, which will result in clinically relevant interactions with multiple drugs since many drugs are metabolized by this enzyme. Mitotane 12-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 21443601-1 2011 BACKGROUND: Based on in vitro data with isolated cytochrome P450 (CYP) isoenzymes, alitretinoin interacts only with CYP3A4, and the potential for drug-drug interactions is considered negligible. Alitretinoin 83-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 21443601-8 2011 The CYP3A4 +- PgP substrates of simvastatin and ciclosporin A did not affect the single or repeated dose PK of alitretinoin. Simvastatin 32-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 21443601-9 2011 The strong CYP3A4/PgP inhibitor ketoconazole led to significant increases in both AUC and C(max) values for alitretinoin. Ketoconazole 32-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 21443601-9 2011 The strong CYP3A4/PgP inhibitor ketoconazole led to significant increases in both AUC and C(max) values for alitretinoin. Alitretinoin 108-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 21443601-13 2011 However, ketoconazole significantly increased the plasma levels of alitretinoin, therefore, co-administration with CYP3A4 inhibitors such as ketoconazole may require a dose reduction of alitretinoin. Ketoconazole 9-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 21443601-13 2011 However, ketoconazole significantly increased the plasma levels of alitretinoin, therefore, co-administration with CYP3A4 inhibitors such as ketoconazole may require a dose reduction of alitretinoin. Alitretinoin 67-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 21443601-13 2011 However, ketoconazole significantly increased the plasma levels of alitretinoin, therefore, co-administration with CYP3A4 inhibitors such as ketoconazole may require a dose reduction of alitretinoin. Ketoconazole 141-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 21443601-13 2011 However, ketoconazole significantly increased the plasma levels of alitretinoin, therefore, co-administration with CYP3A4 inhibitors such as ketoconazole may require a dose reduction of alitretinoin. Alitretinoin 186-198 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 21177984-3 2011 CYP3A4 and CYP3A5 appear to be the enzymes predominantly responsible for the formation of the ticagrelor active and inactive metabolites, AR-C124910XX and AR-C133913XX. Argon 138-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21177984-3 2011 CYP3A4 and CYP3A5 appear to be the enzymes predominantly responsible for the formation of the ticagrelor active and inactive metabolites, AR-C124910XX and AR-C133913XX. Argon 155-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21177985-7 2011 The reaction phenotyping study showed that CYP3A4 and 3A5 were the major cytochrome P450 isozymes involved in the oxidative metabolism of 17-DMAG, whereas CYP2C8, 2D6, 2A6, 2C19, and 1A2 made minor contributions to the formation of metabolites. 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin 138-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-57 21212239-0 2011 Comparison of the inhibitory profiles of itraconazole and cimetidine in cytochrome P450 3A4 genetic variants. Itraconazole 41-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-91 21212239-0 2011 Comparison of the inhibitory profiles of itraconazole and cimetidine in cytochrome P450 3A4 genetic variants. Cimetidine 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-91 21212239-3 2011 In this study, we quantitatively investigated the inhibition kinetics of two typical inhibitors, itraconazole (ITCZ) and cimetidine (CMD), on CYP3A4 variants and evaluated whether the genetic variation leads to interindividual differences in the extent of CYP3A4-mediated drug interactions. Itraconazole 97-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 21212239-3 2011 In this study, we quantitatively investigated the inhibition kinetics of two typical inhibitors, itraconazole (ITCZ) and cimetidine (CMD), on CYP3A4 variants and evaluated whether the genetic variation leads to interindividual differences in the extent of CYP3A4-mediated drug interactions. Itraconazole 111-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 21212239-3 2011 In this study, we quantitatively investigated the inhibition kinetics of two typical inhibitors, itraconazole (ITCZ) and cimetidine (CMD), on CYP3A4 variants and evaluated whether the genetic variation leads to interindividual differences in the extent of CYP3A4-mediated drug interactions. Cimetidine 121-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 21212239-9 2011 Docking simulations could explain the changes in the K(i) values, based on the accessibility of TST and inhibitors to the heme moiety of the CYP3A4 molecule. Heme 122-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 21513075-1 2011 BACKGROUND AND OBJECTIVE: Fentanyl is metabolised by cytochrome P450 (CYP) 3A4 and CYP3A5. Fentanyl 26-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-78 21513075-2 2011 Our previous work demonstrated that the CYP3A4*1G polymorphism significantly affects the post-operative fentanyl analgesic effect in Chinese women undergoing gynaecological surgery. Fentanyl 104-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 21513075-8 2011 Midazolam was used as a probe drug, and CYP3A activity was measured by plasma ratio of 1"-hydroxymidazolam to midazolam 1 h after intravenous administration of 0.1 mg kg-1 midazolam. 1-hydroxymethylmidazolam 87-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 21513075-8 2011 Midazolam was used as a probe drug, and CYP3A activity was measured by plasma ratio of 1"-hydroxymidazolam to midazolam 1 h after intravenous administration of 0.1 mg kg-1 midazolam. Midazolam 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 21513075-8 2011 Midazolam was used as a probe drug, and CYP3A activity was measured by plasma ratio of 1"-hydroxymidazolam to midazolam 1 h after intravenous administration of 0.1 mg kg-1 midazolam. Midazolam 110-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 21513075-13 2011 However, combined with CYP3A4*1G polymorphism, post-operative fentanyl consumption at 24 h was significantly lower for the CYP3A5*1/*3 or CYP3A5*3/*3 group than the CYP3A5*1/*1 group. Fentanyl 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 21348537-6 2011 The presence of a strong CYP3A inhibitor such as ritonavir or cobicistat renders the potential for increase in systemic exposures of CYP3A substrates coadministered with boosted elvitegravir. Ritonavir 49-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-30 21348537-6 2011 The presence of a strong CYP3A inhibitor such as ritonavir or cobicistat renders the potential for increase in systemic exposures of CYP3A substrates coadministered with boosted elvitegravir. Ritonavir 49-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-138 21348537-6 2011 The presence of a strong CYP3A inhibitor such as ritonavir or cobicistat renders the potential for increase in systemic exposures of CYP3A substrates coadministered with boosted elvitegravir. Cobicistat 62-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-30 21348537-6 2011 The presence of a strong CYP3A inhibitor such as ritonavir or cobicistat renders the potential for increase in systemic exposures of CYP3A substrates coadministered with boosted elvitegravir. Cobicistat 62-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-138 21348537-6 2011 The presence of a strong CYP3A inhibitor such as ritonavir or cobicistat renders the potential for increase in systemic exposures of CYP3A substrates coadministered with boosted elvitegravir. elvitegravir 178-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-30 21348537-6 2011 The presence of a strong CYP3A inhibitor such as ritonavir or cobicistat renders the potential for increase in systemic exposures of CYP3A substrates coadministered with boosted elvitegravir. elvitegravir 178-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-138 20466871-2 2011 It is metabolized by CYP1A2 and CYP3A4 to its primary metabolite, roflumilast N-oxide, through which >90% total PDE4 inhibitory activity (tPDE4i) is mediated. n-oxide 78-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20484614-8 2011 The increase in tPDE4i of roflumilast and roflumilast N-oxide following coadministration with cimetidine was mainly due to the inhibitory effect of cimetidine on cytochrome P450 (CYP) isoenzymes CYP1A2, CYP3A, and CYP2C19. n-oxide 54-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-208 20484614-8 2011 The increase in tPDE4i of roflumilast and roflumilast N-oxide following coadministration with cimetidine was mainly due to the inhibitory effect of cimetidine on cytochrome P450 (CYP) isoenzymes CYP1A2, CYP3A, and CYP2C19. Cimetidine 94-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-208 20484614-8 2011 The increase in tPDE4i of roflumilast and roflumilast N-oxide following coadministration with cimetidine was mainly due to the inhibitory effect of cimetidine on cytochrome P450 (CYP) isoenzymes CYP1A2, CYP3A, and CYP2C19. Cimetidine 148-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 203-208 20212519-4 2011 We selected 13 relevant polymorphisms in genes encoding paclitaxel metabolizing enzymes (CYP2C8, CYP3A4 and CYP3A5) and transporters (organic anion transporting polypeptide (OATP) 1B1, OATP1B3 and P-glycoprotein) and genotyped them in 118 Spanish cancer patients treated with paclitaxel. Paclitaxel 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 21383647-11 2011 In three patients treated with potent CYP3A4 inducers, the observed C/D ratios of quetiapine and N-desalkylquetiapine were 77% and 11% lower than the mean C/D ratio in the study population, respectively. Quetiapine Fumarate 82-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 21227907-8 2011 Ex vivo studies showed DEHP and di-isononyl phthalate potently induced CYP2B6 and CYP3A4 expression in human hepatocytes. Diethylhexyl Phthalate 23-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 21227907-8 2011 Ex vivo studies showed DEHP and di-isononyl phthalate potently induced CYP2B6 and CYP3A4 expression in human hepatocytes. diisononyl phthalate 32-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 21383647-11 2011 In three patients treated with potent CYP3A4 inducers, the observed C/D ratios of quetiapine and N-desalkylquetiapine were 77% and 11% lower than the mean C/D ratio in the study population, respectively. norquetiapine 97-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 21383647-13 2011 Age 65 years or older and comedication with CYP3A4 inducers affected the serum levels of both agents, but the relative impact was greater on quetiapine. Quetiapine Fumarate 141-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 21372830-7 2011 Erlotinib also exhibited the time-dependent inhibition on CYP3A, regardless of the probe substrate used: the value of K(I) and k(inact) were 6.3 mumol/L and 0.035 min(-1) for midazolam; 9.0 mumol/L and 0.045 min(-1) for testosterone; and 10.1 mumol/L and 0.058 min(-1) for nifedipine. Erlotinib Hydrochloride 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 19921206-1 2011 PURPOSE: The known importance of testosterone for the development of benign prostatic hyperplasia (BPH) prompted us to test the hypothesis whether polymorphisms of two genes (CYP19A1 and CYP3A4) involved in testosterone metabolism are associated with clinical BPH-parameters. Testosterone 207-219 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 21117944-4 2011 Praeruptorin A and C, salvianolic acid B, sodium danshensu, protocatechuic aldehyde, cryptotanshinone, emodin, morin, and tanshinone IIA significantly transactivated the CYP3A4 reporter gene construct in either HepG2 or Huh7 cells. salvianolic acid 22-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 21117944-4 2011 Praeruptorin A and C, salvianolic acid B, sodium danshensu, protocatechuic aldehyde, cryptotanshinone, emodin, morin, and tanshinone IIA significantly transactivated the CYP3A4 reporter gene construct in either HepG2 or Huh7 cells. Sodium Danshensu 42-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 21117944-4 2011 Praeruptorin A and C, salvianolic acid B, sodium danshensu, protocatechuic aldehyde, cryptotanshinone, emodin, morin, and tanshinone IIA significantly transactivated the CYP3A4 reporter gene construct in either HepG2 or Huh7 cells. Aldehydes 75-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 21117944-4 2011 Praeruptorin A and C, salvianolic acid B, sodium danshensu, protocatechuic aldehyde, cryptotanshinone, emodin, morin, and tanshinone IIA significantly transactivated the CYP3A4 reporter gene construct in either HepG2 or Huh7 cells. cryptotanshinone 85-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 21389905-4 2011 We further evaluated in vitro the contribution of CYP3A4, CYP3A5, and CYP2C8 to everolimus hepatic metabolism using recombinant enzymes. Everolimus 80-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 21389905-7 2011 In vitro data showed that CYP3A4 is a better catalyst of everolimus metabolism than CYP3A5, whereas the opposite was observed for tacrolimus. Everolimus 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 21114969-8 2011 CONCLUSION: CYP3A4 variant alleles are present at a low frequency in the Bangladeshi population whereas 50% of the Bangladeshi population carrying a CYP3A5*3/*3 genotype appear to show lower 6beta-hydroxy-cortisol/cortisol ratios compared with those with a CYP3A5*1/*1 genotype. Hydrocortisone 205-213 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 21372830-0 2011 Substrate-dependent modulation of the catalytic activity of CYP3A by erlotinib. Erlotinib Hydrochloride 69-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 21372830-3 2011 A two-step incubation method was used to examine the time-dependent inhibition of erlotinib on CYP3A. Erlotinib Hydrochloride 82-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-100 21372830-6 2011 Inhibition of CYP3A by erlotinib was substrate-dependent: the IC(50) values for inhibiting testosterone 6beta-hydroxylation and nifedipine metabolism were 31.3+-8.0 and 20.5+-5.3 mumol/L, respectively. Erlotinib Hydrochloride 23-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 20231858-10 2011 A clear gene-dose effect implies plasma 4beta-hydroxycholesterol level as a useful endogenous biomarker for total CYP3A activity (CYP3A5 plus CYP3A4) whereas the omeprazole/omeprazole sulfone ratio reflects mainly CYP3A4 activity. cholest-5-ene-3,4-diol 40-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-119 20231858-10 2011 A clear gene-dose effect implies plasma 4beta-hydroxycholesterol level as a useful endogenous biomarker for total CYP3A activity (CYP3A5 plus CYP3A4) whereas the omeprazole/omeprazole sulfone ratio reflects mainly CYP3A4 activity. cholest-5-ene-3,4-diol 40-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 20231858-10 2011 A clear gene-dose effect implies plasma 4beta-hydroxycholesterol level as a useful endogenous biomarker for total CYP3A activity (CYP3A5 plus CYP3A4) whereas the omeprazole/omeprazole sulfone ratio reflects mainly CYP3A4 activity. cholest-5-ene-3,4-diol 40-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 214-220 21270532-0 2011 CHIP and gp78-mediated ubiquitination of CYP3A4: Implications for the pharmacology of anticancer agents. gp78 9-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 21173180-0 2011 Miconazole oral gel increases exposure to oral oxycodone by inhibition of CYP2D6 and CYP3A4. Miconazole 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 21173180-0 2011 Miconazole oral gel increases exposure to oral oxycodone by inhibition of CYP2D6 and CYP3A4. Oxycodone 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 21173180-4 2011 Pretreatment with miconazole oral gel caused a strong inhibition of the CYP2D6-dependent metabolism and moderate inhibition of the CYP3A4-dependent metabolism of oxycodone. Miconazole 18-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 21173180-4 2011 Pretreatment with miconazole oral gel caused a strong inhibition of the CYP2D6-dependent metabolism and moderate inhibition of the CYP3A4-dependent metabolism of oxycodone. Oxycodone 162-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 21173180-6 2011 The AUC of the CYP2D6-dependent metabolite oxymorphone was greatly decreased (GMR, 0.17; 90% CI, 0.09 to 0.31) by miconazole gel, whereas that of the CYP3A4-dependent metabolite noroxycodone was increased (GMR, 1.30; 90% CI, 1.15 to 1.47) by miconazole gel. Oxymorphone 43-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 21173180-6 2011 The AUC of the CYP2D6-dependent metabolite oxymorphone was greatly decreased (GMR, 0.17; 90% CI, 0.09 to 0.31) by miconazole gel, whereas that of the CYP3A4-dependent metabolite noroxycodone was increased (GMR, 1.30; 90% CI, 1.15 to 1.47) by miconazole gel. noroxycodone 178-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 21173180-6 2011 The AUC of the CYP2D6-dependent metabolite oxymorphone was greatly decreased (GMR, 0.17; 90% CI, 0.09 to 0.31) by miconazole gel, whereas that of the CYP3A4-dependent metabolite noroxycodone was increased (GMR, 1.30; 90% CI, 1.15 to 1.47) by miconazole gel. Miconazole 242-252 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 21075070-2 2011 The diagnostic substrate tetramethylcyclopropane (TMCP) has been reexamined as a substrate with three drug- and xenobiotic-metabolizing cytochrome P450 enzymes, human CYP2E1, CYP3A4 and rat CYP2B1. tetramethylcyclopropane 25-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 21075070-2 2011 The diagnostic substrate tetramethylcyclopropane (TMCP) has been reexamined as a substrate with three drug- and xenobiotic-metabolizing cytochrome P450 enzymes, human CYP2E1, CYP3A4 and rat CYP2B1. tmcp 50-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 21372830-6 2011 Inhibition of CYP3A by erlotinib was substrate-dependent: the IC(50) values for inhibiting testosterone 6beta-hydroxylation and nifedipine metabolism were 31.3+-8.0 and 20.5+-5.3 mumol/L, respectively. Testosterone 91-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 21372830-6 2011 Inhibition of CYP3A by erlotinib was substrate-dependent: the IC(50) values for inhibiting testosterone 6beta-hydroxylation and nifedipine metabolism were 31.3+-8.0 and 20.5+-5.3 mumol/L, respectively. Nifedipine 128-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 21372830-7 2011 Erlotinib also exhibited the time-dependent inhibition on CYP3A, regardless of the probe substrate used: the value of K(I) and k(inact) were 6.3 mumol/L and 0.035 min(-1) for midazolam; 9.0 mumol/L and 0.045 min(-1) for testosterone; and 10.1 mumol/L and 0.058 min(-1) for nifedipine. Midazolam 175-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 21372830-7 2011 Erlotinib also exhibited the time-dependent inhibition on CYP3A, regardless of the probe substrate used: the value of K(I) and k(inact) were 6.3 mumol/L and 0.035 min(-1) for midazolam; 9.0 mumol/L and 0.045 min(-1) for testosterone; and 10.1 mumol/L and 0.058 min(-1) for nifedipine. Testosterone 220-232 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 21372830-7 2011 Erlotinib also exhibited the time-dependent inhibition on CYP3A, regardless of the probe substrate used: the value of K(I) and k(inact) were 6.3 mumol/L and 0.035 min(-1) for midazolam; 9.0 mumol/L and 0.045 min(-1) for testosterone; and 10.1 mumol/L and 0.058 min(-1) for nifedipine. Nifedipine 273-283 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 21372830-8 2011 CONCLUSION: The inhibition of CYP3A by erlotinib was substrate-dependent, while its time-dependent inhibition on CYP3A was substrate-independent. Erlotinib Hydrochloride 39-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-35 21372830-9 2011 The time-dependent inhibition of CYP3A may be a possible cause of drug-drug interaction, suggesting that attention should be paid to the evaluation of erlotinib"s safety, especially in the context of combination therapy. Erlotinib Hydrochloride 151-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 21148251-3 2011 First, the in vitro metabolism of atazanavir was evaluated using human liver microsomes (HLM) and CYP3A4 and CYP3A5 isoforms. Atazanavir Sulfate 34-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 20512335-10 2011 The effect of GJ on CYP3A4 activity was confirmed by an increase of ~50% of mean midazolam exposure (AUC(0-24 h)) from 122.1 to 182.0 ng h/mL (P = 0.034). Midazolam 81-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 21123164-2 2011 In human liver microsomes, formation of oxidative metabolites after incubations with [(14)C]boceprevir was catalyzed by CYP3A4 and CYP3A5. [(14)c]boceprevir 85-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 21148252-0 2011 CYP3A-mediated generation of aldehyde and hydrazine in atazanavir metabolism. Aldehydes 29-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 21148252-0 2011 CYP3A-mediated generation of aldehyde and hydrazine in atazanavir metabolism. hydrazine 42-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 21148252-0 2011 CYP3A-mediated generation of aldehyde and hydrazine in atazanavir metabolism. Atazanavir Sulfate 55-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 21149541-3 2011 Casopitant is shown to be a substrate, an inhibitor, and an inducer of CYP3A4, and, because of this complex behavior, it was difficult to identify the primary mechanism by which it may give rise to drug-drug interactions (DDIs) of clinical relevance. casopitant 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 21294720-10 2011 Human embryonic kidney (HEK) cells were transfected with 4",6-diamidino-2-phenylindole (CYP3A4 to further evaluate the link between CYP3A4 levels, CBZ metabolism, and cell viability. DAPI 57-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 21294720-14 2011 CYP3A4 overexpression in HEK cells conferred resistance to cytotoxic levels of carbamazepine. Carbamazepine 79-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21294720-15 2011 CYP3A4 levels positively correlated with the amount of CBZ metabolized. Carbamazepine 55-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20400651-0 2011 Itraconazole, a P-glycoprotein and CYP3A4 inhibitor, markedly raises the plasma concentrations and enhances the renin-inhibiting effect of aliskiren. Itraconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 20400651-0 2011 Itraconazole, a P-glycoprotein and CYP3A4 inhibitor, markedly raises the plasma concentrations and enhances the renin-inhibiting effect of aliskiren. aliskiren 139-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 24451503-13 2011 This suggests that in the presence of renal function alteration even low doses of fluconazole with an inhibition of only liver CYPA3A4 (without inhibition of intestinal CYP3A4 and P-gp) leads to an increase on tacrolimus concentration and occurrence of adverse effects related to tacrolimus toxicity. Fluconazole 82-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 23251745-7 2011 Pitavastatin"s unique metabolic profile results in a high efficacy at low (1-4 mg) doses and minimal drug interactions with cytochrome CYP3A4 substrates, making it an excellent choice for people requiring multiple medications. pitavastatin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 21131266-5 2011 Consistent with its hPXR agonism, meclizine increased hPXR target gene expression (CYP3A4) in human hepatocytes. Meclizine 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 21163185-5 2011 Laquinimod is metabolised primarily by the CYP3A4 enzyme in the liver. laquinimod 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 20849451-4 2011 The P450 CYP3A4 enzyme is responsible for the major metabolic N-dealkylation pathway. Nitrogen 62-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 21553654-4 2011 In vitro inhibitory effects of DES on CYP isoforms were investigated, and the results showed that DES could competitively inhibit CYP3A4, CYP2C8, CYP2C9 and CYP2E1. Diethylstilbestrol 31-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 21553654-4 2011 In vitro inhibitory effects of DES on CYP isoforms were investigated, and the results showed that DES could competitively inhibit CYP3A4, CYP2C8, CYP2C9 and CYP2E1. Diethylstilbestrol 98-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 21553654-6 2011 Based on peak serum DES level after drip influsion of 500 mg of fosfestrol (DES diphosphate) in patients, [I]/Ki was calculated to be 4.3, 6.2, 3.7 and 2.3 for CYP3A4, CYP2C9, CYP2E1 and CYP2C8, which suggested that DES was likely to induce in vivo DDI through inhibition of these four major CYP isoforms. fosfestrol 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 21553654-6 2011 Based on peak serum DES level after drip influsion of 500 mg of fosfestrol (DES diphosphate) in patients, [I]/Ki was calculated to be 4.3, 6.2, 3.7 and 2.3 for CYP3A4, CYP2C9, CYP2E1 and CYP2C8, which suggested that DES was likely to induce in vivo DDI through inhibition of these four major CYP isoforms. fosfestrol 76-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 20942777-0 2011 Interaction involving tadalafil and CYP3A4 inhibition by ritonavir. Ritonavir 57-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 21749392-8 2011 In agreement with published data, bergamottin, a natural product known to interact with CYP3A4, was shown to inhibit CYP3A4 with an IC50 of 13.63 microm and activate PXR with an EC50 of 6.7 microm. bergamottin 34-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 21749392-8 2011 In agreement with published data, bergamottin, a natural product known to interact with CYP3A4, was shown to inhibit CYP3A4 with an IC50 of 13.63 microm and activate PXR with an EC50 of 6.7 microm. bergamottin 34-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 21225912-2 2011 We have shown in vitro that vincristine is metabolized significantly more efficiently by CYP3A5 than by CYP3A4. Vincristine 28-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 21226652-12 2011 Multiple enzymes including CYP2D6, CYP3A4/5, FMO1 and FMO3 catalyzed AZD0328 metabolism. spiro(1-azabicyclo(2.2.2)octane-3,2'(3H)-furo(2,3-b)pyridine) 69-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-43 21219911-7 2011 KEY FINDINGS: Both diterpenoids inhibited the mRNA and protein expressions of CYP1A2, CYP2D6, and CYP3A4. Diterpenes 19-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 21219911-8 2011 Interestingly, the lowest concentration of both diterpenoids produced a more than 50% reduction in the mRNA and protein expression of CYP3A4 and this reduction was consistent with the enzyme activity. Diterpenes 48-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 21219911-9 2011 Further experiments revealed that both diterpenoids were also capable of attenuating the ability of dexamethasone to induce CYP3A4 expression, and 14-Deoxy-11, 12-Didehydroandrographolide tended to bind to the PXR-LBD site in a concentration-dependent manner. Diterpenes 39-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 21219911-9 2011 Further experiments revealed that both diterpenoids were also capable of attenuating the ability of dexamethasone to induce CYP3A4 expression, and 14-Deoxy-11, 12-Didehydroandrographolide tended to bind to the PXR-LBD site in a concentration-dependent manner. Dexamethasone 100-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 21219911-10 2011 SIGNIFICANCE: These diterpenoids are potential CYP3A4 inhibitors and the effects on CYP3A4 may be clinically significant. Diterpenes 20-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 21219911-10 2011 SIGNIFICANCE: These diterpenoids are potential CYP3A4 inhibitors and the effects on CYP3A4 may be clinically significant. Diterpenes 20-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 21219911-11 2011 14-Deoxy-11, 12-Didehydroandrographolide inhibits CYP3A4 by binding and antagonizing PXR function. 14-deoxy-11,12-didehydroandrographolide 0-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 21242274-10 2011 Erythromycin (the strongest inhibitor of cytochrome P450 3A4) was most strongly associated with hypotension (odds ratio [OR] 5.8, 95% confidence interval [CI] 2.3-15.0), followed by clarithromycin (OR 3.7, 95% CI 2.3-6.1). Erythromycin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-60 21342487-9 2011 This methylation was reversed by treatment with 5-aza-dC, in association with re-expression of PXR and CYP3A4 mRNA, but not VDR mRNA. Decitabine 48-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 21242274-10 2011 Erythromycin (the strongest inhibitor of cytochrome P450 3A4) was most strongly associated with hypotension (odds ratio [OR] 5.8, 95% confidence interval [CI] 2.3-15.0), followed by clarithromycin (OR 3.7, 95% CI 2.3-6.1). Clarithromycin 182-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-60 21207936-2 2011 Resonance Raman (RR) spectroscopy is used to help define active site structural responses of nanodisc-incorporated CYP3A4 to the binding of three substrates: bromocriptine (BC), erythromycin (ERY), and testosterone (TST). Bromocriptine 158-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 21177853-0 2011 Analysis of heterotropic cooperativity in cytochrome P450 3A4 using alpha-naphthoflavone and testosterone. Testosterone 93-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-61 21177853-1 2011 Cytochrome P450 3A4 (CYP3A4) displays non-Michaelis-Menten kinetics for many of the substrates it metabolizes, including testosterone (TST) and alpha-naphthoflavone (ANF). Testosterone 121-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 21177853-1 2011 Cytochrome P450 3A4 (CYP3A4) displays non-Michaelis-Menten kinetics for many of the substrates it metabolizes, including testosterone (TST) and alpha-naphthoflavone (ANF). Testosterone 121-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 21177853-1 2011 Cytochrome P450 3A4 (CYP3A4) displays non-Michaelis-Menten kinetics for many of the substrates it metabolizes, including testosterone (TST) and alpha-naphthoflavone (ANF). Testosterone 135-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 21177853-1 2011 Cytochrome P450 3A4 (CYP3A4) displays non-Michaelis-Menten kinetics for many of the substrates it metabolizes, including testosterone (TST) and alpha-naphthoflavone (ANF). Testosterone 135-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 21177853-1 2011 Cytochrome P450 3A4 (CYP3A4) displays non-Michaelis-Menten kinetics for many of the substrates it metabolizes, including testosterone (TST) and alpha-naphthoflavone (ANF). alpha-naphthoflavone 144-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 21177853-1 2011 Cytochrome P450 3A4 (CYP3A4) displays non-Michaelis-Menten kinetics for many of the substrates it metabolizes, including testosterone (TST) and alpha-naphthoflavone (ANF). alpha-naphthoflavone 144-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 21177853-1 2011 Cytochrome P450 3A4 (CYP3A4) displays non-Michaelis-Menten kinetics for many of the substrates it metabolizes, including testosterone (TST) and alpha-naphthoflavone (ANF). alpha-naphthoflavone 166-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 21177853-1 2011 Cytochrome P450 3A4 (CYP3A4) displays non-Michaelis-Menten kinetics for many of the substrates it metabolizes, including testosterone (TST) and alpha-naphthoflavone (ANF). alpha-naphthoflavone 166-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 21194699-3 2011 Acetaminophen (CYP1A2), dextrorphan (CYP2D6), hydroxy-chlorzoxazone (CYP2E1) and hydroxy-mephenytoin (CYP2C19) can be derivatized because of the presence of a phenolic OH, whereas hydroxy-midazolam (CYP3A4) and hydroxy-tolbutamide (CYP2C9) remain unchanged. hydroxy-chlorzoxazone 46-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 199-205 21194699-3 2011 Acetaminophen (CYP1A2), dextrorphan (CYP2D6), hydroxy-chlorzoxazone (CYP2E1) and hydroxy-mephenytoin (CYP2C19) can be derivatized because of the presence of a phenolic OH, whereas hydroxy-midazolam (CYP3A4) and hydroxy-tolbutamide (CYP2C9) remain unchanged. hydroxy-mephenytoin 81-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 199-205 21194699-3 2011 Acetaminophen (CYP1A2), dextrorphan (CYP2D6), hydroxy-chlorzoxazone (CYP2E1) and hydroxy-mephenytoin (CYP2C19) can be derivatized because of the presence of a phenolic OH, whereas hydroxy-midazolam (CYP3A4) and hydroxy-tolbutamide (CYP2C9) remain unchanged. hydroxy-midazolam 180-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 199-205 21194699-3 2011 Acetaminophen (CYP1A2), dextrorphan (CYP2D6), hydroxy-chlorzoxazone (CYP2E1) and hydroxy-mephenytoin (CYP2C19) can be derivatized because of the presence of a phenolic OH, whereas hydroxy-midazolam (CYP3A4) and hydroxy-tolbutamide (CYP2C9) remain unchanged. hydroxymethyltolbutamide 211-230 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 199-205 21070748-0 2011 The role of CYP3A4 in amiodarone-associated toxicity on HepG2 cells. Amiodarone 22-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 21070748-3 2011 Since cytochrome P450 (CYP) 3A4 is responsible for amiodarone N-deethylation, CYP3A4 induction may represent a risk factor. Amiodarone 51-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-31 21070748-3 2011 Since cytochrome P450 (CYP) 3A4 is responsible for amiodarone N-deethylation, CYP3A4 induction may represent a risk factor. Amiodarone 51-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 21070748-4 2011 Our aim was therefore to investigate the role of CYP3A4 in amiodarone-associated hepatotoxicity. Amiodarone 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 21070748-7 2011 We also used HepG2 wild type cells (HepG2 cells/wt) co-incubated with human CYP3A4 supersomes for amiodarone activation (HepG2 cells/CYP3A4 supersomes). Amiodarone 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 21070748-8 2011 Amiodarone (10-50muM) was cytotoxic for HepG2 cells/CYP3A4 or HepG2 cells/CYP3A4 supersomes, but not for HepG2 cells/wt or less toxic for HepG2 cells/wt incubated with control supersomes without CYP3A4. Amiodarone 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 21070748-8 2011 Amiodarone (10-50muM) was cytotoxic for HepG2 cells/CYP3A4 or HepG2 cells/CYP3A4 supersomes, but not for HepG2 cells/wt or less toxic for HepG2 cells/wt incubated with control supersomes without CYP3A4. Amiodarone 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 21177853-0 2011 Analysis of heterotropic cooperativity in cytochrome P450 3A4 using alpha-naphthoflavone and testosterone. alpha-naphthoflavone 68-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-61 21168483-5 2011 In addition, hyperforin was found to inhibit CYP2D6 and CYP3A4 model activities quite potently. hyperforin 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 21194699-3 2011 Acetaminophen (CYP1A2), dextrorphan (CYP2D6), hydroxy-chlorzoxazone (CYP2E1) and hydroxy-mephenytoin (CYP2C19) can be derivatized because of the presence of a phenolic OH, whereas hydroxy-midazolam (CYP3A4) and hydroxy-tolbutamide (CYP2C9) remain unchanged. Acetaminophen 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 199-205 21070748-8 2011 Amiodarone (10-50muM) was cytotoxic for HepG2 cells/CYP3A4 or HepG2 cells/CYP3A4 supersomes, but not for HepG2 cells/wt or less toxic for HepG2 cells/wt incubated with control supersomes without CYP3A4. Amiodarone 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 21207936-2 2011 Resonance Raman (RR) spectroscopy is used to help define active site structural responses of nanodisc-incorporated CYP3A4 to the binding of three substrates: bromocriptine (BC), erythromycin (ERY), and testosterone (TST). Bromocriptine 173-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 21070748-9 2011 Co-incubation with ketoconazole, attenuated cytotoxicity of amiodarone incubated with HepG2 cells/CYP3A4 or HepG2 cells/CYP3A4 supersomes. Ketoconazole 19-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 21070748-9 2011 Co-incubation with ketoconazole, attenuated cytotoxicity of amiodarone incubated with HepG2 cells/CYP3A4 or HepG2 cells/CYP3A4 supersomes. Ketoconazole 19-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 21070748-9 2011 Co-incubation with ketoconazole, attenuated cytotoxicity of amiodarone incubated with HepG2 cells/CYP3A4 or HepG2 cells/CYP3A4 supersomes. Amiodarone 60-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 21207936-2 2011 Resonance Raman (RR) spectroscopy is used to help define active site structural responses of nanodisc-incorporated CYP3A4 to the binding of three substrates: bromocriptine (BC), erythromycin (ERY), and testosterone (TST). Erythromycin 192-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 21070748-9 2011 Co-incubation with ketoconazole, attenuated cytotoxicity of amiodarone incubated with HepG2 cells/CYP3A4 or HepG2 cells/CYP3A4 supersomes. Amiodarone 60-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 21207936-2 2011 Resonance Raman (RR) spectroscopy is used to help define active site structural responses of nanodisc-incorporated CYP3A4 to the binding of three substrates: bromocriptine (BC), erythromycin (ERY), and testosterone (TST). Testosterone 202-214 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 21070748-10 2011 MDEA and DDEA were formed only in incubations containing HepG2 cells/CYP3A4 or HepG2 cells/CYP3A4 supersomes but not by HepG2 cells/wt or HepG2 cells/wt with control supersomes. 3,4-methylenedioxyethamphetamine 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 21070748-10 2011 MDEA and DDEA were formed only in incubations containing HepG2 cells/CYP3A4 or HepG2 cells/CYP3A4 supersomes but not by HepG2 cells/wt or HepG2 cells/wt with control supersomes. 3,4-methylenedioxyethamphetamine 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 21207936-2 2011 Resonance Raman (RR) spectroscopy is used to help define active site structural responses of nanodisc-incorporated CYP3A4 to the binding of three substrates: bromocriptine (BC), erythromycin (ERY), and testosterone (TST). Testosterone 216-219 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 21070748-10 2011 MDEA and DDEA were formed only in incubations containing HepG2 cells/CYP3A4 or HepG2 cells/CYP3A4 supersomes but not by HepG2 cells/wt or HepG2 cells/wt with control supersomes. Di-N-desethylamiodarone 9-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 21207936-4 2011 While ERY and BC are known to bind to CYP3A4 with a 1:1 stoichiometry, only the BC induces a substantial conversion from low- to high-spin state, as clearly manifested in the RR spectra acquired herein. Bromocriptine 14-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 21070748-10 2011 MDEA and DDEA were formed only in incubations containing HepG2 cells/CYP3A4 or HepG2 cells/CYP3A4 supersomes but not by HepG2 cells/wt or HepG2 cells/wt with control supersomes. Di-N-desethylamiodarone 9-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 21219398-0 2011 4beta-Hydroxycholesterol, an endogenous marker of CYP3A4/5 activity in humans. cholest-5-ene-3,4-diol 0-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 21070748-11 2011 Metabolized amiodarone triggered the production of reactive oxygen species, induced mitochondrial damage and cytochrome c release, and promoted apoptosis/necrosis in HepG2 cells/CYP3A4, but not HepG2 cells/wt. Amiodarone 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 21070748-12 2011 This study supports the hypothesis that a high CYP3A4 activity is a risk factor for amiodarone"s hepatotoxicity. Amiodarone 84-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 21070748-13 2011 Since CYP3A4 inducers are used frequently and amiodarone-associated hepatotoxicity can be fatal, our observations may be clinically relevant. Amiodarone 46-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 21219398-1 2011 We have proposed that 4beta-hydroxycholesterol (4beta-OHC) may be used as an endogenous marker of CYP3A activity. cholest-5-ene-3,4-diol 22-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 21219398-1 2011 We have proposed that 4beta-hydroxycholesterol (4beta-OHC) may be used as an endogenous marker of CYP3A activity. 4beta-ohc 48-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 21219398-2 2011 The cholesterol metabolite 4beta-OHC is formed by CYP3A4. Cholesterol 4-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 21219398-2 2011 The cholesterol metabolite 4beta-OHC is formed by CYP3A4. 4beta-ohc 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 21219398-3 2011 Treatment of patients with strong inducers of CYP3A enzymes, e.g. anti-epileptic drugs, resulted in 10-fold increased concentrations of plasma 4beta-OHC, while treatment with CYP3A inhibitors such as ritonavir or itraconazole resulted in decreased plasma concentrations. 4beta-ohc 143-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-51 21219398-3 2011 Treatment of patients with strong inducers of CYP3A enzymes, e.g. anti-epileptic drugs, resulted in 10-fold increased concentrations of plasma 4beta-OHC, while treatment with CYP3A inhibitors such as ritonavir or itraconazole resulted in decreased plasma concentrations. Itraconazole 213-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-51 21219398-4 2011 There was a relationship between the 4beta-OHC concentration and the number of active CYP3A5*1 alleles showing that 4beta-OHC was not only formed by CYP3A4, but also by CYP3A5. 4beta-ohc 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 21219398-4 2011 There was a relationship between the 4beta-OHC concentration and the number of active CYP3A5*1 alleles showing that 4beta-OHC was not only formed by CYP3A4, but also by CYP3A5. 4beta-ohc 116-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 21219398-5 2011 The concentration of 4beta-OHC was higher in women than in men, confirming previous studies indicating a gender difference in CYP3A4/5-activity. 4beta-ohc 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 21219398-6 2011 The rate of elimination of 4beta-OHC is slow (half-life 17 days) which results in stable plasma concentrations within individuals, but limits its use to study rapid changes in CYP3A activity. 4beta-ohc 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-181 21219398-7 2011 In short-term studies exogenous markers such as midazolam or quinine may be superior, but in long-term studies 4beta-OHC is a sensitive marker of CYP3A activity, especially to assess induction but also inhibition. 4beta-ohc 111-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-151 21056987-2 2011 This information may be important for understanding paclitaxel metabolism in vivo and in the investigation of the role of genetic polymorphisms in the metabolizing enzymes CYP2C8 and CYP3A4/CYP3A5 and the ABCB1 transporter. Paclitaxel 52-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 183-189 21045201-7 2011 Ketoconazole, known to inhibit not only CYP3A but also CYP4F2, was an inhibitor of fingolimod metabolism in HLM with an inhibition constant (K(i)) of 0.74 muM (and by recombinant CYP4F2 with an IC(50) of 1.6 muM), whereas there was only a slight inhibition found with azamulin and none with troleandomycin. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 20955791-0 2011 Transport of 5,5-diphenylbarbituric acid and its precursors and their effect on P-gp, MRP2 and CYP3A4 in Caco-2 and LS180 cells. 5,5-diphenylbarbituric acid 13-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 21147222-9 2011 Studies using itraconazole, a CYP3A4 inhibitor, established its role in curcumin metabolism. Itraconazole 14-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 21147222-9 2011 Studies using itraconazole, a CYP3A4 inhibitor, established its role in curcumin metabolism. Curcumin 72-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 20641061-5 2011 Among seven major CYP isoforms tested, corynoline showed strong inhibitory effects on the activities of CYP3A4 and CYP2C9, with an IC(50) of 3.3 +- 0.9 microm and 31.5 +- 0.5 microm, respectively. corynoline 39-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 20641061-6 2011 Kinetic analysis showed that inhibition of CYP3A4 by corynoline was best fit to a noncompetitive manner with K(i) of 3.2 microm, while inhibition of CYP2C9 by corynoline was best fit to a competitive manner with K(i) of 6.3 microm. corynoline 53-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 20641061-7 2011 Additionally, corynoline exhibited time-dependent inhibition (TDI) toward CYP3A4. corynoline 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 21087116-6 2011 Screening of alpha-thujone metabolism with CYP recombinant enzymes indicated that CYP2A6 was principally responsible for the major 7- and 4-hydroxylation reactions, although CYP3A4 and CYP2B6 participated to a lesser extent and CYP3A4 and CYP2B6 catalyzed minor 2-hydroxylation. beta-thujone 13-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 21087116-6 2011 Screening of alpha-thujone metabolism with CYP recombinant enzymes indicated that CYP2A6 was principally responsible for the major 7- and 4-hydroxylation reactions, although CYP3A4 and CYP2B6 participated to a lesser extent and CYP3A4 and CYP2B6 catalyzed minor 2-hydroxylation. beta-thujone 13-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 21105682-2 2011 While narciclasine was found to possess potent inhibitory activity to human CYP3A4, its dihydro analogue was inactive. narciclasine 6-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 20878151-2 2011 Lopinavir is extensively metabolized by the hepatic cytochrome P450 3A4, and the pharmacokinetics of this protease inhibitor (PI) could be influenced by liver impairment. Lopinavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-71 20931329-2 2011 Like montelukast, zafirlukast is a substrate of CYP2C9 and CYP3A4 and a potent inhibitor of CYP2C8 in vitro. montelukast 5-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 20931329-2 2011 Like montelukast, zafirlukast is a substrate of CYP2C9 and CYP3A4 and a potent inhibitor of CYP2C8 in vitro. zafirlukast 18-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 21235585-0 2011 Mechanism of cytochrome P450-3A inhibition by ketoconazole. Ketoconazole 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-31 21235585-1 2011 OBJECTIVES: Ketoconazole is extensively used as an index inhibitor of cytochrome P450-3A (CYP3A) activity in vitro and in vivo, but the mechanism of ketoconazole inhibition of CYP3A still is not clearly established. Ketoconazole 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-88 21235585-1 2011 OBJECTIVES: Ketoconazole is extensively used as an index inhibitor of cytochrome P450-3A (CYP3A) activity in vitro and in vivo, but the mechanism of ketoconazole inhibition of CYP3A still is not clearly established. Ketoconazole 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 21235585-1 2011 OBJECTIVES: Ketoconazole is extensively used as an index inhibitor of cytochrome P450-3A (CYP3A) activity in vitro and in vivo, but the mechanism of ketoconazole inhibition of CYP3A still is not clearly established. Ketoconazole 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-181 21235585-1 2011 OBJECTIVES: Ketoconazole is extensively used as an index inhibitor of cytochrome P450-3A (CYP3A) activity in vitro and in vivo, but the mechanism of ketoconazole inhibition of CYP3A still is not clearly established. Ketoconazole 149-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 21235585-1 2011 OBJECTIVES: Ketoconazole is extensively used as an index inhibitor of cytochrome P450-3A (CYP3A) activity in vitro and in vivo, but the mechanism of ketoconazole inhibition of CYP3A still is not clearly established. Ketoconazole 149-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-181 20717876-3 2011 Using a systematic in vitro-in vivo approach, a cranberry juice product was identified recently that elicited a pharmacokinetic interaction with the CYP3A probe substrate midazolam in 16 healthy volunteers. Midazolam 171-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-154 20717876-8 2011 The inhibitory potency (IC(50)) of maslinic acid, corosolic acid, and ursolic acid was 7.4, 8.8, and < 10 microM, respectively, using HIM as the enzyme source and 2.8, 4.3, and < 10 microM, respectively, using recombinant CYP3A4 as the enzyme source. maslinic acid 35-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 20717876-8 2011 The inhibitory potency (IC(50)) of maslinic acid, corosolic acid, and ursolic acid was 7.4, 8.8, and < 10 microM, respectively, using HIM as the enzyme source and 2.8, 4.3, and < 10 microM, respectively, using recombinant CYP3A4 as the enzyme source. corosolic acid 50-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 20717876-8 2011 The inhibitory potency (IC(50)) of maslinic acid, corosolic acid, and ursolic acid was 7.4, 8.8, and < 10 microM, respectively, using HIM as the enzyme source and 2.8, 4.3, and < 10 microM, respectively, using recombinant CYP3A4 as the enzyme source. ursolic acid 70-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 20717876-9 2011 These in vitro inhibitory potencies, which are within the range of those reported for two CYP3A inhibitory components in grapefruit juice, suggest that these triterpenes may have contributed to the midazolam-cranberry juice interaction observed in the clinical study. Triterpenes 158-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 20717876-9 2011 These in vitro inhibitory potencies, which are within the range of those reported for two CYP3A inhibitory components in grapefruit juice, suggest that these triterpenes may have contributed to the midazolam-cranberry juice interaction observed in the clinical study. Midazolam 198-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 21138310-2 2011 Among the isolates obtained, alpha-conidendrin (12) showed strong CYP3A4 inhibition with an IC(50) value of 0.2 muM. conidendrin 29-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 20955791-3 2011 P-gp and CYP3A4 activities were assayed by [(3)H]digoxin and rhodamine 123 cellular retention and testosterone 6beta-hydroxylation, respectively. testosterone 6beta 98-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 20955791-8 2011 Changes in expression were confined mostly to MDR1 and CYP3A4: in LS180 cells, treatment for 3 days increased MDR1 and CYP3A4 but not MRP2 mRNA, and elevated P-gp and CYP3A4 protein expression that led to decreased cellular accumulation of [(3)H]digoxin and rhodamine 123, and enhanced testosterone 6beta-hydroxylase activity towards T2007, respectively. [(3)h]digoxin 240-253 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 20955791-8 2011 Changes in expression were confined mostly to MDR1 and CYP3A4: in LS180 cells, treatment for 3 days increased MDR1 and CYP3A4 but not MRP2 mRNA, and elevated P-gp and CYP3A4 protein expression that led to decreased cellular accumulation of [(3)H]digoxin and rhodamine 123, and enhanced testosterone 6beta-hydroxylase activity towards T2007, respectively. Rhodamines 258-267 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 20955791-3 2011 P-gp and CYP3A4 activities were assayed by [(3)H]digoxin and rhodamine 123 cellular retention and testosterone 6beta-hydroxylation, respectively. [(3)h]digoxin 43-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 20955791-3 2011 P-gp and CYP3A4 activities were assayed by [(3)H]digoxin and rhodamine 123 cellular retention and testosterone 6beta-hydroxylation, respectively. Rhodamines 61-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 21177421-8 2011 Everolimus undergoes extensive hepatic metabolism, primarily through the CYP3A4 isoenzyme, which predisposes it to drug interactions with inducers and inhibitors of this enzyme. Everolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 21039635-9 2011 Alcohol caused significant upregulation of ABCC1, CYP2A6, CYP2E1, and CYP3A4 proteins (50 to 85%) and showed >50% increase in the specific activity of CYP2A6 and CYP3A4 in U937 macrophages. Alcohols 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 21039635-3 2011 This study is designed to assess the effect of alcohol on the ABCC1 and CYP enzymes involved in the metabolism of NNRTIs and PIs (CYP2B6, CYP2D6, and CYP3A4) and oxidative stress (CYP1A1, CYP2A6, and CYP2E1) in U937 macrophages. Alcohols 47-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 21039635-8 2011 Alcohol (100 mM) increased the mRNA levels of ABCC1 and CYP2A6 (200%), CYP2B6 and CYP3A4 (150%), and CYP2E1 (400%) compared with the control. Alcohols 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 21039635-9 2011 Alcohol caused significant upregulation of ABCC1, CYP2A6, CYP2E1, and CYP3A4 proteins (50 to 85%) and showed >50% increase in the specific activity of CYP2A6 and CYP3A4 in U937 macrophages. Alcohols 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 20637317-6 2011 Interestingly, both isoforms of CYP3A7 did not metabolize the anti-cancer drug sorafenib (which is approved for the treatment of HCC), while CYP3A4 produced the N-oxide in our system, as expected. n-oxide 161-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 21950148-9 2011 Taiwanese subjects might have lower CYP3A4 activity to metabolize felodipine, which is similar to the phenomenon observed with nifedipine. Felodipine 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 20825389-10 2011 Chemical and mAb inhibition of CYP3A in high 3A activity HLM reduced EDDP formation by 60-85%; inhibition of CYP2B6 in 2B6 high-activity HLM reduced (S)-EDDP formation by 80% and (R)-EDDP formation by 55%. 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine 69-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-36 20825389-12 2011 When CYP3A was inhibited, 2B6 mediated (S)-EDDP formation predominated; S/R stereo-selectivity increased. (s)-eddp 39-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 5-10 20656072-8 2011 In addition, the number of water molecules in the active site cavity of CYP3A4 anomalously decreases under high pressure due to opening of the active site. Water 27-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 25819130-3 2011 For sunitinib, sorafenib, and pazopanib: potential drug interactions are possible with inducers/inhibitors of CYP3A4, anti-hypertensive drugs, antidiabetic drugs, thyroid hormones, and anticoagulant treatments. Sunitinib 4-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 21142269-3 2011 The aim of this study was to determine whether inhibition of CYP2D6 alone by paroxetine or inhibition of both CYP2D6 and CYP3A4 by a combination of paroxetine and itraconazole alters the pharmacokinetics of and pharmacological response to intravenous oxycodone. Paroxetine 148-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 25819130-3 2011 For sunitinib, sorafenib, and pazopanib: potential drug interactions are possible with inducers/inhibitors of CYP3A4, anti-hypertensive drugs, antidiabetic drugs, thyroid hormones, and anticoagulant treatments. Sorafenib 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 25819130-3 2011 For sunitinib, sorafenib, and pazopanib: potential drug interactions are possible with inducers/inhibitors of CYP3A4, anti-hypertensive drugs, antidiabetic drugs, thyroid hormones, and anticoagulant treatments. pazopanib 30-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 22312553-2 2011 We aimed to assess cardiac conduction safety of coadministration of the CYP3A4 inhibitor lopinavir/ritonavir (LPV/r) and the CYP3A4 substrate artemether-lumefantrine (AL) in HIV-positive Ugandans. Lopinavir 89-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 22312553-2 2011 We aimed to assess cardiac conduction safety of coadministration of the CYP3A4 inhibitor lopinavir/ritonavir (LPV/r) and the CYP3A4 substrate artemether-lumefantrine (AL) in HIV-positive Ugandans. Artemether, Lumefantrine Drug Combination 142-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 22312553-2 2011 We aimed to assess cardiac conduction safety of coadministration of the CYP3A4 inhibitor lopinavir/ritonavir (LPV/r) and the CYP3A4 substrate artemether-lumefantrine (AL) in HIV-positive Ugandans. Artemether, Lumefantrine Drug Combination 167-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 21142269-3 2011 The aim of this study was to determine whether inhibition of CYP2D6 alone by paroxetine or inhibition of both CYP2D6 and CYP3A4 by a combination of paroxetine and itraconazole alters the pharmacokinetics of and pharmacological response to intravenous oxycodone. Itraconazole 163-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 21142269-3 2011 The aim of this study was to determine whether inhibition of CYP2D6 alone by paroxetine or inhibition of both CYP2D6 and CYP3A4 by a combination of paroxetine and itraconazole alters the pharmacokinetics of and pharmacological response to intravenous oxycodone. Oxycodone 251-260 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 21177242-7 2011 Lurasidone is primarily metabolized in the liver through the CYP3A4 enzyme system, and coadministration with drugs that are strong inhibitors of CYP3A4 (such as ketoconazole) or strong inducers (such as rifampin) are contraindicated. Lurasidone Hydrochloride 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 21142269-11 2011 If both oxidative metabolic pathways via CYP3A4 and 2D6 are inhibited the exposure to intravenous oxycodone increases substantially. Oxycodone 98-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-55 21177242-7 2011 Lurasidone is primarily metabolized in the liver through the CYP3A4 enzyme system, and coadministration with drugs that are strong inhibitors of CYP3A4 (such as ketoconazole) or strong inducers (such as rifampin) are contraindicated. Lurasidone Hydrochloride 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 20926621-8 2011 The results of screening, inhibition, and correlation studies confirmed that CYP3A4 is the major P450 enzyme responsible for M19 formation from SCH 530348. vorapaxar 144-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 20876785-6 2011 Recombinant CYP3A4 catalyzed MII formation from exemestane with a catalytic efficiency of 840 nl/pmol P450 x min that was at least 4-fold higher than those of other P450s investigated. exemestane 48-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 20876785-7 2011 Among a panel of 10 chemical inhibitors tested, only ketoconazole and troleandomycin (CYP3A-specific chemical inhibitors) significantly inhibited the formation of MII by 45 and 95%, respectively. Ketoconazole 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 20876785-7 2011 Among a panel of 10 chemical inhibitors tested, only ketoconazole and troleandomycin (CYP3A-specific chemical inhibitors) significantly inhibited the formation of MII by 45 and 95%, respectively. Troleandomycin 70-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 20876785-7 2011 Among a panel of 10 chemical inhibitors tested, only ketoconazole and troleandomycin (CYP3A-specific chemical inhibitors) significantly inhibited the formation of MII by 45 and 95%, respectively. Methicillin 163-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 20876785-9 2011 In summary, exemestane seems to be metabolized to MI by multiple P450s that include CYP4A11 and CYP1A1/2, whereas its oxidation to MII is primarily mediated by CYP3A. exemestane 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-165 22287853-6 2011 Mean exposure (AUC) of the CYP3A4-generated active metabolite of saxagliptin, 5-hydroxy saxagliptin, decreased with coadministration of simvastatin, diltiazem, and ketoconazole by 2%, 34%, and 88%, respectively. saxagliptin 65-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 22287853-6 2011 Mean exposure (AUC) of the CYP3A4-generated active metabolite of saxagliptin, 5-hydroxy saxagliptin, decreased with coadministration of simvastatin, diltiazem, and ketoconazole by 2%, 34%, and 88%, respectively. 5-hydroxysaxagliptin 78-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 22287853-6 2011 Mean exposure (AUC) of the CYP3A4-generated active metabolite of saxagliptin, 5-hydroxy saxagliptin, decreased with coadministration of simvastatin, diltiazem, and ketoconazole by 2%, 34%, and 88%, respectively. Simvastatin 136-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 22287853-6 2011 Mean exposure (AUC) of the CYP3A4-generated active metabolite of saxagliptin, 5-hydroxy saxagliptin, decreased with coadministration of simvastatin, diltiazem, and ketoconazole by 2%, 34%, and 88%, respectively. Diltiazem 149-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 22287853-6 2011 Mean exposure (AUC) of the CYP3A4-generated active metabolite of saxagliptin, 5-hydroxy saxagliptin, decreased with coadministration of simvastatin, diltiazem, and ketoconazole by 2%, 34%, and 88%, respectively. Ketoconazole 164-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 22287853-10 2011 The dose of saxagliptin does not need to be adjusted when coadministered with a substrate or moderate inhibitor of CYP3A4. saxagliptin 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 22287853-11 2011 A limitation to the lowest clinical dose of saxagliptin (2.5 mg) is proposed when it is coadministered with a potent CYP3A4 inhibitor such as ketoconazole. saxagliptin 44-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 22287853-11 2011 A limitation to the lowest clinical dose of saxagliptin (2.5 mg) is proposed when it is coadministered with a potent CYP3A4 inhibitor such as ketoconazole. Ketoconazole 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 21568918-4 2011 PPIs might diminish the antiplatelet effects and the clinical effectiveness of clopidogrel possibly through inhibition of CYP2C19 and CYP3A4 isoenzymes. Clopidogrel 79-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 21084763-1 2011 The aim of this study was to investigate the effect of the dipeptidyl peptidase-4 inhibitor linagliptin on the pharmacokinetics of glyburide (a CYP2C9 and CYP3A4 substrate) and vice versa. Linagliptin 92-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 21084763-1 2011 The aim of this study was to investigate the effect of the dipeptidyl peptidase-4 inhibitor linagliptin on the pharmacokinetics of glyburide (a CYP2C9 and CYP3A4 substrate) and vice versa. Glyburide 131-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 21566342-5 2011 An inhibitor of CYP3A4, ketoconazole, significantly suppressed the growth of Hep3B cells overexpressing CYP3A4, but an inhibitor of CYP2D6, quinidine, did not restore Hep3B cell growth to baseline levels. Ketoconazole 24-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 21410294-3 2011 OBJECTIVE: The aim of this study was to investigate the effects of a potent CYP3A4 inducer, rifampicin (Study A), and a potent CYP3A4 inhibitor, itraconazole (Study B), on the pharmacokinetics of a single 300 mg dose of vandetanib in healthy subjects. Itraconazole 145-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 21410294-16 2011 CONCLUSIONS: Exposure to vandetanib, as assessed by AUC(504) in healthy subjects, was reduced by around 40% when a single dose was given in combination with the potent CYP3A4 inducer rifampicin. vandetanib 25-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 21410294-16 2011 CONCLUSIONS: Exposure to vandetanib, as assessed by AUC(504) in healthy subjects, was reduced by around 40% when a single dose was given in combination with the potent CYP3A4 inducer rifampicin. Rifampin 183-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 21178300-3 2011 CYP3A4 and CYP2C8 were involved in the metabolic activation and CYP3A4 was inducible by repeated administrations of troglitazone. Troglitazone 116-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 21178300-3 2011 CYP3A4 and CYP2C8 were involved in the metabolic activation and CYP3A4 was inducible by repeated administrations of troglitazone. Troglitazone 116-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 21178301-6 2011 In addition, phyllanthin and hypophyllanthin were potent mechanism-based inhibitors of CYP3A4 with K(I) values of 1.75 +- 1.20 microM and 2.24 +- 1.84 microM and k(inact) values of 0.18 +- 0.05 min(-1) and 0.15 +- 0.06 min(-1), respectively. phyllanthin 13-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 21178301-6 2011 In addition, phyllanthin and hypophyllanthin were potent mechanism-based inhibitors of CYP3A4 with K(I) values of 1.75 +- 1.20 microM and 2.24 +- 1.84 microM and k(inact) values of 0.18 +- 0.05 min(-1) and 0.15 +- 0.06 min(-1), respectively. hypophyllanthin 29-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 21178301-7 2011 The k(inact)/K(I) ratios of these lignans were higher than those reported for some therapeutic drugs that act as mechanism-based inhibitors of CYP3A4. Lignans 34-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-149 21178302-0 2011 Deglycosylated ginsenosides are more potent inducers of CYP1A1, CYP1A2 and CYP3A4 expression in HepG2 cells than glycosylated ginsenosides. Ginsenosides 15-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 21178302-6 2011 In the present study, we examined the effects of thirteen ginsenosides on the expression of CYP1A1, CYP1A2 and CYP3A4 in HepG2 cells. Ginsenosides 58-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 21178302-8 2011 Moreover, we discovered that deglycosylated ginsenosides, some of which are putative ginsenoside metabolites, were more potent inducers of CYP1A1, CYP1A2 and CYP3A4 than glycosylated ginsenosides. Ginsenosides 44-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 21410294-17 2011 Because of this, it may be appropriate to avoid coadministration of potent CYP3A4 inducers with vandetanib. vandetanib 96-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 21410294-18 2011 Vandetanib exposure was increased by about 9% when it was taken in combination with the CYP3A4 inhibitor itraconazole. vandetanib 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 21566342-5 2011 An inhibitor of CYP3A4, ketoconazole, significantly suppressed the growth of Hep3B cells overexpressing CYP3A4, but an inhibitor of CYP2D6, quinidine, did not restore Hep3B cell growth to baseline levels. Ketoconazole 24-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 21410294-18 2011 Vandetanib exposure was increased by about 9% when it was taken in combination with the CYP3A4 inhibitor itraconazole. Itraconazole 105-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 21178302-8 2011 Moreover, we discovered that deglycosylated ginsenosides, some of which are putative ginsenoside metabolites, were more potent inducers of CYP1A1, CYP1A2 and CYP3A4 than glycosylated ginsenosides. Ginsenosides 44-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 21566342-6 2011 Overexpression of CYP3A4 increased the production of reactive oxygen species, but this was not the cause of the CYP3A4-induced growth. Reactive Oxygen Species 53-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 21566342-7 2011 Previously, we showed that CYP3A4 can produce epoxyeicosatrienoic acids (EETs) from arachidonic acid. epoxyeicosatrienoic acids 46-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 21566342-7 2011 Previously, we showed that CYP3A4 can produce epoxyeicosatrienoic acids (EETs) from arachidonic acid. eets 73-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 21980965-2 2011 This was due to atazanavir and ritonavir therapy for her HIV inhibiting the CYP3A4 hepatic enzyme resulting in accumulation of tacrolimus. Atazanavir Sulfate 16-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 21566342-7 2011 Previously, we showed that CYP3A4 can produce epoxyeicosatrienoic acids (EETs) from arachidonic acid. Arachidonic Acid 84-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 21980965-2 2011 This was due to atazanavir and ritonavir therapy for her HIV inhibiting the CYP3A4 hepatic enzyme resulting in accumulation of tacrolimus. Ritonavir 31-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 21566342-11 2011 The cell growth promoted by CYP3A4 was inhibited by PI3K inhibitor LY294002. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 67-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 21980965-2 2011 This was due to atazanavir and ritonavir therapy for her HIV inhibiting the CYP3A4 hepatic enzyme resulting in accumulation of tacrolimus. Tacrolimus 127-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 20857093-10 2011 CONCLUSIONS: Inhibition of CYP3A4 by ketoconazole increases the exposure and some pharmacodynamic effects of oxycodone. Ketoconazole 37-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 20857093-10 2011 CONCLUSIONS: Inhibition of CYP3A4 by ketoconazole increases the exposure and some pharmacodynamic effects of oxycodone. Oxycodone 109-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 20857093-0 2011 Effect of the inhibition of CYP3A4 or CYP2D6 on the pharmacokinetics and pharmacodynamics of oxycodone. Oxycodone 93-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 20857093-12 2011 Pharmacodynamic changes associated with CYP3A4 inhibition may be clinically important in patients treated with oxycodone. Oxycodone 111-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 20857093-1 2011 PURPOSE: The main metabolic pathways of oxycodone, a potent opioid analgetic, are N-demethylation (CYP3A4) to inactive noroxycodone and O-demethylation (CYP2D6) to active oxymorphone. Oxycodone 40-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 20931330-0 2011 Do CYP3A and ABCB1 genotypes influence the plasma concentration and clinical outcome of donepezil treatment? Donepezil 88-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 3-8 20931330-1 2011 PURPOSE: The aim of our study was to evaluate the impact of CYP3A4, CYP3A5, and ABCB1 polymorphisms on donepezil disposition and clinical outcome. Donepezil 103-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 19906827-5 2011 We now report for the first time the effect of a commercial Echinacea extract (Echinaforce) and four Echinacea alkylamides on the transcription of the major drug metabolizing enzyme CYP3A4. echinacea alkylamides 101-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 182-188 20200269-4 2011 Smoking and CYP3A4 inhibitors as concomitant medications were important predictors of istradefylline exposure. istradefylline 86-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 20980920-0 2011 The effect of St John"s Wort on the pharmacodynamic response of clopidogrel in hyporesponsive volunteers and patients: increased platelet inhibition by enhancement of CYP3A4 metabolic activity. Clopidogrel 64-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 167-173 20702754-2 2011 Previous in vitro studies indicated that nilotinib metabolism is primarily mediated by CYP3A4. nilotinib 41-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 20200269-5 2011 Istradefylline area under the concentration-time curve at steady-state increased 35% (95% confidence interval, 18%-55%) in the presence of CYP3A4 inhibitors and decreased 38% (95% confidence interval, 26%-50%) in smokers. istradefylline 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 20702754-4 2011 In the induction study, administration of rifampin 600 mg once daily for 8 days significantly increased urinary 6beta-hydroxycortisol/ cortisol ratio, from a preinduction baseline of 5.8 +- 2.7 to 18.0 +- 10.2 after 8 days of rifampin treatment, confirming an inductive effect on CYP3A4. Rifampin 42-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 280-286 20702754-7 2011 These results indicate that concurrent use of strong CYP3A4 inducers or inhibitors may necessitate dosage adjustments of nilotinib and should be avoided when possible. nilotinib 121-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 20443129-0 2011 Effect of CYP3A-inducing anti-epileptics on sorafenib exposure: results of a phase II study of sorafenib plus daily temozolomide in adults with recurrent glioblastoma. Sorafenib 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-15 21436605-5 2011 Furthermore, CYP3A4 protein levels were significantly increased by the addition of rifampicin and dexamethasone to the culture media, indicating that the induction potential was maintained. Rifampin 83-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 21436605-5 2011 Furthermore, CYP3A4 protein levels were significantly increased by the addition of rifampicin and dexamethasone to the culture media, indicating that the induction potential was maintained. Dexamethasone 98-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 21126270-4 2011 Based on its considerable CYP3A inhibiting potency, posaconazole may significantly increase plasma concentrations of concomitantly applied drugs which undergo an extensive first-pass effect through gut and liver. posaconazole 52-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-31 21857093-1 2011 The aim of this study was to retrospectively evaluate the effect of polymorphisms in the CYP3A4, CYP3A5 and ABCB1 genes on the dose-adjusted concentration and dose requirement of cyclosporine A(CsA) in Chinese recipients during the early period after bone marrow or hematopoietic stem cell transplantation. Cyclosporine 179-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 21192344-3 2011 CYP2C19 and CYP3A4 play a primary role in citalopram metabolism, whereas CYP2D6 plays a secondary role. Citalopram 42-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 22167207-10 2011 Based on these studies, we attribute most of the enhancing effects of VPA and TSA on ellipticine cytotoxicity to enhanced ellipticine-DNA adduct formation caused by an increase in levels of cytochrome b5, CYP3A4 and CYP1A1 in neuroblastoma cells. ellipticine 85-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 205-211 21190921-1 2011 Carbamazepine is a (CYP1A2 and CYP3A4 enzyme inducer) medicine which is used by epileptic patients for a long time. Carbamazepine 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 21190921-17 2011 This is probably due to the inhibition of CYP3A4 isoenzyme by ciprofloxacin which is responsible for metabolism of CBZ. Ciprofloxacin 62-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21190921-17 2011 This is probably due to the inhibition of CYP3A4 isoenzyme by ciprofloxacin which is responsible for metabolism of CBZ. Carbamazepine 115-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 21857093-1 2011 The aim of this study was to retrospectively evaluate the effect of polymorphisms in the CYP3A4, CYP3A5 and ABCB1 genes on the dose-adjusted concentration and dose requirement of cyclosporine A(CsA) in Chinese recipients during the early period after bone marrow or hematopoietic stem cell transplantation. Cyclosporine 194-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 21462897-4 2011 The results indicated that GA was metabolized mainly by CYP3A4. Glycyrrhetinic Acid 27-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 20954901-2 2011 However, for the CYP3A probe substrate midazolam (MDZ), considerable variability in enzyme kinetic parameters has been observed in different in vitro studies. Midazolam 39-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-22 20954901-2 2011 However, for the CYP3A probe substrate midazolam (MDZ), considerable variability in enzyme kinetic parameters has been observed in different in vitro studies. Midazolam 50-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-22 21462897-6 2011 At concentration up to 50 micromol x L(-1), GA inhibited CYP2C19, CYP2C9 and CYP3A4 enzyme activities with the inhibitory potencies up to 50%. Glycyrrhetinic Acid 44-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 20609441-5 2010 Norketamine was formed by CYP3A4, CYP2C19, CYP2B6, CYP2A6, CYP2D6 and CYP2C9, whereas CYP2B6 and CYP2A6 were identified to be the only enzymes which enable the hydroxylation of norketamine. norketamine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 20609441-7 2010 The kinetic data of ketamine N-demethylation with CYP3A4 and CYP2B6 were best described with the Michaelis-Menten model and the Hill equation, respectively. Ketamine 20-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 20879989-2 2010 In the purified proteoliposomes, CYP3A4 binds testosterone with Kd (app)=36+-6 muM and Hill coefficient=1.5+-0.3, and 75+-4% of the CYP3A4 can be reduced by NADPH in the presence of testosterone. Testosterone 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 20879989-2 2010 In the purified proteoliposomes, CYP3A4 binds testosterone with Kd (app)=36+-6 muM and Hill coefficient=1.5+-0.3, and 75+-4% of the CYP3A4 can be reduced by NADPH in the presence of testosterone. Testosterone 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20879989-2 2010 In the purified proteoliposomes, CYP3A4 binds testosterone with Kd (app)=36+-6 muM and Hill coefficient=1.5+-0.3, and 75+-4% of the CYP3A4 can be reduced by NADPH in the presence of testosterone. NADP 157-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 20879989-2 2010 In the purified proteoliposomes, CYP3A4 binds testosterone with Kd (app)=36+-6 muM and Hill coefficient=1.5+-0.3, and 75+-4% of the CYP3A4 can be reduced by NADPH in the presence of testosterone. Testosterone 182-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 20879989-3 2010 Transfer of the first electron from CPR to CYP3A4 was measured by stopped-flow, trapping the reduced CYP3A4 as its Fe(II)-CO complex and measuring the characteristic absorbance change. ammonium ferrous sulfate 115-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 20879989-3 2010 Transfer of the first electron from CPR to CYP3A4 was measured by stopped-flow, trapping the reduced CYP3A4 as its Fe(II)-CO complex and measuring the characteristic absorbance change. ammonium ferrous sulfate 115-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 20921307-1 2010 Atazanavir (ATV) plasma concentrations are influenced by CYP3A4 and ABCB1, which are regulated by the pregnane X receptor (PXR; NR1I2). Atazanavir Sulfate 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 20861742-5 2010 Darunavir, fosamprenavir, lopinavir, nelfinavir, tipranavir, efavirenz, and abacavir increased CYP3A4 and/or CYP2B6 promoter activity, some through constitutive androstane receptor but mainly through PXR. Darunavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 20861742-5 2010 Darunavir, fosamprenavir, lopinavir, nelfinavir, tipranavir, efavirenz, and abacavir increased CYP3A4 and/or CYP2B6 promoter activity, some through constitutive androstane receptor but mainly through PXR. fosamprenavir 11-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 20861742-5 2010 Darunavir, fosamprenavir, lopinavir, nelfinavir, tipranavir, efavirenz, and abacavir increased CYP3A4 and/or CYP2B6 promoter activity, some through constitutive androstane receptor but mainly through PXR. Lopinavir 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 20861742-5 2010 Darunavir, fosamprenavir, lopinavir, nelfinavir, tipranavir, efavirenz, and abacavir increased CYP3A4 and/or CYP2B6 promoter activity, some through constitutive androstane receptor but mainly through PXR. Nelfinavir 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 20861742-5 2010 Darunavir, fosamprenavir, lopinavir, nelfinavir, tipranavir, efavirenz, and abacavir increased CYP3A4 and/or CYP2B6 promoter activity, some through constitutive androstane receptor but mainly through PXR. efavirenz 61-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 20861742-5 2010 Darunavir, fosamprenavir, lopinavir, nelfinavir, tipranavir, efavirenz, and abacavir increased CYP3A4 and/or CYP2B6 promoter activity, some through constitutive androstane receptor but mainly through PXR. abacavir 76-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 20946203-3 2010 METHOD: In vitro, we examined the impact of CYP2D6 and CYP3A4 inhibitors on zuclopenthixol metabolism in microsomes from six human livers. Clopenthixol 76-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 20946203-10 2010 CONCLUSION: The In vitro study suggests zuclopenthixol is metabolised primarily by CYP2D6 and CYP3A4. Clopenthixol 40-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 20921307-1 2010 Atazanavir (ATV) plasma concentrations are influenced by CYP3A4 and ABCB1, which are regulated by the pregnane X receptor (PXR; NR1I2). Atazanavir Sulfate 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 20861742-7 2010 Some PXR variants displayed lower fosamprenavir- and lopinavir-induced CYP3A4 promoter activity than the PXR reference sequence, whereas efavirenz and nelfinavir induction was unchanged. fosamprenavir 34-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 20861742-7 2010 Some PXR variants displayed lower fosamprenavir- and lopinavir-induced CYP3A4 promoter activity than the PXR reference sequence, whereas efavirenz and nelfinavir induction was unchanged. Lopinavir 53-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 21127497-11 2010 CONCLUSION: the isozymes UGT 1A4, CYP 3A4, 1A2, 2A6 and 2C8 participated in the hepatic metabolism of nuciferine. nuciferine 102-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-41 20921307-3 2010 The PXR single nucleotide polymorphism (SNP) 63396C T (rs2472677) alters PXR expression and CYP3A4 activity in vitro, and we previously showed an association of this polymorphism with unboosted ATV plasma concentrations. Atazanavir Sulfate 194-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 20921307-14 2010 The association is likely to be mediated through an effect on hepatic PXR expression and therefore expression of its target genes (e.g., CYP3A4, SLCO1B1, and ABCB1), which are known to be involved in ATV clearance. Atazanavir Sulfate 200-203 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 21045169-9 2010 DISCUSSION: Simvastatin undergoes extensive first-pass metabolism mediated by CYP3A4, making it susceptible to significant drug interactions. Simvastatin 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 20515961-0 2010 Oxcarbazepine accelerates cortisol elimination via cytochrome P450 3A4 induction. Oxcarbazepine 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-70 20515961-0 2010 Oxcarbazepine accelerates cortisol elimination via cytochrome P450 3A4 induction. Hydrocortisone 26-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-70 21175441-6 2010 Formation of hydroxyanastrozole from anastrozole was markedly inhibited by CYP3A selective chemical inhibitors (by >90%) and significantly correlated with CYP3A activity in a panel of HLMs (r= 0.96, P= 0.0005) and mainly catalyzed by expressed CYP3A4 and CYP3A5. hydroxyanastrozole 13-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 20515961-1 2010 Oxcarbazepine (OXC) induces cytochrome CYP3A4 activity, lowering female sex steroid concentrations. Oxcarbazepine 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 20515961-1 2010 Oxcarbazepine (OXC) induces cytochrome CYP3A4 activity, lowering female sex steroid concentrations. Oxcarbazepine 15-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 20515961-3 2010 The observation of an adolescent boy with Addison"s disease requiring high hydrocortisone replacement doses while on OXC for epilepsy led us to investigate effects of OXC on CYP3A4 induction and steroid metabolism. Oxcarbazepine 167-170 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 20515961-7 2010 This study shows that OXC-induced CYP3A4 activity increases cortisol elimination. Hydrocortisone 60-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 21175441-6 2010 Formation of hydroxyanastrozole from anastrozole was markedly inhibited by CYP3A selective chemical inhibitors (by >90%) and significantly correlated with CYP3A activity in a panel of HLMs (r= 0.96, P= 0.0005) and mainly catalyzed by expressed CYP3A4 and CYP3A5. hydroxyanastrozole 13-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-163 20715157-1 2010 BACKGROUND: CYP3A enzymes, due to their role in the metabolism of steroid hormones, are suggested to affect carcinogenesis of hormone-related cancers. Steroids 66-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 21175441-6 2010 Formation of hydroxyanastrozole from anastrozole was markedly inhibited by CYP3A selective chemical inhibitors (by >90%) and significantly correlated with CYP3A activity in a panel of HLMs (r= 0.96, P= 0.0005) and mainly catalyzed by expressed CYP3A4 and CYP3A5. hydroxyanastrozole 13-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 247-253 21175441-6 2010 Formation of hydroxyanastrozole from anastrozole was markedly inhibited by CYP3A selective chemical inhibitors (by >90%) and significantly correlated with CYP3A activity in a panel of HLMs (r= 0.96, P= 0.0005) and mainly catalyzed by expressed CYP3A4 and CYP3A5. Anastrozole 20-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 21175441-6 2010 Formation of hydroxyanastrozole from anastrozole was markedly inhibited by CYP3A selective chemical inhibitors (by >90%) and significantly correlated with CYP3A activity in a panel of HLMs (r= 0.96, P= 0.0005) and mainly catalyzed by expressed CYP3A4 and CYP3A5. Anastrozole 20-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-163 21175441-6 2010 Formation of hydroxyanastrozole from anastrozole was markedly inhibited by CYP3A selective chemical inhibitors (by >90%) and significantly correlated with CYP3A activity in a panel of HLMs (r= 0.96, P= 0.0005) and mainly catalyzed by expressed CYP3A4 and CYP3A5. Anastrozole 20-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 247-253 21175441-10 2010 CONCLUSION: Anastrozole is oxidized to hydroxyanastrozole mainly by CYP3A4 (and to some extent by CYP3A5 and CYP2C8). Anastrozole 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 21175441-10 2010 CONCLUSION: Anastrozole is oxidized to hydroxyanastrozole mainly by CYP3A4 (and to some extent by CYP3A5 and CYP2C8). hydroxyanastrozole 39-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 21175441-12 2010 Variable activity of CYP3A4 (and probably UGT1A4), possibly due to genetic polymorphisms and drug interactions, may alter anastrozole disposition and its effects in vivo. Anastrozole 122-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 21053990-15 2010 Potent CYP3A inhibitors, gastric acid suppressants and food have been shown to reduce the rate of formation of Pras-AM but not its overall exposure. pras-am 111-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-12 24688155-1 2010 BACKGROUND: Fluoxetine is an inhibitor of the main metabolizing enzymes (cytochrome P450 [CYP] 2C19 and CYP3A4) of omeprazole and thus might influence that drug"s pharmacokinetics. Fluoxetine 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 20583967-3 2010 The concentration-dependent response and time-course for the induction of CYP1A2, CYP2B6 and CYP3A4 by inducing agents beta-naphthoflavone, phenobarbital and rifampicin, respectively were examined in two or more donors using multiple end-points (mRNA, enzyme activity and Western blot analysis). beta-Naphthoflavone 119-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 24688155-1 2010 BACKGROUND: Fluoxetine is an inhibitor of the main metabolizing enzymes (cytochrome P450 [CYP] 2C19 and CYP3A4) of omeprazole and thus might influence that drug"s pharmacokinetics. Omeprazole 115-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 20583967-3 2010 The concentration-dependent response and time-course for the induction of CYP1A2, CYP2B6 and CYP3A4 by inducing agents beta-naphthoflavone, phenobarbital and rifampicin, respectively were examined in two or more donors using multiple end-points (mRNA, enzyme activity and Western blot analysis). Phenobarbital 140-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 20583967-3 2010 The concentration-dependent response and time-course for the induction of CYP1A2, CYP2B6 and CYP3A4 by inducing agents beta-naphthoflavone, phenobarbital and rifampicin, respectively were examined in two or more donors using multiple end-points (mRNA, enzyme activity and Western blot analysis). Rifampin 158-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 20615193-0 2010 Contribution of three CYP3A isoforms to metabolism of R- and S-warfarin. Warfarin 63-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-27 20736323-6 2010 The inhibitory potency of DBZ toward CYP3A4 was greater than that toward other P450 isoforms, including CYP1A2, CYP2C8, CYP2C9, CYP2C19, and CYP2D6. dibenzazepine 26-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 20615193-4 2010 Based on our studies, recombinant CYP3A4, CYP3A5 and CYP3A7 metabolized R- and S-warfarin to 10- and 4"-hydroxywarfarin with efficiencies that depended on the individual enzymes. r- and s-warfarin 72-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 20615193-4 2010 Based on our studies, recombinant CYP3A4, CYP3A5 and CYP3A7 metabolized R- and S-warfarin to 10- and 4"-hydroxywarfarin with efficiencies that depended on the individual enzymes. 10- and 4"-hydroxywarfarin 93-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 20615193-5 2010 For R-warfarin, CYP3A4, CYP3A7, and CYP3A5 demonstrated decreasing preference for 10-hydroxylation over 4"-hydroxylation. Warfarin 4-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 20615193-7 2010 While all enzymes preferentially metabolized R-warfarin, CYP3A4 was the most efficient at metabolizing all reactions. Warfarin 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 20736322-11 2010 In HepaRG cells, N-methylcytisine significantly induced CYP3A4 expression, and this induction was suppressed by the PXR antagonist sulforaphane. N-methylcytisine 17-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 20736322-11 2010 In HepaRG cells, N-methylcytisine significantly induced CYP3A4 expression, and this induction was suppressed by the PXR antagonist sulforaphane. sulforaphane 131-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 20615193-8 2010 Individuals, namely African-Americans and children, with higher relative levels of CYP3A5 and/or CYP3A7, respectively, compared to CYP3A4 may metabolize warfarin less efficiently and thus may require lower doses and be at risk for adverse drug-drug interactions related to the contributions of the respective enzymes. Warfarin 153-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 20924570-0 2010 Systemic uptake of miconazole during vaginal suppository use and effect on CYP1A2 and CYP3A4 associated enzyme activities in women. Miconazole 19-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 20837660-4 2010 The efficacy of MG132 was increased by inclusion of ketoconazole in the hepatocyte incubations and decreased by prior treatment of the cultures with the CYP3A inducers phenobarbital or rifampicin. Phenobarbital 168-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-158 20837660-4 2010 The efficacy of MG132 was increased by inclusion of ketoconazole in the hepatocyte incubations and decreased by prior treatment of the cultures with the CYP3A inducers phenobarbital or rifampicin. Rifampin 185-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-158 20837660-5 2010 Epoxomicin was also rapidly metabolized by CYP3A, whereas bortezomib and lactacystin were much more stable metabolically in human liver microsomes or hepatocyte cultures. epoxomicin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-48 20837660-6 2010 Thus, bortezomib is a better choice than MG132, epoxomicin, or lactacystin in cells with high activities of CYP3A enzymes. Bortezomib 6-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Midazolam 170-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Midazolam 170-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Carbamazepine 181-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Carbamazepine 181-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Atorvastatin 196-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Atorvastatin 196-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Paclitaxel 210-220 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Paclitaxel 210-220 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Docetaxel 222-231 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Docetaxel 222-231 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Irinotecan 233-243 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Irinotecan 233-243 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 20837660-3 2010 The inefficacy of MG132 was due to its metabolism by CYP3A enzymes, as deduced from its rapid, ketoconazole-sensitive clearance by pooled human liver microsomes and cultured hepatocytes. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 18-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 20837660-4 2010 The efficacy of MG132 was increased by inclusion of ketoconazole in the hepatocyte incubations and decreased by prior treatment of the cultures with the CYP3A inducers phenobarbital or rifampicin. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 16-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-158 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Terfenadine 249-260 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 20924570-1 2010 PURPOSE: To investigate if the ordinary use of a vaginal suppository containing miconazole results in systemic absorption that is sufficient to affect the activities of CYP1A2 and CYP3A4, which are major drug- and steroid-metabolising enzymes. Miconazole 80-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 20847137-3 2010 In this study, catalytic activities of the two alleles found in East Asians, CYP3A4*16 (T185S) and CYP3A4*18 (L293P), were assessed using the following seven substrates: midazolam, carbamazepine, atorvastatin, paclitaxel, docetaxel, irinotecan, and terfenadine. Terfenadine 249-260 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 20847137-5 2010 CYP3A4.16 exhibited intrinsic clearances (V(max)/K(m)) that were lowered considerably (by 84-60%) for metabolism of midazolam, carbamazepine, atorvastatin, paclitaxel, and irinotecan compared with CYP3A4.1 due to increased K(m) with or without decreased V(max) values, whereas no apparent decrease in intrinsic clearance was observed for docetaxel. Midazolam 116-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20847137-5 2010 CYP3A4.16 exhibited intrinsic clearances (V(max)/K(m)) that were lowered considerably (by 84-60%) for metabolism of midazolam, carbamazepine, atorvastatin, paclitaxel, and irinotecan compared with CYP3A4.1 due to increased K(m) with or without decreased V(max) values, whereas no apparent decrease in intrinsic clearance was observed for docetaxel. Midazolam 116-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 20924570-1 2010 PURPOSE: To investigate if the ordinary use of a vaginal suppository containing miconazole results in systemic absorption that is sufficient to affect the activities of CYP1A2 and CYP3A4, which are major drug- and steroid-metabolising enzymes. Steroids 214-221 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 20847137-5 2010 CYP3A4.16 exhibited intrinsic clearances (V(max)/K(m)) that were lowered considerably (by 84-60%) for metabolism of midazolam, carbamazepine, atorvastatin, paclitaxel, and irinotecan compared with CYP3A4.1 due to increased K(m) with or without decreased V(max) values, whereas no apparent decrease in intrinsic clearance was observed for docetaxel. Carbamazepine 127-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20847137-5 2010 CYP3A4.16 exhibited intrinsic clearances (V(max)/K(m)) that were lowered considerably (by 84-60%) for metabolism of midazolam, carbamazepine, atorvastatin, paclitaxel, and irinotecan compared with CYP3A4.1 due to increased K(m) with or without decreased V(max) values, whereas no apparent decrease in intrinsic clearance was observed for docetaxel. Carbamazepine 127-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 20924570-3 2010 Enzyme activities of CYP1A2 and CYP3A4 were determined as metabolic ratios of caffeine (CMR = (AFMU + 1MU + 1MX)/17DMU) and quinidine (QMR = 3-hydroxy-quinidine/quinidine) respectively before and 34 h after insertion of the suppository. Caffeine 78-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20847137-5 2010 CYP3A4.16 exhibited intrinsic clearances (V(max)/K(m)) that were lowered considerably (by 84-60%) for metabolism of midazolam, carbamazepine, atorvastatin, paclitaxel, and irinotecan compared with CYP3A4.1 due to increased K(m) with or without decreased V(max) values, whereas no apparent decrease in intrinsic clearance was observed for docetaxel. Atorvastatin 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20924570-3 2010 Enzyme activities of CYP1A2 and CYP3A4 were determined as metabolic ratios of caffeine (CMR = (AFMU + 1MU + 1MX)/17DMU) and quinidine (QMR = 3-hydroxy-quinidine/quinidine) respectively before and 34 h after insertion of the suppository. 3-{[2-(4-Carboxyphenyl)ethyl]sulfamoyl}thiophene-2-Carboxylic Acid 102-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20847137-5 2010 CYP3A4.16 exhibited intrinsic clearances (V(max)/K(m)) that were lowered considerably (by 84-60%) for metabolism of midazolam, carbamazepine, atorvastatin, paclitaxel, and irinotecan compared with CYP3A4.1 due to increased K(m) with or without decreased V(max) values, whereas no apparent decrease in intrinsic clearance was observed for docetaxel. Atorvastatin 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 20847137-5 2010 CYP3A4.16 exhibited intrinsic clearances (V(max)/K(m)) that were lowered considerably (by 84-60%) for metabolism of midazolam, carbamazepine, atorvastatin, paclitaxel, and irinotecan compared with CYP3A4.1 due to increased K(m) with or without decreased V(max) values, whereas no apparent decrease in intrinsic clearance was observed for docetaxel. Paclitaxel 156-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20847137-5 2010 CYP3A4.16 exhibited intrinsic clearances (V(max)/K(m)) that were lowered considerably (by 84-60%) for metabolism of midazolam, carbamazepine, atorvastatin, paclitaxel, and irinotecan compared with CYP3A4.1 due to increased K(m) with or without decreased V(max) values, whereas no apparent decrease in intrinsic clearance was observed for docetaxel. Irinotecan 172-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20924570-3 2010 Enzyme activities of CYP1A2 and CYP3A4 were determined as metabolic ratios of caffeine (CMR = (AFMU + 1MU + 1MX)/17DMU) and quinidine (QMR = 3-hydroxy-quinidine/quinidine) respectively before and 34 h after insertion of the suppository. 17dmu 113-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20847137-5 2010 CYP3A4.16 exhibited intrinsic clearances (V(max)/K(m)) that were lowered considerably (by 84-60%) for metabolism of midazolam, carbamazepine, atorvastatin, paclitaxel, and irinotecan compared with CYP3A4.1 due to increased K(m) with or without decreased V(max) values, whereas no apparent decrease in intrinsic clearance was observed for docetaxel. Irinotecan 172-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 20847137-5 2010 CYP3A4.16 exhibited intrinsic clearances (V(max)/K(m)) that were lowered considerably (by 84-60%) for metabolism of midazolam, carbamazepine, atorvastatin, paclitaxel, and irinotecan compared with CYP3A4.1 due to increased K(m) with or without decreased V(max) values, whereas no apparent decrease in intrinsic clearance was observed for docetaxel. Docetaxel 338-347 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20847137-5 2010 CYP3A4.16 exhibited intrinsic clearances (V(max)/K(m)) that were lowered considerably (by 84-60%) for metabolism of midazolam, carbamazepine, atorvastatin, paclitaxel, and irinotecan compared with CYP3A4.1 due to increased K(m) with or without decreased V(max) values, whereas no apparent decrease in intrinsic clearance was observed for docetaxel. Docetaxel 338-347 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 20847137-6 2010 On the other hand, K(m) values for CYP3A4.18 were comparable to those for CYP3A4.1 for all substrates except terfenadine; but V(max) values were lower for midazolam, paclitaxel, docetaxel, and irinotecan, resulting in partially reduced intrinsic clearance values (by 34-52%). Terfenadine 109-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 20847137-6 2010 On the other hand, K(m) values for CYP3A4.18 were comparable to those for CYP3A4.1 for all substrates except terfenadine; but V(max) values were lower for midazolam, paclitaxel, docetaxel, and irinotecan, resulting in partially reduced intrinsic clearance values (by 34-52%). Terfenadine 109-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 20924570-3 2010 Enzyme activities of CYP1A2 and CYP3A4 were determined as metabolic ratios of caffeine (CMR = (AFMU + 1MU + 1MX)/17DMU) and quinidine (QMR = 3-hydroxy-quinidine/quinidine) respectively before and 34 h after insertion of the suppository. Quinidine 124-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20847137-6 2010 On the other hand, K(m) values for CYP3A4.18 were comparable to those for CYP3A4.1 for all substrates except terfenadine; but V(max) values were lower for midazolam, paclitaxel, docetaxel, and irinotecan, resulting in partially reduced intrinsic clearance values (by 34-52%). Midazolam 155-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 20847137-6 2010 On the other hand, K(m) values for CYP3A4.18 were comparable to those for CYP3A4.1 for all substrates except terfenadine; but V(max) values were lower for midazolam, paclitaxel, docetaxel, and irinotecan, resulting in partially reduced intrinsic clearance values (by 34-52%). Paclitaxel 166-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 20924570-3 2010 Enzyme activities of CYP1A2 and CYP3A4 were determined as metabolic ratios of caffeine (CMR = (AFMU + 1MU + 1MX)/17DMU) and quinidine (QMR = 3-hydroxy-quinidine/quinidine) respectively before and 34 h after insertion of the suppository. 3-hydroxyquinidine 141-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20847137-6 2010 On the other hand, K(m) values for CYP3A4.18 were comparable to those for CYP3A4.1 for all substrates except terfenadine; but V(max) values were lower for midazolam, paclitaxel, docetaxel, and irinotecan, resulting in partially reduced intrinsic clearance values (by 34-52%). Paclitaxel 166-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 20847137-6 2010 On the other hand, K(m) values for CYP3A4.18 were comparable to those for CYP3A4.1 for all substrates except terfenadine; but V(max) values were lower for midazolam, paclitaxel, docetaxel, and irinotecan, resulting in partially reduced intrinsic clearance values (by 34-52%). Docetaxel 178-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 20924570-3 2010 Enzyme activities of CYP1A2 and CYP3A4 were determined as metabolic ratios of caffeine (CMR = (AFMU + 1MU + 1MX)/17DMU) and quinidine (QMR = 3-hydroxy-quinidine/quinidine) respectively before and 34 h after insertion of the suppository. Quinidine 151-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20847137-6 2010 On the other hand, K(m) values for CYP3A4.18 were comparable to those for CYP3A4.1 for all substrates except terfenadine; but V(max) values were lower for midazolam, paclitaxel, docetaxel, and irinotecan, resulting in partially reduced intrinsic clearance values (by 34-52%). Irinotecan 193-203 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 20472816-3 2010 The primary metabolic clearance pathway for dronedarone is via the hepatic enzyme system (primarily cytochrome P450 3A4 [CYP3A4]); the half-life of dronedarone is 27 to 31 hours. Dronedarone 44-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-119 21084035-4 2010 The possible relative risk factors included advanced age, chronic and systemic diseases, and co-administration of cytochrome P450 3A (CYP3A) enzyme-dependent metabolic drugs or its inhibitors such as clopidogrel and diltiazem. Clopidogrel 200-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-132 21084035-4 2010 The possible relative risk factors included advanced age, chronic and systemic diseases, and co-administration of cytochrome P450 3A (CYP3A) enzyme-dependent metabolic drugs or its inhibitors such as clopidogrel and diltiazem. Clopidogrel 200-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-139 21084035-4 2010 The possible relative risk factors included advanced age, chronic and systemic diseases, and co-administration of cytochrome P450 3A (CYP3A) enzyme-dependent metabolic drugs or its inhibitors such as clopidogrel and diltiazem. Diltiazem 216-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-132 21084035-4 2010 The possible relative risk factors included advanced age, chronic and systemic diseases, and co-administration of cytochrome P450 3A (CYP3A) enzyme-dependent metabolic drugs or its inhibitors such as clopidogrel and diltiazem. Diltiazem 216-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-139 20472816-4 2010 Strong CYP3A4 inhibitors, such as ketoconazole, are associated with a marked increase in dronedarone maximum concentration and are thus contraindicated; inducers of CYP3A4 will conversely decrease dronedarone exposure. Dronedarone 197-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 20472816-4 2010 Strong CYP3A4 inhibitors, such as ketoconazole, are associated with a marked increase in dronedarone maximum concentration and are thus contraindicated; inducers of CYP3A4 will conversely decrease dronedarone exposure. Dronedarone 197-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 20472816-3 2010 The primary metabolic clearance pathway for dronedarone is via the hepatic enzyme system (primarily cytochrome P450 3A4 [CYP3A4]); the half-life of dronedarone is 27 to 31 hours. Dronedarone 44-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 20472816-3 2010 The primary metabolic clearance pathway for dronedarone is via the hepatic enzyme system (primarily cytochrome P450 3A4 [CYP3A4]); the half-life of dronedarone is 27 to 31 hours. Dronedarone 148-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-119 20472816-3 2010 The primary metabolic clearance pathway for dronedarone is via the hepatic enzyme system (primarily cytochrome P450 3A4 [CYP3A4]); the half-life of dronedarone is 27 to 31 hours. Dronedarone 148-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 20472816-4 2010 Strong CYP3A4 inhibitors, such as ketoconazole, are associated with a marked increase in dronedarone maximum concentration and are thus contraindicated; inducers of CYP3A4 will conversely decrease dronedarone exposure. Ketoconazole 34-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 20472816-4 2010 Strong CYP3A4 inhibitors, such as ketoconazole, are associated with a marked increase in dronedarone maximum concentration and are thus contraindicated; inducers of CYP3A4 will conversely decrease dronedarone exposure. Dronedarone 89-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 20739453-4 2010 Likewise, in cultured human hepatocytes, only ginkgolide A contributed to the increase in hPXR target gene expression (CYP3A4 mRNA and CYP3A-mediated testosterone 6beta-hydroxylation). ginkgolide A 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 20829393-4 2010 In HepG2 cells, buprenorphine significantly increased human PXR-mediated CYP2B6 and CYP3A4 reporter activities. Buprenorphine 16-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 20829393-6 2010 Real-time reverse transcription-polymerase chain reaction analysis revealed that buprenorphine strongly induced CYP3A4 expression in both PXR- and CAR-transfected HepG2 cells. Buprenorphine 81-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 20829393-8 2010 Further studies indicated that buprenorphine could neither translocate human CAR to the nucleus nor activate CYP2B6/CYP3A4 reporter activities in transfected HPHs. Buprenorphine 31-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 21073556-3 2010 Other interactions between thienopyridines and CYP3A4/5 have also been reported for statins and calcium channel blockers. Thienopyridines 27-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 21073556-11 2010 For the clopidogrel CYP2C19 and CYP3A4/5 interactions, there is good evidence that these interactions occur. Clopidogrel 8-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20153625-4 2010 CM (10(-5) M) activated transcription of a luciferase plasmid containing the distal vitamin D responsive element (VDRE) from the human CYP3A4 gene at levels comparable to 1,25D (10(-8) M) in transfected human colon cancer cells (Caco-2). Vitamin D 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 21062307-5 2010 Monensin, salinomycin and maduramycin had no effect on caffeine metabolism, protein expression and mRNA expression, but did induce dapsone metabolism, increasing CYP3A protein expression. Monensin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-167 21062307-5 2010 Monensin, salinomycin and maduramycin had no effect on caffeine metabolism, protein expression and mRNA expression, but did induce dapsone metabolism, increasing CYP3A protein expression. maduramicin 26-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-167 20621111-1 2010 PURPOSE: To study if polymorphisms in genes encoding for CYP3A enzymes, that play a role in steroid hormone metabolism, affect steroid hormone serum levels and prostate cancer incidence or mortality. Steroids 92-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 20621111-1 2010 PURPOSE: To study if polymorphisms in genes encoding for CYP3A enzymes, that play a role in steroid hormone metabolism, affect steroid hormone serum levels and prostate cancer incidence or mortality. Steroids 127-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 20621111-7 2010 CYP3A4 G-allele carriage was associated with lower levels of estrone sulphate (p=0.005) and higher levels of estradiol (p=0.04) compared to non-carriers. estrone sulfate 61-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20621111-7 2010 CYP3A4 G-allele carriage was associated with lower levels of estrone sulphate (p=0.005) and higher levels of estradiol (p=0.04) compared to non-carriers. Estradiol 109-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20925584-7 2010 Metabolism was mainly CYP3A-mediated and generated a reactive epoxide on the vinylcyclopropyl sulfonamide moiety that could be quenched by glutathione. reactive epoxide 53-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-27 20925584-7 2010 Metabolism was mainly CYP3A-mediated and generated a reactive epoxide on the vinylcyclopropyl sulfonamide moiety that could be quenched by glutathione. vinylcyclopropyl sulfonamide 77-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-27 20925584-7 2010 Metabolism was mainly CYP3A-mediated and generated a reactive epoxide on the vinylcyclopropyl sulfonamide moiety that could be quenched by glutathione. Glutathione 139-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-27 20964620-0 2010 Activation of CYP3A-mediated testosterone 6beta-hydroxylation by tanshinone IIA and midazolam 1-hydroxylation by cryptotanshinone in human liver microsomes. testosterone 6beta 29-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 20964620-0 2010 Activation of CYP3A-mediated testosterone 6beta-hydroxylation by tanshinone IIA and midazolam 1-hydroxylation by cryptotanshinone in human liver microsomes. tanshinone 65-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 20964620-0 2010 Activation of CYP3A-mediated testosterone 6beta-hydroxylation by tanshinone IIA and midazolam 1-hydroxylation by cryptotanshinone in human liver microsomes. cryptotanshinone 113-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 20964620-1 2010 This study evaluated the in vitro activation of CYP3A-mediated midazolam 1-hydroxylation and testosterone 6beta-hydroxylation by tanshinone I, tanshinone IIA, and cryptotanshinone. Midazolam 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 20964620-1 2010 This study evaluated the in vitro activation of CYP3A-mediated midazolam 1-hydroxylation and testosterone 6beta-hydroxylation by tanshinone I, tanshinone IIA, and cryptotanshinone. tanshinone 129-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 20964620-1 2010 This study evaluated the in vitro activation of CYP3A-mediated midazolam 1-hydroxylation and testosterone 6beta-hydroxylation by tanshinone I, tanshinone IIA, and cryptotanshinone. tanshinone 143-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 20964620-1 2010 This study evaluated the in vitro activation of CYP3A-mediated midazolam 1-hydroxylation and testosterone 6beta-hydroxylation by tanshinone I, tanshinone IIA, and cryptotanshinone. cryptotanshinone 163-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 20964620-2 2010 The abilities of tanshinones to activate CYP3A-mediated midazolam 1-hydroxylation and testosterone 6beta-hydroxylation in human liver microsomes (HLMs) were tested. tanshinone 17-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 20964620-2 2010 The abilities of tanshinones to activate CYP3A-mediated midazolam 1-hydroxylation and testosterone 6beta-hydroxylation in human liver microsomes (HLMs) were tested. Midazolam 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 20964620-3 2010 Substrate- and effector-dependent activation of CYP3A by tanshinones were both observed. tanshinone 57-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 20964620-4 2010 Cryptotanshinone was shown to activate CYP3A-mediated midazolam 1-hydroxylation in a concentration-dependent manner. cryptotanshinone 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 20964620-4 2010 Cryptotanshinone was shown to activate CYP3A-mediated midazolam 1-hydroxylation in a concentration-dependent manner. Midazolam 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 20964620-6 2010 In addition, tanshinone IIA activated CYP3A-mediated testosterone 6beta-hydroxylation, whereas cryptotanshinone and tanshinone I did not. tanshinone 13-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 20964620-6 2010 In addition, tanshinone IIA activated CYP3A-mediated testosterone 6beta-hydroxylation, whereas cryptotanshinone and tanshinone I did not. testosterone 6beta 53-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 20964620-6 2010 In addition, tanshinone IIA activated CYP3A-mediated testosterone 6beta-hydroxylation, whereas cryptotanshinone and tanshinone I did not. tanshinone 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 20964620-7 2010 The results from our study enhance the understanding of CYP3A activation by tanshinone IIA and cryptotanshinone in HLMs. tanshinone 76-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 20964620-7 2010 The results from our study enhance the understanding of CYP3A activation by tanshinone IIA and cryptotanshinone in HLMs. cryptotanshinone 95-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-61 20430905-1 2010 BACKGROUND: We previously found 70 mg flat-dose docetaxel coadministered with ketoconazole to modulate CYP3A4 to be the maximum tolerated dose that resulted in comparable docetaxel area under the plasma concentration-time curve (AUC) as 75-100 mg/m2 docetaxel. Docetaxel 48-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 20934334-3 2010 In particular, 2-pyridine, 3-pyridine and pyridazine analogs are potent sEH inhibitors with favorable CYP3A4 inhibitory and microsomal stability profiles. PYRIDINE 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 20934334-3 2010 In particular, 2-pyridine, 3-pyridine and pyridazine analogs are potent sEH inhibitors with favorable CYP3A4 inhibitory and microsomal stability profiles. PYRIDINE 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 20934334-3 2010 In particular, 2-pyridine, 3-pyridine and pyridazine analogs are potent sEH inhibitors with favorable CYP3A4 inhibitory and microsomal stability profiles. pyridazine 42-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 20937259-0 2010 Effect of ethanol on spectral binding, inhibition, and activity of CYP3A4 with an antiretroviral drug nelfinavir. Ethanol 10-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 20937259-0 2010 Effect of ethanol on spectral binding, inhibition, and activity of CYP3A4 with an antiretroviral drug nelfinavir. Nelfinavir 102-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 20937259-2 2010 Although CYP3A4 induction by ethanol and impact of CYP3A4 on drug metabolism and toxicity is known, CYP3A4-ethanol physical interaction and its impact on drug binding, inhibition, or metabolism is not known. Ethanol 29-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 20937259-3 2010 Therefore, we studied the effect of ethanol on binding and inhibition of CYP3A4 with a representative protease inhibitor, nelfinavir, followed by the effect of alcohol on nelfinavir metabolism. Ethanol 36-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 20937259-4 2010 Our initial results showed that methanol, ethanol, isopropanol, isobutanol, and isoamyl alcohol bind in the active site of CYP3A4 and exhibit type I spectra. Methanol 32-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 20937259-4 2010 Our initial results showed that methanol, ethanol, isopropanol, isobutanol, and isoamyl alcohol bind in the active site of CYP3A4 and exhibit type I spectra. Ethanol 33-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 20937259-4 2010 Our initial results showed that methanol, ethanol, isopropanol, isobutanol, and isoamyl alcohol bind in the active site of CYP3A4 and exhibit type I spectra. 2-Propanol 51-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 20937259-4 2010 Our initial results showed that methanol, ethanol, isopropanol, isobutanol, and isoamyl alcohol bind in the active site of CYP3A4 and exhibit type I spectra. isobutyl alcohol 64-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 20937259-4 2010 Our initial results showed that methanol, ethanol, isopropanol, isobutanol, and isoamyl alcohol bind in the active site of CYP3A4 and exhibit type I spectra. isopentyl alcohol 80-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 20937259-5 2010 Among these alcohol compounds, ethanol showed the lowest K(D) (5.9+-0.34mM), suggesting its strong binding affinity with CYP3A4. Alcohols 12-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 20937259-5 2010 Among these alcohol compounds, ethanol showed the lowest K(D) (5.9+-0.34mM), suggesting its strong binding affinity with CYP3A4. Ethanol 31-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 20937259-8 2010 These results suggest that ethanol facilitates binding of nelfinavir with CYP3A4. Ethanol 27-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 20937259-8 2010 These results suggest that ethanol facilitates binding of nelfinavir with CYP3A4. Nelfinavir 58-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 20880704-4 2010 A fluorine substitution at the para-position of the P1 phenyl has contributed to 100-fold decrease of CYP3A4 inhibition and enhancement of compound metabolic stability. Fluorine 2-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 20430905-1 2010 BACKGROUND: We previously found 70 mg flat-dose docetaxel coadministered with ketoconazole to modulate CYP3A4 to be the maximum tolerated dose that resulted in comparable docetaxel area under the plasma concentration-time curve (AUC) as 75-100 mg/m2 docetaxel. Ketoconazole 78-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 20430905-6 2010 Interethnic differences in CYP3A4 inhibition by ketoconazole exist and are important when evaluating the impact of concomitant medications. Ketoconazole 48-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 20977456-8 2010 KEY RESULTS: N-desmethylimatinib formation was correlated with microsomal oxidation of the CYP3A4 substrates testosterone (rho= 0.60; P < 0.01) and midazolam (rho= 0.46; P < 0.05), and the CYP2C8 substrate paclitaxel (rho= 0.58; P < 0.01). N-desmethylimatinib 13-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 20876828-7 2010 DISCUSSION: Ranolazine, an antianginal agent, is both a substrate and a weak inhibitor of CYP3A as well as a substrate and moderate inhibitor of the P-glycoprotein (P-GP) efflux transport system. Ranolazine 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 20876828-8 2010 Tacrolimus, an immunosuppressant, is also a substrate of CYP3A and P-GP. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 20876828-9 2010 Through possible inhibition of both P-GP- and CYP3A-mediated first-pass metabolism and CYP3A systemic metabolism, ranolazine may have significantly increased serum concentrations of tacrolimus necessitating an eventual 70% decrease in the tacrolimus dose. Ranolazine 114-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-51 20876828-9 2010 Through possible inhibition of both P-GP- and CYP3A-mediated first-pass metabolism and CYP3A systemic metabolism, ranolazine may have significantly increased serum concentrations of tacrolimus necessitating an eventual 70% decrease in the tacrolimus dose. Ranolazine 114-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 20959500-0 2010 Induction of CYP3A4 by vinblastine: Role of the nuclear receptor NR1I2. Vinblastine 23-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 20959500-2 2010 OBJECTIVE: To evaluate the CYP3A4 induction potential of vinblastine both clinically and in vitro and determine the involvement of the nuclear receptors NR1I2 and the constitutive androstane receptor (NR1I3). Vinblastine 57-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 21104927-7 2010 Simulations indicated that for a compound with greater metabolism by CYP3A5 than CYP3A4, such as tacrolimus, incorporation of the correlation between CYP3A4 and CYP3A5 does have an impact on the prediction of oral clearance. Tacrolimus 97-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 21104927-7 2010 Simulations indicated that for a compound with greater metabolism by CYP3A5 than CYP3A4, such as tacrolimus, incorporation of the correlation between CYP3A4 and CYP3A5 does have an impact on the prediction of oral clearance. Tacrolimus 97-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 20959500-6 2010 RESULTS: In 6 patients with cancer, vinblastine increased the median (95% CI) clearance of the CYP3A4 phenotyping probe midazolam from 21.7 L/h (12.6 to 28.1) to 32.3 L/h (17.3 to 53.9) (p = 0.0156, Wilcoxon signed-rank test). Vinblastine 36-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 20959500-6 2010 RESULTS: In 6 patients with cancer, vinblastine increased the median (95% CI) clearance of the CYP3A4 phenotyping probe midazolam from 21.7 L/h (12.6 to 28.1) to 32.3 L/h (17.3 to 53.9) (p = 0.0156, Wilcoxon signed-rank test). Midazolam 120-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 20959500-8 2010 In vitro, vinblastine induced CYP3A4 protein. Vinblastine 10-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 20959500-10 2010 CONCLUSIONS: Collectively, these findings suggest that vinblastine is able to induce CYP3A4, at least in part, via an NR1I2-dependent mechanism, and thus has the potential to facilitate its own elimination and cause interactions with other CYP3A4 substrates. Vinblastine 55-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 20959500-10 2010 CONCLUSIONS: Collectively, these findings suggest that vinblastine is able to induce CYP3A4, at least in part, via an NR1I2-dependent mechanism, and thus has the potential to facilitate its own elimination and cause interactions with other CYP3A4 substrates. Vinblastine 55-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 240-246 20978219-10 2010 DISCUSSION: The Horn Drug Interaction Probability Scale demonstrated a possible relationship between the increased aripiprazole concentration and coadministration of darunavir/ritonavir and duloxetine, which inhibit CYP3A4 and 2D6. Aripiprazole 115-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-230 20978219-10 2010 DISCUSSION: The Horn Drug Interaction Probability Scale demonstrated a possible relationship between the increased aripiprazole concentration and coadministration of darunavir/ritonavir and duloxetine, which inhibit CYP3A4 and 2D6. Darunavir 166-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-230 20978219-10 2010 DISCUSSION: The Horn Drug Interaction Probability Scale demonstrated a possible relationship between the increased aripiprazole concentration and coadministration of darunavir/ritonavir and duloxetine, which inhibit CYP3A4 and 2D6. Ritonavir 176-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-230 20978219-10 2010 DISCUSSION: The Horn Drug Interaction Probability Scale demonstrated a possible relationship between the increased aripiprazole concentration and coadministration of darunavir/ritonavir and duloxetine, which inhibit CYP3A4 and 2D6. Duloxetine Hydrochloride 190-200 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-230 20977456-0 2010 Participation of CYP2C8 and CYP3A4 in the N-demethylation of imatinib in human hepatic microsomes. Nitrogen 42-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 20977456-0 2010 Participation of CYP2C8 and CYP3A4 in the N-demethylation of imatinib in human hepatic microsomes. Imatinib Mesylate 61-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 20977456-3 2010 Hepatic cytochrome P450 (CYP) 3A4 has been implicated in imatinib N-demethylation, but the clearance of imatinib decreases during prolonged therapy. Imatinib Mesylate 57-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-33 20977456-4 2010 CYP3A phenotype correlates with imatinib clearance at the commencement of therapy, but not at steady state. Imatinib Mesylate 32-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 20977456-8 2010 KEY RESULTS: N-desmethylimatinib formation was correlated with microsomal oxidation of the CYP3A4 substrates testosterone (rho= 0.60; P < 0.01) and midazolam (rho= 0.46; P < 0.05), and the CYP2C8 substrate paclitaxel (rho= 0.58; P < 0.01). Testosterone 109-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 20977456-8 2010 KEY RESULTS: N-desmethylimatinib formation was correlated with microsomal oxidation of the CYP3A4 substrates testosterone (rho= 0.60; P < 0.01) and midazolam (rho= 0.46; P < 0.05), and the CYP2C8 substrate paclitaxel (rho= 0.58; P < 0.01). Paclitaxel 212-222 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 20977456-10 2010 The CYP3A inhibitors ketoconazole and troleandomycin, and the CYP2C8 inhibitors quercetin and paclitaxel decreased imatinib oxidation. Ketoconazole 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-9 20881954-6 2010 The data suggest that pazopanib is a weak inhibitor of CYP3A4 and CYP2D6 and has no effect on CYP1A2, CYP2C9, and CYP2C19 in patients with advanced cancer. pazopanib 22-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 21254598-5 2010 It is suggested that CYP3A4 activation after mexidol administration occurred only during active drug biotransformation and excretion and ceased after full excretion from the human body. emoxypine succinate 45-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 20669013-10 2010 CONCLUSION: Both CYP2C19 genotypes and CYP3A4 inhibitor erythromycin can influence the plasma concentration of voriconazole, and erythromycin increases plasma concentration of voriconazole in a CYP2C19 genotype-dependent manner. Erythromycin 56-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 20669013-10 2010 CONCLUSION: Both CYP2C19 genotypes and CYP3A4 inhibitor erythromycin can influence the plasma concentration of voriconazole, and erythromycin increases plasma concentration of voriconazole in a CYP2C19 genotype-dependent manner. Voriconazole 111-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 20669013-10 2010 CONCLUSION: Both CYP2C19 genotypes and CYP3A4 inhibitor erythromycin can influence the plasma concentration of voriconazole, and erythromycin increases plasma concentration of voriconazole in a CYP2C19 genotype-dependent manner. Voriconazole 176-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 20680253-0 2010 Proposal of a new limited sampling strategy to predict CYP3A activity using a partial AUC of midazolam. Midazolam 93-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 20680253-1 2010 PURPOSE: Midazolam metabolic clearance to 1"-hydroxymidazolam is an accurate measure of CYP3A activity which requires extensive plasma and urine sampling. Midazolam 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-93 20680253-1 2010 PURPOSE: Midazolam metabolic clearance to 1"-hydroxymidazolam is an accurate measure of CYP3A activity which requires extensive plasma and urine sampling. 1-hydroxymethylmidazolam 42-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-93 20680253-2 2010 The objective of this study was to find a new limited sampling strategy (LSS) to predict midazolam metabolic clearance to 1"-hydroxymidazolam and subsequently CYP3A activity in an easy and reliable way, reducing costs and labour. Midazolam 89-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-164 20680253-10 2010 CONCLUSION: The determination of the partial AUC using four plasma samples from 2 to 4 h after oral administration of a midazolam solution is proposed to be an easy and reliable CYP3A phenotyping measure which of course needs to be validated in prospective clinical trials. Midazolam 120-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-183 20699409-3 2010 Thin-layer (TL) Matrigel was found to yield the highest basal and induced levels of CYP3A activity as determined by testosterone 6beta-hydroxylation. Testosterone 116-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-89 20699409-4 2010 Concentration-dependent CYP3A induction of rifampicin was reproducible with the EC(50) values of 0.36 +- 0.28 muM from four batches of human hepatocytes using the 96-well plate with TL Matrigel. Rifampin 43-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 20699409-6 2010 Cotreatment of avasimibe or efavirenz with 10 muM rifampicin was found to reduce CYP3A activities induced by rifampicin at a lower rate than treatment with rifampicin alone, whereas treatment with phenobarbital and carbamazepine had no effect. avasimibe 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 20699409-6 2010 Cotreatment of avasimibe or efavirenz with 10 muM rifampicin was found to reduce CYP3A activities induced by rifampicin at a lower rate than treatment with rifampicin alone, whereas treatment with phenobarbital and carbamazepine had no effect. efavirenz 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 20699409-6 2010 Cotreatment of avasimibe or efavirenz with 10 muM rifampicin was found to reduce CYP3A activities induced by rifampicin at a lower rate than treatment with rifampicin alone, whereas treatment with phenobarbital and carbamazepine had no effect. Rifampin 50-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 20699409-6 2010 Cotreatment of avasimibe or efavirenz with 10 muM rifampicin was found to reduce CYP3A activities induced by rifampicin at a lower rate than treatment with rifampicin alone, whereas treatment with phenobarbital and carbamazepine had no effect. Rifampin 109-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 20699409-6 2010 Cotreatment of avasimibe or efavirenz with 10 muM rifampicin was found to reduce CYP3A activities induced by rifampicin at a lower rate than treatment with rifampicin alone, whereas treatment with phenobarbital and carbamazepine had no effect. Rifampin 109-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 20699409-6 2010 Cotreatment of avasimibe or efavirenz with 10 muM rifampicin was found to reduce CYP3A activities induced by rifampicin at a lower rate than treatment with rifampicin alone, whereas treatment with phenobarbital and carbamazepine had no effect. Carbamazepine 215-228 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 20699409-8 2010 The cotreatment assay of test compound with rifampicin allows us to exclude the false-negative results caused by the cytotoxicity and/or the mechanism-based inactivation, when the drug candidate"s ability for CYP3A induction is evaluating the enzyme activity. Rifampin 44-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 209-214 20702771-0 2010 Effects of a commonly occurring genetic polymorphism of human CYP3A4 (I118V) on the metabolism of anandamide. anandamide 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 20702771-4 2010 CYP3A4, one of the major P450s involved in the metabolism of AEA, produces four major metabolites. anandamide 61-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20702771-7 2010 Recombinant CYP3A4*4 was expressed in Escherichia coli and was demonstrated to produce 60% less 6-hydroxytestosterone than the wild-type (WT) 3A4 in a reconstituted system. 6-hydroxytestosterone 96-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 20702771-8 2010 The metabolism of AEA by the WT and the CYP3A4.4 variant was investigated. anandamide 18-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 20702771-12 2010 These data indicate that individuals expressing the CYP3A4.4 allele may exhibit significant variations in the metabolism of AEA as well as any other compounds resembling AEA. anandamide 124-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 20702771-12 2010 These data indicate that individuals expressing the CYP3A4.4 allele may exhibit significant variations in the metabolism of AEA as well as any other compounds resembling AEA. anandamide 170-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 20197489-0 2010 Does the long plasma half-life of 4beta-hydroxycholesterol impact its utility as a cytochrome P450 3A (CYP3A) metric? cholest-5-ene-3,4-diol 34-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-101 20955109-5 2010 WHAT THE READER WILL GAIN: Following oral administration, idebenone is rapidly metabolized via oxidative shortening by a number CYP isoenzymes (CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4) to yield QS10, QS8, QS6 and QS4. idebenone 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 21112467-0 2010 Case report: delirium due to a diltiazem-fentanyl CYP3A4 drug interaction. Diltiazem 31-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 21112467-2 2010 Diltiazem inhibits cytochrome P450 3A4 isoenzymes. Diltiazem 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-38 21073811-7 2010 In further studies CYP2D6 and CYP3A4 genotype dependent metabolism of ondansetron enantiomers as well as of co-administered drugs and clinical efficacy of the medication should be tested. Ondansetron 70-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 20197489-0 2010 Does the long plasma half-life of 4beta-hydroxycholesterol impact its utility as a cytochrome P450 3A (CYP3A) metric? cholest-5-ene-3,4-diol 34-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 20197489-1 2010 Plasma 4beta-hydroxycholesterol (4betaHC) has been proposed as an endogenous marker of cytochrome P450 3A (CYP3A). cholest-5-ene-3,4-diol 7-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-105 20197489-1 2010 Plasma 4beta-hydroxycholesterol (4betaHC) has been proposed as an endogenous marker of cytochrome P450 3A (CYP3A). cholest-5-ene-3,4-diol 7-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-112 20197489-1 2010 Plasma 4beta-hydroxycholesterol (4betaHC) has been proposed as an endogenous marker of cytochrome P450 3A (CYP3A). cholest-5-ene-3,4-diol 33-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-105 20197489-1 2010 Plasma 4beta-hydroxycholesterol (4betaHC) has been proposed as an endogenous marker of cytochrome P450 3A (CYP3A). cholest-5-ene-3,4-diol 33-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-112 20197489-2 2010 To assess its utility as a CYP3A metric, a pharmacokinetic model, assuming no alteration in cholesterol plasma concentrations, was developed to simulate the effect of CYP3A induction and inhibition on 4betaHC plasma levels under different treatment durations. cholest-5-ene-3,4-diol 201-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 167-172 20197489-5 2010 On the other hand, simulations indicated that at least 2 weeks of dosing would be needed to detect the potent inhibition of CYP3A (maximal ~40% decrease in 4betaHC plasma levels). cholest-5-ene-3,4-diol 156-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-129 21067331-6 2010 The liver is important in the pharmacological profile of azole drugs, due to metabolic elimination, hepatotoxicity and PK drug-drug interaction (DDI) involving CYP3A4 metabolic inhibition. Azoles 57-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 21031626-3 2010 The inhibition of seven CYP isoforms (CYP3A4, CYP1A2, CYP2A6, CYP2D6, CYP2C9, CYP2C8 and CYP2E1) by tiliroside was investigated using in vitro human liver microsomal incubation assays. tiliroside 100-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 20937004-9 2010 Although AZD2624-induced CYP3A4 activity in hepatocytes, the potential of AZD2624 to cause inductive drug interactions of this enzyme was low at relevant exposure concentration. 3-((methylsulfonyl)amino)-2-phenyl-N-(1-phenylpropyl)quinolin-4-carboxamide 9-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 20937004-11 2010 However, metabolism of AZD2624 might be inhibited when co-administrated with potent CYP3A4/5 inhibitors. 3-((methylsulfonyl)amino)-2-phenyl-N-(1-phenylpropyl)quinolin-4-carboxamide 23-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 20709133-6 2010 Chlorpyrifos metabolism by individual human liver microsomes was significantly correlated with CYP2B6, CYP2C19 and CYP3A4 related activity. Chlorpyrifos 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 20709133-7 2010 CPO formation was best correlated with CYP2B6 related activity at low (20 muM) chlorpyrifos concentrations while CYP3A4 related activity was best correlated with CPO formation at high concentrations (100 muM) of chlorpyrifos. O,O-diethyl O-3,5,6-trichloro-2-pyridyl phosphate 162-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 20709133-7 2010 CPO formation was best correlated with CYP2B6 related activity at low (20 muM) chlorpyrifos concentrations while CYP3A4 related activity was best correlated with CPO formation at high concentrations (100 muM) of chlorpyrifos. Chlorpyrifos 212-224 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 20709133-8 2010 TCP production was best correlated with CYP3A4 activity at all substrate concentrations of chlorpyrifos. 3,5,6-trichloro-2-pyridinol 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 20937004-3 2010 CYP3A4 and CYP3A5 appeared to be the primary enzymes mediating the formation of pharmacologically active ketone metabolite (M1), whereas CYP3A4, CYP3A5, and CYP2C9 appeared to be the enzymes responsible for the formation of the hydroxylated metabolite (M2). Ketones 105-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20937004-3 2010 CYP3A4 and CYP3A5 appeared to be the primary enzymes mediating the formation of pharmacologically active ketone metabolite (M1), whereas CYP3A4, CYP3A5, and CYP2C9 appeared to be the enzymes responsible for the formation of the hydroxylated metabolite (M2). Ketones 105-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 20937004-5 2010 AZD2624 exhibited an inhibitory effect on microsomal CYP3A4/5 activities with apparent IC(50) values of 7.1 and 19.8 microM for midazolam and testosterone assays, respectively. 3-((methylsulfonyl)amino)-2-phenyl-N-(1-phenylpropyl)quinolin-4-carboxamide 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 20937004-5 2010 AZD2624 exhibited an inhibitory effect on microsomal CYP3A4/5 activities with apparent IC(50) values of 7.1 and 19.8 microM for midazolam and testosterone assays, respectively. Midazolam 128-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 20937004-5 2010 AZD2624 exhibited an inhibitory effect on microsomal CYP3A4/5 activities with apparent IC(50) values of 7.1 and 19.8 microM for midazolam and testosterone assays, respectively. Testosterone 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 20709133-8 2010 TCP production was best correlated with CYP3A4 activity at all substrate concentrations of chlorpyrifos. Chlorpyrifos 91-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 21031626-4 2010 The results showed that tiliroside strongly inhibited the activity of CYP3A4 (IC(50) = 9.0 +- 1.7 mum), CYP2C8 (IC(50) = 12.1 +- 0.9 mum) and CYP2C9 (IC(50) = 10.2 +- 0.9 mum) with other CYP isoforms negligibly influenced. tiliroside 24-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 20709133-10 2010 Calculations of percent total normalized rates (% TNR) and the chemical inhibitors ketoconazole and ticlopidine were used to confirm the importance of CYP2B6, CYP2C19, and CYP3A4 for the metabolism of chlorpyrifos. Chlorpyrifos 201-213 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 21031626-8 2010 Therefore, attention should be given to the probable drug-drug interaction between tiliroside-containing herbs and substrates of CYP3A4, CYP2C9 and CYP2C8. tiliroside 83-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 20979644-10 2010 Dig 1, non cytotoxic and not inducing caspases by itself, is able to prevent Roundup-induced cell death in a time-dependant manner with an important efficiency of up to 89%, within 48 h. In addition, we evidenced that it prevents Caspases 3/7 activation and CYP3A4 enhancement, and not GST reduction, but in turn it slightly inhibited CYP2C9 when added before Roundup. dig 1 0-5 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 258-264 20855838-3 2010 The erythromycin breath test was evaluated to determine hepatic activity of cytochrome P450 3A4 (CYP3A4), the main docetaxel-metabolizing enzyme. Erythromycin 4-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-95 20937904-0 2010 Structure and mechanism of the complex between cytochrome P4503A4 and ritonavir. Ritonavir 70-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-65 20937904-1 2010 Ritonavir is a HIV protease inhibitor routinely prescribed to HIV patients that also potently inactivates cytochrome P4503A4 (CYP3A4), the major human drug-metabolizing enzyme. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-124 20937904-1 2010 Ritonavir is a HIV protease inhibitor routinely prescribed to HIV patients that also potently inactivates cytochrome P4503A4 (CYP3A4), the major human drug-metabolizing enzyme. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 20937904-2 2010 By inhibiting CYP3A4, ritonavir increases plasma concentrations of other anti-HIV drugs oxidized by CYP3A4 thereby improving clinical efficacy. Ritonavir 22-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 20937904-2 2010 By inhibiting CYP3A4, ritonavir increases plasma concentrations of other anti-HIV drugs oxidized by CYP3A4 thereby improving clinical efficacy. Ritonavir 22-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 20937904-4 2010 The available data are inconsistent and suggest that ritonavir acts as a mechanism-based, competitive or mixed competitive-noncompetitive CYP3A4 inactivator. Ritonavir 53-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 20937904-6 2010 Our results show that ritonavir is a type II ligand that perfectly fits into the CYP3A4 active site cavity and irreversibly binds to the heme iron via the thiazole nitrogen, which decreases the redox potential of the protein and precludes its reduction with the redox partner, cytochrome P450 reductase. Ritonavir 22-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 20812728-0 2010 Improved cytochrome P450 3A4 molecular models accurately predict the Phe215 requirement for raloxifene dehydrogenation selectivity. Raloxifene Hydrochloride 92-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-28 20812728-3 2010 This study employed a cytochrome P450 3A4 (CYP3A4) crystal structure (Protein Data Bank entry 1W0E) to predict the sites of metabolism of the known CYP3A4 substrate raloxifene. Raloxifene Hydrochloride 165-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-41 20812728-3 2010 This study employed a cytochrome P450 3A4 (CYP3A4) crystal structure (Protein Data Bank entry 1W0E) to predict the sites of metabolism of the known CYP3A4 substrate raloxifene. Raloxifene Hydrochloride 165-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 20812728-3 2010 This study employed a cytochrome P450 3A4 (CYP3A4) crystal structure (Protein Data Bank entry 1W0E) to predict the sites of metabolism of the known CYP3A4 substrate raloxifene. Raloxifene Hydrochloride 165-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 20812728-5 2010 Dehydrogenation of raloxifene to an electrophilic diquinone methide intermediate has been linked to the potent inactivation of CYP3A4. Raloxifene Hydrochloride 19-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 20812728-5 2010 Dehydrogenation of raloxifene to an electrophilic diquinone methide intermediate has been linked to the potent inactivation of CYP3A4. diquinone 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 20855838-3 2010 The erythromycin breath test was evaluated to determine hepatic activity of cytochrome P450 3A4 (CYP3A4), the main docetaxel-metabolizing enzyme. Erythromycin 4-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 20855838-3 2010 The erythromycin breath test was evaluated to determine hepatic activity of cytochrome P450 3A4 (CYP3A4), the main docetaxel-metabolizing enzyme. Docetaxel 115-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-95 20855838-3 2010 The erythromycin breath test was evaluated to determine hepatic activity of cytochrome P450 3A4 (CYP3A4), the main docetaxel-metabolizing enzyme. Docetaxel 115-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 20599501-4 2010 Since Cyclosporin is metabolized by cytochrome P450 CYP3A4, we examined whether interaction between Orlistat and Cyclosporin involves induction of CYP3A4. Cyclosporine 6-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 20599501-7 2010 Rifampicin, a model CYP3A4 inducer, significantly induced CYP3A4 mRNA in both types of cells. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 20599501-7 2010 Rifampicin, a model CYP3A4 inducer, significantly induced CYP3A4 mRNA in both types of cells. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 20599501-8 2010 The level of CYP3A4 protein in human hepatocytes was increased by Orlistat after 48h, while rifampicin strongly induced CYP3A4 protein level. Rifampin 92-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 20599501-10 2010 In conclusion, we report here that Orlistat is weak PXR activator and CYP3A4 inducer in human hepatocytes, but it has no effect on CYP3A4 in intestinal cells, implying no role of CYP3A4 induction in the interaction between Orlistat and Cyclosporin in absorption process. Orlistat 35-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 20600879-2 2010 The inhibition effect of macelignan on the CYP3A4-mediated metabolism was negligible over the concentration range of 0.01-100muM in rat liver microsome while approximately 33% inhibition was observed at 100muM in human liver microsome, implying that the interaction of macelignan with CYP3A4 might be insignificant at the physiologically achievable concentrations. macelignan 25-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 20600879-2 2010 The inhibition effect of macelignan on the CYP3A4-mediated metabolism was negligible over the concentration range of 0.01-100muM in rat liver microsome while approximately 33% inhibition was observed at 100muM in human liver microsome, implying that the interaction of macelignan with CYP3A4 might be insignificant at the physiologically achievable concentrations. macelignan 25-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 285-291 20655369-8 2010 Inhibition of cellular CYP3A4 or CYP1A/1B suppressed the aflatoxin B(1)- and dimethylbenz[a]anthracene-mediated P53 response, respectively, indicating that HepG2 cells are capable of metabolizing these compounds in a CYP1A/B/3A4-dependent manner. Aflatoxin B1 57-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 20655369-8 2010 Inhibition of cellular CYP3A4 or CYP1A/1B suppressed the aflatoxin B(1)- and dimethylbenz[a]anthracene-mediated P53 response, respectively, indicating that HepG2 cells are capable of metabolizing these compounds in a CYP1A/B/3A4-dependent manner. anthracene 92-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 20849814-1 2010 Cytochrome P450 3A4 (CYP3A4), the major P450 present in human liver metabolizes approximately half the drugs in clinical use and requires electrons supplied from NADPH through NADPH-P450 reductase (POR, CPR). NADP 162-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 20849814-1 2010 Cytochrome P450 3A4 (CYP3A4), the major P450 present in human liver metabolizes approximately half the drugs in clinical use and requires electrons supplied from NADPH through NADPH-P450 reductase (POR, CPR). NADP 162-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 20604570-8 2010 Moreover, intrinsic clearance measured with specific CYP3A4 substrates (midazolam and an in-house Servier drug) and intestinal microsomes was well correlated with the amount of CYP3A4 (R(2) > 0.91, p < 0.01). Midazolam 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 20604570-8 2010 Moreover, intrinsic clearance measured with specific CYP3A4 substrates (midazolam and an in-house Servier drug) and intestinal microsomes was well correlated with the amount of CYP3A4 (R(2) > 0.91, p < 0.01). Midazolam 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 20655369-8 2010 Inhibition of cellular CYP3A4 or CYP1A/1B suppressed the aflatoxin B(1)- and dimethylbenz[a]anthracene-mediated P53 response, respectively, indicating that HepG2 cells are capable of metabolizing these compounds in a CYP1A/B/3A4-dependent manner. dimethylbenz 77-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 20840439-4 2010 Based on the ability of posaconazole to inhibit cytochrome P450 3A4, several drug interactions can be expected, especially with agents that undergo extensive first-pass effect through the gut and the liver. posaconazole 24-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-67 20840445-1 2010 AIM: To evaluate the impact of single and repeated doses casopitant on the pharmacokinetics of single dose midazolam and nifedipine (CYP3A substrates) in healthy subjects. Nifedipine 121-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-138 20969505-7 2010 In particular, atorvastatin, an inhibitor of P-glycoprotein and cytochrome P450 3A4, was likely responsible for an increased severity of rhabdomyolysis. Atorvastatin 15-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-83 20739919-0 2010 Accurate prediction of dose-dependent CYP3A4 inhibition by itraconazole and its metabolites from in vitro inhibition data. Itraconazole 59-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 20578904-0 2010 Common variants of HMGCR, CETP, APOAI, ABCB1, CYP3A4, and CYP7A1 genes as predictors of lipid-lowering response to atorvastatin therapy. Atorvastatin 115-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 20739919-2 2010 The aim of this study was to determine the importance of inhibitory metabolites of itraconazole (ITZ) in in vivo cytochrome P450 (CYP) 3A4 inhibition. Itraconazole 83-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-138 20739919-2 2010 The aim of this study was to determine the importance of inhibitory metabolites of itraconazole (ITZ) in in vivo cytochrome P450 (CYP) 3A4 inhibition. Itraconazole 97-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-138 20739919-6 2010 The metabolites of ITZ were estimated to account for ~50% of the total CYP3A4 inhibition, with the relative contribution increasing with time after ITZ dosing. Itraconazole 19-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 20811346-1 2010 Ambrisentan (ABS), approved for the treatment of pulmonary arterial hypertension and administered as an oral dose once daily, is an ET(A)-selective endothelin receptor antagonist (ERA) and a potential substrate for cytochrome P450 (CYP) 3A4, organic anion-transporting polypeptide (OATP), and P-glycoprotein (P-gp). ambrisentan 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-240 20942779-10 2010 Several studies have also demonstrated that CYP3A4/5 and CYP1A2 are important in clopidogrel bioactivation and should also be considered as potential targets for unwanted drug-drug interactions. Clopidogrel 81-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 20942779-11 2010 Prasugrel bioactivation is mainly related to CYP3A4 and 2B6 activity and therefore the question of the effect of drug-drug interaction on its activity is open. Prasugrel Hydrochloride 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-59 20639434-6 2010 Both chemical inhibition and human recombinant P450 isoform assays indicated that CYP3A4 was the predominant isozyme responsible for the oxygenation metabolism of PPT ginsenosides. protopanaxatriol 163-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 20837591-4 2010 Coadministration of clarithromycin (a potent cytochrome P450 3A4 inhibitor) for an ear infection and valproic acid for seizures since birth further prevented drug elimination from the body. Clarithromycin 20-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-64 20639434-6 2010 Both chemical inhibition and human recombinant P450 isoform assays indicated that CYP3A4 was the predominant isozyme responsible for the oxygenation metabolism of PPT ginsenosides. Ginsenosides 167-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 20639434-8 2010 Results obtained from this study suggest that CYP3A4-catalyzed oxygenation metabolism plays an important role in the hepatic disposition of ginsenosides and that glycosyl substitution, especially at the C20 hydroxy group, determines their intrinsic clearances by CYP3A4. Ginsenosides 140-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 20624855-2 2010 We investigated the inhibition of CYP3A4 by lapatinib as a possible cause of its idiosyncratic toxicity. Lapatinib 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 20624855-3 2010 Inhibition of CYP3A4 was time-, concentration-, and NADPH-dependent, with k(inact) = 0.0202 min(-1) and K(i) = 1.709 muM. NADP 52-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 20624855-6 2010 Testosterone protected CYP3A4 from inactivation by lapatinib. Testosterone 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 20624855-6 2010 Testosterone protected CYP3A4 from inactivation by lapatinib. Lapatinib 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 20624855-8 2010 However, reduced carbon monoxide (CO)-difference spectroscopy did reveal a 43% loss of the spectrally detectable CYP3A4-CO complex in the presence of lapatinib. Carbon Monoxide 17-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 20624855-8 2010 However, reduced carbon monoxide (CO)-difference spectroscopy did reveal a 43% loss of the spectrally detectable CYP3A4-CO complex in the presence of lapatinib. Carbon Monoxide 34-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 20624855-8 2010 However, reduced carbon monoxide (CO)-difference spectroscopy did reveal a 43% loss of the spectrally detectable CYP3A4-CO complex in the presence of lapatinib. Lapatinib 150-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 20624855-11 2010 In conclusion, we demonstrated for the first time that lapatinib is a mechanism-based inactivator of CYP3A4, most likely via the formation and further oxidation of its O-dealkylated metabolite to a quinoneimine that covalently modifies the CYP3A4 apoprotein and/or heme moiety. Lapatinib 55-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 20624855-11 2010 In conclusion, we demonstrated for the first time that lapatinib is a mechanism-based inactivator of CYP3A4, most likely via the formation and further oxidation of its O-dealkylated metabolite to a quinoneimine that covalently modifies the CYP3A4 apoprotein and/or heme moiety. Lapatinib 55-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 240-246 20624855-11 2010 In conclusion, we demonstrated for the first time that lapatinib is a mechanism-based inactivator of CYP3A4, most likely via the formation and further oxidation of its O-dealkylated metabolite to a quinoneimine that covalently modifies the CYP3A4 apoprotein and/or heme moiety. quinoneimine 198-210 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 20624855-11 2010 In conclusion, we demonstrated for the first time that lapatinib is a mechanism-based inactivator of CYP3A4, most likely via the formation and further oxidation of its O-dealkylated metabolite to a quinoneimine that covalently modifies the CYP3A4 apoprotein and/or heme moiety. quinoneimine 198-210 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 240-246 20624855-11 2010 In conclusion, we demonstrated for the first time that lapatinib is a mechanism-based inactivator of CYP3A4, most likely via the formation and further oxidation of its O-dealkylated metabolite to a quinoneimine that covalently modifies the CYP3A4 apoprotein and/or heme moiety. Heme 265-269 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 20697309-7 2010 The A503 V polymorphism reduced the CYP3A4 activity to 61-77% of WT with testosterone and midazolam, but had nearly WT activity with quinidine and erythromycin. Testosterone 73-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 20697309-7 2010 The A503 V polymorphism reduced the CYP3A4 activity to 61-77% of WT with testosterone and midazolam, but had nearly WT activity with quinidine and erythromycin. Midazolam 90-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 20578904-3 2010 We studied the association between 18 single-nucleotide polymorphisms (SNPs) in six genes (HMGCR, CETP, APOAI, ABCB1, CYP3A4, CYP7A1) in response to atorvastatin therapy (20 mg/day) in 265 newly diagnosed CAD patients using multivariable adjusted general linear regression. Atorvastatin 149-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 20150526-1 2010 Diltiazem increases systemic exposure to simvastatin via inhibition of CYP3A. Diltiazem 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-76 20150526-1 2010 Diltiazem increases systemic exposure to simvastatin via inhibition of CYP3A. Simvastatin 41-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-76 21047202-4 2010 RESULTS: Four polymorphisms in CYP3A5 and one polymorphism in CYP3A4 were identified to be significantly associated with tacrolimus stable dose (p < 8.46 x 10(-5)). Tacrolimus 121-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 21047202-9 2010 Age, ethnicity and CYP3A inhibitor use could predict 30% of tacrolimus dosing variability. Tacrolimus 60-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-24 20642349-1 2010 Voriconazole (VRC), a triazole agent is extensively metabolized by CYP2C19, CYP2C9, and to a lesser extent, by CYP3A4. Voriconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 20642349-1 2010 Voriconazole (VRC), a triazole agent is extensively metabolized by CYP2C19, CYP2C9, and to a lesser extent, by CYP3A4. Voriconazole 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 20683390-5 2010 Sotrastaurin is primarily metabolized through CYP3A4. sotrastaurin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 20673718-0 2010 Addressing time-dependent CYP 3A4 inhibition observed in a novel series of substituted amino propanamide renin inhibitors, a case study. amino propanamide 87-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-33 20513361-2 2010 Several P450 enzymes including CYP26A1, CYP2C8, and CYP3A4 have been proposed to be responsible for RA clearance in the liver but their quantitative importance has not been demonstrated. Tretinoin 100-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 20513361-6 2010 CYP2C8, CYP3A4, CYP3A5 and CYP3A7 metabolized RA with unbound K(m) values of 3.4-7.2microM and V(max) values of 2.3-4.9pmol/min/pmol P450, but were less efficient than CYP26A1 in clearing RA. Tretinoin 46-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 20513361-8 2010 HLM incubation data showed that 4-OH RA formation velocity varied from 0.2 to 15.3pmol/min/mg microsomal protein and velocity in HLMs was significantly correlated (p<0.01) to CYP26A1, CYP3A4, and CYP3A5 protein content, but not to CYP2C8. 4-oh 32-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 20513361-8 2010 HLM incubation data showed that 4-OH RA formation velocity varied from 0.2 to 15.3pmol/min/mg microsomal protein and velocity in HLMs was significantly correlated (p<0.01) to CYP26A1, CYP3A4, and CYP3A5 protein content, but not to CYP2C8. Tretinoin 37-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 20856845-3 2010 Sertindole undergoes extensive hepatic metabolism by the cytochrome P450 isoenzymes CYP2D6 and CYP3A4 and has an elimination half-life of approximately three days. sertindole 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 21254628-2 2010 In the contrast to 15-ketocholestane derivative (I), 15-ketoergostane derivatives (II - IV) decreased the HMG- CoA reductase mRNA level; (22R,23R)-22,23-oxido-5alpha-ergost-8(14)-en-15-on-3beta-ol (IV) significantly increased CYP3A4 mRNA level (320% from control). 15-ketoergostane 53-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 226-232 20642349-1 2010 Voriconazole (VRC), a triazole agent is extensively metabolized by CYP2C19, CYP2C9, and to a lesser extent, by CYP3A4. Triazoles 22-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 20712450-0 2010 Sources of variability in ketoconazole inhibition of human cytochrome P450 3A in vitro. Ketoconazole 26-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-77 20712450-1 2010 Despite the extensive use of ketoconazole as an index inhibitor of human cytochrome P450 3A (CYP3A) isoforms in vitro, literature reports of the quantitative inhibitory potency of ketoconazole are highly variable. Ketoconazole 29-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-91 20712450-1 2010 Despite the extensive use of ketoconazole as an index inhibitor of human cytochrome P450 3A (CYP3A) isoforms in vitro, literature reports of the quantitative inhibitory potency of ketoconazole are highly variable. Ketoconazole 29-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 20716241-1 2010 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: The anticancer agent irinotecan is a prodrug that is hydrolyzed by hepatic carboxylesterase to its active and toxic metabolite SN-38 and oxidized by CYP3A4 to its inactive metabolite APC. Irinotecan 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-197 20716241-1 2010 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: The anticancer agent irinotecan is a prodrug that is hydrolyzed by hepatic carboxylesterase to its active and toxic metabolite SN-38 and oxidized by CYP3A4 to its inactive metabolite APC. Irinotecan 169-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-197 20716241-2 2010 Irinotecan therapy is complicated by co-administered drugs that inhibit CYP3A4 and decrease APC formation and that indirectly increase SN-38 formation. Irinotecan 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 20716241-4 2010 WHAT THIS STUDY ADDS: In microsomal fractions from patients with severe hepatic dysfunction both APC and SN-38 formation were decreased due to down-regulation of CYP3A4 and carboxylesterase enzymes. Irinotecan 105-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 20716241-14 2010 CONCLUSIONS: Down-regulation of CYP3A4 in liver disease decreased APC formation from irinotecan. Irinotecan 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20716241-16 2010 However, in a subset of disease samples SN-38 production was relatively high because CYP3A4 activity was markedly impaired. Irinotecan 40-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 20673718-2 2010 After finding that several leading compounds in a novel series of substituted amino propanamide renin inhibitors inactivated CYP3A4 in an NADPH-dependent and time-dependent manner, a search to identify the cause of this liability was initiated. amino propanamide 78-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 20673718-2 2010 After finding that several leading compounds in a novel series of substituted amino propanamide renin inhibitors inactivated CYP3A4 in an NADPH-dependent and time-dependent manner, a search to identify the cause of this liability was initiated. NADP 138-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 20716633-4 2010 CYP1A2, CYP2D6, CYP2C9, and CYP3A4 enzyme activities were measured by the metabolism of caffeine, dextromethorphan, losartan, and buspirone, respectively. Caffeine 88-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 20735423-4 2010 KEY RESULTS: Experiments using HLM or specific CYPs (3A4, 2C19) revealed that at clopidogrel concentrations >10 microM, CYP3A4 was primarily responsible for clopidogrel biotransformation. Clopidogrel 81-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 20735423-4 2010 KEY RESULTS: Experiments using HLM or specific CYPs (3A4, 2C19) revealed that at clopidogrel concentrations >10 microM, CYP3A4 was primarily responsible for clopidogrel biotransformation. Clopidogrel 160-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 20735423-6 2010 Clarithromycin, another CYP3A4 inhibitor, impaired clopidogrel biotransformation and antiplatelet activity almost as effectively as ketoconazole. Clarithromycin 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 20735423-6 2010 Clarithromycin, another CYP3A4 inhibitor, impaired clopidogrel biotransformation and antiplatelet activity almost as effectively as ketoconazole. Clopidogrel 51-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 20735423-7 2010 The CYP3A4 substrates atorvastatin and simvastatin both inhibited clopidogrel biotransformation and antiplatelet activity, less potently than ketoconazole. Atorvastatin 22-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 20735423-7 2010 The CYP3A4 substrates atorvastatin and simvastatin both inhibited clopidogrel biotransformation and antiplatelet activity, less potently than ketoconazole. Clopidogrel 66-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 20735423-11 2010 CONCLUSIONS AND IMPLICATIONS: At clopidogrel concentrations >10 microM, CYP3A4 is mainly responsible for clopidogrel biotransformation, whereas CYP2C19 contributes only at clopidogrel concentrations < or =10 microM. Clopidogrel 33-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 20735423-11 2010 CONCLUSIONS AND IMPLICATIONS: At clopidogrel concentrations >10 microM, CYP3A4 is mainly responsible for clopidogrel biotransformation, whereas CYP2C19 contributes only at clopidogrel concentrations < or =10 microM. Clopidogrel 108-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 20735423-11 2010 CONCLUSIONS AND IMPLICATIONS: At clopidogrel concentrations >10 microM, CYP3A4 is mainly responsible for clopidogrel biotransformation, whereas CYP2C19 contributes only at clopidogrel concentrations < or =10 microM. Clopidogrel 108-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 20716633-4 2010 CYP1A2, CYP2D6, CYP2C9, and CYP3A4 enzyme activities were measured by the metabolism of caffeine, dextromethorphan, losartan, and buspirone, respectively. Dextromethorphan 98-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 20716633-4 2010 CYP1A2, CYP2D6, CYP2C9, and CYP3A4 enzyme activities were measured by the metabolism of caffeine, dextromethorphan, losartan, and buspirone, respectively. Losartan 116-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 20716633-4 2010 CYP1A2, CYP2D6, CYP2C9, and CYP3A4 enzyme activities were measured by the metabolism of caffeine, dextromethorphan, losartan, and buspirone, respectively. Buspirone 130-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 20716633-8 2010 Resveratrol intervention was found to inhibit the phenotypic indices of CYP3A4, CYP2D6, and CYP2C9 and to induce the phenotypic index of 1A2. Resveratrol 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 20818746-7 2010 Upon activation of PXR by rifampicin, the messenger RNA levels of CYP3A4, CYP3A5, and CYP3A7 increased 49- to 213-fold versus HepG2 cells. Rifampin 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 20501911-3 2010 The kinetics of metabolite formation from phenacetin, tolbutamide, and alprazolam and midazolam, selected as substrates probes for CYP1A2, CYP2C9, and CYP3A4, respectively, were characterized in this in vitro system. Phenacetin 42-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 20501911-3 2010 The kinetics of metabolite formation from phenacetin, tolbutamide, and alprazolam and midazolam, selected as substrates probes for CYP1A2, CYP2C9, and CYP3A4, respectively, were characterized in this in vitro system. Tolbutamide 54-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 20501911-3 2010 The kinetics of metabolite formation from phenacetin, tolbutamide, and alprazolam and midazolam, selected as substrates probes for CYP1A2, CYP2C9, and CYP3A4, respectively, were characterized in this in vitro system. Alprazolam 71-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 20501911-3 2010 The kinetics of metabolite formation from phenacetin, tolbutamide, and alprazolam and midazolam, selected as substrates probes for CYP1A2, CYP2C9, and CYP3A4, respectively, were characterized in this in vitro system. Midazolam 86-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 20552178-0 2010 Zolpidem pharmacokinetics and pharmacodynamics in metabolic interactions involving CYP3A: sex as a differentiating factor. Zolpidem 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 20653496-15 2010 Ritonavir, a potent CYP3A4 inhibitor, may inhibit corticosteroid degradation and increase its accumulation. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 20690781-11 2010 The only exception concerns saxagliptin, which is metabolized to an active metabolite by CYP3A4/5. saxagliptin 28-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 20690781-12 2010 Therefore, exposure to saxagliptin and its primary metabolite may be significantly modified when saxagliptin is coadministered with specific strong inhibitors (ketoconazole, diltiazem) or inducers (rifampicin) of CYP3A4/5 isoforms. saxagliptin 23-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 213-219 20690781-12 2010 Therefore, exposure to saxagliptin and its primary metabolite may be significantly modified when saxagliptin is coadministered with specific strong inhibitors (ketoconazole, diltiazem) or inducers (rifampicin) of CYP3A4/5 isoforms. saxagliptin 97-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 213-219 20690781-12 2010 Therefore, exposure to saxagliptin and its primary metabolite may be significantly modified when saxagliptin is coadministered with specific strong inhibitors (ketoconazole, diltiazem) or inducers (rifampicin) of CYP3A4/5 isoforms. Rifampin 198-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 213-219 20551241-5 2010 We demonstrate highly selective atorvastatin ortho-hydroxylation by CYP3A4 by recombinant P450s. Atorvastatin 32-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 20551241-6 2010 In human liver microsomes ortho-hydroxyatorvastatin formation was highly correlated with CYP3A4 protein content (r(s) = 0.78, p < 0.0001, n = 150). ortho 26-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 20551241-6 2010 In human liver microsomes ortho-hydroxyatorvastatin formation was highly correlated with CYP3A4 protein content (r(s) = 0.78, p < 0.0001, n = 150). hydroxyatorvastatin 32-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 20106684-3 2010 AIMS: The aim of this study was to assess the potential of St John"s wort to alter the CYP3A-mediated metabolism of a mu-opioid receptor agonist, oxycodone. Oxycodone 146-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 20504912-0 2010 Camptothecin attenuates cytochrome P450 3A4 induction by blocking the activation of human pregnane X receptor. Camptothecin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-43 20504912-3 2010 Camptothecin (CPT) was demonstrated as a novel and potent inhibitor (IC(50) = 0.58 microM) of an hPXR-mediated transcriptional regulation on CYP3A4 in this study. Camptothecin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 20504912-3 2010 Camptothecin (CPT) was demonstrated as a novel and potent inhibitor (IC(50) = 0.58 microM) of an hPXR-mediated transcriptional regulation on CYP3A4 in this study. Camptothecin 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 20504912-6 2010 CPT treatment resulted in delayed metabolism of nifedipine in human hepatocytes treated with rifampicin, suggesting a potential prevention of drug-drug interactions between CYP3A4 inducers and CYP3A4-metabolized drugs. Rifampin 93-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 20504912-6 2010 CPT treatment resulted in delayed metabolism of nifedipine in human hepatocytes treated with rifampicin, suggesting a potential prevention of drug-drug interactions between CYP3A4 inducers and CYP3A4-metabolized drugs. Rifampin 93-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 193-199 20629947-9 2010 Oleic acid is primarily oxidized to oleic acid oxide (cis-EODA) by CYP2C and CYP3A mono-oxygenases. Oleic Acid 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 20629947-9 2010 Oleic acid is primarily oxidized to oleic acid oxide (cis-EODA) by CYP2C and CYP3A mono-oxygenases. oleic acid oxide 36-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 20629947-9 2010 Oleic acid is primarily oxidized to oleic acid oxide (cis-EODA) by CYP2C and CYP3A mono-oxygenases. 9,10-epoxystearic acid 54-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 20505544-3 2010 We evaluated the relationship between steroid hormone metabolism genotypes at COMT, CYP1A2, CYP1B1, CYP3A4, CYP19, SULT1A1, and SULT1E1 with hormone levels and menopausal features. Steroids 38-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 20818746-8 2010 According to reporter gene assays with different inducers, the highest increase in CYP3A4 promoter activity (131-fold) was observed upon induction with rifampicin. Rifampin 152-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 20818746-10 2010 The rate of testosterone 6beta-hydroxylation, a measure of CYP3A function inside BALs, increased 4-fold in cBAL119 BALs versus HepG2 BALs. Testosterone 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 20664903-2 2010 Drug-drug interaction between statins metabolised by cytochrome P450 3A4 and clopidogrel have been claimed to attenuate the inhibitory effect of clopidogrel. Clopidogrel 145-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-72 20638257-3 2010 Dihydrotanshinone was a competitive inhibitor of human CYP1A2 (K(i)=0.53 microM) and CYP2C9 (K(i)=1.92 microM), a noncompetitive inhibitor of CYP3A4 (K(i)=2.11 microM) but an uncompetitive CYP2E1 inhibitor. DIHYDROTANSHINONE 0-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 21351567-8 2010 The selective CYP3A4 inhibitors, ketoconazole, troleandomycin and ritonavir demonstrated significant inhibitory effects on CMDCK intestinal metabolism, which suggested that co-administration of CMDCK with potent CYP3A inhibitors, such as ritonavir, might decrease its intestinal metabolic clearance and subsequently improve its bioavailability in body. Ritonavir 66-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 20832577-3 2010 Both tacrolimus and micafungin are substrates of cytochrome P450 3A4 in vitro. Tacrolimus 5-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-68 20832577-3 2010 Both tacrolimus and micafungin are substrates of cytochrome P450 3A4 in vitro. Micafungin 20-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-68 21351567-8 2010 The selective CYP3A4 inhibitors, ketoconazole, troleandomycin and ritonavir demonstrated significant inhibitory effects on CMDCK intestinal metabolism, which suggested that co-administration of CMDCK with potent CYP3A inhibitors, such as ritonavir, might decrease its intestinal metabolic clearance and subsequently improve its bioavailability in body. Ritonavir 238-247 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 20580705-0 2010 Induction of CYP3A4 and MDR1 gene expression by baicalin, baicalein, chlorogenic acid, and ginsenoside Rf through constitutive androstane receptor- and pregnane X receptor-mediated pathways. baicalein 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 20580705-0 2010 Induction of CYP3A4 and MDR1 gene expression by baicalin, baicalein, chlorogenic acid, and ginsenoside Rf through constitutive androstane receptor- and pregnane X receptor-mediated pathways. Chlorogenic Acid 69-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 20580705-2 2010 The present study investigated whether baicalin, baicalein, chlorogenic acid, and ginsenoside Rf induced the expression of the cytochrome P450 3A4 (CYP3A4) and multi-drug resistance 1 (MDR1) genes through the pregnane X receptor and constitutive androstane receptor pathways. baicalein 49-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 20580705-0 2010 Induction of CYP3A4 and MDR1 gene expression by baicalin, baicalein, chlorogenic acid, and ginsenoside Rf through constitutive androstane receptor- and pregnane X receptor-mediated pathways. Ginsenosides 92-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 20580705-2 2010 The present study investigated whether baicalin, baicalein, chlorogenic acid, and ginsenoside Rf induced the expression of the cytochrome P450 3A4 (CYP3A4) and multi-drug resistance 1 (MDR1) genes through the pregnane X receptor and constitutive androstane receptor pathways. Chlorogenic Acid 60-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-146 20580705-2 2010 The present study investigated whether baicalin, baicalein, chlorogenic acid, and ginsenoside Rf induced the expression of the cytochrome P450 3A4 (CYP3A4) and multi-drug resistance 1 (MDR1) genes through the pregnane X receptor and constitutive androstane receptor pathways. Chlorogenic Acid 60-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 20580705-2 2010 The present study investigated whether baicalin, baicalein, chlorogenic acid, and ginsenoside Rf induced the expression of the cytochrome P450 3A4 (CYP3A4) and multi-drug resistance 1 (MDR1) genes through the pregnane X receptor and constitutive androstane receptor pathways. Ginsenosides 82-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-146 20580705-2 2010 The present study investigated whether baicalin, baicalein, chlorogenic acid, and ginsenoside Rf induced the expression of the cytochrome P450 3A4 (CYP3A4) and multi-drug resistance 1 (MDR1) genes through the pregnane X receptor and constitutive androstane receptor pathways. Ginsenosides 82-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 20580705-5 2010 Baicalein induced the expression of CYP3A4 and MDR1 mRNA by activating pregnane X receptor and constitutive androstane receptor. baicalein 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 20580705-6 2010 Chlorogenic acid and ginsenoside Rf showed a relatively weak effect on CYP3A4 promoter activation only in HepG2 cells cotransfected with constitutive androstane receptor and demonstrated no effects on MDR1 via either the constitutive androstane receptor or pregnane X receptor pathway. Chlorogenic Acid 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 20580705-2 2010 The present study investigated whether baicalin, baicalein, chlorogenic acid, and ginsenoside Rf induced the expression of the cytochrome P450 3A4 (CYP3A4) and multi-drug resistance 1 (MDR1) genes through the pregnane X receptor and constitutive androstane receptor pathways. baicalin 39-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-146 20580705-6 2010 Chlorogenic acid and ginsenoside Rf showed a relatively weak effect on CYP3A4 promoter activation only in HepG2 cells cotransfected with constitutive androstane receptor and demonstrated no effects on MDR1 via either the constitutive androstane receptor or pregnane X receptor pathway. Ginsenosides 21-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 20580705-9 2010 Chlorogenic acid and ginsenoside Rf only induced constitutive androstane receptor-mediated CYP3A4 expression. Chlorogenic Acid 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 20580705-2 2010 The present study investigated whether baicalin, baicalein, chlorogenic acid, and ginsenoside Rf induced the expression of the cytochrome P450 3A4 (CYP3A4) and multi-drug resistance 1 (MDR1) genes through the pregnane X receptor and constitutive androstane receptor pathways. baicalin 39-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 20580705-2 2010 The present study investigated whether baicalin, baicalein, chlorogenic acid, and ginsenoside Rf induced the expression of the cytochrome P450 3A4 (CYP3A4) and multi-drug resistance 1 (MDR1) genes through the pregnane X receptor and constitutive androstane receptor pathways. baicalein 49-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-146 20580705-9 2010 Chlorogenic acid and ginsenoside Rf only induced constitutive androstane receptor-mediated CYP3A4 expression. ginsenoside Rf 21-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 19966851-5 2010 SNPs in ABCB1, CYP3A4 and TP53BP2 were associated with response to VAD induction therapy (P<0.01). VAD I protocol 67-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 23616707-8 2010 The concurrent use of drugs that inhibit or induce the cytochrome P450 enzyme CYP3A4 can alter concentrations of eszopiclone and the dose may need to be adjusted. Eszopiclone 113-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 20718999-5 2010 Tibolone is known to be a weak competitive inhibitor of CYP3A4, which is involved in tacrolimus metabolism. tibolone 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 20718999-5 2010 Tibolone is known to be a weak competitive inhibitor of CYP3A4, which is involved in tacrolimus metabolism. Tacrolimus 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 20590741-17 2010 However, the daily dose of saxagliptin should be reduced when coadministered with potent CYP 3A4 inhibitors. saxagliptin 27-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-96 20478852-7 2010 Ramelteon metabolism was catalyzed by CYP1A2, CYP2C19, and CYP3A4 as shown through the use of recombinant human cytochrome P450 enzymes and specific inhibitors. ramelteon 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 20592724-1 2010 According to available information, montelukast is metabolized by cytochrome P450 (CYP) 3A4 and 2C9. montelukast 36-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-99 20393696-0 2010 Effect of glycyrrhizin on the activity of CYP3A enzyme in humans. Glycyrrhizic Acid 10-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 20642445-0 2010 Induction of CYP2B6 and CYP3A4 expression by 1-aminobenzotriazole (ABT) in human hepatocytes. 1-aminobenzotriazole 45-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 20642445-0 2010 Induction of CYP2B6 and CYP3A4 expression by 1-aminobenzotriazole (ABT) in human hepatocytes. 1-aminobenzotriazole 67-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 20642445-3 2010 In this study, we show that ABT up-regulates expression of CYP2B6 and CYP3A4 potentially by activating nuclear receptor CAR. 1-aminobenzotriazole 28-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 20642445-4 2010 In freshly isolated human hepatocytes, ABT increased mRNA expression of CYP2B6 and CYP3A4 in a concentration-dependent manner. 1-aminobenzotriazole 39-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 20642445-5 2010 ABT also modulated CYP-inducing actions of CITCO and rifampin, the known inducers of CYP2B6 and CYP3A4. 1-aminobenzotriazole 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 20642445-5 2010 ABT also modulated CYP-inducing actions of CITCO and rifampin, the known inducers of CYP2B6 and CYP3A4. 6-(4-chlorophenyl)imidazo(2,1-b)(1,3)thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime 43-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 20642445-5 2010 ABT also modulated CYP-inducing actions of CITCO and rifampin, the known inducers of CYP2B6 and CYP3A4. Rifampin 53-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 20393696-12 2010 CONCLUSIONS: Administration of glycyrrhizin resulted in a modest induction of CYP3A that was clinically relevant according to the bioequivalence analysis. Glycyrrhizic Acid 31-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 20393696-2 2010 Licorice or glycyrrhizin has been shown to alter the activity of CYP3A in rodents. Glycyrrhizic Acid 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 20393696-3 2010 The influence of glycyrrhizin on CYP3A has not been elucidated in humans. Glycyrrhizic Acid 17-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 20124517-1 2010 Casopitant, an antiemetic, is a neurokinin-1 receptor antagonist metabolized primarily by cytochrome P450 3A4 (CYP3A4). casopitant 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-109 20374039-6 2010 Similarly, high-salt diet increases intestinal CYP3A function in humans, but it is not known whether these changes are mediated directly by NFAT5. Salts 16-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 20124517-1 2010 Casopitant, an antiemetic, is a neurokinin-1 receptor antagonist metabolized primarily by cytochrome P450 3A4 (CYP3A4). casopitant 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 20124517-8 2010 Coadministration of casopitant with strong inhibitors of CYP3A is likely to increase plasma exposure of casopitant, whereas coadministration with strong inducers of CYP3A is likely to decrease casopitant exposure and compromise efficacy. casopitant 20-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 20507880-6 2010 Second, by using these transformants, beta-endosulfan, a chemical for which the CYP isoforms contributing to its genotoxicity are unknown, was found to induce MN through the CYP3A4-mediated pathway. Endosulfan 38-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 20839617-0 2010 Cytochrome P450 3A4 inhibitory activity studies within the lycorine series of alkaloids. lycorine 59-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 20839617-0 2010 Cytochrome P450 3A4 inhibitory activity studies within the lycorine series of alkaloids. Alkaloids 78-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 20839617-1 2010 A mini-panel of semi-synthetic analogs of the Amaryllidaceae alkaloid lycorine was screened for cytochrome P450 3A4 (CYP3A4) inhibitory activity, the most potent of which exhibited inhibition as low as 0.21 microM. lycorine 70-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-115 20839617-1 2010 A mini-panel of semi-synthetic analogs of the Amaryllidaceae alkaloid lycorine was screened for cytochrome P450 3A4 (CYP3A4) inhibitory activity, the most potent of which exhibited inhibition as low as 0.21 microM. lycorine 70-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 20442190-0 2010 Sulforaphane- and phenethyl isothiocyanate-induced inhibition of aflatoxin B1-mediated genotoxicity in human hepatocytes: role of GSTM1 genotype and CYP3A4 gene expression. sulforaphane 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 20442190-7 2010 Transcriptional repression of genes involved in AFB bioactivation (CYP3A4 and CYP1A2), but not transcriptional activation of GSTs, may be responsible for the protective effects of SFN. sulforaphane 180-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 20442190-9 2010 The downregulation of CYP3A4 by SFN may have important implications for drug interactions. sulforaphane 32-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 20148399-3 2010 In this study, the inhibitory effects of curcumenol on seven CYP isoforms were investigated, and the results demonstrated that only CYP3A4 was strongly inhibited (IC(50) = 12.6 +/- 1.3 microM). curcumenol 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20507880-7 2010 This result was confirmed by the facts that the decreased CYP3A4 activity using a inhibitor or short interfering RNA (siRNA) repressed MN induction by beta-endosulfan and that endosulfan sulfate, one of the metabolites produced by CYP3A4, induced MN in the transformants harboring an empty vector. Endosulfan 151-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 20507880-7 2010 This result was confirmed by the facts that the decreased CYP3A4 activity using a inhibitor or short interfering RNA (siRNA) repressed MN induction by beta-endosulfan and that endosulfan sulfate, one of the metabolites produced by CYP3A4, induced MN in the transformants harboring an empty vector. endosulfan sulfate 176-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 231-237 20507880-8 2010 Third, the interaction between phase I and II drug-metabolizing enzymes was demonstrated by MN induction with inhibitors of uridine diphosphate (UDP)-glucuronosyltransferases in tamoxifen-treated transformants harboring the corresponding CYP3A4 or with inhibitors of glutathione S-transferase in safrole-treated transformants harboring the corresponding CYP2D6, whereas neither tamoxifen nor safrole alone induced MN in any transformant. Uridine Diphosphate 124-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 238-244 20507880-8 2010 Third, the interaction between phase I and II drug-metabolizing enzymes was demonstrated by MN induction with inhibitors of uridine diphosphate (UDP)-glucuronosyltransferases in tamoxifen-treated transformants harboring the corresponding CYP3A4 or with inhibitors of glutathione S-transferase in safrole-treated transformants harboring the corresponding CYP2D6, whereas neither tamoxifen nor safrole alone induced MN in any transformant. Uridine Diphosphate 145-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 238-244 20507880-8 2010 Third, the interaction between phase I and II drug-metabolizing enzymes was demonstrated by MN induction with inhibitors of uridine diphosphate (UDP)-glucuronosyltransferases in tamoxifen-treated transformants harboring the corresponding CYP3A4 or with inhibitors of glutathione S-transferase in safrole-treated transformants harboring the corresponding CYP2D6, whereas neither tamoxifen nor safrole alone induced MN in any transformant. Tamoxifen 178-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 238-244 20617557-3 2010 CYP3A activity has been related with the risk for hypertension in pregnancy, a major cause of morbidity and mortality among women, and CYP3A5*3 could reduce the risk for this disease in populations from regions with high sodium and water availability. Sodium 221-227 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 20617557-3 2010 CYP3A activity has been related with the risk for hypertension in pregnancy, a major cause of morbidity and mortality among women, and CYP3A5*3 could reduce the risk for this disease in populations from regions with high sodium and water availability. Water 232-237 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 20642550-2 2010 So far, the effects of CYP2D6 or CYP3A4 inhibitors on the pharmacokinetics of oxycodone in humans have not been systematically studied. Oxycodone 78-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 20590614-10 2010 CYP3A4 activity in intestine or liver, separately, reduced lopinavir AUC(oral) (>100-fold), compared with Cyp3a(-/-) mice. Lopinavir 59-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20642550-5 2010 AIM: The aim of this study was to find out whether the inhibition of cytochrome P450 2D6 (CYP2D6) with paroxetine or concomitant inhibition of CYP2D6 and CYP3A4 with paroxetine and itraconazole, altered the pharmacokinetics and pharmacological response of orally administered oxycodone. Paroxetine 166-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 20642550-4 2010 When both of CYP2D6 and CYP3A4 pathways are inhibited, the exposure to oral oxycodone is increased substantially. Oxycodone 76-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 20642550-5 2010 AIM: The aim of this study was to find out whether the inhibition of cytochrome P450 2D6 (CYP2D6) with paroxetine or concomitant inhibition of CYP2D6 and CYP3A4 with paroxetine and itraconazole, altered the pharmacokinetics and pharmacological response of orally administered oxycodone. Itraconazole 181-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 20388857-7 2010 Inhibition of COMT by 2"-fluoro-3,4-dihydroxy-5-nitrobenzophenone (Ro-41-0960) and GST by buthionine sulfoximine showed that COMT is mainly involved in detoxification of CYP2D6-formed MDMA metabolites, whereas glutathione (GSH) is mainly involved in detoxification of CYP3A4-formed MDMA metabolites. Glutathione 210-221 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 268-274 20642550-5 2010 AIM: The aim of this study was to find out whether the inhibition of cytochrome P450 2D6 (CYP2D6) with paroxetine or concomitant inhibition of CYP2D6 and CYP3A4 with paroxetine and itraconazole, altered the pharmacokinetics and pharmacological response of orally administered oxycodone. Oxycodone 276-285 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 20642550-12 2010 CONCLUSIONS: Drug interactions arising from CYP2D6 inhibition most likely have minor clinical importance for oral oxycodone if the function of the CYP3A4 pathway is normal. Oxycodone 114-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 20642550-13 2010 When both CYP2D6 and CYP3A4 pathways are inhibited, the exposure to oral oxycodone is increased substantially. Oxycodone 73-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 20678684-2 2010 Preclinical in vitro studies suggest that zibotentan has the potential to act as a time-dependent inhibitor of the cytochrome P450 isozyme 3A4 (CYP3A4) metabolic pathway. ZD4054 42-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-142 20678684-2 2010 Preclinical in vitro studies suggest that zibotentan has the potential to act as a time-dependent inhibitor of the cytochrome P450 isozyme 3A4 (CYP3A4) metabolic pathway. ZD4054 42-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 20678684-6 2010 The potency of zibotentan as a CYP3A4 inhibitor was also assessed. ZD4054 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 20678684-24 2010 The results indicate that once-daily zibotentan 10 mg acted as a weak inhibitor of the CYP3A4 pathway. ZD4054 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 20388857-7 2010 Inhibition of COMT by 2"-fluoro-3,4-dihydroxy-5-nitrobenzophenone (Ro-41-0960) and GST by buthionine sulfoximine showed that COMT is mainly involved in detoxification of CYP2D6-formed MDMA metabolites, whereas glutathione (GSH) is mainly involved in detoxification of CYP3A4-formed MDMA metabolites. Ro 41-0960 22-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 268-274 20052538-2 2010 Orally administered tamoxifen, is extensively metabolized by cytochrome P450 (CYP) enzymes, namely CYP3A4 and CYP2D6, into active metabolites, especially endoxifen. Tamoxifen 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 20052538-2 2010 Orally administered tamoxifen, is extensively metabolized by cytochrome P450 (CYP) enzymes, namely CYP3A4 and CYP2D6, into active metabolites, especially endoxifen. 4-hydroxy-N-desmethyltamoxifen 154-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 20375180-5 2010 A subsequent in vitro study using ketoconazole as an inhibitor of CJ-13,610 sulfoxidation corroborated the CYP3A4/5-mediated pathway (IC(50) = 7 nM). Ketoconazole 34-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 20388857-7 2010 Inhibition of COMT by 2"-fluoro-3,4-dihydroxy-5-nitrobenzophenone (Ro-41-0960) and GST by buthionine sulfoximine showed that COMT is mainly involved in detoxification of CYP2D6-formed MDMA metabolites, whereas glutathione (GSH) is mainly involved in detoxification of CYP3A4-formed MDMA metabolites. RO-41 67-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 268-274 20388857-7 2010 Inhibition of COMT by 2"-fluoro-3,4-dihydroxy-5-nitrobenzophenone (Ro-41-0960) and GST by buthionine sulfoximine showed that COMT is mainly involved in detoxification of CYP2D6-formed MDMA metabolites, whereas glutathione (GSH) is mainly involved in detoxification of CYP3A4-formed MDMA metabolites. Buthionine Sulfoximine 90-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 268-274 20388857-7 2010 Inhibition of COMT by 2"-fluoro-3,4-dihydroxy-5-nitrobenzophenone (Ro-41-0960) and GST by buthionine sulfoximine showed that COMT is mainly involved in detoxification of CYP2D6-formed MDMA metabolites, whereas glutathione (GSH) is mainly involved in detoxification of CYP3A4-formed MDMA metabolites. N-Methyl-3,4-methylenedioxyamphetamine 184-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 268-274 20388857-7 2010 Inhibition of COMT by 2"-fluoro-3,4-dihydroxy-5-nitrobenzophenone (Ro-41-0960) and GST by buthionine sulfoximine showed that COMT is mainly involved in detoxification of CYP2D6-formed MDMA metabolites, whereas glutathione (GSH) is mainly involved in detoxification of CYP3A4-formed MDMA metabolites. Glutathione 223-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 268-274 20388857-7 2010 Inhibition of COMT by 2"-fluoro-3,4-dihydroxy-5-nitrobenzophenone (Ro-41-0960) and GST by buthionine sulfoximine showed that COMT is mainly involved in detoxification of CYP2D6-formed MDMA metabolites, whereas glutathione (GSH) is mainly involved in detoxification of CYP3A4-formed MDMA metabolites. N-Methyl-3,4-methylenedioxyamphetamine 282-286 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 268-274 20553089-7 2010 Interactions with UDP-glucuronosyl transferase inducers, CYP2C8 and CYP3A4 substrates and drugs affecting enterohepatic recycling are likely to affect deferasirox"s efficacy and toxicity. Deferasirox 151-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 19395426-0 2010 Relationship between response to risperidone, plasma concentrations of risperidone and CYP3A4 polymorphisms in schizophrenia patients. Risperidone 33-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 19897389-0 2010 Clarithromycin, a potent inhibitor of CYP3A, greatly increases exposure to oral S-ketamine. Clarithromycin 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 19897389-0 2010 Clarithromycin, a potent inhibitor of CYP3A, greatly increases exposure to oral S-ketamine. Ketamine 80-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 19897389-9 2010 The relative amount of the CYP3A dependent metabolite norketamine was decreased by 54% by clarithromycin (p=0.004). norketamine 54-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 19897389-9 2010 The relative amount of the CYP3A dependent metabolite norketamine was decreased by 54% by clarithromycin (p=0.004). Clarithromycin 90-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 19897389-11 2010 CONCLUSIONS: Clarithromycin strongly increases plasma concentrations of oral S-ketamine probably by inhibiting its CYP3A-mediated N-demethylation. Clarithromycin 13-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 19897389-11 2010 CONCLUSIONS: Clarithromycin strongly increases plasma concentrations of oral S-ketamine probably by inhibiting its CYP3A-mediated N-demethylation. Ketamine 77-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 19897389-11 2010 CONCLUSIONS: Clarithromycin strongly increases plasma concentrations of oral S-ketamine probably by inhibiting its CYP3A-mediated N-demethylation. Nitrogen 2-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 19395426-1 2010 In this study, we examined the relationships between plasma concentrations of risperidone and 9-hydroxyrisperidone and polymorphisms of CYP3A4. Risperidone 78-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 19395426-5 2010 Our study has, for the first time, conducted a genetic association study of the CYP3A4 gene with risperidone response. Risperidone 97-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 20456080-0 2010 Triamcinolone acetonide induced secondary adrenal insufficiency related to impaired CYP3A4 metabolism by coadministration of nefazodone. Triamcinolone Acetonide 0-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 20456080-0 2010 Triamcinolone acetonide induced secondary adrenal insufficiency related to impaired CYP3A4 metabolism by coadministration of nefazodone. nefazodone 125-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 20456080-4 2010 Recently, there has been a greater appreciation of the potential drug interactions between CYP3A4 inhibitors and corticosteroid medications including topical steroid preparations. Steroids 120-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 20456080-5 2010 We report a case of triamcinolone acetonide induced secondary adrenal insufficiency related to impaired CYP3A4 metabolism by coadministration of nefazodone. Triamcinolone Acetonide 20-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 20456080-5 2010 We report a case of triamcinolone acetonide induced secondary adrenal insufficiency related to impaired CYP3A4 metabolism by coadministration of nefazodone. nefazodone 145-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 20089387-0 2010 Inhibition of cytochrome P450 3A4 activity by schisandrol A and gomisin A isolated from Fructus Schisandrae chinensis. schizandrol B 64-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-33 20575631-1 2010 STUDY OBJECTIVE: To investigate whether a drug interaction exists between bortezomib and the cytochrome P450 (CYP) 3A4 inhibitor itraconazole and/or the CYP2C19 inhibitor lansoprazole that results in increased severity of bortezomib-induced peripheral neuropathy and thrombocytopenia. Bortezomib 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-118 20575631-10 2010 We further assessed whether a drug interaction between bortezomib and itraconazole and/or lansoprazole had occurred involving the CYP3A4 and/or the CYP2C19 pathways, respectively-resulting in increased severity of the bortezomib-induced peripheral neuropathy and thrombocytopenia-by using the Horn drug interaction probability scale. Bortezomib 55-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 20575631-10 2010 We further assessed whether a drug interaction between bortezomib and itraconazole and/or lansoprazole had occurred involving the CYP3A4 and/or the CYP2C19 pathways, respectively-resulting in increased severity of the bortezomib-induced peripheral neuropathy and thrombocytopenia-by using the Horn drug interaction probability scale. Itraconazole 70-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 20575631-10 2010 We further assessed whether a drug interaction between bortezomib and itraconazole and/or lansoprazole had occurred involving the CYP3A4 and/or the CYP2C19 pathways, respectively-resulting in increased severity of the bortezomib-induced peripheral neuropathy and thrombocytopenia-by using the Horn drug interaction probability scale. Lansoprazole 90-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 20089387-0 2010 Inhibition of cytochrome P450 3A4 activity by schisandrol A and gomisin A isolated from Fructus Schisandrae chinensis. schisandrol A 46-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-33 20575631-10 2010 We further assessed whether a drug interaction between bortezomib and itraconazole and/or lansoprazole had occurred involving the CYP3A4 and/or the CYP2C19 pathways, respectively-resulting in increased severity of the bortezomib-induced peripheral neuropathy and thrombocytopenia-by using the Horn drug interaction probability scale. Bortezomib 218-228 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-136 20089387-1 2010 We studied the effects of schisandrol A (SCH) and gomisin A (GOM), two of the main bioactive components of Fructus Schisandrae chinensis, on cytochrome P450-3A4 (CYP3A4) activity and cellular glutathione (GSH) level. schisandrol A 26-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 20575631-13 2010 Clinicians should closely monitor for bortezomib-induced adverse effects when itraconazole, or any other potent CYP3A4 inhibitor, is administered concomitantly with bortezomib. Bortezomib 38-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 20089387-1 2010 We studied the effects of schisandrol A (SCH) and gomisin A (GOM), two of the main bioactive components of Fructus Schisandrae chinensis, on cytochrome P450-3A4 (CYP3A4) activity and cellular glutathione (GSH) level. schisandrol A 41-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-160 20089387-1 2010 We studied the effects of schisandrol A (SCH) and gomisin A (GOM), two of the main bioactive components of Fructus Schisandrae chinensis, on cytochrome P450-3A4 (CYP3A4) activity and cellular glutathione (GSH) level. schisandrol A 41-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 20089387-1 2010 We studied the effects of schisandrol A (SCH) and gomisin A (GOM), two of the main bioactive components of Fructus Schisandrae chinensis, on cytochrome P450-3A4 (CYP3A4) activity and cellular glutathione (GSH) level. schizandrol B 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-160 20089387-1 2010 We studied the effects of schisandrol A (SCH) and gomisin A (GOM), two of the main bioactive components of Fructus Schisandrae chinensis, on cytochrome P450-3A4 (CYP3A4) activity and cellular glutathione (GSH) level. schizandrol B 50-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 20089387-1 2010 We studied the effects of schisandrol A (SCH) and gomisin A (GOM), two of the main bioactive components of Fructus Schisandrae chinensis, on cytochrome P450-3A4 (CYP3A4) activity and cellular glutathione (GSH) level. schizandrol B 61-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-160 20089387-1 2010 We studied the effects of schisandrol A (SCH) and gomisin A (GOM), two of the main bioactive components of Fructus Schisandrae chinensis, on cytochrome P450-3A4 (CYP3A4) activity and cellular glutathione (GSH) level. schizandrol B 61-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 20089387-2 2010 In a cell-free system both SCH and GOM inhibited CYP3A4 activity with IC(50) values of 32.02 microM and 1.39 microM, respectively. schisandrol A 27-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 20089387-2 2010 In a cell-free system both SCH and GOM inhibited CYP3A4 activity with IC(50) values of 32.02 microM and 1.39 microM, respectively. schizandrol B 35-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 20405834-0 2010 CYP3A4-Mediated oxygenation versus dehydrogenation of raloxifene. Raloxifene Hydrochloride 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20361990-0 2010 Endosulfan induces CYP2B6 and CYP3A4 by activating the pregnane X receptor. Endosulfan 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 20361990-11 2010 These data support the role of endosulfan-alpha as a strong activator of PXR and inducer of CYP2B6 and CYP3A4, which may impact metabolism of CYP2B6 or CYP3A4 substrates. Endosulfan 31-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 20361990-11 2010 These data support the role of endosulfan-alpha as a strong activator of PXR and inducer of CYP2B6 and CYP3A4, which may impact metabolism of CYP2B6 or CYP3A4 substrates. Endosulfan 31-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 20405834-8 2010 These findings not only confirm CYP3A4-mediated dehydrogenation of raloxifene to a reactive diquinone methide but also suggest a novel route of raloxifene toxicity. diquinone 92-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20405834-8 2010 These findings not only confirm CYP3A4-mediated dehydrogenation of raloxifene to a reactive diquinone methide but also suggest a novel route of raloxifene toxicity. Raloxifene Hydrochloride 144-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20507089-9 2010 Characterization of the GSH conjugate structures allowed insight(s) into the bioactivation pathway, which involved CYP3A4-mediated phenol ring oxidation to the catechol, followed by further oxidation to the electrophilic ortho-quinone species. Glutathione 24-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 20507089-9 2010 Characterization of the GSH conjugate structures allowed insight(s) into the bioactivation pathway, which involved CYP3A4-mediated phenol ring oxidation to the catechol, followed by further oxidation to the electrophilic ortho-quinone species. Phenol 131-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 20507089-9 2010 Characterization of the GSH conjugate structures allowed insight(s) into the bioactivation pathway, which involved CYP3A4-mediated phenol ring oxidation to the catechol, followed by further oxidation to the electrophilic ortho-quinone species. catechol 160-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 20507089-9 2010 Characterization of the GSH conjugate structures allowed insight(s) into the bioactivation pathway, which involved CYP3A4-mediated phenol ring oxidation to the catechol, followed by further oxidation to the electrophilic ortho-quinone species. ortho 221-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 20507089-9 2010 Characterization of the GSH conjugate structures allowed insight(s) into the bioactivation pathway, which involved CYP3A4-mediated phenol ring oxidation to the catechol, followed by further oxidation to the electrophilic ortho-quinone species. quinone 227-234 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 20553580-0 2010 Flavonoids activate pregnane x receptor-mediated CYP3A4 gene expression by inhibiting cyclin-dependent kinases in HepG2 liver carcinoma cells. Flavonoids 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 20553580-5 2010 RESULTS: In a cell-based screen designed to identify compounds that activate PXR-mediated CYP3A4 gene expression in HepG2 human carcinoma cells, we identified several flavonoids, such as luteolin and apigenin, as PXR activators. Flavonoids 167-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 20553580-9 2010 The Cdk5-mediated downregulation of CYP3A4 promoter activity was restored by flavonoids, suggesting that flavonoids activate PXR by inactivating Cdk5. Flavonoids 77-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 20553580-9 2010 The Cdk5-mediated downregulation of CYP3A4 promoter activity was restored by flavonoids, suggesting that flavonoids activate PXR by inactivating Cdk5. Flavonoids 105-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 20188793-4 2010 Here we are reporting that mutations in the FMN binding domain of POR may reduce CYP3A4 activity, potentially influencing drug and steroid metabolism; and the loss of CYP3A4 activity may be correlated to the reduction of cytochrome b(5) by POR. Steroids 131-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 20405834-3 2010 However, recent studies have demonstrated the ability of raloxifene to form reactive intermediates and act as a mechanism-based inhibitor of cytochrome P450 3A4 (CYP3A4) by forming adducts with the apoprotein. Raloxifene Hydrochloride 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-160 20405834-3 2010 However, recent studies have demonstrated the ability of raloxifene to form reactive intermediates and act as a mechanism-based inhibitor of cytochrome P450 3A4 (CYP3A4) by forming adducts with the apoprotein. Raloxifene Hydrochloride 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 20405834-4 2010 However, previous studies could not differentiate between dehydrogenation to a diquinone methide and the more common oxygenation pathway to an arene oxide as the most likely intermediate to inactivate CYP3A4. Benzene oxide 143-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-207 20405834-6 2010 These studies established that 3"-hydroxyraloxifene is produced exclusively via CYP3A4-mediated oxygenation and provide convincing evidence for the mechanism of CYP3A4-mediated dehydrogenation of raloxifene to a reactive diquinone methide, while excluding the alternative arene oxide pathway. 3"-hydroxyraloxifene 31-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 20405834-6 2010 These studies established that 3"-hydroxyraloxifene is produced exclusively via CYP3A4-mediated oxygenation and provide convincing evidence for the mechanism of CYP3A4-mediated dehydrogenation of raloxifene to a reactive diquinone methide, while excluding the alternative arene oxide pathway. 3"-hydroxyraloxifene 31-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 20405834-6 2010 These studies established that 3"-hydroxyraloxifene is produced exclusively via CYP3A4-mediated oxygenation and provide convincing evidence for the mechanism of CYP3A4-mediated dehydrogenation of raloxifene to a reactive diquinone methide, while excluding the alternative arene oxide pathway. Raloxifene Hydrochloride 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 19898510-5 2010 Concomitant administration of oral voriconazole (n=4) significantly increased the bioavailability of Neoral (median 0.87 vs 0.54, P=0.017), probably due to the inhibition of gut CYP3A4 by voriconazole. Voriconazole 35-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 20405834-6 2010 These studies established that 3"-hydroxyraloxifene is produced exclusively via CYP3A4-mediated oxygenation and provide convincing evidence for the mechanism of CYP3A4-mediated dehydrogenation of raloxifene to a reactive diquinone methide, while excluding the alternative arene oxide pathway. Raloxifene Hydrochloride 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 20405834-6 2010 These studies established that 3"-hydroxyraloxifene is produced exclusively via CYP3A4-mediated oxygenation and provide convincing evidence for the mechanism of CYP3A4-mediated dehydrogenation of raloxifene to a reactive diquinone methide, while excluding the alternative arene oxide pathway. diquinone 221-230 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 20405834-6 2010 These studies established that 3"-hydroxyraloxifene is produced exclusively via CYP3A4-mediated oxygenation and provide convincing evidence for the mechanism of CYP3A4-mediated dehydrogenation of raloxifene to a reactive diquinone methide, while excluding the alternative arene oxide pathway. arene 272-277 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 20405834-6 2010 These studies established that 3"-hydroxyraloxifene is produced exclusively via CYP3A4-mediated oxygenation and provide convincing evidence for the mechanism of CYP3A4-mediated dehydrogenation of raloxifene to a reactive diquinone methide, while excluding the alternative arene oxide pathway. arene 272-277 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 20590587-12 2010 Blocking CYP3A4 (with ketoconazole) tripled oxymorphone AUC(infinity) and reduced noroxycodone and noroxymorphone AUCs by 80%. Ketoconazole 22-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 20405834-7 2010 Furthermore, it was demonstrated that 7-hydroxyraloxifene, which was previously believed to be a typical O(2)-derived metabolite of CYP3A4, is in fact produced by a highly unusual hydrolysis pathway from a putative ester, formed by the conjugation of raloxifene diquinone methide with a carboxylic acid moiety of CYP3A4, or other proteins in the reconstituted system. 7-hydroxyraloxifene 38-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20590587-12 2010 Blocking CYP3A4 (with ketoconazole) tripled oxymorphone AUC(infinity) and reduced noroxycodone and noroxymorphone AUCs by 80%. Oxymorphone 44-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 20405834-7 2010 Furthermore, it was demonstrated that 7-hydroxyraloxifene, which was previously believed to be a typical O(2)-derived metabolite of CYP3A4, is in fact produced by a highly unusual hydrolysis pathway from a putative ester, formed by the conjugation of raloxifene diquinone methide with a carboxylic acid moiety of CYP3A4, or other proteins in the reconstituted system. 7-hydroxyraloxifene 38-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 313-319 20590587-12 2010 Blocking CYP3A4 (with ketoconazole) tripled oxymorphone AUC(infinity) and reduced noroxycodone and noroxymorphone AUCs by 80%. noroxycodone 82-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 20590587-12 2010 Blocking CYP3A4 (with ketoconazole) tripled oxymorphone AUC(infinity) and reduced noroxycodone and noroxymorphone AUCs by 80%. noroxymorphone 99-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-15 20405834-7 2010 Furthermore, it was demonstrated that 7-hydroxyraloxifene, which was previously believed to be a typical O(2)-derived metabolite of CYP3A4, is in fact produced by a highly unusual hydrolysis pathway from a putative ester, formed by the conjugation of raloxifene diquinone methide with a carboxylic acid moiety of CYP3A4, or other proteins in the reconstituted system. o(2) 105-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20590587-14 2010 CONCLUSIONS AND IMPLICATIONS: Drug-drug interactions via CYP2D6 and CYP3A affected oxycodone pharmacokinetics and its magnitude depended on CYP2D6 genotype. Oxycodone 83-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 20405834-7 2010 Furthermore, it was demonstrated that 7-hydroxyraloxifene, which was previously believed to be a typical O(2)-derived metabolite of CYP3A4, is in fact produced by a highly unusual hydrolysis pathway from a putative ester, formed by the conjugation of raloxifene diquinone methide with a carboxylic acid moiety of CYP3A4, or other proteins in the reconstituted system. o(2) 105-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 313-319 20590588-0 2010 Genetic polymorphisms and drug interactions modulating CYP2D6 and CYP3A activities have a major effect on oxycodone analgesic efficacy and safety. Oxycodone 106-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 20405834-7 2010 Furthermore, it was demonstrated that 7-hydroxyraloxifene, which was previously believed to be a typical O(2)-derived metabolite of CYP3A4, is in fact produced by a highly unusual hydrolysis pathway from a putative ester, formed by the conjugation of raloxifene diquinone methide with a carboxylic acid moiety of CYP3A4, or other proteins in the reconstituted system. Esters 215-220 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20590588-1 2010 BACKGROUND AND PURPOSE: The major drug-metabolizing enzymes for the oxidation of oxycodone are CYP2D6 and CYP3A. Oxycodone 81-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-111 20590588-13 2010 CONCLUSIONS AND IMPLICATIONS: The modulation of CYP2D6 and CYP3A activities had clear effects on oxycodone pharmacodynamics and these effects were dependent on CYP2D6 genetic polymorphism. Oxycodone 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 20405834-7 2010 Furthermore, it was demonstrated that 7-hydroxyraloxifene, which was previously believed to be a typical O(2)-derived metabolite of CYP3A4, is in fact produced by a highly unusual hydrolysis pathway from a putative ester, formed by the conjugation of raloxifene diquinone methide with a carboxylic acid moiety of CYP3A4, or other proteins in the reconstituted system. Esters 215-220 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 313-319 20405834-7 2010 Furthermore, it was demonstrated that 7-hydroxyraloxifene, which was previously believed to be a typical O(2)-derived metabolite of CYP3A4, is in fact produced by a highly unusual hydrolysis pathway from a putative ester, formed by the conjugation of raloxifene diquinone methide with a carboxylic acid moiety of CYP3A4, or other proteins in the reconstituted system. raloxifene diquinone 251-271 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20405834-7 2010 Furthermore, it was demonstrated that 7-hydroxyraloxifene, which was previously believed to be a typical O(2)-derived metabolite of CYP3A4, is in fact produced by a highly unusual hydrolysis pathway from a putative ester, formed by the conjugation of raloxifene diquinone methide with a carboxylic acid moiety of CYP3A4, or other proteins in the reconstituted system. raloxifene diquinone 251-271 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 313-319 20405834-7 2010 Furthermore, it was demonstrated that 7-hydroxyraloxifene, which was previously believed to be a typical O(2)-derived metabolite of CYP3A4, is in fact produced by a highly unusual hydrolysis pathway from a putative ester, formed by the conjugation of raloxifene diquinone methide with a carboxylic acid moiety of CYP3A4, or other proteins in the reconstituted system. Carboxylic Acids 287-302 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20405834-7 2010 Furthermore, it was demonstrated that 7-hydroxyraloxifene, which was previously believed to be a typical O(2)-derived metabolite of CYP3A4, is in fact produced by a highly unusual hydrolysis pathway from a putative ester, formed by the conjugation of raloxifene diquinone methide with a carboxylic acid moiety of CYP3A4, or other proteins in the reconstituted system. Carboxylic Acids 287-302 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 313-319 20405834-8 2010 These findings not only confirm CYP3A4-mediated dehydrogenation of raloxifene to a reactive diquinone methide but also suggest a novel route of raloxifene toxicity. Raloxifene Hydrochloride 67-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20219851-6 2010 K(i, u) values of sarizotan against CYP2C8, CYP2C19, and CYP3A4 were >10 microM, whereas those against CYP2D6 and CYP1A2 were 0.43 and 8.7 microM, respectively. sarizotan 18-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 20200233-7 2010 The ratios were 2.9 (DES-CYP2C11), 3.6 [(S)-FLX-CYP2C19], and 0.8 (MA-CYP3A4), indicating that secondary hydroxylamines are significant metabolites of the P450-mediated metabolism of secondary alkyl amines. Hydroxylamines 105-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 20590587-0 2010 The effects of CYP2D6 and CYP3A activities on the pharmacokinetics of immediate release oxycodone. Oxycodone 88-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-31 20203109-3 2010 In response to studies that suggested the presence of several binding regions within the CYP3A4 active site, multiple probe substrates are often used for in vitro CYP3A4 DDI studies, including midazolam (the clinical standard), felodipine/nifedipine, and testosterone. Midazolam 193-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 20402562-0 2010 Using drug probes to monitor hepatic drug metabolism in critically ill patients: midazolam, a flawed but useful tool for clinical investigation of CYP3A activity? Midazolam 81-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-152 20203109-3 2010 In response to studies that suggested the presence of several binding regions within the CYP3A4 active site, multiple probe substrates are often used for in vitro CYP3A4 DDI studies, including midazolam (the clinical standard), felodipine/nifedipine, and testosterone. Felodipine 228-238 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 20203109-3 2010 In response to studies that suggested the presence of several binding regions within the CYP3A4 active site, multiple probe substrates are often used for in vitro CYP3A4 DDI studies, including midazolam (the clinical standard), felodipine/nifedipine, and testosterone. Nifedipine 239-249 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 20203109-3 2010 In response to studies that suggested the presence of several binding regions within the CYP3A4 active site, multiple probe substrates are often used for in vitro CYP3A4 DDI studies, including midazolam (the clinical standard), felodipine/nifedipine, and testosterone. Testosterone 255-267 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 20203109-8 2010 Buspirone, sildenafil, and simvastatin exhibited similar or greater sensitivity than midazolam to CYP3A4 inhibition in vivo. Simvastatin 27-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 20203109-8 2010 Buspirone, sildenafil, and simvastatin exhibited similar or greater sensitivity than midazolam to CYP3A4 inhibition in vivo. Midazolam 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 20203109-9 2010 Finally, Simcyp was used to predict the in vivo magnitude of CYP3A4 DDIs caused by AMG 458 using midazolam, sildenafil, simvastatin, and testosterone as probe substrates. Midazolam 97-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 20203109-9 2010 Finally, Simcyp was used to predict the in vivo magnitude of CYP3A4 DDIs caused by AMG 458 using midazolam, sildenafil, simvastatin, and testosterone as probe substrates. Sildenafil Citrate 108-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 20203109-9 2010 Finally, Simcyp was used to predict the in vivo magnitude of CYP3A4 DDIs caused by AMG 458 using midazolam, sildenafil, simvastatin, and testosterone as probe substrates. Simvastatin 120-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 20203109-9 2010 Finally, Simcyp was used to predict the in vivo magnitude of CYP3A4 DDIs caused by AMG 458 using midazolam, sildenafil, simvastatin, and testosterone as probe substrates. Testosterone 137-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 20215413-4 2010 CYP2C9-mediated metabolism of S-naproxen and S-flurbiprofen was inhibited up to 80% by coincubation with CYP3A4, although K(m) values were unchanged. Naproxen 30-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 20215413-4 2010 CYP2C9-mediated metabolism of S-naproxen and S-flurbiprofen was inhibited up to 80% by coincubation with CYP3A4, although K(m) values were unchanged. Flurbiprofen 45-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 20402562-4 2010 AREAS COVERED IN THIS REVIEW: Midazolam as a drug probe of CYP3A activity is reviewed, with discussion of its limitations and alternatives in critically ill patients. Midazolam 30-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 20233841-5 2010 By using the CYP3A4-specific substrates luciferin 6" benzyl ether, testosterone, and midazolam, we could confirm that the increased CYP3A4 gene expression also was accompanied by a similar increase in catalytic activity, inhibitable by the CYP3A4-selective inhibitor ketoconazole. luciferin 6" benzyl ether 40-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 20233841-5 2010 By using the CYP3A4-specific substrates luciferin 6" benzyl ether, testosterone, and midazolam, we could confirm that the increased CYP3A4 gene expression also was accompanied by a similar increase in catalytic activity, inhibitable by the CYP3A4-selective inhibitor ketoconazole. luciferin 6" benzyl ether 40-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20233841-5 2010 By using the CYP3A4-specific substrates luciferin 6" benzyl ether, testosterone, and midazolam, we could confirm that the increased CYP3A4 gene expression also was accompanied by a similar increase in catalytic activity, inhibitable by the CYP3A4-selective inhibitor ketoconazole. luciferin 6" benzyl ether 40-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20233841-5 2010 By using the CYP3A4-specific substrates luciferin 6" benzyl ether, testosterone, and midazolam, we could confirm that the increased CYP3A4 gene expression also was accompanied by a similar increase in catalytic activity, inhibitable by the CYP3A4-selective inhibitor ketoconazole. Testosterone 67-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 20233841-5 2010 By using the CYP3A4-specific substrates luciferin 6" benzyl ether, testosterone, and midazolam, we could confirm that the increased CYP3A4 gene expression also was accompanied by a similar increase in catalytic activity, inhibitable by the CYP3A4-selective inhibitor ketoconazole. Testosterone 67-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20233841-5 2010 By using the CYP3A4-specific substrates luciferin 6" benzyl ether, testosterone, and midazolam, we could confirm that the increased CYP3A4 gene expression also was accompanied by a similar increase in catalytic activity, inhibitable by the CYP3A4-selective inhibitor ketoconazole. Testosterone 67-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20233841-5 2010 By using the CYP3A4-specific substrates luciferin 6" benzyl ether, testosterone, and midazolam, we could confirm that the increased CYP3A4 gene expression also was accompanied by a similar increase in catalytic activity, inhibitable by the CYP3A4-selective inhibitor ketoconazole. Midazolam 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 20233841-5 2010 By using the CYP3A4-specific substrates luciferin 6" benzyl ether, testosterone, and midazolam, we could confirm that the increased CYP3A4 gene expression also was accompanied by a similar increase in catalytic activity, inhibitable by the CYP3A4-selective inhibitor ketoconazole. Midazolam 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20233841-5 2010 By using the CYP3A4-specific substrates luciferin 6" benzyl ether, testosterone, and midazolam, we could confirm that the increased CYP3A4 gene expression also was accompanied by a similar increase in catalytic activity, inhibitable by the CYP3A4-selective inhibitor ketoconazole. Midazolam 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20233841-5 2010 By using the CYP3A4-specific substrates luciferin 6" benzyl ether, testosterone, and midazolam, we could confirm that the increased CYP3A4 gene expression also was accompanied by a similar increase in catalytic activity, inhibitable by the CYP3A4-selective inhibitor ketoconazole. Ketoconazole 267-279 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 20233841-5 2010 By using the CYP3A4-specific substrates luciferin 6" benzyl ether, testosterone, and midazolam, we could confirm that the increased CYP3A4 gene expression also was accompanied by a similar increase in catalytic activity, inhibitable by the CYP3A4-selective inhibitor ketoconazole. Ketoconazole 267-279 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20233841-5 2010 By using the CYP3A4-specific substrates luciferin 6" benzyl ether, testosterone, and midazolam, we could confirm that the increased CYP3A4 gene expression also was accompanied by a similar increase in catalytic activity, inhibitable by the CYP3A4-selective inhibitor ketoconazole. Ketoconazole 267-279 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 20233841-6 2010 The CYP3A4 activity in confluent cells was also inducible by rifampicin. Rifampin 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 20233841-7 2010 Finally, the cell system could support the CYP3A4-dependent hepatotoxic activation of aflatoxin B(1), which was effectively inhibited by ketoconazole. Aflatoxin B1 86-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 20233841-7 2010 Finally, the cell system could support the CYP3A4-dependent hepatotoxic activation of aflatoxin B(1), which was effectively inhibited by ketoconazole. Ketoconazole 137-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 20350051-0 2010 Effect of glycyrrhizin on CYP2C19 and CYP3A4 activity in healthy volunteers with different CYP2C19 genotypes. Glycyrrhizic Acid 10-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 20497744-1 2010 OBJECTIVE: Itraconazole is a potent inhibitor of cytochrome P450 (CYP) 3A with an elimination half-life of more than 30 hours. Itraconazole 11-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-73 20497744-2 2010 Therefore, itraconazole may cause persistent CYP3A inhibition. Itraconazole 11-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-50 20497744-3 2010 Triazolam is primarily metabolized by CYP3A and its plasma concentration is increased remarkably by itraconazole. Triazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 20350051-9 2010 Glycyrrhizin induces CYP3A4-catalyzed sulfoxidation of omeprazole and leads to decreased omeprazole plasma concentrations, but has no significant impact on CYP2C19-dependent hydroxylation of omeprazole. Glycyrrhizic Acid 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 20350051-9 2010 Glycyrrhizin induces CYP3A4-catalyzed sulfoxidation of omeprazole and leads to decreased omeprazole plasma concentrations, but has no significant impact on CYP2C19-dependent hydroxylation of omeprazole. Omeprazole 55-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 20416375-8 2010 Using a PXR reporter gene assay, cyclosporin A - but not FK506 - was shown to be a direct PXR activator, and also to induce expression of the classic PXR-regulated CYP3A4 gene in human hepatocytes and in a cell line null for the FXR, a nuclear receptor with similar properties to the PXR. Cyclosporine 33-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 20399649-1 2010 A series of 3-[6-(4-substituted-piperazin-1-yl)-4-methyl-1H-benzimidazol-2-yl]-1H-pyridine-2-one were synthesized to modulate CYP3A4 inhibition and improve aqueous solubility of our prototypical compound BMS-536924 (1), while maintaining potent IGF-1R inhibitory activity. 3-[6-(4-substituted-piperazin-1-yl)-4-methyl-1h-benzimidazol-2-yl]-1h-pyridine-2-one 12-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 20408551-4 2010 Unwanted side effects are preventable without remarkable loss of activity when the responsible constituent(s) are carefully removed during the extraction process, as demonstrated for hyperforin (3), which is responsible for the induction of cytochrome P450 (CYP)-metabolizing enzymes (CYP3A4, in particular). hyperforin 183-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 285-291 24900196-1 2010 Cobicistat (3, GS-9350) is a newly discovered, potent, and selective inhibitor of human cytochrome P450 3A (CYP3A) enzymes. Cobicistat 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-106 20429590-8 2010 Compared to the substrate, CYP2C9 bound its hydroxywarfarin products with less affinity but retained high affinity for 10- and 4"-hydroxywarfarins, products from CYP3A4 reactions. 10- and 4"-hydroxywarfarins 119-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 24900196-1 2010 Cobicistat (3, GS-9350) is a newly discovered, potent, and selective inhibitor of human cytochrome P450 3A (CYP3A) enzymes. Cobicistat 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-113 24900196-0 2010 Cobicistat (GS-9350): A Potent and Selective Inhibitor of Human CYP3A as a Novel Pharmacoenhancer. Cobicistat 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 20359891-1 2010 For the purpose of reducing the strong CYP3A4 inhibitory potency of diamide prodrug 4, cyclic prodrugs of tricyclic-based FBPase inhibitors were synthesized. Diamide 68-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 20167382-6 2010 Killifish have significantly higher metabolic rates for all tested substrates except 7-benzyloxyquinoline and 7-benzyloxy-4-trifluoromethylcoumarin (both mammalian CYP3A substrates); significant differences were also seen between male and female killifish. 7-benzyloxy-4-trifluoromethylcoumarin 110-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-169 20307514-7 2010 CYP3A5 and CYP2B6 had the greatest efficiency to form carbosulfan sulfinamide, while CYP3A4 and CYP3A5 were the most efficient in the generation of the carbofuran metabolic pathway. carbosulfan sulfinamide 54-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 20307514-7 2010 CYP3A5 and CYP2B6 had the greatest efficiency to form carbosulfan sulfinamide, while CYP3A4 and CYP3A5 were the most efficient in the generation of the carbofuran metabolic pathway. Carbofuran 152-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 20307514-8 2010 Based on average abundances of CYP enzymes in human liver, CYP3A4 contributed to 98% of carbosulfan activation, while CYP3A4 and CYP2B6 contributed 57 and 37% to detoxification, respectively. carbosulfan 88-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 20307514-9 2010 Significant correlations between carbosulfan activation and CYP marker activities were seen with CYP3A4 (omeprazole sulfoxidation), CYP2C19 (omeprazole 5-hydroxylation) and CYP3A4 (midazolam 1"-hydroxylation), displaying r(2)=0.96, 0.87 and 0.82, respectively. carbosulfan 33-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 20307514-9 2010 Significant correlations between carbosulfan activation and CYP marker activities were seen with CYP3A4 (omeprazole sulfoxidation), CYP2C19 (omeprazole 5-hydroxylation) and CYP3A4 (midazolam 1"-hydroxylation), displaying r(2)=0.96, 0.87 and 0.82, respectively. carbosulfan 33-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 20307514-9 2010 Significant correlations between carbosulfan activation and CYP marker activities were seen with CYP3A4 (omeprazole sulfoxidation), CYP2C19 (omeprazole 5-hydroxylation) and CYP3A4 (midazolam 1"-hydroxylation), displaying r(2)=0.96, 0.87 and 0.82, respectively. Omeprazole 105-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 20307514-10 2010 Activation and detoxification pathways were inhibited by ketoconazole, a specific CYP3A4 inhibitor, by 90-97% and 47-94%, respectively. Ketoconazole 57-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 20307514-11 2010 Carbosulfan inhibited relatively potently CYP3A4 and moderately CYP1A1/2 and CYP2C19 in pooled HLM. carbosulfan 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 20307514-12 2010 These results suggest that the carbosulfan activation pathway is more important than the detoxification pathway, and that carbosulfan activation is predominantly catalyzed in humans by CYP3A4. carbosulfan 122-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 185-191 20387782-0 2010 How does the reductase help to regulate the catalytic cycle of cytochrome P450 3A4 using the conserved water channel? Water 103-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-82 20387782-2 2010 Here, we locate the preferred water pathways and their gating mechanisms for the human cytochrome P450 3A4 (CYP3A4) and elucidate the role of the cytochrome P450 reductase (CPR) in turning on and activating these water channels. Water 30-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-106 20387782-2 2010 Here, we locate the preferred water pathways and their gating mechanisms for the human cytochrome P450 3A4 (CYP3A4) and elucidate the role of the cytochrome P450 reductase (CPR) in turning on and activating these water channels. Water 30-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 20387782-2 2010 Here, we locate the preferred water pathways and their gating mechanisms for the human cytochrome P450 3A4 (CYP3A4) and elucidate the role of the cytochrome P450 reductase (CPR) in turning on and activating these water channels. Water 213-218 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-106 20387782-2 2010 Here, we locate the preferred water pathways and their gating mechanisms for the human cytochrome P450 3A4 (CYP3A4) and elucidate the role of the cytochrome P450 reductase (CPR) in turning on and activating these water channels. Water 213-218 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 20387782-8 2010 Indeed, we find that when the FMN domain of CPR binds to CYP3A4, the aqueduct fully opens up, thereby allowing a flow of water molecules. Water 121-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 19636246-5 2010 Polymorphisms in the hepatic enzymes involved in the metabolism of clopidogrel (e.g., CYP 1A2, CYP3A4, CYP2C19) or within the platelet membrane receptor (P2Y12) and/or polymorphism of platelet integrin alphaIIbbeta3 or integrin alpha2beta1 may affect platelet responses and could influence response to clopidogrel administration. Clopidogrel 67-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 20437462-5 2010 The present study systematically investigated the contributions of various human CYP isoforms (CYP3A4, CYP3A5, CYP2C8, CYP2C9 and CYP2C19) to in vitro metabolism of GLB. Glyburide 165-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 20437462-6 2010 GLB depletion and metabolite formation in human liver microsomes were most significantly inhibited by the CYP3A inhibitor ketoconazole compared with the inhibitors of other CYP isoforms. Glyburide 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-111 20437462-6 2010 GLB depletion and metabolite formation in human liver microsomes were most significantly inhibited by the CYP3A inhibitor ketoconazole compared with the inhibitors of other CYP isoforms. Ketoconazole 122-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-111 20437462-7 2010 Furthermore, multiple correlation analysis between GLB depletion and individual CYP activities was performed, demonstrating a significant correlation between GLB depletion and the CYP3A probe activity in 16 individual human liver microsomal preparations, but not between GLB depletion and the CYP2C19, CYP2C8 or CYP2C9 probe activity. Glyburide 158-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-185 20437462-7 2010 Furthermore, multiple correlation analysis between GLB depletion and individual CYP activities was performed, demonstrating a significant correlation between GLB depletion and the CYP3A probe activity in 16 individual human liver microsomal preparations, but not between GLB depletion and the CYP2C19, CYP2C8 or CYP2C9 probe activity. Glyburide 158-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-185 20437462-8 2010 By using recombinant supersomes overexpressing individual human CYP isoforms, it was found that GLB could be depleted by all the enzymes tested; however, the intrinsic clearance (V(max)/K(m)) of CYP3A4 for GLB depletion was 4-17 times greater than that of other CYP isoforms. Glyburide 96-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 20437462-8 2010 By using recombinant supersomes overexpressing individual human CYP isoforms, it was found that GLB could be depleted by all the enzymes tested; however, the intrinsic clearance (V(max)/K(m)) of CYP3A4 for GLB depletion was 4-17 times greater than that of other CYP isoforms. Glyburide 206-209 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 20437462-9 2010 These results confirm that human CYP3A4 is the major enzyme involved in the in vitro metabolism of GLB. Glyburide 99-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 20359891-2 2010 Extensive SAR studies led to the discovery of pyridine-containing cyclic prodrug 20, which strongly inhibited glucose production in monkey hepatocytes and also showed weak CYP3A4 inhibitory potency. pyridine 46-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 20218903-3 2010 The goal of this study was to analyze the genotype frequency of 10 SNPs related to mirtazapine metabolism [CYP3A4*17, CYP3A4*18, CYP3A5*3A, CYP1A2*1F, pregnane/steroid X receptor (PXR) (rs3814055, rs38114057, rs3814058) and constitutive androstane receptor (CAR) (rs4073054, rs2307424, rs2502815)]. Mirtazapine 83-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 20573082-1 2010 AIM: Docetaxel has a low oral bioavailability due to affinity for P-glycoprotein and cytochrome P450 (CYP) 3A4 enzymes. Docetaxel 5-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-110 20573082-2 2010 Inhibition of the CYP3A4 enzymes by ritonavir resulted in increased oral bioavailability. Ritonavir 36-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 20218903-3 2010 The goal of this study was to analyze the genotype frequency of 10 SNPs related to mirtazapine metabolism [CYP3A4*17, CYP3A4*18, CYP3A5*3A, CYP1A2*1F, pregnane/steroid X receptor (PXR) (rs3814055, rs38114057, rs3814058) and constitutive androstane receptor (CAR) (rs4073054, rs2307424, rs2502815)]. Mirtazapine 83-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 20156150-9 2010 Co-administration of galantamine with ketoconazole (CYP 3A4 strong inhibitor) or paroxetine (CYP 2D6 strong inhibitor) leads to a 30% and 40% increase, respectively, in galantamine exposure compared to galantamine given alone. Galantamine 21-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-59 20100816-0 2010 Bioactivation of a novel 2-methylindole-containing dual chemoattractant receptor-homologous molecule expressed on T-helper type-2 cells/D-prostanoid receptor antagonist leads to mechanism-based CYP3A inactivation: glutathione adduct characterization and prediction of in vivo drug-drug interaction. 2-methylindole 25-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-199 20100816-0 2010 Bioactivation of a novel 2-methylindole-containing dual chemoattractant receptor-homologous molecule expressed on T-helper type-2 cells/D-prostanoid receptor antagonist leads to mechanism-based CYP3A inactivation: glutathione adduct characterization and prediction of in vivo drug-drug interaction. Glutathione 214-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-199 20100816-3 2010 The inactivation was shown to be irreversible by dialysis and accompanied by an NADPH-dependent increase in 2MI covalent binding to a 55- to 60-kDa microsomal protein, consistent with irreversible binding to CYP3A4. NADP 80-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 208-214 20100816-5 2010 The potential for a clinical drug-drug interaction arising from mechanism-based inactivation of CYP3A4 by 2MI was predicted using a steady-state model, and a 4.3- to 7.5-fold increase in the exposure of midazolam was predicted at anticipated therapeutic concentrations. Midazolam 203-212 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 20124396-9 2010 In vitro studies showed that UGT2B7 and CYP3A4 are responsible for the majority of lersivirine metabolism in humans. UK 453,061 83-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 20097724-5 2010 Previous studies have shown that CYP3A is involved in the metabolism of 17-OHPC. 17 alpha-Hydroxyprogesterone Caproate 72-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-38 20097724-9 2010 Expressed CYP3A4 demonstrated a significantly higher (>10 times) capacity to metabolize 17-OHPC than CYP3A7. 17 alpha-Hydroxyprogesterone Caproate 91-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 20097724-12 2010 In summary, this study demonstrates that fetal hepatocytes and, in particular, the fetal form of CYP3A (i.e., CYP3A7) can metabolize 17-OHPC. 17 alpha-Hydroxyprogesterone Caproate 133-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-102 20164110-2 2010 Human CYP1A1 and CYP3A4 have also been shown to contribute to CLZ metabolism. Chlorzoxazone 62-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 20164112-3 2010 To gain insight into the potential effects of hypothermia on drug metabolism and disposition, we evaluated the pharmacokinetics of midazolam as a probe for CYP3A4/5 activity during mild hypothermia in human volunteers. Midazolam 131-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 20156150-9 2010 Co-administration of galantamine with ketoconazole (CYP 3A4 strong inhibitor) or paroxetine (CYP 2D6 strong inhibitor) leads to a 30% and 40% increase, respectively, in galantamine exposure compared to galantamine given alone. Ketoconazole 38-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-59 20156150-9 2010 Co-administration of galantamine with ketoconazole (CYP 3A4 strong inhibitor) or paroxetine (CYP 2D6 strong inhibitor) leads to a 30% and 40% increase, respectively, in galantamine exposure compared to galantamine given alone. Galantamine 169-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-59 20156150-9 2010 Co-administration of galantamine with ketoconazole (CYP 3A4 strong inhibitor) or paroxetine (CYP 2D6 strong inhibitor) leads to a 30% and 40% increase, respectively, in galantamine exposure compared to galantamine given alone. Galantamine 169-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-59 19960413-0 2010 Inhibitory effects of deoxypodophyllotoxin from Anthriscus sylvestris on human CYP2C9 and CYP3A4. deoxypodophyllotoxin 22-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 20609060-1 2010 OBJECTIVES: Nateglinide is metabolized by CYP2C9 and CYP3A4, therefore drug-drug interactions through cytochrome P450 (CYP) inhibition may occur. Nateglinide 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 20091056-5 2010 It also highlights the key role in tacrolimus pharmacokinetics of the CYP3A system and P-gp polymorphisms, and their influence in high-risk situations when enzyme activity is already affected by enterocyte damage due to diarrhoea and CCB competition. Tacrolimus 35-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-75 20179914-1 2010 PURPOSE: This study aimed to investigate the effect of rifampicin, an inducer of CYP3A4 and P-glycoprotein, on the pharmacokinetics and pharmacodynamics of aliskiren, a renin inhibitor used in the treatment of hypertension. Rifampin 55-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 20179914-1 2010 PURPOSE: This study aimed to investigate the effect of rifampicin, an inducer of CYP3A4 and P-glycoprotein, on the pharmacokinetics and pharmacodynamics of aliskiren, a renin inhibitor used in the treatment of hypertension. aliskiren 156-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 20609060-7 2010 The influence of pre-incubation on the inhibition by nateglinide of CYP3A4, CYP2C9 and CYP2C19 was examined. Nateglinide 53-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 19960413-3 2010 When a mixture of specific CYP substrates was incubated with DPT in HLM, CYP2C9-catalyzed diclofenac 4-hydroxylation and CYP3A4-catalyzed midazolam 1-hydroxylation were strongly inhibited by DPT, with IC (50) values of 6.3 and 9.2 microM, respectively. deoxypodophyllotoxin 61-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 19960413-3 2010 When a mixture of specific CYP substrates was incubated with DPT in HLM, CYP2C9-catalyzed diclofenac 4-hydroxylation and CYP3A4-catalyzed midazolam 1-hydroxylation were strongly inhibited by DPT, with IC (50) values of 6.3 and 9.2 microM, respectively. Midazolam 138-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 19960413-3 2010 When a mixture of specific CYP substrates was incubated with DPT in HLM, CYP2C9-catalyzed diclofenac 4-hydroxylation and CYP3A4-catalyzed midazolam 1-hydroxylation were strongly inhibited by DPT, with IC (50) values of 6.3 and 9.2 microM, respectively. deoxypodophyllotoxin 191-194 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 19960413-5 2010 From these results, DPT was characterized to be a competitive inhibitor of CYP2C9 and CYP3A4, with K(i) values of 3.5 and 10.8 microM in HLM and 24.9 and 3.5 microM in baculovirus-insect cell-expressed human CYPs, respectively. deoxypodophyllotoxin 20-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 20699073-3 2010 However, the absence of response among patients and the metabolic profile of imatinib (involving the CYP3A4) suggested the existence of a great interindividual variability. Imatinib Mesylate 77-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 27392989-3 2010 However, the absence of response among patients and the metabolic profile of imatinib (involving the CYP3A4) suggested the existence of a great interindividual variability. Imatinib Mesylate 77-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 20097278-6 2010 Furthermore, 100 microM of WZ extract almost completely inhibited FK506 metabolism in rat and human liver microsomes, indicating WZ extract potently inhibited the CYP3A-mediated metabolism of FK506. 3-(2-(Diethylamino)ethyl)-5-ethyl-5-phenylbarbituric acid hydrochloride 27-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-168 20097278-6 2010 Furthermore, 100 microM of WZ extract almost completely inhibited FK506 metabolism in rat and human liver microsomes, indicating WZ extract potently inhibited the CYP3A-mediated metabolism of FK506. 3-(2-(Diethylamino)ethyl)-5-ethyl-5-phenylbarbituric acid hydrochloride 129-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-168 20097278-6 2010 Furthermore, 100 microM of WZ extract almost completely inhibited FK506 metabolism in rat and human liver microsomes, indicating WZ extract potently inhibited the CYP3A-mediated metabolism of FK506. Tacrolimus 192-197 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-168 20097278-7 2010 In conclusion, WZ inhibited P-gp-mediated efflux and CYP3A-mediated metabolism of FK506, and the reduction of intestinal first-pass effect by WZ was the major cause of the increased FK506 oral bioavailability. 3-(2-(Diethylamino)ethyl)-5-ethyl-5-phenylbarbituric acid hydrochloride 15-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 20097278-7 2010 In conclusion, WZ inhibited P-gp-mediated efflux and CYP3A-mediated metabolism of FK506, and the reduction of intestinal first-pass effect by WZ was the major cause of the increased FK506 oral bioavailability. Tacrolimus 82-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 20446912-0 2010 Assessment of competitive and mechanism-based inhibition by clarithromycin: use of domperidone as a CYP3A probe-drug substrate and various enzymatic sources including a new cell-based assay with freshly isolated human hepatocytes. Domperidone 83-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 20189386-0 2010 Potent and selective inhibition of human cytochrome P450 3A4 by seco-pancratistatin structural analogs. seco-pancratistatin 64-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-60 20189386-2 2010 Structure-activity relationships reveal important insights into the seco-pancratistatin pharmacophore as a potent and selective inhibitor of human cytochrome P450 3A4 (CYP3A4), and highlight features of concern in advancing a potent, selective anticancer agent in the pancratistatin series. seco-pancratistatin 68-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-166 20189386-2 2010 Structure-activity relationships reveal important insights into the seco-pancratistatin pharmacophore as a potent and selective inhibitor of human cytochrome P450 3A4 (CYP3A4), and highlight features of concern in advancing a potent, selective anticancer agent in the pancratistatin series. seco-pancratistatin 68-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 20189386-2 2010 Structure-activity relationships reveal important insights into the seco-pancratistatin pharmacophore as a potent and selective inhibitor of human cytochrome P450 3A4 (CYP3A4), and highlight features of concern in advancing a potent, selective anticancer agent in the pancratistatin series. pancratistatin 73-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-166 20189386-2 2010 Structure-activity relationships reveal important insights into the seco-pancratistatin pharmacophore as a potent and selective inhibitor of human cytochrome P450 3A4 (CYP3A4), and highlight features of concern in advancing a potent, selective anticancer agent in the pancratistatin series. pancratistatin 73-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 168-174 20086031-18 2010 The initial ketone formation was CYP3A4-dependent and rate-limiting for the overall reaction to CD1790. Ketones 12-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 21281268-0 2010 Characterization of CYP3A isozymes involved in the metabolism of domperidone: role of cytochrome b5 and inhibition by ketoconazole. Domperidone 65-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-25 21281268-0 2010 Characterization of CYP3A isozymes involved in the metabolism of domperidone: role of cytochrome b5 and inhibition by ketoconazole. Ketoconazole 118-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-25 20446912-5 2010 At high concentrations (100 microM), clarithromycin had weak competitive inhibition potency towards CYP3A4 and CYP3A5. Clarithromycin 37-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 21281268-1 2010 Previous studies have indicated that CYP3As are involved in the metabolism of the prokinetic agent domperidone.The objectives of our study were to characterize further the role of specific CYP3A isoforms in the metabolism of domperidone and to compare the kinetic parameters of domperidone to those of the CYP3A probe drug midazolam. Domperidone 99-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-42 20446912-9 2010 Drug interactions between clarithromycin and several CYP3A substrates are predicted to be insidious; the risk of severe adverse events should increase over time and persist for a few days after cessation of the drug. Clarithromycin 26-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 21281268-1 2010 Previous studies have indicated that CYP3As are involved in the metabolism of the prokinetic agent domperidone.The objectives of our study were to characterize further the role of specific CYP3A isoforms in the metabolism of domperidone and to compare the kinetic parameters of domperidone to those of the CYP3A probe drug midazolam. Domperidone 99-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-194 21281268-1 2010 Previous studies have indicated that CYP3As are involved in the metabolism of the prokinetic agent domperidone.The objectives of our study were to characterize further the role of specific CYP3A isoforms in the metabolism of domperidone and to compare the kinetic parameters of domperidone to those of the CYP3A probe drug midazolam. Domperidone 225-236 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-42 21281268-1 2010 Previous studies have indicated that CYP3As are involved in the metabolism of the prokinetic agent domperidone.The objectives of our study were to characterize further the role of specific CYP3A isoforms in the metabolism of domperidone and to compare the kinetic parameters of domperidone to those of the CYP3A probe drug midazolam. Domperidone 225-236 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-194 21281268-1 2010 Previous studies have indicated that CYP3As are involved in the metabolism of the prokinetic agent domperidone.The objectives of our study were to characterize further the role of specific CYP3A isoforms in the metabolism of domperidone and to compare the kinetic parameters of domperidone to those of the CYP3A probe drug midazolam. Domperidone 225-236 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-42 21281268-1 2010 Previous studies have indicated that CYP3As are involved in the metabolism of the prokinetic agent domperidone.The objectives of our study were to characterize further the role of specific CYP3A isoforms in the metabolism of domperidone and to compare the kinetic parameters of domperidone to those of the CYP3A probe drug midazolam. Domperidone 225-236 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-194 21281268-1 2010 Previous studies have indicated that CYP3As are involved in the metabolism of the prokinetic agent domperidone.The objectives of our study were to characterize further the role of specific CYP3A isoforms in the metabolism of domperidone and to compare the kinetic parameters of domperidone to those of the CYP3A probe drug midazolam. Midazolam 323-332 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-42 21281268-1 2010 Previous studies have indicated that CYP3As are involved in the metabolism of the prokinetic agent domperidone.The objectives of our study were to characterize further the role of specific CYP3A isoforms in the metabolism of domperidone and to compare the kinetic parameters of domperidone to those of the CYP3A probe drug midazolam. Midazolam 323-332 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-194 20076952-1 2010 BACKGROUND: The aim of this study was to investigate the effects of the cytochrome P450 3A4 (CYP34A) inhibitor itraconazole on the pharmacokinetics and pharmacodynamics of orally and intravenously administered oxycodone. Itraconazole 111-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-91 21281268-6 2010 Ketoconazole more potently inhibited CYP3A4 than CYP3A5 for both domperidone and midazolam. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 21281268-6 2010 Ketoconazole more potently inhibited CYP3A4 than CYP3A5 for both domperidone and midazolam. Domperidone 65-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 21281268-6 2010 Ketoconazole more potently inhibited CYP3A4 than CYP3A5 for both domperidone and midazolam. Midazolam 81-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 21281268-7 2010 However, the addition of cytochrome b5 to the incubation mixture appeared to decrease the inhibitory potency of ketoconazole towards CYP3A4 for domperidone but not for midazolam. Ketoconazole 112-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 21281268-7 2010 However, the addition of cytochrome b5 to the incubation mixture appeared to decrease the inhibitory potency of ketoconazole towards CYP3A4 for domperidone but not for midazolam. Domperidone 144-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 21281268-8 2010 Our results indicate that CYP3A4 plays major role in the metabolism of domperidone. Domperidone 71-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 21281268-9 2010 We demonstrated a modulatory role of cytochrome b5mostly for the metabolism of domperidone and confirmed selective inhibition of CYP3A4 over CYP3A5 by ketoconazole. Ketoconazole 151-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 21281268-10 2010 Comparison of domperidone kinetic parameters to those of the CYP3A probe drug midazolam suggests that domperidone exhibits a much higher CYP3A4/CYP3A5 selectivity ratio than midazolam. Midazolam 78-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-66 21281268-10 2010 Comparison of domperidone kinetic parameters to those of the CYP3A probe drug midazolam suggests that domperidone exhibits a much higher CYP3A4/CYP3A5 selectivity ratio than midazolam. Domperidone 102-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-66 21281268-10 2010 Comparison of domperidone kinetic parameters to those of the CYP3A probe drug midazolam suggests that domperidone exhibits a much higher CYP3A4/CYP3A5 selectivity ratio than midazolam. Domperidone 102-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 20054526-0 2010 CYP3A activity influences imatinib response in patients with chronic myeloid leukemia: a pilot study on in vivo CYP3A activity. Imatinib Mesylate 26-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 20054526-2 2010 The main metabolite CGP74588 has similar potency to that of imatinib and is a product of CYP3A4 and CYP3A5 metabolism. CGP 74588 20-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 20054526-4 2010 We designed this study to investigate the role of the CYP3A activity in the response to imatinib therapy. Imatinib Mesylate 88-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-59 20054526-5 2010 METHODS: Fourteen CML patients were phenotyped for in vivo CYP3A activity using quinine as a probe drug. Quinine 80-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 20054526-6 2010 The plasma concentration ratio of quinine and its CYP3A metabolite was used for assessing CYP3A activity. Quinine 34-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 20054526-8 2010 RESULTS: Patients that achieved complete molecular response showed significantly (Mann-Whitney U-test, p=0.013) higher in vivo CYP3A activity (median quinine metabolic ratio = 10.1) than patients achieving partial molecular response (median = 15.9). Quinine 150-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 20076952-1 2010 BACKGROUND: The aim of this study was to investigate the effects of the cytochrome P450 3A4 (CYP34A) inhibitor itraconazole on the pharmacokinetics and pharmacodynamics of orally and intravenously administered oxycodone. Oxycodone 210-219 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-91 20054526-9 2010 CONCLUSIONS: These results indicate a clinical significance of the CYP3A activity and its metabolic products in CML patients treated with imatinib. Imatinib Mesylate 138-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-72 20214408-0 2010 Predictions of metabolic drug-drug interactions using physiologically based modelling: Two cytochrome P450 3A4 substrates coadministered with ketoconazole or verapamil. Ketoconazole 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-110 20345925-8 2010 We found that CYP3A is also expressed in SH-SY5Y cells and inhibiting CYP3A with ketoconazole significantly increased the cell death caused by 10 and 25 microM of MPP+ by between 8 +/- 1 and 30 +/- 3% (P < 0.001). Ketoconazole 81-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 20214408-0 2010 Predictions of metabolic drug-drug interactions using physiologically based modelling: Two cytochrome P450 3A4 substrates coadministered with ketoconazole or verapamil. Verapamil 158-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-110 20345925-8 2010 We found that CYP3A is also expressed in SH-SY5Y cells and inhibiting CYP3A with ketoconazole significantly increased the cell death caused by 10 and 25 microM of MPP+ by between 8 +/- 1 and 30 +/- 3% (P < 0.001). Ketoconazole 81-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-75 20345925-8 2010 We found that CYP3A is also expressed in SH-SY5Y cells and inhibiting CYP3A with ketoconazole significantly increased the cell death caused by 10 and 25 microM of MPP+ by between 8 +/- 1 and 30 +/- 3% (P < 0.001). mangion-purified polysaccharide (Candida albicans) 163-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 20345925-8 2010 We found that CYP3A is also expressed in SH-SY5Y cells and inhibiting CYP3A with ketoconazole significantly increased the cell death caused by 10 and 25 microM of MPP+ by between 8 +/- 1 and 30 +/- 3% (P < 0.001). mangion-purified polysaccharide (Candida albicans) 163-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-75 19727863-2 2010 Recently, a CYP3A4 structure with two molecules of ketoconazole (2KT) was identified. Ketoconazole 51-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 19727863-7 2010 F215 and F220 are known as entrance blockers of channel-2 in metyrapone-bound CYP3A4. Metyrapone 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 20171174-6 2010 TRalpha1, TRbeta1, COUP-TFI, and COUP-TFII further demonstrated dose-dependent repression of PXR-mediated CYP3A4 enhancer/promoter reporter activity in transient transfection in the presence and absence of the PXR inducer rifampin, while VDR showed this effect only in the absence of treatment. Rifampin 222-230 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 20026040-0 2010 Electron transfer in the complex of membrane-bound human cytochrome P450 3A4 with the flavin domain of P450BM-3: the effect of oligomerization of the heme protein and intermittent modulation of the spin equilibrium. 4,6-dinitro-o-cresol 86-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-76 20080160-9 2010 In conclusion, Alprazolam, Bromazepam, Chlordiazepoxide, Clonazepam, Diazepam, Lorazepam, Nitrazepam, Oxazepam, Tetrazepam and Triazolam can be considered as safe drugs in term of their inability to induce PXR- and AhR-dependent cytochrome P450 enzymes CYP1A2 and CYP3A4. Clonazepam 57-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 264-270 20080160-9 2010 In conclusion, Alprazolam, Bromazepam, Chlordiazepoxide, Clonazepam, Diazepam, Lorazepam, Nitrazepam, Oxazepam, Tetrazepam and Triazolam can be considered as safe drugs in term of their inability to induce PXR- and AhR-dependent cytochrome P450 enzymes CYP1A2 and CYP3A4. Lorazepam 79-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 264-270 20080160-9 2010 In conclusion, Alprazolam, Bromazepam, Chlordiazepoxide, Clonazepam, Diazepam, Lorazepam, Nitrazepam, Oxazepam, Tetrazepam and Triazolam can be considered as safe drugs in term of their inability to induce PXR- and AhR-dependent cytochrome P450 enzymes CYP1A2 and CYP3A4. Oxazepam 102-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 264-270 20080160-9 2010 In conclusion, Alprazolam, Bromazepam, Chlordiazepoxide, Clonazepam, Diazepam, Lorazepam, Nitrazepam, Oxazepam, Tetrazepam and Triazolam can be considered as safe drugs in term of their inability to induce PXR- and AhR-dependent cytochrome P450 enzymes CYP1A2 and CYP3A4. tetrazepam 112-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 264-270 20080160-9 2010 In conclusion, Alprazolam, Bromazepam, Chlordiazepoxide, Clonazepam, Diazepam, Lorazepam, Nitrazepam, Oxazepam, Tetrazepam and Triazolam can be considered as safe drugs in term of their inability to induce PXR- and AhR-dependent cytochrome P450 enzymes CYP1A2 and CYP3A4. Triazolam 127-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 264-270 20080160-10 2010 Medazepam and Midazolam slightly activated pregnane X receptor and displayed weak potency to induce CYP3A4 mRNA in human hepatocytes. Midazolam 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 20211808-12 2010 CYP3A4 enzyme plays a primary role in the metabolism of nifedipine. Nifedipine 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20211808-14 2010 Nifedipine dosage was based on the value of CYP3A4 gene expression. Nifedipine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 20108303-2 2010 Preclinical data have indicated that dasatinib is metabolized primarily through cytochrome P450 3A4 (CYP3A4) and may cause QT prolongation. Dasatinib 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-99 20108303-2 2010 Preclinical data have indicated that dasatinib is metabolized primarily through cytochrome P450 3A4 (CYP3A4) and may cause QT prolongation. Dasatinib 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 20108303-5 2010 Segment 1 of the trial was short term and sequential and was designed to determine whether the coadministration of the potent CYP3A4 inhibitor ketoconazole had an effect on the pharmacokinetics of dasatinib. Ketoconazole 143-155 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 20108303-5 2010 Segment 1 of the trial was short term and sequential and was designed to determine whether the coadministration of the potent CYP3A4 inhibitor ketoconazole had an effect on the pharmacokinetics of dasatinib. Dasatinib 197-206 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 20108303-14 2010 The pharmacokinetic and cardiac studies indicated that coadministration of dasatinib with potent CYP3A4 inhibitors or agents that prolong the QTc interval should be avoided if possible. Dasatinib 75-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 20080160-0 2010 Benzodiazepines medazepam and midazolam are activators of pregnane X receptor and weak inducers of CYP3A4: investigation in primary cultures of human hepatocytes and hepatocarcinoma cell lines. Benzodiazepines 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 20080160-0 2010 Benzodiazepines medazepam and midazolam are activators of pregnane X receptor and weak inducers of CYP3A4: investigation in primary cultures of human hepatocytes and hepatocarcinoma cell lines. Medazepam 16-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 20080160-0 2010 Benzodiazepines medazepam and midazolam are activators of pregnane X receptor and weak inducers of CYP3A4: investigation in primary cultures of human hepatocytes and hepatocarcinoma cell lines. Midazolam 30-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 20080160-5 2010 We found weak but significant induction of CYP3A4 mRNA by Midazolam and Medazepam, while other benzodiazepines did not induce CYP3A4 expression. Midazolam 58-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 20080160-5 2010 We found weak but significant induction of CYP3A4 mRNA by Midazolam and Medazepam, while other benzodiazepines did not induce CYP3A4 expression. Medazepam 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 20080160-9 2010 In conclusion, Alprazolam, Bromazepam, Chlordiazepoxide, Clonazepam, Diazepam, Lorazepam, Nitrazepam, Oxazepam, Tetrazepam and Triazolam can be considered as safe drugs in term of their inability to induce PXR- and AhR-dependent cytochrome P450 enzymes CYP1A2 and CYP3A4. Alprazolam 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 264-270 20080160-9 2010 In conclusion, Alprazolam, Bromazepam, Chlordiazepoxide, Clonazepam, Diazepam, Lorazepam, Nitrazepam, Oxazepam, Tetrazepam and Triazolam can be considered as safe drugs in term of their inability to induce PXR- and AhR-dependent cytochrome P450 enzymes CYP1A2 and CYP3A4. Bromazepam 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 264-270 20026040-6 2010 The effect of the surface density of CYP3A4 in proteoliposomes on the oligomerization equilibrium was confirmed with a FRET-based assay employing a cysteine-depleted mutant labeled on Cys-468 with BODIPY iodoacetamide. Cysteine 148-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 20026040-6 2010 The effect of the surface density of CYP3A4 in proteoliposomes on the oligomerization equilibrium was confirmed with a FRET-based assay employing a cysteine-depleted mutant labeled on Cys-468 with BODIPY iodoacetamide. Cysteine 184-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 20026040-6 2010 The effect of the surface density of CYP3A4 in proteoliposomes on the oligomerization equilibrium was confirmed with a FRET-based assay employing a cysteine-depleted mutant labeled on Cys-468 with BODIPY iodoacetamide. bodipy iodoacetamide 197-217 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 19719748-2 2010 Midazolam, a short-acting benzodiazepine, has been considered a probe for estimating hepatic and intestinal cytochrome P450 (CYP) 3A activity in humans. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-132 20233203-2 2010 It is metabolized to DA-8164, a major metabolite, by CYP3A4. DA-8164 21-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 20233203-3 2010 This study was performed to investigate the effect of ketoconazole, a known CYP3A4 inhibitor, on the pharmacokinetics of udenafil. Ketoconazole 54-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 20233203-3 2010 This study was performed to investigate the effect of ketoconazole, a known CYP3A4 inhibitor, on the pharmacokinetics of udenafil. udenafil 121-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 19719748-2 2010 Midazolam, a short-acting benzodiazepine, has been considered a probe for estimating hepatic and intestinal cytochrome P450 (CYP) 3A activity in humans. Benzodiazepines 26-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-132 20170205-9 2010 CYP3A4 may play a more dominant role than CYP3A5 in the metabolism of ciclosporin. Cyclosporine 70-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20007670-2 2010 CYP1A2, CYP2C19, CYP2D6, CYP3A4, and CYP3A5 were identified as paroxetine-catechol-forming P450 isoforms, and CYP2C19 and CYP2D6 were identified as metabolizing P450 isoforms by substrate depletion. catechol 74-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 19940026-6 2010 Experiments with human cDNA-expressed P450 enzymes and P450 chemical inhibitors and correlation with P450 activities in individual human liver microsomes demonstrated that the oxidative metabolism of apixaban for formation of all metabolites was predominantly catalyzed by CYP3A4/5 with a minor contribution of CYP1A2 and CYP2J2 for formation of M2. apixaban 200-208 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 273-279 20007670-2 2010 CYP1A2, CYP2C19, CYP2D6, CYP3A4, and CYP3A5 were identified as paroxetine-catechol-forming P450 isoforms, and CYP2C19 and CYP2D6 were identified as metabolizing P450 isoforms by substrate depletion. Paroxetine 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 20007670-8 2010 Considering the kinetic parameters, inhibition results, relative activity factor calculations, and Simcyp simulations, CYP2D6 (high affinity) and CYP3A4 (low affinity) are most likely to be the major contributors to paroxetine metabolism in humans. Paroxetine 216-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 20016053-9 2010 In vitro data indicated that anacetrapib is metabolized mainly by CYP3A4 to form M1, M2, and M3. anacetrapib 29-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 20016053-10 2010 Overall, these data, along with those from other preclinical and clinical studies, indicate that anacetrapib probably exhibits a low-to-moderate degree of oral absorption in humans and the absorbed fraction of the dose is eliminated largely via CYP3A4-catalyzed oxidative metabolism, followed by excretion of metabolites by the biliary-fecal route. anacetrapib 97-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 245-251 20019244-7 2010 Thus, CYP1A2, CYP2B6, and CYP3A4 were found to accurately respond to their respective prototypical inducers, i.e., omeprazole, phenobarbital, and rifampicin. Omeprazole 115-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 20019244-7 2010 Thus, CYP1A2, CYP2B6, and CYP3A4 were found to accurately respond to their respective prototypical inducers, i.e., omeprazole, phenobarbital, and rifampicin. Phenobarbital 127-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 20019244-7 2010 Thus, CYP1A2, CYP2B6, and CYP3A4 were found to accurately respond to their respective prototypical inducers, i.e., omeprazole, phenobarbital, and rifampicin. Rifampin 146-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 20369030-7 2010 AEDs, such as phenytoin, phenobarbital, carbamazepine, felbamate, topiramate, oxcarbazepine and primidone, induce cytochrome P450 3A4, leading to enhanced metabolism of either or both the estrogenic and progestogenic component of OCs, thereby reducing their efficacy in preventing pregnancy. Phenytoin 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-133 20369030-7 2010 AEDs, such as phenytoin, phenobarbital, carbamazepine, felbamate, topiramate, oxcarbazepine and primidone, induce cytochrome P450 3A4, leading to enhanced metabolism of either or both the estrogenic and progestogenic component of OCs, thereby reducing their efficacy in preventing pregnancy. Phenobarbital 25-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-133 20369030-7 2010 AEDs, such as phenytoin, phenobarbital, carbamazepine, felbamate, topiramate, oxcarbazepine and primidone, induce cytochrome P450 3A4, leading to enhanced metabolism of either or both the estrogenic and progestogenic component of OCs, thereby reducing their efficacy in preventing pregnancy. Carbamazepine 40-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-133 20369030-7 2010 AEDs, such as phenytoin, phenobarbital, carbamazepine, felbamate, topiramate, oxcarbazepine and primidone, induce cytochrome P450 3A4, leading to enhanced metabolism of either or both the estrogenic and progestogenic component of OCs, thereby reducing their efficacy in preventing pregnancy. Felbamate 55-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-133 20369030-7 2010 AEDs, such as phenytoin, phenobarbital, carbamazepine, felbamate, topiramate, oxcarbazepine and primidone, induce cytochrome P450 3A4, leading to enhanced metabolism of either or both the estrogenic and progestogenic component of OCs, thereby reducing their efficacy in preventing pregnancy. Topiramate 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-133 20369030-7 2010 AEDs, such as phenytoin, phenobarbital, carbamazepine, felbamate, topiramate, oxcarbazepine and primidone, induce cytochrome P450 3A4, leading to enhanced metabolism of either or both the estrogenic and progestogenic component of OCs, thereby reducing their efficacy in preventing pregnancy. Oxcarbazepine 78-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-133 20369030-7 2010 AEDs, such as phenytoin, phenobarbital, carbamazepine, felbamate, topiramate, oxcarbazepine and primidone, induce cytochrome P450 3A4, leading to enhanced metabolism of either or both the estrogenic and progestogenic component of OCs, thereby reducing their efficacy in preventing pregnancy. Primidone 96-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-133 20012601-2 2010 Verapamil is a substrate of both P-gp and CYP3A4. Verapamil 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 20388821-0 2010 Studies of the toxicological potential of capsinoids, XIII: inhibitory effects of capsaicin and capsinoids on cytochrome P450 3A4 in human liver microsomes. Capsaicin 82-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-129 20012601-11 2010 CONCLUSION: Lovastatin increased the absorption of verapamil by inhibiting P-gp and inhibited the first-pass metabolism of verapamil by inhibiting CYP3A4 in the intestine and/or liver in humans. Lovastatin 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 20012601-11 2010 CONCLUSION: Lovastatin increased the absorption of verapamil by inhibiting P-gp and inhibited the first-pass metabolism of verapamil by inhibiting CYP3A4 in the intestine and/or liver in humans. Verapamil 123-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 20012430-0 2010 In vitro-in vivo extrapolation of zolpidem as a perpetrator of metabolic interactions involving CYP3A. Zolpidem 34-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-101 20012430-1 2010 OBJECTIVES: To evaluate zolpidem as a mechanism-based inactivator of human CYP3A in vitro, and to assess its metabolic interaction potential with CYP3A drugs (in vitro-in vivo extrapolation; IV-IVE). Zolpidem 24-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 20012430-2 2010 METHODS: A co- vs. pre-incubation strategy was used to quantify time-dependent inhibition of human liver microsomal (HLM) and recombinant CYP3A4 (rCYP3A4) by zolpidem. Zolpidem 158-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 20012430-5 2010 RESULTS: Consistent with MBI, the inhibitory potency of zolpidem toward CYP3A was increased following pre-incubation. Zolpidem 56-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-77 20012430-11 2010 CONCLUSIONS: Zolpidem is a relatively weak mechanism-based inactivator of human CYP3A in vitro. Zolpidem 13-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-85 20388821-0 2010 Studies of the toxicological potential of capsinoids, XIII: inhibitory effects of capsaicin and capsinoids on cytochrome P450 3A4 in human liver microsomes. capsinoids 96-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-129 20388821-3 2010 Capsaicin clearly inhibited cytochrome P450 3A4 activity, losing 50% of the activity at 21.5 micromol/L. Capsaicin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-47 20388821-5 2010 Preincubation increased the capsaicin inhibitory activity against cytochrome P450 3A4 in a time-dependent manner. Capsaicin 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-85 20388821-7 2010 Capsaicin was shown to inhibit cytochrome P450 3A4, probably through a mechanism-based inhibition. Capsaicin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-50 20135071-8 2010 However, alterations of rivaroxaban and apixaban pharmacokinetics upon interactions with inhibitors and inducers of CYP3A4 or P-glycoprotein may complicate the use of these compounds in daily practice, whereas dabigatran elimination largely depends on renal function. Rivaroxaban 24-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 20159579-0 2010 Bioconversion of the antihistaminc drug loratadine by tobacco cell suspension cultures expressing human cytochrome P450 3A4. Loratadine 40-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-123 19934400-7 2010 A common silent polymorphism and a polymorphic trinucleotide (CCT) repeat in FoxA2 were associated with CYP3A4 expression. trinucleotide 47-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 20035846-5 2010 CYP3A was induced by EMD in human HepG2 cells exceeding the level induced by rifampicin, but was not induced in rat H4IIE cells. Rifampin 77-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 20305307-6 2010 The reason of this effect is that tramadol is the substrate and clarithromycin is the inhibitor of the CYP 3A4 enzyme. Tramadol 34-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-110 20305307-6 2010 The reason of this effect is that tramadol is the substrate and clarithromycin is the inhibitor of the CYP 3A4 enzyme. Clarithromycin 64-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-110 19790032-5 2010 All clones showed potent inhibition of CYP3A4 and P-gp activities, with IC (50) values ranging from 1.7 to 3.1 microg/mL and from 16.7 to 51.7 microg/mL, respectively, being below that reported for other herbs and some known classic drug inhibitors, such as St. John"s wort and fluoxetine. Fluoxetine 278-288 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 19854261-0 2010 Effects of dinuclear copper(II) complexes with 6-(benzylamino)purine derivatives on AhR and PXR dependent expression of cytochromes P450 CYP1A2 and CYP3A4 genes in primary cultures of human hepatocytes. cupric ion 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 19854261-0 2010 Effects of dinuclear copper(II) complexes with 6-(benzylamino)purine derivatives on AhR and PXR dependent expression of cytochromes P450 CYP1A2 and CYP3A4 genes in primary cultures of human hepatocytes. benzylaminopurine 47-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 19854261-5 2010 On the other hand, the model inducers, i.e. 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD) and rifampicin, significantly increased the levels of CYP1A2 and CYP3A4 mRNAs in all cultures. Polychlorinated Dibenzodioxins 44-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 19854261-5 2010 On the other hand, the model inducers, i.e. 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD) and rifampicin, significantly increased the levels of CYP1A2 and CYP3A4 mRNAs in all cultures. Polychlorinated Dibenzodioxins 82-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 19854261-5 2010 On the other hand, the model inducers, i.e. 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD) and rifampicin, significantly increased the levels of CYP1A2 and CYP3A4 mRNAs in all cultures. Rifampin 92-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 153-159 20135071-8 2010 However, alterations of rivaroxaban and apixaban pharmacokinetics upon interactions with inhibitors and inducers of CYP3A4 or P-glycoprotein may complicate the use of these compounds in daily practice, whereas dabigatran elimination largely depends on renal function. apixaban 40-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 20025923-6 2010 The CYP3A-mediated benzyloxyquinoline dealkylation was inhibited by PEITC in only two of the four human donors, whereas a rise in CYP3A4 apoprotein levels was noted in all human livers, albeit to different extent. 2-(benzyloxy)quinoline 19-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-9 20025923-6 2010 The CYP3A-mediated benzyloxyquinoline dealkylation was inhibited by PEITC in only two of the four human donors, whereas a rise in CYP3A4 apoprotein levels was noted in all human livers, albeit to different extent. phenethyl isothiocyanate 68-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-9 20040700-9 2010 Cyclophosphamide and vincristine are metabolized via the CYP3A4 isoenzyme. Cyclophosphamide 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 20169036-4 2010 Etravirine is a substrate of CYP3A4, CYP2C9, CYP2C19, and uridine diphosphate glucuronyltransferase, and induces CYP3A4, weakly inhibits CYP2C9 and moderately inhibits CYP2C19. etravirine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 20169036-4 2010 Etravirine is a substrate of CYP3A4, CYP2C9, CYP2C19, and uridine diphosphate glucuronyltransferase, and induces CYP3A4, weakly inhibits CYP2C9 and moderately inhibits CYP2C19. etravirine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 20103024-6 2010 CONCLUSIONS: Initiation of a fibrate or statin that inhibits CYP3A4 enzymes, including atorvastatin, was associated with an increased risk of hospitalization for gastrointestinal bleeding. Atorvastatin 87-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 20040700-9 2010 Cyclophosphamide and vincristine are metabolized via the CYP3A4 isoenzyme. Vincristine 21-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 20022493-1 2010 A variety of N-linked tertiary amines and heteroarylamines were examined at the 4-position of sulfonylated proline dipeptides in order to improve VLA-4 receptor off-rates and overcome the issue of CYP3A4 time-dependent inhibition of ester prodrugs. Esters 233-238 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 19603168-1 2010 PURPOSE: Axitinib, a potent and selective inhibitor of vascular endothelial growth factor receptors 1, 2, 3, is metabolized by cytochrome P450 3A4 and glucuronidation. Axitinib 9-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-146 20233183-0 2010 Time-dependent inhibition (TDI) of CYP3A4 and CYP2C9 by noscapine potentially explains clinical noscapine-warfarin interaction. Noscapine 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 20233183-0 2010 Time-dependent inhibition (TDI) of CYP3A4 and CYP2C9 by noscapine potentially explains clinical noscapine-warfarin interaction. Noscapine 96-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 20233183-0 2010 Time-dependent inhibition (TDI) of CYP3A4 and CYP2C9 by noscapine potentially explains clinical noscapine-warfarin interaction. Warfarin 106-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 20233183-10 2010 CONCLUSIONS: TDI of CYP3A4 and CYP2C9 by noscapine potentially explains clinical noscapine-warfarin interaction. Warfarin 91-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 20233183-6 2010 Kinetic analysis showed that inhibition of CYP2C9 by noscapine was best fit to a noncompetitive type with K(i) value of 8.8 microm, while inhibition of CYP3A4 by noscapine was best fit to a competitive manner with K(i) value of 5.2 microm. Noscapine 162-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 19924124-0 2010 Effect of simultaneous induction and inhibition of CYP3A by St John"s Wort and ritonavir on CYP3A activity. Ritonavir 79-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-97 20233183-7 2010 Noscapine also exhibited TDI to CYP3A4 and CYP2C9. Noscapine 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20233183-10 2010 CONCLUSIONS: TDI of CYP3A4 and CYP2C9 by noscapine potentially explains clinical noscapine-warfarin interaction. Noscapine 41-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 20233183-10 2010 CONCLUSIONS: TDI of CYP3A4 and CYP2C9 by noscapine potentially explains clinical noscapine-warfarin interaction. Noscapine 81-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 19769955-5 2010 RESULTS: Zn(2+)-Phos-tag PAGE permitted identification of the following allele genotypes: the A/A homozygote (CYP3A51/1) in 3 individuals, the G/G homozygote (CYP3A53/3) in 14 individuals, and the A/G heterozygote (CYP3A51/3) in 2 individuals. Zinc 9-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-168 19769955-5 2010 RESULTS: Zn(2+)-Phos-tag PAGE permitted identification of the following allele genotypes: the A/A homozygote (CYP3A51/1) in 3 individuals, the G/G homozygote (CYP3A53/3) in 14 individuals, and the A/G heterozygote (CYP3A51/3) in 2 individuals. Zinc 9-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-224 19924124-1 2010 We aimed to assess the effect of coadministration and withdrawal of a potent cytochrome P450 3A (CYP3A) inhibitor (ritonavir) and a potent CYP3A inducer (St John"s wort) on CYP3A enzyme activity in an open, fixed-sequence study design. Ritonavir 115-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-95 19924124-1 2010 We aimed to assess the effect of coadministration and withdrawal of a potent cytochrome P450 3A (CYP3A) inhibitor (ritonavir) and a potent CYP3A inducer (St John"s wort) on CYP3A enzyme activity in an open, fixed-sequence study design. Ritonavir 115-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-102 19884323-0 2010 Physiologically based pharmacokinetic model of mechanism-based inhibition of CYP3A by clarithromycin. Clarithromycin 86-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 19884323-7 2010 The incorporation of CYP3A-dependent metabolism of clarithromycin enabled prediction of its nonlinear pharmacokinetics. Clarithromycin 51-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-26 19884323-11 2010 This semiphysiologically based pharmacokinetic model incorporating CYP3A inactivation in the intestine and liver accurately predicts the nonlinear pharmacokinetics of clarithromycin and the DDI observed between clarithromycin and midazolam. Clarithromycin 167-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-72 19884323-11 2010 This semiphysiologically based pharmacokinetic model incorporating CYP3A inactivation in the intestine and liver accurately predicts the nonlinear pharmacokinetics of clarithromycin and the DDI observed between clarithromycin and midazolam. Clarithromycin 211-225 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-72 19817679-2 2010 However, our recent studies have suggested that CYP3A4 specifically associates with UGT2B7 and alters the regioselectivity of morphine glucuronidation. Morphine 126-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 19884323-1 2010 The prediction of clinical drug-drug interactions (DDIs) due to mechanism-based inhibitors of CYP3A is complicated when the inhibitor itself is metabolized by CYP3Aas in the case of clarithromycin. Clarithromycin 182-196 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-99 19884323-11 2010 This semiphysiologically based pharmacokinetic model incorporating CYP3A inactivation in the intestine and liver accurately predicts the nonlinear pharmacokinetics of clarithromycin and the DDI observed between clarithromycin and midazolam. Midazolam 230-239 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-72 19884323-2 2010 Previous attempts to predict the effects of clarithromycin on CYP3A substrates, e.g., midazolam, failed to account for nonlinear metabolism of clarithromycin. Clarithromycin 44-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 19884323-3 2010 A semiphysiologically based pharmacokinetic model was developed for clarithromycin and midazolam metabolism, incorporating hepatic and intestinal metabolism by CYP3A and non-CYP3A mechanisms. Clarithromycin 68-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-165 19923256-7 2010 Extracted ion chromatograms of metabolites observed for albendazole, amiodarone, astemizole, thioridazine, mesoridazine, and danazol showed marked differences in the regioselectivity of CYP2J2 and CYP3A4. Albendazole 56-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 19884323-3 2010 A semiphysiologically based pharmacokinetic model was developed for clarithromycin and midazolam metabolism, incorporating hepatic and intestinal metabolism by CYP3A and non-CYP3A mechanisms. Clarithromycin 68-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-179 19923256-7 2010 Extracted ion chromatograms of metabolites observed for albendazole, amiodarone, astemizole, thioridazine, mesoridazine, and danazol showed marked differences in the regioselectivity of CYP2J2 and CYP3A4. Amiodarone 69-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 19889885-6 2010 In vitro experiments showed that FK1706 inhibited CYP3A4/5 in a time-dependent and irreversible manner. FK1706 33-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 19884323-4 2010 CYP3A inactivation by clarithromycin occurred at both sites. Clarithromycin 22-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 19889885-10 2010 In conclusion, FK1706 weakly or moderately inhibited the activity of CYP3A4/5 in vitro and vivo at the tested dose. FK1706 15-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 20137762-2 2010 The authors determined whether a pharmacokinetic interaction occurs between sotrastaurin and everolimus, both of which are substrates and inhibitors of CYP3A4. sotrastaurin 76-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 19823813-2 2010 It has been reported that, in humans, CyA is metabolized by cytochrome P450 (CYP) 3A or excreted by P-glycoprotein/multidrug resistant protein (MRP) 2. Cyclosporine 38-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-84 19923256-7 2010 Extracted ion chromatograms of metabolites observed for albendazole, amiodarone, astemizole, thioridazine, mesoridazine, and danazol showed marked differences in the regioselectivity of CYP2J2 and CYP3A4. Astemizole 81-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 19923256-7 2010 Extracted ion chromatograms of metabolites observed for albendazole, amiodarone, astemizole, thioridazine, mesoridazine, and danazol showed marked differences in the regioselectivity of CYP2J2 and CYP3A4. Thioridazine 93-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 19923256-7 2010 Extracted ion chromatograms of metabolites observed for albendazole, amiodarone, astemizole, thioridazine, mesoridazine, and danazol showed marked differences in the regioselectivity of CYP2J2 and CYP3A4. Mesoridazine 107-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 19923256-7 2010 Extracted ion chromatograms of metabolites observed for albendazole, amiodarone, astemizole, thioridazine, mesoridazine, and danazol showed marked differences in the regioselectivity of CYP2J2 and CYP3A4. Danazol 125-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 19923256-9 2010 Although the CYP2J2 active site can accommodate large substrates, it may be more narrow than CYP3A4, limiting metabolism to moieties that can extend closer toward the active heme iron. Heme 174-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 19923256-9 2010 Although the CYP2J2 active site can accommodate large substrates, it may be more narrow than CYP3A4, limiting metabolism to moieties that can extend closer toward the active heme iron. Iron 179-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 19923256-10 2010 For albendazole, CYP2J2 forms a unique metabolite compared with CYP3A4. Albendazole 4-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 19923256-12 2010 The Michaelis-Menten-derived intrinsic clearance of N-desethyl amiodarone was 4.6 greater in HLM than in HIM and 17-fold greater in recombinant CYP3A4 than in recombinant CYP2J2. desethylamiodarone 52-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 20137762-2 2010 The authors determined whether a pharmacokinetic interaction occurs between sotrastaurin and everolimus, both of which are substrates and inhibitors of CYP3A4. Everolimus 93-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 19948947-4 2010 Whereas ticlopidine and clopidogrel are metabolized to their thiolactones in the liver by cytochromes P450, prasugrel proceeds to its thiolactone following hydrolysis by carboxylesterase 2 during absorption, and a portion of prasugrel"s active metabolite is also formed by intestinal CYP3A. Prasugrel Hydrochloride 108-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 284-289 19864617-1 2010 Saquinavir exhibits paradoxical transport across modified Caco-2 cell monolayers (doi: 10.1124/jpet.103.056390) expressing P-glycoprotein and Cyp3A4. Saquinavir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 19940232-6 2010 Upon coadministration of midazolam, there was a modest reduction of up to 22% in midazolam exposure (AUC, C(max)), suggesting a modest induction of CYP3A4/5 by deferasirox. Midazolam 25-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 19940232-6 2010 Upon coadministration of midazolam, there was a modest reduction of up to 22% in midazolam exposure (AUC, C(max)), suggesting a modest induction of CYP3A4/5 by deferasirox. Deferasirox 160-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 20175821-6 2010 The present drug-drug interaction can be attributed to a strong inhibitory effect on cytochrome P450-3A4 activity by voriconazole. Voriconazole 117-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-104 19889796-0 2010 Quantitative prediction and clinical observation of a CYP3A inhibitor-based drug-drug interactions with MLN3897, a potent C-C chemokine receptor-1 antagonist. MLN3897 104-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-59 19889796-2 2010 This approach, using inhibition data from human hepatocytes incubated in human plasma, and quantitative P450 phenotyping data from hepatic microsomal incubations, successfully predicted DDIs for 15 marketed drugs with ketoconazole, a strong competitive inhibitor of CYP3A4/5, generally used to demonstrate a "worst-case scenario" for CYP3A inhibition. Ketoconazole 218-230 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 266-272 19838691-1 2010 PURPOSE: In preterm infants, the biotransformation of midazolam (M) to 1-OH-midazolam (OHM) by cytochrome P450 3A4 (CYP3A4) is developmentally immature, but it is currently unknown whether the glucuronidation of OHM to 1-OH-midazolam glucuronide (OHMG) is also decreased. Midazolam 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-114 19838691-1 2010 PURPOSE: In preterm infants, the biotransformation of midazolam (M) to 1-OH-midazolam (OHM) by cytochrome P450 3A4 (CYP3A4) is developmentally immature, but it is currently unknown whether the glucuronidation of OHM to 1-OH-midazolam glucuronide (OHMG) is also decreased. Midazolam 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 19838691-1 2010 PURPOSE: In preterm infants, the biotransformation of midazolam (M) to 1-OH-midazolam (OHM) by cytochrome P450 3A4 (CYP3A4) is developmentally immature, but it is currently unknown whether the glucuronidation of OHM to 1-OH-midazolam glucuronide (OHMG) is also decreased. 1-oh-midazolam 71-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-114 19838691-1 2010 PURPOSE: In preterm infants, the biotransformation of midazolam (M) to 1-OH-midazolam (OHM) by cytochrome P450 3A4 (CYP3A4) is developmentally immature, but it is currently unknown whether the glucuronidation of OHM to 1-OH-midazolam glucuronide (OHMG) is also decreased. 1-oh-midazolam 71-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 19838691-1 2010 PURPOSE: In preterm infants, the biotransformation of midazolam (M) to 1-OH-midazolam (OHM) by cytochrome P450 3A4 (CYP3A4) is developmentally immature, but it is currently unknown whether the glucuronidation of OHM to 1-OH-midazolam glucuronide (OHMG) is also decreased. 1-oh-midazolam glucuronide 219-245 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-114 19838691-1 2010 PURPOSE: In preterm infants, the biotransformation of midazolam (M) to 1-OH-midazolam (OHM) by cytochrome P450 3A4 (CYP3A4) is developmentally immature, but it is currently unknown whether the glucuronidation of OHM to 1-OH-midazolam glucuronide (OHMG) is also decreased. 1-oh-midazolam glucuronide 219-245 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 19838691-1 2010 PURPOSE: In preterm infants, the biotransformation of midazolam (M) to 1-OH-midazolam (OHM) by cytochrome P450 3A4 (CYP3A4) is developmentally immature, but it is currently unknown whether the glucuronidation of OHM to 1-OH-midazolam glucuronide (OHMG) is also decreased. ohmg 247-251 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-114 19838691-1 2010 PURPOSE: In preterm infants, the biotransformation of midazolam (M) to 1-OH-midazolam (OHM) by cytochrome P450 3A4 (CYP3A4) is developmentally immature, but it is currently unknown whether the glucuronidation of OHM to 1-OH-midazolam glucuronide (OHMG) is also decreased. ohmg 247-251 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 19889796-2 2010 This approach, using inhibition data from human hepatocytes incubated in human plasma, and quantitative P450 phenotyping data from hepatic microsomal incubations, successfully predicted DDIs for 15 marketed drugs with ketoconazole, a strong competitive inhibitor of CYP3A4/5, generally used to demonstrate a "worst-case scenario" for CYP3A inhibition. Ketoconazole 218-230 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 266-271 19889796-3 2010 In addition, this approach was successfully extended to DDI predictions with the moderate competitive CYP3A inhibitor fluconazole for nine marketed drugs. Fluconazole 118-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-107 19686701-6 2010 Chromatin immunoprecipitation assay showed that retinoids recruit RXRalpha and CAR to the proximal ER6 and distal XREM nuclear receptor response elements of the CYP3A4 gene promoter. Retinoids 48-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 161-167 20099988-1 2010 STUDY OBJECTIVE: To examine the effect of telavancin, a lipoglycopeptide antibiotic with potent gram-positive activity, on the pharmacokinetics of midazolam, a cytochrome P450 (CYP) 3A probe substrate. telavancin 42-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-184 20455331-11 2010 Dapoxetine is strongly metabolised by the cytochrome P450 isoenzymes CYP 3A4 and CYP 2D6, and thus carries a risk of numerous pharmacokinetic interactions. dapoxetine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-76 19699225-0 2010 The algal hepatoxoxin okadaic acid is a substrate for human cytochromes CYP3A4 and CYP3A5. algal 4-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 19699225-0 2010 The algal hepatoxoxin okadaic acid is a substrate for human cytochromes CYP3A4 and CYP3A5. hepatoxoxin 10-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 19699225-0 2010 The algal hepatoxoxin okadaic acid is a substrate for human cytochromes CYP3A4 and CYP3A5. Okadaic Acid 22-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 20082577-6 2010 Based on the simulation and rat in vitro-in vivo extrapolation, it is predicted that co-administration of domperidone in humans could modestly increase (approximately 50%) the exposure of drugs that are primarily cleared by CYP3A. Domperidone 106-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 224-229 19712670-2 2010 Pregnane X receptor (PXR) dominantly controls CYP3A4 inducibility in the liver, whereas vitamin D receptor (VDR) transactivates CYP3A4 in the intestine by secondary bile acids. Bile Acids and Salts 165-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 19712670-7 2010 In contrast, eNR3A4 is involved only in the basal transactivation in intestinal cells and in the PXR-mediated rifampicin-induced transactivation of CYP3A4 in LS174T intestinal cells. Rifampin 110-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 19593786-6 2010 Microsomal M1 and M2 formation was most sensitive to the inhibition by a CYP2D6 inhibitor, paroxetine and a CYP3A4 inhibitor, ketoconazole, respectively. Ketoconazole 126-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 19497360-3 2010 Fold-induction of CYP3A4/5 by 1000muM PB and 10microM RIF were equivalent. Lead 38-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 19686701-0 2010 Retinoids activate RXR/CAR-mediated pathway and induce CYP3A. Retinoids 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 19686701-7 2010 The experimental data demonstrate that retinoids can effectively regulate CYP3A gene expression through the RXR/CAR-mediated pathway. Retinoids 39-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-79 19686701-2 2010 In this study, a panel of retinoids and carotenoids was examined to determine their effects on activation of RXR/CAR-mediated pathway and regulation of CYP3A gene expression. Retinoids 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-157 19686701-2 2010 In this study, a panel of retinoids and carotenoids was examined to determine their effects on activation of RXR/CAR-mediated pathway and regulation of CYP3A gene expression. Carotenoids 40-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-157 19898817-10 2010 Exposure of fathead minnow (FHM) cells with the CYP3A inducer rifampicin leads to dose-dependent increase in putative CYP3A enzyme activity. Rifampin 62-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 19686701-3 2010 Transient transfection assays of HepG2 cells revealed that five out of thirteen studied retinoids significantly induced RXRalpha/CAR-mediated activation of luciferase activity that is driven by the thymidine kinase promoter linked with a PXR binding site in the CYP3A4 gene [tk-(3A4)(3)-Luc reporter]. Retinoids 88-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 262-268 20068078-0 2010 A CYP3A4 phenotype-based dosing algorithm for individualized treatment of irinotecan. Irinotecan 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 2-8 20068078-1 2010 PURPOSE: Irinotecan, the prodrug of SN-38, is extensively metabolized by cytochrome P450-3A4 (CYP3A4). Irinotecan 9-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-92 20068078-1 2010 PURPOSE: Irinotecan, the prodrug of SN-38, is extensively metabolized by cytochrome P450-3A4 (CYP3A4). Irinotecan 9-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 20068078-1 2010 PURPOSE: Irinotecan, the prodrug of SN-38, is extensively metabolized by cytochrome P450-3A4 (CYP3A4). Irinotecan 36-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-92 20068078-1 2010 PURPOSE: Irinotecan, the prodrug of SN-38, is extensively metabolized by cytochrome P450-3A4 (CYP3A4). Irinotecan 36-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 20068078-2 2010 A randomized trial was done to assess the utility of an algorithm for individualized irinotecan dose calculation based on a priori CYP3A4 activity measurements by the midazolam clearance test. Irinotecan 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-137 20068078-11 2010 CONCLUSIONS: Incorporation of CYP3A4 phenotyping in dose calculation resulted in an improved predictability of the pharmacokinetic and toxicity profile of irinotecan, thereby lowering the incidence of severe neutropenia. Irinotecan 155-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 20068078-12 2010 In combination with UGT1A1*28 genotyping, CYP3A4 phenotype determination should be explored further as a strategy for the individualization of irinotecan treatment. Irinotecan 143-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 19907160-1 2010 PURPOSE: To explore the association between CYP3A4 and CYP3A5 gene polymorphisms and blood pressure response to amlodipine among participants from the African-American Study of Kidney Disease and Hypertension Trial randomized to amlodipine (n = 164). Amlodipine 112-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 19907160-8 2010 CONCLUSIONS: Our findings suggest that blood pressure response to amlodipine among high-risk African-Americans appears to be determined by CYP3A4 genotypes, and sex specificity may be an important consideration. Amlodipine 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 20305320-1 2010 BACKGROUND: Induction of the hepatic and intestinal cytochrome P450-3A4 system and intestinal P-glycoprotein is an unavoidable consequence of rifampin administration which requires substantial increase in tacrolimus dose when given concurrently. Rifampin 142-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-71 20305320-1 2010 BACKGROUND: Induction of the hepatic and intestinal cytochrome P450-3A4 system and intestinal P-glycoprotein is an unavoidable consequence of rifampin administration which requires substantial increase in tacrolimus dose when given concurrently. Tacrolimus 205-215 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-71 20040702-11 2010 Boosting of elvitegravir through inhibition of CYP3A4 metabolism has been investigated and suggests a pharmacokinetic profile conducive to once-daily-dosing. elvitegravir 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 19898817-10 2010 Exposure of fathead minnow (FHM) cells with the CYP3A inducer rifampicin leads to dose-dependent increase in putative CYP3A enzyme activity. Rifampin 62-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-123 19898817-11 2010 In contrast, inhibitory effects of diazepam treatment were observed on putative CYP3A enzyme activity and additionally on CYP3A126 mRNA expression. Diazepam 35-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-85 21041912-4 2010 RESULTS: Among the HIV-infected patients, the overall CYP3A activity (apparent oral midazolam clearance) was approximately 50% of the activity observed in healthy volunteers (point estimate 0.490, 90% confidence interval [CI] 0.377-0.638). Midazolam 84-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-59 20834094-3 2010 Etravirine is a weak inducer of cytochrome P450 (CYP)3A and a weak inhibitor of CYP2C9/CYP2C19 and P-glycoprotein, and although etravirine is metabolized by the CYP enzyme system, the extent of clinically relevant interactions with other antiretrovirals is limited. etravirine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-55 20000889-4 2010 OBJECTIVES: To accomplish a semi-mechanistic DDI model for a long-elimination-half-life drug substrate, tesofensine, and the cytochrome P450 (CYP) 3A4 inhibitor itraconazole, and to compare the results of the semi-mechanistic model with the results obtained from the standard NCA approach. Itraconazole 161-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-150 20157218-4 2010 Solifenacin is metabolized only by the CYP3A4, giving three inactive metabolites and one with a similar activity to the original compound. Solifenacin Succinate 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 20686242-3 2010 On the other hand, as ETV is a substrate and inducer of cytochrome P450 3A4 (CYP3A4), ETV may induce metabolism of PI and alter the concentrations of co-administered PIs. etravirine 22-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-75 20686242-3 2010 On the other hand, as ETV is a substrate and inducer of cytochrome P450 3A4 (CYP3A4), ETV may induce metabolism of PI and alter the concentrations of co-administered PIs. etravirine 22-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 20686242-3 2010 On the other hand, as ETV is a substrate and inducer of cytochrome P450 3A4 (CYP3A4), ETV may induce metabolism of PI and alter the concentrations of co-administered PIs. etravirine 86-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-75 20686242-3 2010 On the other hand, as ETV is a substrate and inducer of cytochrome P450 3A4 (CYP3A4), ETV may induce metabolism of PI and alter the concentrations of co-administered PIs. etravirine 86-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 20686242-3 2010 On the other hand, as ETV is a substrate and inducer of cytochrome P450 3A4 (CYP3A4), ETV may induce metabolism of PI and alter the concentrations of co-administered PIs. Monothiopyrophosphoric acid 166-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-75 20686242-3 2010 On the other hand, as ETV is a substrate and inducer of cytochrome P450 3A4 (CYP3A4), ETV may induce metabolism of PI and alter the concentrations of co-administered PIs. Monothiopyrophosphoric acid 166-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 20923245-15 2010 No dose adjustment of ambrisentan should be required when it is co-administered with rifampicin, a strong inducer of CYP3A4 activity and inhibitor of OATPs. Rifampin 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 20078610-2 2010 * Cilostazol undergoes extensive hepatic metabolism via the P450 enzymes, primarily CYP3A and, to a lesser extent, CYP2C19. Cilostazol 2-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-89 20923245-3 2010 OBJECTIVE: To assess the effects of rifampicin (rifampin), a potent inducer of CYP3A4 and inhibitor of organic anion transporter polypeptides (OATPs), on the steady-state pharmacokinetics, safety and tolerability of ambrisentan. Rifampin 36-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 20923245-3 2010 OBJECTIVE: To assess the effects of rifampicin (rifampin), a potent inducer of CYP3A4 and inhibitor of organic anion transporter polypeptides (OATPs), on the steady-state pharmacokinetics, safety and tolerability of ambrisentan. Rifampin 48-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 19833845-7 2010 Second, two known human CYP3A4 inducers, rifampicin and hyperforin, were tested in monkey and human primary hepatocytes for induction of CYP3A enzymes. Rifampin 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 20171411-1 2010 BACKGROUND: Bosentan is an endothelin-receptor antagonist that reportedly induces both cytochrome P450 (CYP) 3A4 and CYP2C9 enzymes, which are also involved in warfarin metabolism. Bosentan 12-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-112 20171411-1 2010 BACKGROUND: Bosentan is an endothelin-receptor antagonist that reportedly induces both cytochrome P450 (CYP) 3A4 and CYP2C9 enzymes, which are also involved in warfarin metabolism. Warfarin 160-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-112 20171411-7 2010 CONCLUSIONS: Bosentan has CYP3A4- and CYP2C9-inducing properties and is therefore likely to cause decreased concentrations of warfarin. Bosentan 13-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 19797611-6 2010 In cells arrested in S phase by a thymidine block and then released into a synchronous cell cycle, there was a clear dissociation among the activation of CDK2 and the expression of UGT1A1, CYP2B6, and CYP3A4. Thymidine 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-207 19833845-7 2010 Second, two known human CYP3A4 inducers, rifampicin and hyperforin, were tested in monkey and human primary hepatocytes for induction of CYP3A enzymes. Rifampin 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 19797611-7 2010 Furthermore, the induction of CYP3A4 but not UGT1A1 or CYP2B6 mRNA expression by roscovitine was repressed in pregnane X receptor (PXR) siRNA-transfected HepG2 cells. Roscovitine 81-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 19797609-0 2010 Exploration of catalytic properties of CYP2D6 and CYP3A4 through metabolic studies of levorphanol and levallorphan. Levorphanol 86-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 19833845-7 2010 Second, two known human CYP3A4 inducers, rifampicin and hyperforin, were tested in monkey and human primary hepatocytes for induction of CYP3A enzymes. hyperforin 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 19797609-0 2010 Exploration of catalytic properties of CYP2D6 and CYP3A4 through metabolic studies of levorphanol and levallorphan. Levallorphan 102-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 19797609-4 2010 Detailed metabolite identification, reversible inhibition, and time-dependent inhibition were examined for levorphanol and levallorphan with CYP2D6 and CYP3A4. Levorphanol 107-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 19797609-4 2010 Detailed metabolite identification, reversible inhibition, and time-dependent inhibition were examined for levorphanol and levallorphan with CYP2D6 and CYP3A4. Levallorphan 123-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 19797609-6 2010 The metabolite identification revealed that CYP3A4 catalyzed the formation of a variety of metabolites as a result of presenting different parts of the substrates to the heme. Heme 170-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 19797609-9 2010 Levallorphan acted as a time-dependent inhibitor on CYP3A4, indicating a productive binding mode with this enzyme not observed with CYP2D6 that presumably resulted from close interactions of the N-allyl moiety oriented toward the heme. Levallorphan 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 19797609-9 2010 Levallorphan acted as a time-dependent inhibitor on CYP3A4, indicating a productive binding mode with this enzyme not observed with CYP2D6 that presumably resulted from close interactions of the N-allyl moiety oriented toward the heme. Heme 230-234 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 19812348-10 2010 These studies showed that CYP2C19 contributed substantially to both oxidative steps required in the formation of clopidogrel active metabolite and that CYP3A4 contributed substantially to the second oxidative step. Clopidogrel 113-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 19833845-7 2010 Second, two known human CYP3A4 inducers, rifampicin and hyperforin, were tested in monkey and human primary hepatocytes for induction of CYP3A enzymes. hyperforin 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 19797611-3 2010 The CDK inhibitor roscovitine also enhanced the expression of UGT1A1, CYP2B6, and CYP3A4. Roscovitine 18-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 19841059-3 2010 Voriconazole is cleared predominantly via hepatic metabolism in adults, mainly by CYP3A4, CYP2C19, and flavin-containing monooxygenase 3 (FMO3). Voriconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 20201779-0 2010 An evaluation of ondansetron binding interactions with human cytochrome P450 enzymes CYP3A4 and CYP2D6. Ondansetron 17-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 20201779-1 2010 The results of an evaluation study of ondansetron binding to human cytochromes P450 CYP3A4 and CYP2D6 is reported. Ondansetron 38-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 20201775-1 2010 OBJECTIVE: To investigate the effects of black seed on the metabolic activities of CYP3A4 and CYP2D6 in human liver microsomes and in human subjects using dextromethorphan as a probe drug. Dextromethorphan 155-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 20201775-2 2010 METHODS: CYP2D6-mediated O-demethylation and CYP3A4-mediated N-demethylation of dextromethorphan (DEX) to dextrorphan (DOR) and 3-methoxymorphinan (3-MM), respectively, were utilized to assess the metabolic activities of the two enzymatic pathways. Dextromethorphan 80-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 20201775-2 2010 METHODS: CYP2D6-mediated O-demethylation and CYP3A4-mediated N-demethylation of dextromethorphan (DEX) to dextrorphan (DOR) and 3-methoxymorphinan (3-MM), respectively, were utilized to assess the metabolic activities of the two enzymatic pathways. Dextromethorphan 98-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 20201775-2 2010 METHODS: CYP2D6-mediated O-demethylation and CYP3A4-mediated N-demethylation of dextromethorphan (DEX) to dextrorphan (DOR) and 3-methoxymorphinan (3-MM), respectively, were utilized to assess the metabolic activities of the two enzymatic pathways. Dextrorphan 106-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 20201779-3 2010 It is shown that there is a generally good agreement between the experimental and calculated binding affinities for ondansetron towards CYP2D6 and CYP3A4 enzymes, based on interactive docking studies. Ondansetron 116-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 20814160-2 2010 Low activities for dealkylation of ethoxyresorufin and pentoxyresorufin were seen in recombinant monkey mfCYP3A4 and mfCYP3A5 and in recombinant human CYP3A4 and CYP3A5 expressed in bacterial membranes. ethoxyresorufin 35-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 20201779-4 2010 Moreover, the modelled binding orientations for ondansetron in CYP2D6 and CYP3A4 are largely consistent with the NMR data and with the known routes for P450-mediated metabolism of this compound. Ondansetron 48-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 20208386-5 2010 Gemfibrozil and bupropion represent examples of glucuronidation-dependent and reduction-dependent activation to metabolites that inhibit CYP2C8 and CYP2D6, respectively, whereas ezetimibe represents an example of glucuronidation-dependent protection against metabolism-dependent inhibition of CYP3A4. Gemfibrozil 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 293-299 20208386-5 2010 Gemfibrozil and bupropion represent examples of glucuronidation-dependent and reduction-dependent activation to metabolites that inhibit CYP2C8 and CYP2D6, respectively, whereas ezetimibe represents an example of glucuronidation-dependent protection against metabolism-dependent inhibition of CYP3A4. Ezetimibe 178-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 293-299 20201775-2 2010 METHODS: CYP2D6-mediated O-demethylation and CYP3A4-mediated N-demethylation of dextromethorphan (DEX) to dextrorphan (DOR) and 3-methoxymorphinan (3-MM), respectively, were utilized to assess the metabolic activities of the two enzymatic pathways. Dextrorphan 119-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 20201775-2 2010 METHODS: CYP2D6-mediated O-demethylation and CYP3A4-mediated N-demethylation of dextromethorphan (DEX) to dextrorphan (DOR) and 3-methoxymorphinan (3-MM), respectively, were utilized to assess the metabolic activities of the two enzymatic pathways. 3-methoxymorphinan 128-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 20201775-10 2010 CONCLUSION: Black seed significantly inhibited CYP2D6 and CYP3A4 mediated metabolism of DEX in human liver microsomes and healthy human volunteers indicating that it has the potential to interact with CYP2D6 and CYP3A4 substrates. Dextromethorphan 88-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 20201775-10 2010 CONCLUSION: Black seed significantly inhibited CYP2D6 and CYP3A4 mediated metabolism of DEX in human liver microsomes and healthy human volunteers indicating that it has the potential to interact with CYP2D6 and CYP3A4 substrates. Dextromethorphan 88-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 212-218 20201776-3 2010 Since EFV is most commonly used with ATV and RTV, the known CYP inhibitors, we evaluated the effects of combinations of these agents on the CYP3A4 induction by EFV. efavirenz 160-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 20201776-4 2010 We determined the induction of CYP3A4 by EFV, RTV, ATV, EFV+RTV, EFV+ATV, EFV+RTV+ATV and rifampicin (RIF) employing primary human hepatocytes from 3 donors. efavirenz 41-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 20201776-4 2010 We determined the induction of CYP3A4 by EFV, RTV, ATV, EFV+RTV, EFV+ATV, EFV+RTV+ATV and rifampicin (RIF) employing primary human hepatocytes from 3 donors. Ritonavir 46-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 20201776-4 2010 We determined the induction of CYP3A4 by EFV, RTV, ATV, EFV+RTV, EFV+ATV, EFV+RTV+ATV and rifampicin (RIF) employing primary human hepatocytes from 3 donors. efavirenz 56-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 20201776-4 2010 We determined the induction of CYP3A4 by EFV, RTV, ATV, EFV+RTV, EFV+ATV, EFV+RTV+ATV and rifampicin (RIF) employing primary human hepatocytes from 3 donors. Ritonavir 60-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 20201776-4 2010 We determined the induction of CYP3A4 by EFV, RTV, ATV, EFV+RTV, EFV+ATV, EFV+RTV+ATV and rifampicin (RIF) employing primary human hepatocytes from 3 donors. efavirenz 56-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 20201776-4 2010 We determined the induction of CYP3A4 by EFV, RTV, ATV, EFV+RTV, EFV+ATV, EFV+RTV+ATV and rifampicin (RIF) employing primary human hepatocytes from 3 donors. Atazanavir Sulfate 69-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 20201776-4 2010 We determined the induction of CYP3A4 by EFV, RTV, ATV, EFV+RTV, EFV+ATV, EFV+RTV+ATV and rifampicin (RIF) employing primary human hepatocytes from 3 donors. efavirenz 56-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 20814160-3 2010 Hydroxylation activities of mfCYP3A4 and mfCYP3A5 toward coumarin, paclitaxel, diclofenac, flurbiprofen, and S-mephenytoin were below detectable levels, as was also true for CYP3A4 and CYP3A5. coumarin 57-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 20814160-3 2010 Hydroxylation activities of mfCYP3A4 and mfCYP3A5 toward coumarin, paclitaxel, diclofenac, flurbiprofen, and S-mephenytoin were below detectable levels, as was also true for CYP3A4 and CYP3A5. Paclitaxel 67-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 20814160-3 2010 Hydroxylation activities of mfCYP3A4 and mfCYP3A5 toward coumarin, paclitaxel, diclofenac, flurbiprofen, and S-mephenytoin were below detectable levels, as was also true for CYP3A4 and CYP3A5. Diclofenac 79-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 20814160-3 2010 Hydroxylation activities of mfCYP3A4 and mfCYP3A5 toward coumarin, paclitaxel, diclofenac, flurbiprofen, and S-mephenytoin were below detectable levels, as was also true for CYP3A4 and CYP3A5. Flurbiprofen 91-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 20814160-3 2010 Hydroxylation activities of mfCYP3A4 and mfCYP3A5 toward coumarin, paclitaxel, diclofenac, flurbiprofen, and S-mephenytoin were below detectable levels, as was also true for CYP3A4 and CYP3A5. Mephenytoin 109-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 20201776-4 2010 We determined the induction of CYP3A4 by EFV, RTV, ATV, EFV+RTV, EFV+ATV, EFV+RTV+ATV and rifampicin (RIF) employing primary human hepatocytes from 3 donors. Ritonavir 60-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 20201776-4 2010 We determined the induction of CYP3A4 by EFV, RTV, ATV, EFV+RTV, EFV+ATV, EFV+RTV+ATV and rifampicin (RIF) employing primary human hepatocytes from 3 donors. Atazanavir Sulfate 69-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 20201776-4 2010 We determined the induction of CYP3A4 by EFV, RTV, ATV, EFV+RTV, EFV+ATV, EFV+RTV+ATV and rifampicin (RIF) employing primary human hepatocytes from 3 donors. Rifampin 90-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 20201776-4 2010 We determined the induction of CYP3A4 by EFV, RTV, ATV, EFV+RTV, EFV+ATV, EFV+RTV+ATV and rifampicin (RIF) employing primary human hepatocytes from 3 donors. Rifampin 102-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 20814160-2 2010 Low activities for dealkylation of ethoxyresorufin and pentoxyresorufin were seen in recombinant monkey mfCYP3A4 and mfCYP3A5 and in recombinant human CYP3A4 and CYP3A5 expressed in bacterial membranes. pentoxyresorufin 55-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 20201776-6 2010 CYP3A4 activity (testosterone-6beta-hydroxylation) was induced by EFV (3 fold) and RIF (4 fold), but was significantly suppressed in the presence of RTV and ATV. testosterone-6beta 17-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 19883715-0 2010 Inhibitory effects of polyphenols on human cytochrome P450 3A4 and 2C9 activity. Polyphenols 22-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-70 20201776-6 2010 CYP3A4 activity (testosterone-6beta-hydroxylation) was induced by EFV (3 fold) and RIF (4 fold), but was significantly suppressed in the presence of RTV and ATV. efavirenz 66-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20201776-6 2010 CYP3A4 activity (testosterone-6beta-hydroxylation) was induced by EFV (3 fold) and RIF (4 fold), but was significantly suppressed in the presence of RTV and ATV. Ritonavir 149-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20201776-6 2010 CYP3A4 activity (testosterone-6beta-hydroxylation) was induced by EFV (3 fold) and RIF (4 fold), but was significantly suppressed in the presence of RTV and ATV. Atazanavir Sulfate 157-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 20201776-9 2010 However, in primary hepatocytes the net effect was suppression of EFV mediated CYP3A4 induction by RTV and ATV. Ritonavir 99-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 20201776-9 2010 However, in primary hepatocytes the net effect was suppression of EFV mediated CYP3A4 induction by RTV and ATV. Atazanavir Sulfate 107-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 20201776-10 2010 This observation corresponds to the clinical observations of attenuated CYP3A4 induction by EFV induction in the presence of RTV and other protease inhibitors (PIs). efavirenz 92-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 19883715-3 2010 In this study, we systematically evaluated the inhibitory effects of 60 polyphenols and related compounds on human cytochrome P450 (CYP) 3A4 and CYP2C9 activity by in vitro assay to investigate whether some polyphenols induce drug interactions. Polyphenols 72-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-140 19959402-3 2010 The metabolic ratio (MR) of the concentration of 6beta-hydroxycortisol (6beta-OHC) to cortisol (MR 6beta-OHC/cortisol) in human urine had been proposed as an endogenous marker for CYP3A activity. Hydrocortisone 86-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-185 19784640-0 2010 CYP3A4*1G genetic polymorphism influences CYP3A activity and response to fentanyl in Chinese gynecologic patients. Fentanyl 73-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 19784640-0 2010 CYP3A4*1G genetic polymorphism influences CYP3A activity and response to fentanyl in Chinese gynecologic patients. Fentanyl 73-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 19784640-1 2010 PURPOSE: To investigate whether the CYP3A4*1G genetic polymorphism contributes to the variability in CYP3A activity and response to fentanyl. Fentanyl 132-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 19784640-1 2010 PURPOSE: To investigate whether the CYP3A4*1G genetic polymorphism contributes to the variability in CYP3A activity and response to fentanyl. Fentanyl 132-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 19784640-6 2010 CYP3A activity was measured by plasma 1"-hydroxymidazolam-to-midazolam ratio 1 h after intravenous administration of 0.1 mg/kg midazolam. 1-hydroxymethylmidazolam 38-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 19784640-6 2010 CYP3A activity was measured by plasma 1"-hydroxymidazolam-to-midazolam ratio 1 h after intravenous administration of 0.1 mg/kg midazolam. Midazolam 60-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 19784640-6 2010 CYP3A activity was measured by plasma 1"-hydroxymidazolam-to-midazolam ratio 1 h after intravenous administration of 0.1 mg/kg midazolam. Midazolam 48-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 19784640-10 2010 The patients with the CYP3A4*1G/*1G genotype needed less fentanyl (227.8 +/- 55.2 microg) to achieve pain control than patients carrying the CYP3A4*1/*1 (381.6 +/- 163.6 microg) and CYP3A4*1/*1G (371.9 +/- 180.1 microg) genotypes (P < 0.05) during the first 24 h postoperatively. Fentanyl 57-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 19784640-12 2010 CONCLUSIONS: CYP3A4*1G genetic polymorphism decreases CYP3A activity and fentanyl consumption for postoperative pain control. Fentanyl 73-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 19784640-12 2010 CONCLUSIONS: CYP3A4*1G genetic polymorphism decreases CYP3A activity and fentanyl consumption for postoperative pain control. Fentanyl 73-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-18 19959402-3 2010 The metabolic ratio (MR) of the concentration of 6beta-hydroxycortisol (6beta-OHC) to cortisol (MR 6beta-OHC/cortisol) in human urine had been proposed as an endogenous marker for CYP3A activity. 6 beta-hydroxycortisol 49-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-185 19959402-3 2010 The metabolic ratio (MR) of the concentration of 6beta-hydroxycortisol (6beta-OHC) to cortisol (MR 6beta-OHC/cortisol) in human urine had been proposed as an endogenous marker for CYP3A activity. 6beta-ohc 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-185 19959402-3 2010 The metabolic ratio (MR) of the concentration of 6beta-hydroxycortisol (6beta-OHC) to cortisol (MR 6beta-OHC/cortisol) in human urine had been proposed as an endogenous marker for CYP3A activity. Hydrocortisone 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-185 20016682-2 2010 1,25-dihydroxycholecalciferol activates CYP3A4, an enzyme of the cytochrome P450 system, which metabolizes atorvastatin to its main metabolites. Calcitriol 0-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 20016682-2 2010 1,25-dihydroxycholecalciferol activates CYP3A4, an enzyme of the cytochrome P450 system, which metabolizes atorvastatin to its main metabolites. Atorvastatin 107-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 21152245-9 2010 Strong correlations between allelic variation in the tamoxifen pathway at CYP1A1-CYP3A4, CYP3A4-CYP2C9, and CYP2C9-SULT1A2, in addition to CYP2D6 and its adjacent genes, were seen in the placebo-arm but not the tamoxifen-arm. Tamoxifen 53-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-102 19943026-3 2010 All protease inhibitors are inhibitors of CYP3A, which is important in the metabolism of approximately 50% of all drugs, e.g. simvastatin, atorvastatin, sildenafil, and clarithromycin. Simvastatin 126-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 19943026-3 2010 All protease inhibitors are inhibitors of CYP3A, which is important in the metabolism of approximately 50% of all drugs, e.g. simvastatin, atorvastatin, sildenafil, and clarithromycin. Atorvastatin 139-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 19943026-3 2010 All protease inhibitors are inhibitors of CYP3A, which is important in the metabolism of approximately 50% of all drugs, e.g. simvastatin, atorvastatin, sildenafil, and clarithromycin. Sildenafil Citrate 153-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 19943026-3 2010 All protease inhibitors are inhibitors of CYP3A, which is important in the metabolism of approximately 50% of all drugs, e.g. simvastatin, atorvastatin, sildenafil, and clarithromycin. Clarithromycin 169-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 19943026-4 2010 Among the protease inhibitors, ritonavir is the strongest inhibitor of CYP3A activity. Ritonavir 31-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-76 19959402-3 2010 The metabolic ratio (MR) of the concentration of 6beta-hydroxycortisol (6beta-OHC) to cortisol (MR 6beta-OHC/cortisol) in human urine had been proposed as an endogenous marker for CYP3A activity. 6beta-ohc 99-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-185 19755414-1 2010 The aim of this study is to determine whether the inhibition of CYP2D6 and CYP3A4 enzyme activity with telithromycin affects the pharmacokinetics and pharmacodynamics of orally administered oxycodone in a randomized 2-phase crossover study. telithromycin 103-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 19755414-1 2010 The aim of this study is to determine whether the inhibition of CYP2D6 and CYP3A4 enzyme activity with telithromycin affects the pharmacokinetics and pharmacodynamics of orally administered oxycodone in a randomized 2-phase crossover study. Oxycodone 190-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 19959402-5 2010 [(2)H(2)]6beta-OHC was prepared by incubation of human recombinant CYP3A4 with commercially available [(2)H(2)]cortisol. [(2)h(2)]6beta-ohc 0-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 19959402-5 2010 [(2)H(2)]6beta-OHC was prepared by incubation of human recombinant CYP3A4 with commercially available [(2)H(2)]cortisol. [(2)h(2)]cortisol 102-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 19585271-2 2010 Genetic variants of CYP3A7 are associated with serum estrone level, bone density, and hepatic CYP3A activity in adults. Estrone 53-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-25 21105332-4 2010 In this review we present results of studies assessing effect of various allele variants of CYP3A4 and CYP3A5 on efficacy and tolerability of atorvastatin, lovastatin,, and simvastatin in different populations of patients. Atorvastatin 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 21105332-4 2010 In this review we present results of studies assessing effect of various allele variants of CYP3A4 and CYP3A5 on efficacy and tolerability of atorvastatin, lovastatin,, and simvastatin in different populations of patients. Lovastatin 156-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 21105332-4 2010 In this review we present results of studies assessing effect of various allele variants of CYP3A4 and CYP3A5 on efficacy and tolerability of atorvastatin, lovastatin,, and simvastatin in different populations of patients. Simvastatin 173-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 19931478-9 2010 We have shown that HIV-1 protease drugs such as tipranavir, nelfinavir, lopinavir, and atazanavir differ in their binding modes on each other for metabolic clearance in CYP3A4, whereas ritonavir, amprenavir, indinavir, saquinavir, fosamprenavir, and darunavir share the same binding mode. Nelfinavir 60-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 19931478-9 2010 We have shown that HIV-1 protease drugs such as tipranavir, nelfinavir, lopinavir, and atazanavir differ in their binding modes on each other for metabolic clearance in CYP3A4, whereas ritonavir, amprenavir, indinavir, saquinavir, fosamprenavir, and darunavir share the same binding mode. Lopinavir 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 19931478-9 2010 We have shown that HIV-1 protease drugs such as tipranavir, nelfinavir, lopinavir, and atazanavir differ in their binding modes on each other for metabolic clearance in CYP3A4, whereas ritonavir, amprenavir, indinavir, saquinavir, fosamprenavir, and darunavir share the same binding mode. Atazanavir Sulfate 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 19931478-9 2010 We have shown that HIV-1 protease drugs such as tipranavir, nelfinavir, lopinavir, and atazanavir differ in their binding modes on each other for metabolic clearance in CYP3A4, whereas ritonavir, amprenavir, indinavir, saquinavir, fosamprenavir, and darunavir share the same binding mode. Saquinavir 219-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 19931478-9 2010 We have shown that HIV-1 protease drugs such as tipranavir, nelfinavir, lopinavir, and atazanavir differ in their binding modes on each other for metabolic clearance in CYP3A4, whereas ritonavir, amprenavir, indinavir, saquinavir, fosamprenavir, and darunavir share the same binding mode. fosamprenavir 231-244 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 19931478-9 2010 We have shown that HIV-1 protease drugs such as tipranavir, nelfinavir, lopinavir, and atazanavir differ in their binding modes on each other for metabolic clearance in CYP3A4, whereas ritonavir, amprenavir, indinavir, saquinavir, fosamprenavir, and darunavir share the same binding mode. Darunavir 250-259 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 19802823-0 2010 Influence of genetic variation in CYP3A4 and ABCB1 on dose decrease or switching during simvastatin and atorvastatin therapy. Simvastatin 88-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 20829626-7 2010 The use of ketoconazole, a potent inhibitor of cytochrome P450 3A4 (CYP3A4), may significantly increase plasma concentrations of certain statins (such as simvastatin and atorvastatin) that undergo metabolism by the same pathway, thus increasing the risk of complications and side effects. Ketoconazole 11-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-66 20829626-7 2010 The use of ketoconazole, a potent inhibitor of cytochrome P450 3A4 (CYP3A4), may significantly increase plasma concentrations of certain statins (such as simvastatin and atorvastatin) that undergo metabolism by the same pathway, thus increasing the risk of complications and side effects. Ketoconazole 11-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 20829626-7 2010 The use of ketoconazole, a potent inhibitor of cytochrome P450 3A4 (CYP3A4), may significantly increase plasma concentrations of certain statins (such as simvastatin and atorvastatin) that undergo metabolism by the same pathway, thus increasing the risk of complications and side effects. Simvastatin 154-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-66 20829626-7 2010 The use of ketoconazole, a potent inhibitor of cytochrome P450 3A4 (CYP3A4), may significantly increase plasma concentrations of certain statins (such as simvastatin and atorvastatin) that undergo metabolism by the same pathway, thus increasing the risk of complications and side effects. Simvastatin 154-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 20829626-7 2010 The use of ketoconazole, a potent inhibitor of cytochrome P450 3A4 (CYP3A4), may significantly increase plasma concentrations of certain statins (such as simvastatin and atorvastatin) that undergo metabolism by the same pathway, thus increasing the risk of complications and side effects. Atorvastatin 170-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-66 20829626-7 2010 The use of ketoconazole, a potent inhibitor of cytochrome P450 3A4 (CYP3A4), may significantly increase plasma concentrations of certain statins (such as simvastatin and atorvastatin) that undergo metabolism by the same pathway, thus increasing the risk of complications and side effects. Atorvastatin 170-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-74 22966274-3 2010 The purpose of this study was to evaluate the possible relationship between paclitaxel-induced neurotoxicity and the distribution of genetic variations with reported functional significance in the ABCB1, CYP2C8 and CYP3A4 genes that are all implicated in taxol metabolism. Paclitaxel 76-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-221 22966274-3 2010 The purpose of this study was to evaluate the possible relationship between paclitaxel-induced neurotoxicity and the distribution of genetic variations with reported functional significance in the ABCB1, CYP2C8 and CYP3A4 genes that are all implicated in taxol metabolism. Paclitaxel 255-260 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-221 19802823-0 2010 Influence of genetic variation in CYP3A4 and ABCB1 on dose decrease or switching during simvastatin and atorvastatin therapy. Atorvastatin 104-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 19802823-1 2010 PURPOSE: Simvastatin and atorvastatin are metabolized by the CYP3A4 enzyme and transported by the ABCB1 transporter. Simvastatin 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 19802823-1 2010 PURPOSE: Simvastatin and atorvastatin are metabolized by the CYP3A4 enzyme and transported by the ABCB1 transporter. Atorvastatin 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 19802823-5 2010 Associations between the polymorphisms in the CYP3A4 and ABCB1 gene and the time to a decrease in dose or a switch to another cholesterol lowering drug were studied using Cox proportional hazards. Cholesterol 126-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 19802823-6 2010 RESULTS: Simvastatin and atorvastatin users with the CYP3A4*1B variant G allele had a lower risk (HR 0.46; 95%CI 0.24-0.90) for these events than users with the wild-type AA genotype. Simvastatin 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 19802823-6 2010 RESULTS: Simvastatin and atorvastatin users with the CYP3A4*1B variant G allele had a lower risk (HR 0.46; 95%CI 0.24-0.90) for these events than users with the wild-type AA genotype. Atorvastatin 25-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 19802823-10 2010 CONCLUSION: In simvastatin and atorvastatin users, the CYP3A4*1B G allele is associated with a lower risk of elevated statin plasma levels, particularly in women and in users with the ABCB1 3435T variant allele. Simvastatin 15-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 20523106-0 2010 CYP3A4 genetic polymorphism influences repaglinide"s pharmacokinetics. repaglinide 39-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 19802823-10 2010 CONCLUSION: In simvastatin and atorvastatin users, the CYP3A4*1B G allele is associated with a lower risk of elevated statin plasma levels, particularly in women and in users with the ABCB1 3435T variant allele. Atorvastatin 31-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 20523106-1 2010 AIM: To investigate the effects of CYP3A4 and CYP2C8 enzymes on repaglinide"s pharmacokinetics in healthy Malaysian subjects. repaglinide 64-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 19905875-6 2010 In conclusion, the time-dependent inhibition of CYP3A4 by diazepam was attenuated by DMSO, while acetonitrile and methanol had no effect. Diazepam 58-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 20523106-8 2010 However, the CYP3A4 genotype significantly influenced some of repaglinide"s pharmacokinetics, where the mean elimination rate constant was 44.0% lower (p = 0.04) and the mean half-life was 33.8% higher (p = 0.04) in subjects with the CYP3A4*1/*18 genotype as compared to those with the normal CYP3A4*1/*1 genotype. repaglinide 62-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 20523106-8 2010 However, the CYP3A4 genotype significantly influenced some of repaglinide"s pharmacokinetics, where the mean elimination rate constant was 44.0% lower (p = 0.04) and the mean half-life was 33.8% higher (p = 0.04) in subjects with the CYP3A4*1/*18 genotype as compared to those with the normal CYP3A4*1/*1 genotype. repaglinide 62-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 234-240 20523106-8 2010 However, the CYP3A4 genotype significantly influenced some of repaglinide"s pharmacokinetics, where the mean elimination rate constant was 44.0% lower (p = 0.04) and the mean half-life was 33.8% higher (p = 0.04) in subjects with the CYP3A4*1/*18 genotype as compared to those with the normal CYP3A4*1/*1 genotype. repaglinide 62-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 234-240 20523106-9 2010 This result confirms that CYP3A4 plays a large role in metabolizing repaglinide. repaglinide 68-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 20523106-10 2010 CONCLUSION: Genetic polymorphisms of CYP3A4, specifically CYP3A4*18, play a major role in contributing to the interindividual variability in repaglinide"s pharmacokinetics. repaglinide 141-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 20523106-10 2010 CONCLUSION: Genetic polymorphisms of CYP3A4, specifically CYP3A4*18, play a major role in contributing to the interindividual variability in repaglinide"s pharmacokinetics. repaglinide 141-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 20205992-4 2010 Zonisamide is well absorbed with maximum concentration achieved in 2 to 5 h. It is partly metabolized by the CYP3A4. Zonisamide 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 19883238-3 2010 Although the safety profile of resveratrol has been minimally investigated in humans, resveratrol has been associated with observations of toxicity in vitro, and has been identified as a mechanism-based inhibitor of cytochrome P450 3A4. Resveratrol 86-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-235 19905875-0 2010 Effects of organic solvents on the time-dependent inhibition of CYP3A4 by diazepam. Diazepam 74-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 19905875-6 2010 In conclusion, the time-dependent inhibition of CYP3A4 by diazepam was attenuated by DMSO, while acetonitrile and methanol had no effect. Dimethyl Sulfoxide 85-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 19905875-2 2010 The inactivation kinetics of CYP3A4 by diazepam dissolved in acetonitrile and methanol were almost equal with k(inact)/K(I) values, 0.095 and 0.15 min(-1) mM(-1) for HLM and 1.1 and 1.4 min(-1) mM(-1) for rCYP3A4, respectively. Diazepam 39-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 19905875-7 2010 The metabolite formation profile under the conditions tested suggested that DMSO competitively inhibit the formation of the reactive metabolites of diazepam by CYP3A4. Dimethyl Sulfoxide 76-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 19905875-2 2010 The inactivation kinetics of CYP3A4 by diazepam dissolved in acetonitrile and methanol were almost equal with k(inact)/K(I) values, 0.095 and 0.15 min(-1) mM(-1) for HLM and 1.1 and 1.4 min(-1) mM(-1) for rCYP3A4, respectively. acetonitrile 61-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 19905875-2 2010 The inactivation kinetics of CYP3A4 by diazepam dissolved in acetonitrile and methanol were almost equal with k(inact)/K(I) values, 0.095 and 0.15 min(-1) mM(-1) for HLM and 1.1 and 1.4 min(-1) mM(-1) for rCYP3A4, respectively. Methanol 78-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 19905875-7 2010 The metabolite formation profile under the conditions tested suggested that DMSO competitively inhibit the formation of the reactive metabolites of diazepam by CYP3A4. Diazepam 148-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 20001672-0 2010 CYP3A catalyses schizandrin biotransformation in human, minipig and rat liver microsomes. schizandrin 16-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 20001672-4 2010 A combination of correlation analysis, chemical inhibition studies, assays with recombinant CYPs, and enzyme kinetics indicated that CYP3A4 was the main hepatic isoform that cleared schizandrin. schizandrin 182-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 20001672-6 2010 In conclusion, CYP3A4 plays a major role in the biotransformation of schizandrin in human liver microsomes. schizandrin 69-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 19766177-0 2009 CYP1A1 and CYP3A4 modulation by dietary flavonoids in human intestinal Caco-2 cells. Flavonoids 40-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 21042038-0 2010 In vitro and in vivo inhibitory effects of glycyrrhetinic acid on cytochrome P450 3A activity. Glycyrrhetinic Acid 43-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-84 21042038-3 2010 We have assessed the ability of GA to inhibit the enzyme cytochrome P450 3A (CYP3A). Glycyrrhetinic Acid 32-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-75 21042038-3 2010 We have assessed the ability of GA to inhibit the enzyme cytochrome P450 3A (CYP3A). Glycyrrhetinic Acid 32-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 21042038-4 2010 A Lineweaver-Burk plot showed that GA was a mixed inhibitor of CYP3A, with an IC50 of 7.25 mumol/l, a K(m) of 4.3 mumol/l and a K(i) of 6.4 mumol/l by non-linear regression analysis. Glycyrrhetinic Acid 35-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 21042038-5 2010 CYP3A activity was also affected by intragastric administration of GA, which resulted in increases in area under the plasma concentration-time curve (AUC)(0-t) and in apparent elimination half-time (t1/2) and significant decreases in body clearance, as well as in the formation of 1-hydroxy-midazolam after intragastric or intravenous administration of midazolam (p < 0.05). Glycyrrhetinic Acid 67-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 21042038-5 2010 CYP3A activity was also affected by intragastric administration of GA, which resulted in increases in area under the plasma concentration-time curve (AUC)(0-t) and in apparent elimination half-time (t1/2) and significant decreases in body clearance, as well as in the formation of 1-hydroxy-midazolam after intragastric or intravenous administration of midazolam (p < 0.05). 1-hydroxymethylmidazolam 281-300 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 21042038-5 2010 CYP3A activity was also affected by intragastric administration of GA, which resulted in increases in area under the plasma concentration-time curve (AUC)(0-t) and in apparent elimination half-time (t1/2) and significant decreases in body clearance, as well as in the formation of 1-hydroxy-midazolam after intragastric or intravenous administration of midazolam (p < 0.05). Midazolam 291-300 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 19679108-7 2009 The data revealed that the major hepatic isozymes responsible for the formation of each metabolite are as follows: CYP3A4 (ethylene-hydroxylated glyburide (M5), 3-trans-(M3) and 2-trans-(M4) cyclohexyl glyburide); CYP2C9 (M1, M2a (4-cis-) and M2b); CYP2C8 (M1 and M2b); and CYP2C19 (M2a). ethylene-hydroxylated glyburide 123-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 19766177-9 2009 Quercetin was also shown to significantly inhibit the constitutive CYP3A4 activity, measured by the 6beta-(OH)-testosterone assay, and to impair its induction by 1,25-vitamin D(3). Quercetin 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 19766177-9 2009 Quercetin was also shown to significantly inhibit the constitutive CYP3A4 activity, measured by the 6beta-(OH)-testosterone assay, and to impair its induction by 1,25-vitamin D(3). 6beta-(oh)-testosterone 100-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 19766177-10 2009 Chrysin, quercetin and genistein, were detected as significant inhibitors of the 1,25-vitamin D(3)-induced CYP3A4 activity. chrysin 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 19766177-10 2009 Chrysin, quercetin and genistein, were detected as significant inhibitors of the 1,25-vitamin D(3)-induced CYP3A4 activity. Quercetin 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 19766177-10 2009 Chrysin, quercetin and genistein, were detected as significant inhibitors of the 1,25-vitamin D(3)-induced CYP3A4 activity. Genistein 23-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 19766177-10 2009 Chrysin, quercetin and genistein, were detected as significant inhibitors of the 1,25-vitamin D(3)-induced CYP3A4 activity. 1,25-vitamin d(3) 81-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 19775168-3 2009 We have discovered a novel series of azetidinyl ketolides that focus on mitigation of hepatotoxicity by minimizing hepatic turnover and time-dependent inactivation of CYP3A isoforms in the liver without compromising the potency and efficacy of 1. azetidinyl ketolides 37-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 167-172 19664894-0 2009 Validation of a new HPLC method for determination of midazolam and its metabolites: application to determine its pharmacokinetics in human and measure hepatic CYP3A activity in rabbits. Midazolam 53-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-164 20002085-1 2009 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: * Pharmacokinetic variability of voriconazole is largely caused by CYP3A4- and CYP2C19-mediated metabolism. Voriconazole 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 20002087-4 2009 * Therefore ritonavir is an appropriate positive control inhibitor for clinical drug interaction studies involving CYP3A substrates. Ritonavir 12-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 20002087-7 2009 The study also determined whether 4,4-dimethyl-benziso-(2H)-selenazine (ALT-2074), an investigational organoselenium compound that acts as a catalytic mimic of glutathione oxidase, inhibits CYP3A metabolism in vivo. 4,4-dimethyl-benziso-(2h)-selenazine 34-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-195 20002087-7 2009 The study also determined whether 4,4-dimethyl-benziso-(2H)-selenazine (ALT-2074), an investigational organoselenium compound that acts as a catalytic mimic of glutathione oxidase, inhibits CYP3A metabolism in vivo. BXT-51072 72-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 190-195 20002087-11 2009 CONCLUSIONS: Low-dose ritonavir produces extensive CYP3A inhibition exceeding that of ketoconazole (typically 10- to 15-fold midazolam AUC enhancement), and is a suitable positive control index inhibitor for drug-drug interaction studies. Ritonavir 22-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-56 20002088-4 2009 * This cocktail can be used to test the effects of a new chemical entity on multiple CYP isoforms in a single clinical study: CYP1A2 (caffeine), CYP2C9 (warfarin), CYP2C19 (omeprazole), CYP2D6 (metoprolol), and CYP3A (midazolam) and was designed to overcome potential liabilities of other reported cocktails. Caffeine 134-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-216 20002088-4 2009 * This cocktail can be used to test the effects of a new chemical entity on multiple CYP isoforms in a single clinical study: CYP1A2 (caffeine), CYP2C9 (warfarin), CYP2C19 (omeprazole), CYP2D6 (metoprolol), and CYP3A (midazolam) and was designed to overcome potential liabilities of other reported cocktails. Warfarin 153-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-216 20002088-4 2009 * This cocktail can be used to test the effects of a new chemical entity on multiple CYP isoforms in a single clinical study: CYP1A2 (caffeine), CYP2C9 (warfarin), CYP2C19 (omeprazole), CYP2D6 (metoprolol), and CYP3A (midazolam) and was designed to overcome potential liabilities of other reported cocktails. Metoprolol 194-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-216 20002088-4 2009 * This cocktail can be used to test the effects of a new chemical entity on multiple CYP isoforms in a single clinical study: CYP1A2 (caffeine), CYP2C9 (warfarin), CYP2C19 (omeprazole), CYP2D6 (metoprolol), and CYP3A (midazolam) and was designed to overcome potential liabilities of other reported cocktails. Midazolam 218-227 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-216 20002088-5 2009 AIMS: To assess the pharmacokinetics (PK) of selective substrates of CYP1A2 (caffeine), CYP2C9 (S-warfarin), CYP2C19 (omeprazole), CYP2D6 (metoprolol) and CYP3A (midazolam) when administered orally and concurrently as a cocktail relative to the drugs administered alone. Sulfur 3-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-160 19664894-10 2009 Although less sensitive than GC-MS, the proposed method was adequately sensitive to measure midazolam hydroxylase activity as a marker for CYP3A activity, and was applied to measure midazolam pharmacokinetics in human plasma. Midazolam 92-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-144 20110038-3 2009 OBJECTIVE: The aim of this study was to investigate the effects of a potent inhibitor (ketoconazole) and inducer (rifampicin) of the CYP3A4 isozyme on the pharmacokinetics of mirodenafil to meet the regulatory requirements for the marketing of mirodenafil in Korea. Ketoconazole 87-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 20110038-3 2009 OBJECTIVE: The aim of this study was to investigate the effects of a potent inhibitor (ketoconazole) and inducer (rifampicin) of the CYP3A4 isozyme on the pharmacokinetics of mirodenafil to meet the regulatory requirements for the marketing of mirodenafil in Korea. Rifampin 114-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 20110038-3 2009 OBJECTIVE: The aim of this study was to investigate the effects of a potent inhibitor (ketoconazole) and inducer (rifampicin) of the CYP3A4 isozyme on the pharmacokinetics of mirodenafil to meet the regulatory requirements for the marketing of mirodenafil in Korea. mirodenafil 175-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 20110038-3 2009 OBJECTIVE: The aim of this study was to investigate the effects of a potent inhibitor (ketoconazole) and inducer (rifampicin) of the CYP3A4 isozyme on the pharmacokinetics of mirodenafil to meet the regulatory requirements for the marketing of mirodenafil in Korea. mirodenafil 244-255 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 20175801-1 2009 BACKGROUND: Halofantrine, an antimalarial drug used in endemic areas such as the tropics is mainly metabolized by CYP3A4 to the active metabolite N-desbutylhalofantrine. halofantrine 12-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 19245271-4 2009 Here, we report on the development of a fluorescent-based CYP3A high-throughput assay for four fish cell lines cultivated in 96-well plates based on 7-benzyloxy-4-trifluoromethylcoumarin as a CYP3A substrate. 7-benzyloxy-4-trifluoromethylcoumarin 149-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 19245271-4 2009 Here, we report on the development of a fluorescent-based CYP3A high-throughput assay for four fish cell lines cultivated in 96-well plates based on 7-benzyloxy-4-trifluoromethylcoumarin as a CYP3A substrate. 7-benzyloxy-4-trifluoromethylcoumarin 149-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 192-197 19755916-2 2009 Vitamin E may increase the production of CYP3A4 in the liver, and this could lead to an increase in drug metabolism, potentially lowering the efficacy of therapeutic drugs. Vitamin E 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 19755916-3 2009 We hypothesized that upregulation of CYP3A4 by alpha-tocopherol (alpha-TOH) would decrease the plasma concentration of the CYP3A4 substrate midazolam. alpha-Tocopherol 47-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 19755916-3 2009 We hypothesized that upregulation of CYP3A4 by alpha-tocopherol (alpha-TOH) would decrease the plasma concentration of the CYP3A4 substrate midazolam. alpha-Tocopherol 47-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 19755916-3 2009 We hypothesized that upregulation of CYP3A4 by alpha-tocopherol (alpha-TOH) would decrease the plasma concentration of the CYP3A4 substrate midazolam. alpha-Tocopherol 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 19755916-3 2009 We hypothesized that upregulation of CYP3A4 by alpha-tocopherol (alpha-TOH) would decrease the plasma concentration of the CYP3A4 substrate midazolam. alpha-Tocopherol 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 19755916-3 2009 We hypothesized that upregulation of CYP3A4 by alpha-tocopherol (alpha-TOH) would decrease the plasma concentration of the CYP3A4 substrate midazolam. Midazolam 140-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 19755916-3 2009 We hypothesized that upregulation of CYP3A4 by alpha-tocopherol (alpha-TOH) would decrease the plasma concentration of the CYP3A4 substrate midazolam. Midazolam 140-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 20175801-1 2009 BACKGROUND: Halofantrine, an antimalarial drug used in endemic areas such as the tropics is mainly metabolized by CYP3A4 to the active metabolite N-desbutylhalofantrine. 1,3-dichloro-6-trifluoromethyl-9-phenanthryl-3-(n-butyl)aminopropanol 146-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 20175801-2 2009 Fluconazole, an antifungal agent and an inhibitor of CYP3A4 is an established part of the therapy in HIV patients, who in turn are prone to malaria in the tropics. Fluconazole 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 20175801-10 2009 CONCLUSION: The decreased plasma concentrations of the metabolite are presumably caused by metabolic inhibition of CYP3A4 by fluconazole. Fluconazole 125-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 19958586-1 2009 OBJECTIVES: It has been reported that hepatic cytochrome P450 (CYP)2C9 and CYP3A4 are responsible for the metabolism of sildenafil and formation of its metabolite, N-desmethylsildenafil, in humans. Sildenafil Citrate 120-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 19958586-1 2009 OBJECTIVES: It has been reported that hepatic cytochrome P450 (CYP)2C9 and CYP3A4 are responsible for the metabolism of sildenafil and formation of its metabolite, N-desmethylsildenafil, in humans. Sildenafil Citrate 164-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 19729463-3 2009 Pharmacokinetic studies have demonstrated that cyclosporine increases statin drug levels, presumably via competitive inhibition of cytochrome P450 3A4. Cyclosporine 47-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-150 20183988-17 2009 The risk is strongly intensified by drug interactions through CYP3A4 (for simvastatin and atorvastatin), high doses, and combination therapy with fibrates. Simvastatin 74-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 20183988-17 2009 The risk is strongly intensified by drug interactions through CYP3A4 (for simvastatin and atorvastatin), high doses, and combination therapy with fibrates. Atorvastatin 90-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 19954708-0 2009 4beta-hydroxycholesterol as a marker of CYP3A4 inhibition in vivo - effects of itraconazole in man. cholest-5-ene-3,4-diol 0-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 19954708-1 2009 OBJECTIVE: Itraconazole, a triazole antifungal agent, has been demonstrated to act as an inhibitor of the ligand induced pregnane X receptor-mediated transcriptional regulation of the CYP3A4 gene. Itraconazole 11-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 19954708-1 2009 OBJECTIVE: Itraconazole, a triazole antifungal agent, has been demonstrated to act as an inhibitor of the ligand induced pregnane X receptor-mediated transcriptional regulation of the CYP3A4 gene. Triazoles 27-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 184-190 19954708-2 2009 Here, we study the potential endogenous serum marker of CYP3A4 activity, 4beta-hydroxycholesterol, during therapy with itraconazole. cholest-5-ene-3,4-diol 73-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 19954708-2 2009 Here, we study the potential endogenous serum marker of CYP3A4 activity, 4beta-hydroxycholesterol, during therapy with itraconazole. Itraconazole 119-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 19954708-9 2009 Absolute and cholesterol-corrected concentrations of 4beta-hydroxycholesterol, formed by CYP3A4-mediated oxidation, decreased significantly during both cycles, on average by 29.1% (p = 0.0006) and 20.8% (p = 0.0062), respectively. Cholesterol 13-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 19954708-9 2009 Absolute and cholesterol-corrected concentrations of 4beta-hydroxycholesterol, formed by CYP3A4-mediated oxidation, decreased significantly during both cycles, on average by 29.1% (p = 0.0006) and 20.8% (p = 0.0062), respectively. cholest-5-ene-3,4-diol 53-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 19954708-11 2009 CONCLUSIONS: In conclusion, 4beta-hydroxycholesterol appears to be a sensitive endogenous surrogate marker in human serum for inhibition of CYP3A4 by itraconazole. cholest-5-ene-3,4-diol 28-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 19954708-11 2009 CONCLUSIONS: In conclusion, 4beta-hydroxycholesterol appears to be a sensitive endogenous surrogate marker in human serum for inhibition of CYP3A4 by itraconazole. Itraconazole 150-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 19795923-4 2009 In human liver microsomes, 7-epi-cephalomannine was subject to C-13 lateral chain (M-1) and diterpenoid core monohydroxylation (M-2), mediated by cytochrome P450 (CYP) 3A4 and CYP2C8, respectively. Diterpenes 92-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-171 19686824-6 2009 The levels of CYP1A1, CYP1A2, CY2C9 and CYP3A4 mRNAs were not altered by Zolpidem, whereas model inducers dioxin and rifampicin significantly induced CYP1A and CYP2/3 gene expression, respectively. Rifampin 117-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 19795924-6 2009 The transactivation of the CYP3A4 promoter by prednisolone via the glucocorticoid receptor might be especially responsive for intestinal CYP3A4. Prednisolone 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 19795923-4 2009 In human liver microsomes, 7-epi-cephalomannine was subject to C-13 lateral chain (M-1) and diterpenoid core monohydroxylation (M-2), mediated by cytochrome P450 (CYP) 3A4 and CYP2C8, respectively. 7-epi-Cephalomannine 27-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-171 19795924-6 2009 The transactivation of the CYP3A4 promoter by prednisolone via the glucocorticoid receptor might be especially responsive for intestinal CYP3A4. Prednisolone 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 19616568-10 2009 This was further confirmed by significant inhibition of primaquine hemotoxicity by the selective CYP inhibitors, namely thiotepa (CYP2B6), fluoxetine (CYP2D6) and troleandomycin (CYP3A4). Troleandomycin 163-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 19616568-9 2009 Multiple CYP isoforms (CYP2E1, CYP2B6, CYP1A2, CYP2D6 and CYP3A4) variably contributed to the hemotoxicity of primaquine. Primaquine 110-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 19616568-10 2009 This was further confirmed by significant inhibition of primaquine hemotoxicity by the selective CYP inhibitors, namely thiotepa (CYP2B6), fluoxetine (CYP2D6) and troleandomycin (CYP3A4). Primaquine 56-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 179-185 19444798-0 2009 A validated SIM GC/MS method for the simultaneous determination of dextromethorphan and its metabolites dextrorphan, 3-methoxymorphinan and 3-hydroxymorphinan in biological matrices and its application to in vitro CYP2D6 and CYP3A4 inhibition study. Dextromethorphan 67-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 225-231 19444798-1 2009 Dextromethorphan is used as a probe drug for assessing CYP2D6 and CYP3A4 activity in vivo and in vitro. Dextromethorphan 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 19444798-7 2009 The method has been successfully applied for the in vitro inhibition of metabolism of dextromethorphan by CYP2D6 and CYP3A4 using known inhibitors of CYPs such as quinidine and verapamil. Dextromethorphan 86-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 19444798-7 2009 The method has been successfully applied for the in vitro inhibition of metabolism of dextromethorphan by CYP2D6 and CYP3A4 using known inhibitors of CYPs such as quinidine and verapamil. Quinidine 163-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 19686543-3 2009 Recent studies have revealed that triclosan is able to activate the human pregnane X receptor in vitro and thus possibly affecting metabolism of drugs in humans via the induction of CYP3A4. Triclosan 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 182-188 19444798-7 2009 The method has been successfully applied for the in vitro inhibition of metabolism of dextromethorphan by CYP2D6 and CYP3A4 using known inhibitors of CYPs such as quinidine and verapamil. Verapamil 177-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 19686543-5 2009 In the present study, we investigated if an everyday exposure to triclosan via triclosan-containing toothpaste for 14 days in 12 adult humans caused an increase in plasma 4beta-hydroxycholesterol, indicative of CYP3A4 induction, and/or alterations in thyroid hormonal status. Triclosan 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-217 19686543-5 2009 In the present study, we investigated if an everyday exposure to triclosan via triclosan-containing toothpaste for 14 days in 12 adult humans caused an increase in plasma 4beta-hydroxycholesterol, indicative of CYP3A4 induction, and/or alterations in thyroid hormonal status. Triclosan 79-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 211-217 22478935-11 2009 Drug-drug interactions with other substrates of CYP2C9, CYP2C19, and CYP3A4 can also alter voriconazole concentrations. Voriconazole 91-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 19916995-1 2009 AIMS: To investigate in vivo the influence of the potent CYP2C19 and CYP3A4 inhibitor voriconazole on the pharmacokinetics and analgesic effects of tilidine. Voriconazole 86-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 19916995-1 2009 AIMS: To investigate in vivo the influence of the potent CYP2C19 and CYP3A4 inhibitor voriconazole on the pharmacokinetics and analgesic effects of tilidine. Tilidine 148-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 19695866-8 2009 In addition, a new role for HIF-1alpha in the repression of CYP3A4 is demonstrated in cells treated with chemical inducers of HIF-1alpha, cobalt chloride or desferrioxamine, and by transfecting untreated HepaRG cells with HIF-1alpha expression vector. cobaltous chloride 138-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 19639308-6 2009 Analysis of 61 patients using only CYP3A4 metabolised benzodiazepines showed this class to be associated with higher (R)-concentration/dose, which is consistent with a potential competitive inhibition of CYP3A4. Benzodiazepines 54-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 19695866-8 2009 In addition, a new role for HIF-1alpha in the repression of CYP3A4 is demonstrated in cells treated with chemical inducers of HIF-1alpha, cobalt chloride or desferrioxamine, and by transfecting untreated HepaRG cells with HIF-1alpha expression vector. Deferoxamine 157-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 19639308-6 2009 Analysis of 61 patients using only CYP3A4 metabolised benzodiazepines showed this class to be associated with higher (R)-concentration/dose, which is consistent with a potential competitive inhibition of CYP3A4. Benzodiazepines 54-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 204-210 20038391-1 2009 OBJECTIVE: To determine how single nucleotide polymorphisms located on genes MDR1, CYP3A4 and CYP3A5 affect the absorption kinetics of cyclosporine in cardiac transplant patients. Cyclosporine 135-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 19801957-0 2009 The P450 oxidoreductase genotype is associated with CYP3A activity in vivo as measured by the midazolam phenotyping test. Midazolam 94-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-57 20088394-3 2009 Although no association of any CYP3A4 polymorphisms and breast cancer has been documented, the CYP3A4*1B (392A>G) variant, correlates with earlier menarche and endometrial cancer secondary to tamoxifen therapy. Tamoxifen 195-204 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 19713357-7 2009 Other cytochromes P450, including CYP1A1, CYP1B1, CYP1A2, and CYP3A4, were also able to epoxidize BaP-7,8-diol using various fatty acid hydroperoxides, although at slower rates than CYP2S1. benzo(a)pyrene 7,8-dihydrodiol 98-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 19713357-7 2009 Other cytochromes P450, including CYP1A1, CYP1B1, CYP1A2, and CYP3A4, were also able to epoxidize BaP-7,8-diol using various fatty acid hydroperoxides, although at slower rates than CYP2S1. Lipid Peroxides 125-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 19801957-3 2009 METHODS: We phenotyped 251 individuals from two independent studies (182 patients treated with methadone and 69 patients with clozapine) for CYP3A activity using the midazolam phenotyping test and genotyped them for CYP3A4, CYP3A5, and CYP3A7 genetic variants, including the single nucleotide polymorphism (SNP) rs4646437C>T in intron 7 of CYP3A4. Methadone 95-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-146 19801957-3 2009 METHODS: We phenotyped 251 individuals from two independent studies (182 patients treated with methadone and 69 patients with clozapine) for CYP3A activity using the midazolam phenotyping test and genotyped them for CYP3A4, CYP3A5, and CYP3A7 genetic variants, including the single nucleotide polymorphism (SNP) rs4646437C>T in intron 7 of CYP3A4. Clozapine 126-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-146 19801957-3 2009 METHODS: We phenotyped 251 individuals from two independent studies (182 patients treated with methadone and 69 patients with clozapine) for CYP3A activity using the midazolam phenotyping test and genotyped them for CYP3A4, CYP3A5, and CYP3A7 genetic variants, including the single nucleotide polymorphism (SNP) rs4646437C>T in intron 7 of CYP3A4. Midazolam 166-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-146 19845431-7 2009 Using rifampicin as a reference standard, compounds with a C(ss,u)/RF value greater than 7.31 nmol l(-1) may induce CYP3A in vivo in humans. Rifampin 6-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-121 19480428-1 2009 Testosterone hydroxylation is a prototypical reaction of human cytochrome P450 3A4, which metabolizes about 50% of oral drugs on the market. Testosterone 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-82 19843060-5 2009 RESULTS: (i) The CYP3A4 and CYP1A2 inhibitors ketoconazole and fluvoxamine inhibited CLZ oxidation to varying extents in individual microsomal fractions. Ketoconazole 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 19700319-4 2009 Rational optimization of time dependent inactivation of CYP 3A4 and clearance was accomplished by incorporation of electron-withdrawing groups to the benzothiazine core. benzothiazine 150-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-63 19713107-0 2009 Structure-activity studies on seco-pancratistatin analogs: potent inhibitors of human cytochrome P450 3A4. seco-pancratistatin 30-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-105 19843060-5 2009 RESULTS: (i) The CYP3A4 and CYP1A2 inhibitors ketoconazole and fluvoxamine inhibited CLZ oxidation to varying extents in individual microsomal fractions. Fluvoxamine 63-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 19283354-0 2009 Delivery of high levels of anti-proliferative nucleoside triphosphates to CYP3A-expressing cells as a potential treatment for hepatocellular carcinoma. nucleoside triphosphates 46-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-79 19283354-3 2009 The aim of our studies was to explore the utility of CYP3A-activated prodrugs of cytarabine and fludarabine monophosphate for the treatment of HCC. Cytarabine 81-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 19283354-3 2009 The aim of our studies was to explore the utility of CYP3A-activated prodrugs of cytarabine and fludarabine monophosphate for the treatment of HCC. fludarabine phosphate 96-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 19843060-5 2009 RESULTS: (i) The CYP3A4 and CYP1A2 inhibitors ketoconazole and fluvoxamine inhibited CLZ oxidation to varying extents in individual microsomal fractions. Clozapine 85-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 19562329-3 2009 The aim of the present study was to investigate potential drug interactions between the benzimidazoles albendazole and mebendazole and the potent CYP3A4 inhibitor ritonavir. benzimidazoles albendazole 88-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 19608694-4 2009 Milnacipran inhibited CYP3A4/5 in a substrate-dependent manner (i.e., midazolam 1"-hydroxylation IC(50) approximately 30 microM; testosterone 6beta-hydroxylation IC(50) approximately 100 microM); whereas, duloxetine inhibited both CYP3A4/5 activities with equal potency (IC(50) = 37 and 38 microM, respectively). Duloxetine Hydrochloride 205-215 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 19608694-8 2009 The highest concentration of milnacipran (30 microM; >10 times plasma C(max)) produced 2.6- and 2.2-fold increases in CYP2B6 and CYP3A4/5 activity (making it 26 and 34% as effective as phenobarbital and rifampin, respectively). Milnacipran 29-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 19608694-4 2009 Milnacipran inhibited CYP3A4/5 in a substrate-dependent manner (i.e., midazolam 1"-hydroxylation IC(50) approximately 30 microM; testosterone 6beta-hydroxylation IC(50) approximately 100 microM); whereas, duloxetine inhibited both CYP3A4/5 activities with equal potency (IC(50) = 37 and 38 microM, respectively). Milnacipran 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 19608694-4 2009 Milnacipran inhibited CYP3A4/5 in a substrate-dependent manner (i.e., midazolam 1"-hydroxylation IC(50) approximately 30 microM; testosterone 6beta-hydroxylation IC(50) approximately 100 microM); whereas, duloxetine inhibited both CYP3A4/5 activities with equal potency (IC(50) = 37 and 38 microM, respectively). Milnacipran 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 231-237 19608694-4 2009 Milnacipran inhibited CYP3A4/5 in a substrate-dependent manner (i.e., midazolam 1"-hydroxylation IC(50) approximately 30 microM; testosterone 6beta-hydroxylation IC(50) approximately 100 microM); whereas, duloxetine inhibited both CYP3A4/5 activities with equal potency (IC(50) = 37 and 38 microM, respectively). Midazolam 70-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 19562329-3 2009 The aim of the present study was to investigate potential drug interactions between the benzimidazoles albendazole and mebendazole and the potent CYP3A4 inhibitor ritonavir. Mebendazole 119-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 19562329-3 2009 The aim of the present study was to investigate potential drug interactions between the benzimidazoles albendazole and mebendazole and the potent CYP3A4 inhibitor ritonavir. Ritonavir 163-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 19506580-2 2009 Midazolam (MDZ) is a substrate for both CYP3A4 and CYP3A5. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 19744012-1 2009 BACKGROUND AND OBJECTIVE: Carbamazepine (CBZ) is metabolized mainly by the CYP3A family of enzymes, which includes CYP3A4 and CYP3A5. Carbamazepine 26-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 19744012-1 2009 BACKGROUND AND OBJECTIVE: Carbamazepine (CBZ) is metabolized mainly by the CYP3A family of enzymes, which includes CYP3A4 and CYP3A5. Carbamazepine 41-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 19728720-0 2009 Theoretical characterization of substrate access/exit channels in the human cytochrome P450 3A4 enzyme: involvement of phenylalanine residues in the gating mechanism. Phenylalanine 119-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-95 19506580-2 2009 Midazolam (MDZ) is a substrate for both CYP3A4 and CYP3A5. Midazolam 11-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 19622022-8 2009 Studies using recombinant human CYP isozymes established that the rate-limiting step in the oxidative metabolism of 1 to the major primary alcohol metabolite M1 was catalysed by CYP3A4. Alcohols 139-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-184 19792991-0 2009 Effect of saquinavir-ritonavir on cytochrome P450 3A4 activity in healthy volunteers using midazolam as a probe. saquinavir-ritonavir 10-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-53 19792991-15 2009 CONCLUSION: Administration of ritonavir-boosted saquinavir markedly increased the exposure of midazolam by inhibiting its metabolism, confirming that the combination of saquinavir and ritonavir at steady state strongly inhibits CYP3A4 activity. Ritonavir 30-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 19792991-15 2009 CONCLUSION: Administration of ritonavir-boosted saquinavir markedly increased the exposure of midazolam by inhibiting its metabolism, confirming that the combination of saquinavir and ritonavir at steady state strongly inhibits CYP3A4 activity. Saquinavir 48-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 19792991-15 2009 CONCLUSION: Administration of ritonavir-boosted saquinavir markedly increased the exposure of midazolam by inhibiting its metabolism, confirming that the combination of saquinavir and ritonavir at steady state strongly inhibits CYP3A4 activity. Midazolam 94-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 19792991-15 2009 CONCLUSION: Administration of ritonavir-boosted saquinavir markedly increased the exposure of midazolam by inhibiting its metabolism, confirming that the combination of saquinavir and ritonavir at steady state strongly inhibits CYP3A4 activity. Saquinavir 169-179 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 19792991-15 2009 CONCLUSION: Administration of ritonavir-boosted saquinavir markedly increased the exposure of midazolam by inhibiting its metabolism, confirming that the combination of saquinavir and ritonavir at steady state strongly inhibits CYP3A4 activity. Ritonavir 184-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 19679477-1 2009 The HIV protease inhibitor ritonavir (RTV) is also a potent inhibitor of the metabolizing enzyme cytochrome P450 3A (CYP3A) and is clinically useful in HIV therapy in its ability to enhance human plasma levels of other HIV protease inhibitors (PIs). Ritonavir 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-115 19694439-10 2009 Much tighter binding of the inhibitor to the verdoheme intermediate differentiates it from inhibition of, for example, CYP3A4 and offers a possible route to more selective inhibitor design. verdoheme 45-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 19467820-5 2009 Our study using human hepatocyte suspensions showed that both DP and PRED were metabolized by CYP3A4 isozymes, resulting in the formation of diverse arrays of both oxidative and oxidative-reduced metabolites. Dipyridamole 62-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 19575604-4 2009 Erythromycin is a CYP3A4 inhibitor. Erythromycin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 19467820-6 2009 Within phase 1 biotransformation, CYP3A4 was one of the pathways responsible for the metabolism of PRED, while phase 2 biotransformation played a significant role in the metabolism of DP. Dipyridamole 184-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 19467820-10 2009 DP, but not PRED, exerted a minimal inhibitory effect on the drug-metabolizing CYP isoforms, including CYP3A4, which was determined using a panel of CYP isoform-preferred substrate activities in pooled human liver microsomal (HLM) preparations and microsomal preparations containing the recombinant enzymes (K(i) approximately 2-12 microM). Dipyridamole 0-2 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 19679477-1 2009 The HIV protease inhibitor ritonavir (RTV) is also a potent inhibitor of the metabolizing enzyme cytochrome P450 3A (CYP3A) and is clinically useful in HIV therapy in its ability to enhance human plasma levels of other HIV protease inhibitors (PIs). Ritonavir 27-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-122 19679477-1 2009 The HIV protease inhibitor ritonavir (RTV) is also a potent inhibitor of the metabolizing enzyme cytochrome P450 3A (CYP3A) and is clinically useful in HIV therapy in its ability to enhance human plasma levels of other HIV protease inhibitors (PIs). Ritonavir 38-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-115 19679477-1 2009 The HIV protease inhibitor ritonavir (RTV) is also a potent inhibitor of the metabolizing enzyme cytochrome P450 3A (CYP3A) and is clinically useful in HIV therapy in its ability to enhance human plasma levels of other HIV protease inhibitors (PIs). Ritonavir 38-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-122 19500085-8 2009 Both nelfinavir and ritonavir decreased both M1 and M3, consistent with their ability to inhibit CYP3A and 2C8. Ritonavir 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-102 19701237-0 2009 Evaluation of CYP3A activity in humans using three different parameters based on endogenous cortisol metabolism. Hydrocortisone 92-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 19701237-1 2009 AIM: Currently, there is considerable debate as to which method is more accurate for measuring the activity of CYP3A in vivo: cortisol 6beta-hydroxylation clearance (Cl(m(6beta))) or the urinary ratio of 6beta-OHF to F (6beta-OHF/F). cortisol 6beta 126-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-116 19701237-1 2009 AIM: Currently, there is considerable debate as to which method is more accurate for measuring the activity of CYP3A in vivo: cortisol 6beta-hydroxylation clearance (Cl(m(6beta))) or the urinary ratio of 6beta-OHF to F (6beta-OHF/F). 6beta-ohf 204-213 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-116 19701237-1 2009 AIM: Currently, there is considerable debate as to which method is more accurate for measuring the activity of CYP3A in vivo: cortisol 6beta-hydroxylation clearance (Cl(m(6beta))) or the urinary ratio of 6beta-OHF to F (6beta-OHF/F). Fluorine 212-213 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-116 19701237-1 2009 AIM: Currently, there is considerable debate as to which method is more accurate for measuring the activity of CYP3A in vivo: cortisol 6beta-hydroxylation clearance (Cl(m(6beta))) or the urinary ratio of 6beta-OHF to F (6beta-OHF/F). 6beta-ohf 220-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-116 19701237-8 2009 The ratio of 1-hydroxymidazolam (1-OHMDZ) concentration to MDZ concentration at 1 h (MR) was taken as a measure of the in vivo CYP3A activity. 1-hydroxymethylmidazolam 13-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 19701237-11 2009 After 4 d of clarithromycin administration, CYP3A activity (MR) decreased by 75% (P=0.000), whereas AUC(F) increased by 19% (P=0.040), and Cl(m(6beta)) and 6beta-OHF/F decreased by 54.2% (P=0.000) and 50% (P=0.003), respectively. Clarithromycin 13-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-49 19500085-7 2009 Delavirdine increased M1 and decreased M3 consistent with its ability to inhibit CYP3A. Delavirdine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 19740395-0 2009 The effect on sotrastaurin pharmacokinetics of strong CYP3A inhibition by ketoconazole. sotrastaurin 14-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-59 19500085-8 2009 Both nelfinavir and ritonavir decreased both M1 and M3, consistent with their ability to inhibit CYP3A and 2C8. Nelfinavir 5-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-102 19740395-0 2009 The effect on sotrastaurin pharmacokinetics of strong CYP3A inhibition by ketoconazole. Ketoconazole 74-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-59 19740395-2 2009 The effect of CYP3A4 inhibition by ketoconazole on the pharmacokinetics of sotrastaurin, a CYP3A4 substrate, was investigated. sotrastaurin 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 19740395-2 2009 The effect of CYP3A4 inhibition by ketoconazole on the pharmacokinetics of sotrastaurin, a CYP3A4 substrate, was investigated. sotrastaurin 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 19740395-8 2009 CONCLUSIONS: The strong CYP3A4 inhibitor ketoconazole increased sotrastaurin AUC by 4.6-fold. Ketoconazole 41-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 19740395-8 2009 CONCLUSIONS: The strong CYP3A4 inhibitor ketoconazole increased sotrastaurin AUC by 4.6-fold. sotrastaurin auc 64-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 19740395-9 2009 A compensatory reduction in the dose of sotrastaurin is warranted when strong CYP3A4 inhibitors are co-administered. sotrastaurin 40-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 19594405-6 2009 CYP1A2 and CYP3A4 appear to be the major P450 enzymes catalyzing the oxidation of all-trans-retinol to all-trans-retinoic acid in human liver, and CYP3A4 is one of the vitamin D3 25-hydroxylases. Vitamin A 82-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 19487251-7 2009 Incubation of lithocholic acid with a of human recombinant P450 enzymes revealed that all five metabolites were formed by recombinant CYP3A4. Lithocholic Acid 14-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 19487251-8 2009 Chemical inhibition studies with human liver microsomes and recombinant P450 enzymes confirmed that CYP3A4 was the predominant enzyme involved in hepatic microsomal biotransformation of lithocholic acid. Lithocholic Acid 186-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 19520774-6 2009 Laromustine caused direct inhibition of CYP2B6 and CYP3A4/5 (the two enzymes involved in C-7 formation) as well as of CYP2C19. laromustine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 19520774-7 2009 K(i) values were 125 microM for CYP2B6, 297 muM for CYP3A4/5, and 349 microM for CYP2C19 and were greater than the average clinical plasma C(max) of laromustine (25 microM). laromustine 149-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 19520774-10 2009 The results of this study suggest the laromustine has 1) negligible victim potential with respect to metabolism by cytochrome P450 enzymes, 2) negligible enzyme-inducing potential, and 3) the potential in some cases to cause inhibition of CYP2B6, CYP3A4, and possibly CYP2C19 during and shortly after the duration of intravenous administration of this anticancer drug, but the clinical effects of such interactions are likely to be insignificant. laromustine 38-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 247-253 19594405-6 2009 CYP1A2 and CYP3A4 appear to be the major P450 enzymes catalyzing the oxidation of all-trans-retinol to all-trans-retinoic acid in human liver, and CYP3A4 is one of the vitamin D3 25-hydroxylases. Vitamin A 82-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 19594405-6 2009 CYP1A2 and CYP3A4 appear to be the major P450 enzymes catalyzing the oxidation of all-trans-retinol to all-trans-retinoic acid in human liver, and CYP3A4 is one of the vitamin D3 25-hydroxylases. Tretinoin 103-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 21217856-12 2009 VPA also induced the expression of CYP3A4 in this neuroblastoma cell line. Valproic Acid 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 19801894-0 2009 Inhibitory effects of ketoconazole, cimetidine and erythromycin on hepatic CYP3A activities in cats. Ketoconazole 22-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 19734738-11 2009 Metabolism of colchicine by the cytochrome P450 3A4 system has been previously described, but this is the first published report of colchicine associated rhabdomyolysis secondary to drug metabolism interactions with an antibiotic. Colchicine 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-51 19734738-11 2009 Metabolism of colchicine by the cytochrome P450 3A4 system has been previously described, but this is the first published report of colchicine associated rhabdomyolysis secondary to drug metabolism interactions with an antibiotic. Colchicine 132-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-51 19689106-0 2009 Minor furanocoumarins and coumarins in grapefruit peel oil as inhibitors of human cytochrome P450 3A4. Furocoumarins 6-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-101 19689106-0 2009 Minor furanocoumarins and coumarins in grapefruit peel oil as inhibitors of human cytochrome P450 3A4. Coumarins 12-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-101 19801894-0 2009 Inhibitory effects of ketoconazole, cimetidine and erythromycin on hepatic CYP3A activities in cats. Cimetidine 36-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 19801894-0 2009 Inhibitory effects of ketoconazole, cimetidine and erythromycin on hepatic CYP3A activities in cats. Erythromycin 51-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 19801894-1 2009 Inhibitory effects of ketoconazole (KTZ), cimetidine (CIM), and erythromycin (ERY) were examined on CYP3A activities. Ketoconazole 22-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 19801894-1 2009 Inhibitory effects of ketoconazole (KTZ), cimetidine (CIM), and erythromycin (ERY) were examined on CYP3A activities. Ketoconazole 36-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 19801894-1 2009 Inhibitory effects of ketoconazole (KTZ), cimetidine (CIM), and erythromycin (ERY) were examined on CYP3A activities. Cimetidine 42-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 19801894-1 2009 Inhibitory effects of ketoconazole (KTZ), cimetidine (CIM), and erythromycin (ERY) were examined on CYP3A activities. Cimetidine 54-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 19801894-1 2009 Inhibitory effects of ketoconazole (KTZ), cimetidine (CIM), and erythromycin (ERY) were examined on CYP3A activities. Erythromycin 64-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 19801894-1 2009 Inhibitory effects of ketoconazole (KTZ), cimetidine (CIM), and erythromycin (ERY) were examined on CYP3A activities. Erythromycin 78-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 19801894-12 2009 These results suggest that, KTZ inhibits CYP3A activities (both in vitro and in vivo), but CIM does not. Ketoconazole 28-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 19801894-13 2009 In clinical practice, therefore, KTZ may result in inhibition based drug-drug interaction with CYP3A substrates in cat patients, whereas CIM and ERY are unlikely to lead to interaction involving CYP3A substrates. Ketoconazole 33-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-100 19813492-3 2009 Tacrolimus is metabolized by cytochrome P450 3A4 in both the liver and small intestine. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-48 19761365-4 2009 MATERIALS & METHODS: Seven polymorphic variations in four genes that encode enzymes from phase I (CYP2C9, CYP3A4 and CYP3A5) or phase III (ABCB1) of drug metabolism were analyzed in population samples from Cabinda (n = 107), Mozambique (n = 109) and Sao Tome e Principe (n = 126). Adenosine Monophosphate 11-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 19813492-4 2009 Drugs that are substrates of cytochrome P450 3A4, as well as inhibitors and inducers of cytochrome P450 3A4, can cause significant interactions with tacrolimus. Tacrolimus 149-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-48 19813492-4 2009 Drugs that are substrates of cytochrome P450 3A4, as well as inhibitors and inducers of cytochrome P450 3A4, can cause significant interactions with tacrolimus. Tacrolimus 149-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-107 19084030-5 2009 The present study investigates the effect of sodium arsenite and its metabolites monomethylarsonous acid (MMA(III)) and dimethylarsinous acid (DMA(III)) on CYP3A4, PXR, and RXR alpha expression in the small intestine of CYP3A4 transgenic mice. sodium arsenite 45-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 19084030-5 2009 The present study investigates the effect of sodium arsenite and its metabolites monomethylarsonous acid (MMA(III)) and dimethylarsinous acid (DMA(III)) on CYP3A4, PXR, and RXR alpha expression in the small intestine of CYP3A4 transgenic mice. monomethylarsonous acid 81-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 19084030-0 2009 Arsenite and its metabolites, MMA(III) and DMA(III), modify CYP3A4, PXR and RXR alpha expression in the small intestine of CYP3A4 transgenic mice. arsenite 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 19084030-0 2009 Arsenite and its metabolites, MMA(III) and DMA(III), modify CYP3A4, PXR and RXR alpha expression in the small intestine of CYP3A4 transgenic mice. arsenite 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 19084030-5 2009 The present study investigates the effect of sodium arsenite and its metabolites monomethylarsonous acid (MMA(III)) and dimethylarsinous acid (DMA(III)) on CYP3A4, PXR, and RXR alpha expression in the small intestine of CYP3A4 transgenic mice. monomethylarsonous acid 81-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 19084030-0 2009 Arsenite and its metabolites, MMA(III) and DMA(III), modify CYP3A4, PXR and RXR alpha expression in the small intestine of CYP3A4 transgenic mice. mma 30-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 19084030-5 2009 The present study investigates the effect of sodium arsenite and its metabolites monomethylarsonous acid (MMA(III)) and dimethylarsinous acid (DMA(III)) on CYP3A4, PXR, and RXR alpha expression in the small intestine of CYP3A4 transgenic mice. dimethylarsinous acid 120-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 19084030-0 2009 Arsenite and its metabolites, MMA(III) and DMA(III), modify CYP3A4, PXR and RXR alpha expression in the small intestine of CYP3A4 transgenic mice. mma 30-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 19084030-0 2009 Arsenite and its metabolites, MMA(III) and DMA(III), modify CYP3A4, PXR and RXR alpha expression in the small intestine of CYP3A4 transgenic mice. N-myristoyl-alaninol 43-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 19084030-5 2009 The present study investigates the effect of sodium arsenite and its metabolites monomethylarsonous acid (MMA(III)) and dimethylarsinous acid (DMA(III)) on CYP3A4, PXR, and RXR alpha expression in the small intestine of CYP3A4 transgenic mice. dimethylarsinous acid 120-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 19084030-0 2009 Arsenite and its metabolites, MMA(III) and DMA(III), modify CYP3A4, PXR and RXR alpha expression in the small intestine of CYP3A4 transgenic mice. N-myristoyl-alaninol 43-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 19084030-6 2009 Sodium arsenite treatment increases mRNA, protein and CYP3A4 activity in a dose-dependent manner. sodium arsenite 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 19084030-5 2009 The present study investigates the effect of sodium arsenite and its metabolites monomethylarsonous acid (MMA(III)) and dimethylarsinous acid (DMA(III)) on CYP3A4, PXR, and RXR alpha expression in the small intestine of CYP3A4 transgenic mice. sodium arsenite 45-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 19084030-8 2009 Arsenite treatment induces the accumulation of Ub-protein conjugates, indicating that the activation of this mechanism may explain the differences observed between the mRNA and protein expression of CYP3A4 induction. arsenite 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 199-205 19084030-9 2009 Treatment with 0.05 mg/kg of DMA(III) induces CYP3A4 in a similar way, while treatment with 0.05 mg/kg of MMA(III) increases mostly mRNA, and to a lesser degree, CYP3A4 activity. N-myristoyl-alaninol 29-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 19084030-11 2009 Overall, these results suggest that sodium arsenite and its metabolites induce CYP3A4 expression by increasing PXR expression in the small intestine of CYP3A4 transgenic mice. sodium arsenite 36-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 19084030-11 2009 Overall, these results suggest that sodium arsenite and its metabolites induce CYP3A4 expression by increasing PXR expression in the small intestine of CYP3A4 transgenic mice. sodium arsenite 36-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 19393727-5 2009 In the CYP3A4-, CYP1A2-, CYP1A1-, and CYP1B1-expressing strains, DNBeP was found to be activated to reactive metabolites that cause the induction of umuC gene expression compared with the parent strain. 3,6-dinitrobenzopyrene 65-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 7-13 20095333-1 2009 OBJECTIVE: To evaluate the long-term therapeutic effects of atorvastatin via cytochrome P450 (CYP)3A4 pathway or a non-CYP 3A4 pathway statin, pravastatin, combined with clopidogrel for the patients undergoing coronary stenting. Atorvastatin 60-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-101 20719167-2 2009 Irinotecan, oxidized by CYP3A4 to produce inactive compounds, is used for treatment of various cancers including advanced non small cell lung cancer (NSCLC) patients. Irinotecan 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 20719167-3 2009 CYP3A4(*)16B polymorphism was associated with decreased metabolism of irrinotecan. Irinotecan 70-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 19557931-2 2009 The purpose of this study was to investigate the effect of Shenmai injection (SMI) on the CYP3A-mediated metabolism of midazolam (MDZ). Midazolam 119-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 19557931-2 2009 The purpose of this study was to investigate the effect of Shenmai injection (SMI) on the CYP3A-mediated metabolism of midazolam (MDZ). Midazolam 130-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 19557931-3 2009 The present study demonstrated that SMI could significantly inhibit MDZ 4-hydroxylation but activate its 1"-hydroxylation in human liver microsomes (HLMs), rat liver microsomes (RLM) and recombinant human CYP3A4 and CYP3A5. SMI496 36-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 205-211 19667964-8 2009 Cyclosporine A and Tac are metabolized by CYP3A4 and CYP3A5, and several single nucleotide polymorphisms in the two genes have been associated with differences in drug clearance. Cyclosporine 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 19667964-8 2009 Cyclosporine A and Tac are metabolized by CYP3A4 and CYP3A5, and several single nucleotide polymorphisms in the two genes have been associated with differences in drug clearance. Tacrolimus 19-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 19393727-7 2009 Collectively, these results suggest that nitroreduction by human CYP1A2, CYP3A4, and CYP1A1 and O-acetylation by human NAT2 contributed to the genotoxic activation of DNBeP to its metabolites. 3,6-dinitrobenzopyrene 167-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 19817686-5 2009 Reconstitution of catalytic activity of cytochrome P450 3A4 in the reaction of testosterone 6beta-hydroxylation in the presence of Hmwb(5)-EGFP indicates that cytochrome b(5) in the fusion protein is able to stimulate the hydroxylation reaction. testosterone 6beta 79-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-59 19652384-3 2009 Lansoprazole is metabolized to Lansoprazole sulfone (LS) by CYP3A, while to 5-hydroxylansoprasole by CYP2C19. Lansoprazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 19652384-3 2009 Lansoprazole is metabolized to Lansoprazole sulfone (LS) by CYP3A, while to 5-hydroxylansoprasole by CYP2C19. Lansoprazole Sulfone 31-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 19458613-0 2009 Plasma 4beta-hydroxycholesterol: an endogenous CYP3A metric? cholest-5-ene-3,4-diol 7-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 19652384-3 2009 Lansoprazole is metabolized to Lansoprazole sulfone (LS) by CYP3A, while to 5-hydroxylansoprasole by CYP2C19. Lansoprazole Sulfone 53-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 19652384-9 2009 Lansoprazole sulfoxidation activity was significantly correlated with T6beta-OH activity and CYP3A protein level. Lansoprazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-98 19652384-12 2009 These results suggest that metabolism of lansoprazole to LS by CYP3A occurs independently of metabolism by CYP2C19. Lansoprazole 41-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 19652384-12 2009 These results suggest that metabolism of lansoprazole to LS by CYP3A occurs independently of metabolism by CYP2C19. Lansoprazole Sulfone 57-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 19694743-1 2009 AIMS: We aimed to describe the pharmacokinetic interaction between phenytoin, a potent CYP3A4 and P-glycoprotein (P-gp) (ABCB1) inducer, and gefitinib, a CYP3A4, CYP2D6 and P-gp substrate. Phenytoin 67-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 19694743-1 2009 AIMS: We aimed to describe the pharmacokinetic interaction between phenytoin, a potent CYP3A4 and P-glycoprotein (P-gp) (ABCB1) inducer, and gefitinib, a CYP3A4, CYP2D6 and P-gp substrate. Phenytoin 67-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 19694743-5 2009 Hepatic CYP3A4 activity was evaluated by the (14)C-erythromycin breath test (ERMBT) and the ABCB1 and CYP2D6 genetic polymorphisms were determined by the TaqMan allelic discrimination assay and long polymerase chain reaction, respectively. Erythromycin 51-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 19694743-10 2009 CONCLUSIONS: The significant interaction between gefitinib and phenytoin was not correlated with the erythromycin breath test and was independent of ABCB1 polymorphism, but may involve presystemic CYP3A-mediated intestinal first-pass. Gefitinib 49-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-202 19694743-10 2009 CONCLUSIONS: The significant interaction between gefitinib and phenytoin was not correlated with the erythromycin breath test and was independent of ABCB1 polymorphism, but may involve presystemic CYP3A-mediated intestinal first-pass. Phenytoin 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-202 19530977-2 2009 Since cytochrome P450 enzymes CYP3A4 and CYP2B6 play a major role in prasugrel"s active metabolite formation, the effect of potent CYP induction by rifampin on the pharmacokinetics of prasugrel and on the pharmacodynamic response to prasugrel was evaluated in healthy male subjects. Prasugrel Hydrochloride 69-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 19649922-1 2009 The HIV protease inhibitor (PI) ritonavir is a potent, mechanism-based inhibitor of cytochrome P450 CYP3A4, an enzyme that is responsible for metabolizing most HIV PIs. Ritonavir 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 19649929-3 2009 Schering-Plough Corp is developing vicriviroc, a CCR5 inhibitor that has demonstrated good oral bioavailability, has a long half-life that allows once daily dosing, and is primarily metabolized by cytochrome P450 CYP3A4. vicriviroc 35-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 213-219 19406954-2 2009 In this study, the prediction of clinical DDIs for 30 drugs on the pharmacokinetics of midazolam, a probe substrate for CYP3A4, was done using in vitro inhibition, inactivation, and induction data. Midazolam 87-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 120-126 19420129-1 2009 Prediction of the extent and time course of drug-drug interactions (DDIs) between the mechanism-based inhibitor diltiazem (DTZ) and the CYP3A4 substrate midazolam (MDZ) is confounded by time- and concentration-dependent clearance of the inhibitor. Diltiazem 112-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 19420129-1 2009 Prediction of the extent and time course of drug-drug interactions (DDIs) between the mechanism-based inhibitor diltiazem (DTZ) and the CYP3A4 substrate midazolam (MDZ) is confounded by time- and concentration-dependent clearance of the inhibitor. Diltiazem 123-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 19420129-1 2009 Prediction of the extent and time course of drug-drug interactions (DDIs) between the mechanism-based inhibitor diltiazem (DTZ) and the CYP3A4 substrate midazolam (MDZ) is confounded by time- and concentration-dependent clearance of the inhibitor. Midazolam 153-162 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 19420129-1 2009 Prediction of the extent and time course of drug-drug interactions (DDIs) between the mechanism-based inhibitor diltiazem (DTZ) and the CYP3A4 substrate midazolam (MDZ) is confounded by time- and concentration-dependent clearance of the inhibitor. Midazolam 164-167 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 19420129-3 2009 Enzyme kinetic parameters (k(inact) and K(I)) for DTZ and nd-DTZ were estimated in vitro and used to model the time course of changes in the amount of CYP3A4 in the liver and gut wall, which in turn, determined the nonlinear elimination of MDZ and DTZ, and the corresponding DDI. Diltiazem 50-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 19420129-3 2009 Enzyme kinetic parameters (k(inact) and K(I)) for DTZ and nd-DTZ were estimated in vitro and used to model the time course of changes in the amount of CYP3A4 in the liver and gut wall, which in turn, determined the nonlinear elimination of MDZ and DTZ, and the corresponding DDI. nd-dtz 58-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 19420129-3 2009 Enzyme kinetic parameters (k(inact) and K(I)) for DTZ and nd-DTZ were estimated in vitro and used to model the time course of changes in the amount of CYP3A4 in the liver and gut wall, which in turn, determined the nonlinear elimination of MDZ and DTZ, and the corresponding DDI. Midazolam 240-243 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 19420129-3 2009 Enzyme kinetic parameters (k(inact) and K(I)) for DTZ and nd-DTZ were estimated in vitro and used to model the time course of changes in the amount of CYP3A4 in the liver and gut wall, which in turn, determined the nonlinear elimination of MDZ and DTZ, and the corresponding DDI. Diltiazem 61-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 151-157 19420129-9 2009 Moreover, model simulation suggested that both DTZ and nd-DTZ contributed to the overall inhibitory effect after DTZ administration, and the values of the in vitro estimated inhibition parameters and CYP3A4 turnover rate are critical for the prediction. Diltiazem 47-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 19531897-1 2009 BACKGROUND: The P2Y(12) adenosine diphosphate (ADP) receptor blocker, clopidogrel, an essential drug for the prevention of stent thrombosis after percutaneous coronary intervention (PCI), is a prodrug that requires CYP2C19- and CYP3A4-mediating activation. Clopidogrel 70-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 19531897-4 2009 The effect of polymorphisms of CYP2C19, CYP3A4 and P2Y(12) on the antiplatelet effect of clopidogrel in clinical patients was examined in the present study. Clopidogrel 89-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 19420129-9 2009 Moreover, model simulation suggested that both DTZ and nd-DTZ contributed to the overall inhibitory effect after DTZ administration, and the values of the in vitro estimated inhibition parameters and CYP3A4 turnover rate are critical for the prediction. nd-dtz 55-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 19420129-9 2009 Moreover, model simulation suggested that both DTZ and nd-DTZ contributed to the overall inhibitory effect after DTZ administration, and the values of the in vitro estimated inhibition parameters and CYP3A4 turnover rate are critical for the prediction. Diltiazem 58-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 19454483-1 2009 17alpha-Ethinyl estradiol (EE) was systematically evaluated as a reversible and time-dependent inhibitor of 11 human drug-metabolizing cytochromes P450 (P450s) (CYP1A1, CYP1A2, CYP1B1, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2J2, CYP3A4, and CYP3A5) in vitro. Ethinyl Estradiol 0-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 234-240 19451401-0 2009 Evaluation of luciferin-isopropyl acetal as a CYP3A4 substrate for human hepatocytes: effects of organic solvents, cytochrome P450 (P450) inhibitors, and P450 inducers. luciferin-isopropyl acetal 14-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 19451401-1 2009 This study represents the first report on the characterization of luciferin-isopropyl acetal (LIPA) as a CYP3A4 substrate in human hepatocytes. luciferin-isopropyl acetal 66-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 19621007-2 2009 However, one should not expect any prediction success for drugs primarily metabolized by the major cytochrome P450 enzyme, CYP3A4, whether one uses an exogenous drug or an endogenous metabolic process, such as the oxidation of cortisol. Hydrocortisone 227-235 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 19460945-0 2009 Rifampicin-activated human pregnane X receptor and CYP3A4 induction enhance acetaminophen-induced toxicity. Acetaminophen 76-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Rifampin 247-257 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Acetaminophen 262-266 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 19451401-1 2009 This study represents the first report on the characterization of luciferin-isopropyl acetal (LIPA) as a CYP3A4 substrate in human hepatocytes. luciferin-isopropyl acetal 94-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 19451401-3 2009 The nonspecific cytochrome P450 (P450) inhibitor 1-aminobenzotriazole (ABT) and the CYP3A4-selective inhibitor ketoconazole (KTZ) caused concentration-dependent inhibition of LIPA metabolism, with more than 50% inhibition observed at the lowest concentrations evaluated of 7.8 microM (ABT) and 0.78 microM (KTZ), and near 100% inhibition observed at higher concentrations. Ketoconazole 111-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 19451401-3 2009 The nonspecific cytochrome P450 (P450) inhibitor 1-aminobenzotriazole (ABT) and the CYP3A4-selective inhibitor ketoconazole (KTZ) caused concentration-dependent inhibition of LIPA metabolism, with more than 50% inhibition observed at the lowest concentrations evaluated of 7.8 microM (ABT) and 0.78 microM (KTZ), and near 100% inhibition observed at higher concentrations. Ketoconazole 125-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Acetaminophen 262-266 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 19460945-3 2009 Human PXR activation and CYP3A4 induction enhanced APAP-induced hepatotoxicity as revealed by hepatic alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated in serum, and hepatic necrosis after coadministration of rifampicin and APAP, compared with APAP administration alone. Acetaminophen 51-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 19460945-6 2009 Moreover, mRNA analysis demonstrated that CYP3A4 and other PXR target genes were significantly induced by rifampicin treatment. Rifampin 106-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 19451401-3 2009 The nonspecific cytochrome P450 (P450) inhibitor 1-aminobenzotriazole (ABT) and the CYP3A4-selective inhibitor ketoconazole (KTZ) caused concentration-dependent inhibition of LIPA metabolism, with more than 50% inhibition observed at the lowest concentrations evaluated of 7.8 microM (ABT) and 0.78 microM (KTZ), and near 100% inhibition observed at higher concentrations. 1-aminobenzotriazole 285-288 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 19451401-3 2009 The nonspecific cytochrome P450 (P450) inhibitor 1-aminobenzotriazole (ABT) and the CYP3A4-selective inhibitor ketoconazole (KTZ) caused concentration-dependent inhibition of LIPA metabolism, with more than 50% inhibition observed at the lowest concentrations evaluated of 7.8 microM (ABT) and 0.78 microM (KTZ), and near 100% inhibition observed at higher concentrations. Ketoconazole 307-310 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 19451401-4 2009 Substantially lower inhibitory effects were observed for the non-CYP3A4 inhibitors diethyldithiocarbamate, furafylline, omeprazole, orphenadrine, sulfaphenazole, and quinidine. Ditiocarb 83-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 19702548-1 2009 The present study demonstrated that in addition to CYP3A4 and CYP2D6, the metabolism of loratadine is also catalyzed by CYP1A1, CYP2C19, and to a lesser extent by CYP1A2, CYP2B6, CYP2C8, CYP2C9 and CYP3A5. Loratadine 88-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 19451401-4 2009 Substantially lower inhibitory effects were observed for the non-CYP3A4 inhibitors diethyldithiocarbamate, furafylline, omeprazole, orphenadrine, sulfaphenazole, and quinidine. furafylline 107-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 19451401-4 2009 Substantially lower inhibitory effects were observed for the non-CYP3A4 inhibitors diethyldithiocarbamate, furafylline, omeprazole, orphenadrine, sulfaphenazole, and quinidine. Omeprazole 120-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 19451401-4 2009 Substantially lower inhibitory effects were observed for the non-CYP3A4 inhibitors diethyldithiocarbamate, furafylline, omeprazole, orphenadrine, sulfaphenazole, and quinidine. Orphenadrine 132-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 19451401-4 2009 Substantially lower inhibitory effects were observed for the non-CYP3A4 inhibitors diethyldithiocarbamate, furafylline, omeprazole, orphenadrine, sulfaphenazole, and quinidine. Sulfaphenazole 146-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 19451401-4 2009 Substantially lower inhibitory effects were observed for the non-CYP3A4 inhibitors diethyldithiocarbamate, furafylline, omeprazole, orphenadrine, sulfaphenazole, and quinidine. Quinidine 166-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 19451401-6 2009 The comparatively higher inhibitory effects of DMSO relative to that for acetonitrile and methanol on LIPA metabolism were consistent with its known CYP3A4 inhibitory effects reported by others. Dimethyl Sulfoxide 47-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 19451401-6 2009 The comparatively higher inhibitory effects of DMSO relative to that for acetonitrile and methanol on LIPA metabolism were consistent with its known CYP3A4 inhibitory effects reported by others. acetonitrile 73-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 19451401-6 2009 The comparatively higher inhibitory effects of DMSO relative to that for acetonitrile and methanol on LIPA metabolism were consistent with its known CYP3A4 inhibitory effects reported by others. Methanol 90-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 19451401-7 2009 LIPA metabolism in human hepatocytes was found to be induced by the treatment of human hepatocytes with the prototypical CYP3A4 inducers rifampin, carbamazepine, omeprazole, phenobarbital, and phenytoin but not by the CYP1A2 inducer 3-methylcholanthrene. Rifampin 137-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 19451401-7 2009 LIPA metabolism in human hepatocytes was found to be induced by the treatment of human hepatocytes with the prototypical CYP3A4 inducers rifampin, carbamazepine, omeprazole, phenobarbital, and phenytoin but not by the CYP1A2 inducer 3-methylcholanthrene. Carbamazepine 147-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 19451401-7 2009 LIPA metabolism in human hepatocytes was found to be induced by the treatment of human hepatocytes with the prototypical CYP3A4 inducers rifampin, carbamazepine, omeprazole, phenobarbital, and phenytoin but not by the CYP1A2 inducer 3-methylcholanthrene. Phenobarbital 174-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 19451401-7 2009 LIPA metabolism in human hepatocytes was found to be induced by the treatment of human hepatocytes with the prototypical CYP3A4 inducers rifampin, carbamazepine, omeprazole, phenobarbital, and phenytoin but not by the CYP1A2 inducer 3-methylcholanthrene. Phenytoin 193-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 19451401-7 2009 LIPA metabolism in human hepatocytes was found to be induced by the treatment of human hepatocytes with the prototypical CYP3A4 inducers rifampin, carbamazepine, omeprazole, phenobarbital, and phenytoin but not by the CYP1A2 inducer 3-methylcholanthrene. Methylcholanthrene 233-253 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 19451401-8 2009 Although the selectivity toward CYP3A4 needs to be definitively evaluated using cDNA-expressed P450 isoforms, the results suggest that LIPA is a suitable substrate to be used with human hepatocytes for the evaluation of CYP3A4 activities. luciferin-isopropyl acetal 135-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 19460945-10 2009 These findings demonstrated that human PXR is involved in regulation of APAP-induced toxicity through CYP3A4-mediated hepatic metabolism of APAP in the presence of PXR ligands. Acetaminophen 72-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 19460945-10 2009 These findings demonstrated that human PXR is involved in regulation of APAP-induced toxicity through CYP3A4-mediated hepatic metabolism of APAP in the presence of PXR ligands. Acetaminophen 140-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 19702548-5 2009 High inter-subject variability in loratadine steady-state data is probably due to the phenotypical characteristics of CYP2D6, CYP2C19, and CYP3A4. Loratadine 34-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 19702548-6 2009 The relative abundance of CYP3A4 in the human liver exceeds that of CYP2C19 and CYP2D6 and therefore the contribution of CYP3A4 in the metabolism of loratadine should be major (approximately 70%). Loratadine 149-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 19702548-6 2009 The relative abundance of CYP3A4 in the human liver exceeds that of CYP2C19 and CYP2D6 and therefore the contribution of CYP3A4 in the metabolism of loratadine should be major (approximately 70%). Loratadine 149-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 19490052-6 2009 RESULTS: In both, humans and cell lines, the expression of testosterone metabolising CYP3A4 (human) or CYP3A11 (mouse) and AR was up-regulated when P450-inducing AEDs and/or prednisolone had been applied. Testosterone 59-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 19799546-5 2009 Reaction phenotyping shows that most of the metabolites arise from CYP3A4, the enzyme known to be well inhibited by ketoconazole. Ketoconazole 116-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 19490052-6 2009 RESULTS: In both, humans and cell lines, the expression of testosterone metabolising CYP3A4 (human) or CYP3A11 (mouse) and AR was up-regulated when P450-inducing AEDs and/or prednisolone had been applied. Prednisolone 174-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 19625112-7 2009 Macrolides and ketolides are metabolized in the liver through CYP3A4 and they can partially block the activity of the enzyme, interfering with the metabolism of other drugs that use the same metabolic pathway. Macrolides 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 19625112-7 2009 Macrolides and ketolides are metabolized in the liver through CYP3A4 and they can partially block the activity of the enzyme, interfering with the metabolism of other drugs that use the same metabolic pathway. Ketolides 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 19743543-5 2009 It is also associated with gastrointestinal disorders (constipation, nausea, vomiting) and dizziness; (6) Ranolazine is metabolised by the cytochrome P450 isoenzymes CYP 3A4 and CYP 2D6 and is also a P-glycoprotein substrate. Ranolazine 106-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-173 20183062-5 2009 Deltamethrin and fenvalerate were potent inhibitors of CYP2D6 (IC(50) values of approximately 3 micro M) while lambda-cyhalothrin potently inhibited both CYP2D6 and CYP3A4-mediated activities (IC(50)"s about 3-4 micro M). cyhalothrin 118-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-171 19593168-4 2009 In patients comedicated with fluvoxamine, a strong CYP1A2 inhibitor, clozapine and norclozapine concentrations correlate with CYP3A activity (r = 0.44, P = 0.075; r = 0.63, P = 0.007, respectively). Fluvoxamine 29-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-131 19593168-4 2009 In patients comedicated with fluvoxamine, a strong CYP1A2 inhibitor, clozapine and norclozapine concentrations correlate with CYP3A activity (r = 0.44, P = 0.075; r = 0.63, P = 0.007, respectively). Clozapine 69-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-131 19593168-4 2009 In patients comedicated with fluvoxamine, a strong CYP1A2 inhibitor, clozapine and norclozapine concentrations correlate with CYP3A activity (r = 0.44, P = 0.075; r = 0.63, P = 0.007, respectively). norclozapine 83-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-131 19478134-3 2009 Nelfinavir is cleared from the body predominantly by CYP3A metabolism and P-glycoprotein (P-gp) efflux. Nelfinavir 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 19478134-9 2009 Assuming that MDZ and DIG are selective substrates of the macaque CYP3A enzymes and P-gp, respectively, these results suggest that factors other than increased CYP3A or P-gp activity contribute to the increased clearance of protease inhibitors during M. nemestrina pregnancy. Midazolam 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 19478134-9 2009 Assuming that MDZ and DIG are selective substrates of the macaque CYP3A enzymes and P-gp, respectively, these results suggest that factors other than increased CYP3A or P-gp activity contribute to the increased clearance of protease inhibitors during M. nemestrina pregnancy. Digoxin 22-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 18294936-8 2009 Since buprenorphine is metabolized through cytochrome P450 3A4, we genotyped six genetic polymorphisms previously described in poor metabolizers but could not confirm these pharmacogenetic bases in this case. Buprenorphine 6-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-62 19575493-3 2009 RESULTS: Serum levels of hyodeoxycholic acid, the CYP3A4-mediated detoxification product of the secondary BA lithocholic acid (LCA), was increased significantly in Crohn"s disease (CD) and ulcerative colitis (UC), while most other serum BA species were decreased significantly. hyodeoxycholic acid 25-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 19575493-3 2009 RESULTS: Serum levels of hyodeoxycholic acid, the CYP3A4-mediated detoxification product of the secondary BA lithocholic acid (LCA), was increased significantly in Crohn"s disease (CD) and ulcerative colitis (UC), while most other serum BA species were decreased significantly. Lithocholic Acid 109-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 19575493-3 2009 RESULTS: Serum levels of hyodeoxycholic acid, the CYP3A4-mediated detoxification product of the secondary BA lithocholic acid (LCA), was increased significantly in Crohn"s disease (CD) and ulcerative colitis (UC), while most other serum BA species were decreased significantly. Lithocholic Acid 127-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 19575493-3 2009 RESULTS: Serum levels of hyodeoxycholic acid, the CYP3A4-mediated detoxification product of the secondary BA lithocholic acid (LCA), was increased significantly in Crohn"s disease (CD) and ulcerative colitis (UC), while most other serum BA species were decreased significantly. Bile Acids and Salts 106-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 19414584-1 2009 Clarithromycin decreases CYP3A4 activity and thus gradually inhibits its own metabolism as well as that of coadministered drugs. Clarithromycin 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 19414584-9 2009 The proposed semimechanistic population pharmacokinetic model successfully described the autoinhibition of clarithromycin metabolism and may be used to adjust the doses of other drugs that are metabolized by CYP3A4 and that are coadministered with clarithromycin. Clarithromycin 107-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 208-214 19414584-9 2009 The proposed semimechanistic population pharmacokinetic model successfully described the autoinhibition of clarithromycin metabolism and may be used to adjust the doses of other drugs that are metabolized by CYP3A4 and that are coadministered with clarithromycin. Clarithromycin 248-262 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 208-214 19309762-3 2009 Since both itraconazole and hydroxyitraconazole are effective inhibitors of cytochrome P450 (CYP) 3A4 and p-glycoprotein (pgp)-mediated efflux transporters, they have the potential to elicit drug-drug interaction with a number of CYP3A4 and/or pgp substrates. Itraconazole 11-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-236 19309762-3 2009 Since both itraconazole and hydroxyitraconazole are effective inhibitors of cytochrome P450 (CYP) 3A4 and p-glycoprotein (pgp)-mediated efflux transporters, they have the potential to elicit drug-drug interaction with a number of CYP3A4 and/or pgp substrates. hydroxyitraconazole 28-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-236 19339377-11 2009 Taken together, glucuronidation of cannabinoids depends on upstream processing including enzymes such as CYP2C9 and CYP3A4. Cannabinoids 35-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 19225771-1 2009 PURPOSE: Fluvoxamine (FVX) is metabolized by cytochrome P450 (CYP) 2D6 and CYP1A2 and inhibits CYP3A4. Fluvoxamine 9-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 19225771-1 2009 PURPOSE: Fluvoxamine (FVX) is metabolized by cytochrome P450 (CYP) 2D6 and CYP1A2 and inhibits CYP3A4. Fluvoxamine 22-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 19440701-12 2009 CONCLUSION: The CYP3A4*1B polymorphism was found to influence the pharmacokinetics of indinavir and, to some extent, the biochemical safety of indinavir. Indinavir 86-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 19440701-12 2009 CONCLUSION: The CYP3A4*1B polymorphism was found to influence the pharmacokinetics of indinavir and, to some extent, the biochemical safety of indinavir. Indinavir 143-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 19414624-5 2009 Marked increase in 6beta-hydroxylation of testosterone by CYP3A4 was also observed in the 6-day 1,25(OH)(2)D(3)-treated (100 nM) cell lysate. Testosterone 42-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 19414624-8 2009 Higher protein expression of CYP3A4, MRP2, P-gp, and MRP4 was also observed after a 6-day treatment with other vitamin D analogs (100 nM 1alpha-hydroxyvitamin D(3),1alpha-hydroxyvitamin D(2) or Hectorol, and 25-hydroxyvitamin D(3)) in Caco-2 cells, suggesting a role of 1,25(OH)(2)D(3) and analogs in the activation of enzymes and transporters via the vitamin D receptor. Vitamin D 111-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 19414624-8 2009 Higher protein expression of CYP3A4, MRP2, P-gp, and MRP4 was also observed after a 6-day treatment with other vitamin D analogs (100 nM 1alpha-hydroxyvitamin D(3),1alpha-hydroxyvitamin D(2) or Hectorol, and 25-hydroxyvitamin D(3)) in Caco-2 cells, suggesting a role of 1,25(OH)(2)D(3) and analogs in the activation of enzymes and transporters via the vitamin D receptor. 1alpha-hydroxyvitamin d 137-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 19414624-8 2009 Higher protein expression of CYP3A4, MRP2, P-gp, and MRP4 was also observed after a 6-day treatment with other vitamin D analogs (100 nM 1alpha-hydroxyvitamin D(3),1alpha-hydroxyvitamin D(2) or Hectorol, and 25-hydroxyvitamin D(3)) in Caco-2 cells, suggesting a role of 1,25(OH)(2)D(3) and analogs in the activation of enzymes and transporters via the vitamin D receptor. 1alpha-hydroxyvitamin d 164-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 19414624-8 2009 Higher protein expression of CYP3A4, MRP2, P-gp, and MRP4 was also observed after a 6-day treatment with other vitamin D analogs (100 nM 1alpha-hydroxyvitamin D(3),1alpha-hydroxyvitamin D(2) or Hectorol, and 25-hydroxyvitamin D(3)) in Caco-2 cells, suggesting a role of 1,25(OH)(2)D(3) and analogs in the activation of enzymes and transporters via the vitamin D receptor. 1 alpha-hydroxyergocalciferol 194-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 19414624-8 2009 Higher protein expression of CYP3A4, MRP2, P-gp, and MRP4 was also observed after a 6-day treatment with other vitamin D analogs (100 nM 1alpha-hydroxyvitamin D(3),1alpha-hydroxyvitamin D(2) or Hectorol, and 25-hydroxyvitamin D(3)) in Caco-2 cells, suggesting a role of 1,25(OH)(2)D(3) and analogs in the activation of enzymes and transporters via the vitamin D receptor. 25-hydroxyvitamin D 208-227 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 19501215-1 2009 BACKGROUND: Etravirine, a non-nucleoside reverse transcriptase inhibitor (NNRTI) active against NNRTI-resistant HIV, is an inducer of CYP3A4 and an inhibitor of CYP2C9/19. etravirine 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 19364830-7 2009 Formation of the nevirapine GSH conjugate was primarily catalyzed by heterologously expressed recombinant CYP3A4 and, to a lesser extent, CYP2D6, CYP2C19, and CYP2A6. Glutathione 28-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 19364830-8 2009 In addition, the quinone methide reactive metabolite was a mechanism-based inactivator of CYP3A4, with inactivation parameters K(I) = 31 microM and k(inact) = 0.029 min(-1), respectively. quinone 17-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 19379727-0 2009 DP7, a novel dihydropyridine multidrug resistance reverter, shows only weak inhibitory activity on human CYP3A enzyme(s). DP7 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-110 19379727-9 2009 The moderate inhibition of CYP isoforms of rat liver microsomes and the weak inhibition of human CYP3A4 enzyme activity operated by DP7, suggest that DP7 in man should not give rise to important, unpredictable pharmacokinetic interactions. DP7 132-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 19589229-9 2009 CONCLUSIONS: Fluorophenylpiperazine, methoxyphenylpiperazine, chlorophenylpiperazine, methylbenzylpiperazine and methylenedioxybenzylpiperazine had significant inhibitory effects on CYP2D6, CYP1A2, CYP3A4, CYP2C19 and CYP2C9 isoenzymes but each piperazine had a different inhibitory profile. diethyl 4-methylbenzylphosphonate 86-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 198-204 19589229-7 2009 The metabolism of benzylpiperazine (BZP) and trifluoromethylphenylpiperazine (TFMPP) involved CYP2D6, CYP1A2 and CYP3A4. 1-benzylpiperazine 18-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 19589229-9 2009 CONCLUSIONS: Fluorophenylpiperazine, methoxyphenylpiperazine, chlorophenylpiperazine, methylbenzylpiperazine and methylenedioxybenzylpiperazine had significant inhibitory effects on CYP2D6, CYP1A2, CYP3A4, CYP2C19 and CYP2C9 isoenzymes but each piperazine had a different inhibitory profile. Piperazine 25-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 198-204 19589229-7 2009 The metabolism of benzylpiperazine (BZP) and trifluoromethylphenylpiperazine (TFMPP) involved CYP2D6, CYP1A2 and CYP3A4. 1-benzylpiperazine 36-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 19589229-7 2009 The metabolism of benzylpiperazine (BZP) and trifluoromethylphenylpiperazine (TFMPP) involved CYP2D6, CYP1A2 and CYP3A4. 1-(3-trifluoromethylphenyl)piperazine 45-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 19589229-7 2009 The metabolism of benzylpiperazine (BZP) and trifluoromethylphenylpiperazine (TFMPP) involved CYP2D6, CYP1A2 and CYP3A4. 1-(3-trifluoromethylphenyl)piperazine 78-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 19409404-6 2009 Differentially expressed genes included the Phase I xenobiotic, fatty acid, sterol and steroid metabolism genes Cyp2b2 and CYP2B6, Cyp3a1 and CYP3A4, and Cyp4a22 and CYP4A11; Phase II conjugation enzyme genes Ugt1a1 and UGT1A1; and Phase III ABC transporter genes Abcb1 and ABCB1. Steroids 87-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 19589229-9 2009 CONCLUSIONS: Fluorophenylpiperazine, methoxyphenylpiperazine, chlorophenylpiperazine, methylbenzylpiperazine and methylenedioxybenzylpiperazine had significant inhibitory effects on CYP2D6, CYP1A2, CYP3A4, CYP2C19 and CYP2C9 isoenzymes but each piperazine had a different inhibitory profile. fluorophenylpiperazine 13-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 198-204 19589229-9 2009 CONCLUSIONS: Fluorophenylpiperazine, methoxyphenylpiperazine, chlorophenylpiperazine, methylbenzylpiperazine and methylenedioxybenzylpiperazine had significant inhibitory effects on CYP2D6, CYP1A2, CYP3A4, CYP2C19 and CYP2C9 isoenzymes but each piperazine had a different inhibitory profile. methoxyphenylpiperazine 37-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 198-204 19589229-9 2009 CONCLUSIONS: Fluorophenylpiperazine, methoxyphenylpiperazine, chlorophenylpiperazine, methylbenzylpiperazine and methylenedioxybenzylpiperazine had significant inhibitory effects on CYP2D6, CYP1A2, CYP3A4, CYP2C19 and CYP2C9 isoenzymes but each piperazine had a different inhibitory profile. chlorophenylpiperazine 62-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 198-204 19694183-6 2009 The ability of diphenytriazol to inhibit rat liver CYP1A and CYP3A suggests that in human patients complex interactions may result from co-adiministration of diphenytriazol with other agents which are also substrates for CYP1A or CYP3A enzymes. 3-(2-ethylphenyl)-5-(3-methoxyphenyl)-1H,2,4-triazol 15-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-235 19694183-6 2009 The ability of diphenytriazol to inhibit rat liver CYP1A and CYP3A suggests that in human patients complex interactions may result from co-adiministration of diphenytriazol with other agents which are also substrates for CYP1A or CYP3A enzymes. 3-(2-ethylphenyl)-5-(3-methoxyphenyl)-1H,2,4-triazol 158-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 230-235 19428250-0 2009 Selective cytochrome P450 3A4 inhibitory activity of Amaryllidaceae alkaloids. Amaryllidaceae Alkaloids 53-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-29 19332043-0 2009 Side effects after docetaxel treatment in Taiwanese breast cancer patients with CYP3A4, CYP3A5, and ABCB1 gene polymorphisms. Docetaxel 19-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 19428250-1 2009 A library of natural and semi-synthetic Amaryllidaceae alkaloids was screened for cytochrome P450 3A4 (CYP3A4) inhibitory activity. Amaryllidaceae Alkaloids 40-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-101 19428250-1 2009 A library of natural and semi-synthetic Amaryllidaceae alkaloids was screened for cytochrome P450 3A4 (CYP3A4) inhibitory activity. Amaryllidaceae Alkaloids 40-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 18839173-2 2009 In addition to rifampicin and hyperforin, the anticancer drug paclitaxel has also been shown to be an inducer of CYP3A4 via activation of the pregnane X receptor (PXR). Paclitaxel 62-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 19433356-1 2009 Previous studies have demonstrated the CYP3A4 mediated oxidation of the 5-aminooxindole motif, present in the trifluoromethylpyrimidine class of PYK-2 inhibitors, to a reactive bis-imine species, which can be trapped with glutathione (GSH) in human liver microsomal incubations. bis-imine 177-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 19433356-1 2009 Previous studies have demonstrated the CYP3A4 mediated oxidation of the 5-aminooxindole motif, present in the trifluoromethylpyrimidine class of PYK-2 inhibitors, to a reactive bis-imine species, which can be trapped with glutathione (GSH) in human liver microsomal incubations. Glutathione 222-233 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 19433356-1 2009 Previous studies have demonstrated the CYP3A4 mediated oxidation of the 5-aminooxindole motif, present in the trifluoromethylpyrimidine class of PYK-2 inhibitors, to a reactive bis-imine species, which can be trapped with glutathione (GSH) in human liver microsomal incubations. Glutathione 235-238 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 19457725-2 2009 Rifampicin is a CYP3A4 inducer while clarithromycin is known to inhibit CYP3A4. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 19457725-2 2009 Rifampicin is a CYP3A4 inducer while clarithromycin is known to inhibit CYP3A4. Clarithromycin 37-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 19489632-6 2009 CYP3A4, CYP3A5, CYP3A7, and CYP19 (aromatase) inhibition to the log concentration of beta-acid content was significant with r(2) > 0.37, suggesting that these components can account for some of the variation in inhibition of CYP metabolism. 6-Hydroxy-2-oxo-1,2-dihydroquinoline-4-carboxylic acid 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 19458107-1 2009 BACKGROUND: osartan is metabolized by CYP2C9 and CYP3A4 to an active metabolite, E-3174, which has greater antihypertensive activity than the parent compound. osartan 12-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 19458107-1 2009 BACKGROUND: osartan is metabolized by CYP2C9 and CYP3A4 to an active metabolite, E-3174, which has greater antihypertensive activity than the parent compound. losartan carboxylic acid 81-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 19371336-8 2009 Rifampicin is a strong inducer of human CYP3A; thus, the increase in 4-NP activity in human hepatocytes could be due to the induction of CYP3A. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 19371336-8 2009 Rifampicin is a strong inducer of human CYP3A; thus, the increase in 4-NP activity in human hepatocytes could be due to the induction of CYP3A. Rifampin 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-142 19433356-0 2009 Differences in CYP3A4 catalyzed bioactivation of 5-aminooxindole and 5-aminobenzsultam scaffolds in proline-rich tyrosine kinase 2 (PYK2) inhibitors: retrospective analysis by CYP3A4 molecular docking, quantum chemical calculations and glutathione adduct detection using linear ion trap/orbitrap mass spectrometry. 5-Aminooxindole 49-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 19433356-0 2009 Differences in CYP3A4 catalyzed bioactivation of 5-aminooxindole and 5-aminobenzsultam scaffolds in proline-rich tyrosine kinase 2 (PYK2) inhibitors: retrospective analysis by CYP3A4 molecular docking, quantum chemical calculations and glutathione adduct detection using linear ion trap/orbitrap mass spectrometry. 5-aminobenzsultam 69-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 19433356-1 2009 Previous studies have demonstrated the CYP3A4 mediated oxidation of the 5-aminooxindole motif, present in the trifluoromethylpyrimidine class of PYK-2 inhibitors, to a reactive bis-imine species, which can be trapped with glutathione (GSH) in human liver microsomal incubations. 5-Aminooxindole 72-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 19433356-1 2009 Previous studies have demonstrated the CYP3A4 mediated oxidation of the 5-aminooxindole motif, present in the trifluoromethylpyrimidine class of PYK-2 inhibitors, to a reactive bis-imine species, which can be trapped with glutathione (GSH) in human liver microsomal incubations. 2-(trifluoromethyl)pyrimidine 110-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 19417618-4 2009 Their hypothesis was that rifampin enhances the CYP3A-mediated metabolism of oxycodone and attenuates its pharmacologic effect. Rifampin 26-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 19417618-4 2009 Their hypothesis was that rifampin enhances the CYP3A-mediated metabolism of oxycodone and attenuates its pharmacologic effect. Oxycodone 77-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 18839173-6 2009 Finally, the effect of pre-treatment with these agents on the 1"-hydroxylation of midazolam (a specific CYP3A4 probe) was determined. Midazolam 82-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 18839173-7 2009 RESULTS: Paclitaxel, erlotinib, tamoxifen, ifosfamide, flutamide and docetaxel are able to activate PXR, while only strong PXR activation leads to significant induction of CYP3A4 activity. Paclitaxel 9-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 18839173-7 2009 RESULTS: Paclitaxel, erlotinib, tamoxifen, ifosfamide, flutamide and docetaxel are able to activate PXR, while only strong PXR activation leads to significant induction of CYP3A4 activity. Erlotinib Hydrochloride 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 18839173-7 2009 RESULTS: Paclitaxel, erlotinib, tamoxifen, ifosfamide, flutamide and docetaxel are able to activate PXR, while only strong PXR activation leads to significant induction of CYP3A4 activity. Tamoxifen 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 18839173-7 2009 RESULTS: Paclitaxel, erlotinib, tamoxifen, ifosfamide, flutamide and docetaxel are able to activate PXR, while only strong PXR activation leads to significant induction of CYP3A4 activity. Ifosfamide 43-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 18839173-7 2009 RESULTS: Paclitaxel, erlotinib, tamoxifen, ifosfamide, flutamide and docetaxel are able to activate PXR, while only strong PXR activation leads to significant induction of CYP3A4 activity. Flutamide 55-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 18839173-7 2009 RESULTS: Paclitaxel, erlotinib, tamoxifen, ifosfamide, flutamide and docetaxel are able to activate PXR, while only strong PXR activation leads to significant induction of CYP3A4 activity. Docetaxel 69-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 19251823-5 2009 Olomoucine II significantly inhibited the enzymatic activities of CYP1A2, CYP2C9, and (to a lesser degree) CYP3A4. olomoucine II 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 19299527-0 2009 Ligand diversity of human and chimpanzee CYP3A4: activation of human CYP3A4 by lithocholic acid results from positive selection. Lithocholic Acid 79-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 19299527-5 2009 Upon addition of alpha-naphthoflavone (25 microM), human CYP3A4 showed a slightly decreased substrate concentration at which 50% of the maximal rate V(max) is reached for 7-BFC, whereas chimpanzee CYP3A4 showed a >2-fold increase. alpha-naphthoflavone 17-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 19299527-7 2009 A striking exception was the hepatotoxic secondary bile acid lithocholic acid, which at saturation caused a 5-fold increase in 7-BFC debenzylation by human CYP3A4 but not by chimpanzee CYP3A4. Bile Acids and Salts 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 19299527-7 2009 A striking exception was the hepatotoxic secondary bile acid lithocholic acid, which at saturation caused a 5-fold increase in 7-BFC debenzylation by human CYP3A4 but not by chimpanzee CYP3A4. Lithocholic Acid 61-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 19299527-7 2009 A striking exception was the hepatotoxic secondary bile acid lithocholic acid, which at saturation caused a 5-fold increase in 7-BFC debenzylation by human CYP3A4 but not by chimpanzee CYP3A4. 7-benzyloxy-4-trifluoromethylcoumarin 127-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 19299527-8 2009 Mutagenesis of human CYP3A4 revealed that at least four of the six amino acids positively selected in the human lineage contribute to the activating effect of lithocholic acid. Lithocholic Acid 159-175 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 19299527-10 2009 Positive selection on the human CYP3A4 may have been triggered by an increased load of dietary steroids, which led to a novel defense mechanism against cholestasis. Steroids 95-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 19307295-2 2009 Over half of the compounds tested (14 of 24) were identified as time-dependent inhibitors of CYP3A4 and high mRNA/activity ratios (>10) were consistent with CYP3A4 time-dependent inhibition for compounds such as troleandomycin, ritonavir, and verapamil. Troleandomycin 215-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 19307295-2 2009 Over half of the compounds tested (14 of 24) were identified as time-dependent inhibitors of CYP3A4 and high mRNA/activity ratios (>10) were consistent with CYP3A4 time-dependent inhibition for compounds such as troleandomycin, ritonavir, and verapamil. Troleandomycin 215-229 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 19307295-2 2009 Over half of the compounds tested (14 of 24) were identified as time-dependent inhibitors of CYP3A4 and high mRNA/activity ratios (>10) were consistent with CYP3A4 time-dependent inhibition for compounds such as troleandomycin, ritonavir, and verapamil. Ritonavir 231-240 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 19307295-2 2009 Over half of the compounds tested (14 of 24) were identified as time-dependent inhibitors of CYP3A4 and high mRNA/activity ratios (>10) were consistent with CYP3A4 time-dependent inhibition for compounds such as troleandomycin, ritonavir, and verapamil. Ritonavir 231-240 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 19307295-2 2009 Over half of the compounds tested (14 of 24) were identified as time-dependent inhibitors of CYP3A4 and high mRNA/activity ratios (>10) were consistent with CYP3A4 time-dependent inhibition for compounds such as troleandomycin, ritonavir, and verapamil. Verapamil 246-255 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 19307295-2 2009 Over half of the compounds tested (14 of 24) were identified as time-dependent inhibitors of CYP3A4 and high mRNA/activity ratios (>10) were consistent with CYP3A4 time-dependent inhibition for compounds such as troleandomycin, ritonavir, and verapamil. Verapamil 246-255 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 19282395-0 2009 Characterization of dasatinib and its structural analogs as CYP3A4 mechanism-based inactivators and the proposed bioactivation pathways. Dasatinib 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 19282395-2 2009 Dasatinib is extensively metabolized in humans by CYP3A4. Dasatinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 19282395-3 2009 In this study, we report that the bioactivation of dasatinib by CYP3A4 proceeds through a reactive intermediate that leads to CYP3A4 inactivation with K(I) = 6.3 microM and k(inact) = 0.034 min(-1). Dasatinib 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 19282395-3 2009 In this study, we report that the bioactivation of dasatinib by CYP3A4 proceeds through a reactive intermediate that leads to CYP3A4 inactivation with K(I) = 6.3 microM and k(inact) = 0.034 min(-1). Dasatinib 51-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 19282395-9 2009 Numerous analogs are presented that did effectively block the formation of glutathione adducts and prevent the inactivation of CYP3A4. Glutathione 75-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 19299523-7 2009 The highest contributions to both metabolic steps as calculated from the enzyme kinetic data were obtained for CYP3A4 and CYP2D6 at substrate concentrations corresponding to plasma concentrations of recreational users after intake of racemic MDEA. 3,4-methylenedioxyethamphetamine 242-246 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 19172254-0 2009 Effects of allicin on CYP2C19 and CYP3A4 activity in healthy volunteers with different CYP2C19 genotypes. allicin 11-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 19251823-6 2009 The results indicate that use of olomoucine II as a drug could affect the activities of CYP3A4, CYP1A2, and CYP2C9 in vivo. olomoucine II 33-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 19251824-5 2009 In HepG2 and LS180 cells stably transduced with PXR.1, PXR target genes (CYP3A4, MDR1, CYP2B6, and UGT1A1) were higher than mock-transduced cells in the absence of ligand and were further induced in the presence of rifampin. Rifampin 215-223 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 19298836-1 2009 A novel aflatoxin B(1) bioassay was created by introducing a Lipomyces kononenkoae alpha-amylase gene into a strain of S. cerevisiae capable of expressing the human cytochrome P450 3A4 (CYP3A4), and the cognate human CYP450 reductase. Aflatoxin B1 8-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 165-184 19347334-7 2009 CONCLUSIONS: Fesoterodine dosage should not exceed 4 mg once daily when taken concomitantly with potent CYP3A4 inhibitors. fesoterodine 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 19347334-8 2009 Coadministration of CYP3A4 inducers with fesoterodine may produce subtherapeutic 5-HMT exposures. fesoterodine 41-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 19298836-1 2009 A novel aflatoxin B(1) bioassay was created by introducing a Lipomyces kononenkoae alpha-amylase gene into a strain of S. cerevisiae capable of expressing the human cytochrome P450 3A4 (CYP3A4), and the cognate human CYP450 reductase. Aflatoxin B1 8-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 186-192 19402636-6 2009 Furthermore, electrochemically driven drug metabolism reactions of CYP3A4 were clearly observed by voltammetry, and these reactions were inhibited by a CYP3A4 inhibitor, ketoconazole. Ketoconazole 170-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 19293388-7 2009 Human CYP3A inhibitors erythromycin (0.5 mM), ketoconazole (0.5 microM), and troleandomycin (0.01-1 mM), but not the CYP2C inhibitor, sulfaphenazole (3 microM), significantly inhibited the depletion of NFV in hepatic S-9 fractions and expressed rhesus CYP3A64 enzyme. Erythromycin 23-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-11 19293388-7 2009 Human CYP3A inhibitors erythromycin (0.5 mM), ketoconazole (0.5 microM), and troleandomycin (0.01-1 mM), but not the CYP2C inhibitor, sulfaphenazole (3 microM), significantly inhibited the depletion of NFV in hepatic S-9 fractions and expressed rhesus CYP3A64 enzyme. Ketoconazole 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-11 19293388-7 2009 Human CYP3A inhibitors erythromycin (0.5 mM), ketoconazole (0.5 microM), and troleandomycin (0.01-1 mM), but not the CYP2C inhibitor, sulfaphenazole (3 microM), significantly inhibited the depletion of NFV in hepatic S-9 fractions and expressed rhesus CYP3A64 enzyme. Troleandomycin 77-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-11 19302272-2 2009 Azole antifungal drugs inhibit CYP3A4, resulting in significant metabolic drug-drug interactions. Azoles 0-5 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 19389876-1 2009 Ambrisentan is an endothelin type A (ET(A))-selective receptor antagonist that is metabolized primarily by glucuronidation but also undergoes oxidative metabolism by CYP3A4. ambrisentan 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 166-172 19389876-2 2009 The potential for ketoconazole, the archetypal strong inhibitor of CYP3A4, to alter the pharmacokinetic profile of ambrisentan and its oxidative metabolite, 4-hydroxymethyl ambrisentan, was assessed in an open-label, nonrandomized, 2-period, single-sequence study in 16 healthy men. Ketoconazole 18-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 19389876-2 2009 The potential for ketoconazole, the archetypal strong inhibitor of CYP3A4, to alter the pharmacokinetic profile of ambrisentan and its oxidative metabolite, 4-hydroxymethyl ambrisentan, was assessed in an open-label, nonrandomized, 2-period, single-sequence study in 16 healthy men. ambrisentan 115-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 19530969-2 2009 Statins are cholesterol-lowering drugs that are extensively metabolized by CYP3A4 and CYP3A5. Cholesterol 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 19402636-6 2009 Furthermore, electrochemically driven drug metabolism reactions of CYP3A4 were clearly observed by voltammetry, and these reactions were inhibited by a CYP3A4 inhibitor, ketoconazole. Ketoconazole 170-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 152-158 19249324-0 2009 Pyrethroid insecticides: isoform-dependent hydrolysis, induction of cytochrome P450 3A4 and evidence on the involvement of the pregnane X receptor. Pyrethrins 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-87 19364136-6 2009 On the basis of the coupling between the LSPR of the Ag nanoparticles and the electronic resonances of the heme chromophore in CYP3A4-Nanodiscs, LSPR spectroscopy is used to detect drug binding with high sensitivity. Heme 107-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 19135037-9 2009 Herein, we report that there is low potential for DDI with SR13668 and PMCol due to enzyme induction of CYP1A2, CYP2B6, and CYP3A4 expression at the concentrations examined. SR 13668 59-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 19135037-9 2009 Herein, we report that there is low potential for DDI with SR13668 and PMCol due to enzyme induction of CYP1A2, CYP2B6, and CYP3A4 expression at the concentrations examined. 2,2,5,7,8-pentamethyl-1-hydroxychroman 71-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 19249324-4 2009 The aim of this study was to determine whether pyrethroids induce carboxylesterases and CYP3A4, and whether the induction is correlated inversely with their hydrolysis. Pyrethrins 47-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 19249324-8 2009 In primary human hepatocytes, all pyrethroids except tetramethrin significantly induced CYP3A4. Pyrethrins 34-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 19249324-8 2009 In primary human hepatocytes, all pyrethroids except tetramethrin significantly induced CYP3A4. tetramethrin 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 19429418-5 2009 In human ileum and liver, 1,25(OH)(2)D(3) and DEX induced CYP3A4 expression, whereas CDCA induced CYP3A4 expression in liver only. Dexamethasone 46-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 19429418-5 2009 In human ileum and liver, 1,25(OH)(2)D(3) and DEX induced CYP3A4 expression, whereas CDCA induced CYP3A4 expression in liver only. Chenodeoxycholic Acid 85-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 19429419-4 2009 Simvastatin lactone, but not the acid form, exhibited a strong inductive effect on the mRNA expression of MDR1 and CYP3A in a dose-dependent manner. Simvastatin 0-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-120 19429419-5 2009 Sulforaphane significantly suppressed the expression of MDR1 and CYP3A mRNAs induced by atorvastatin lactone, lovastatin acid, and lovastatin lactone, comparable to the control level, and moderately inhibited that by cerivastatin acid, fluvastatin acid and simvastatin lactone. sulforaphane 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 19429419-5 2009 Sulforaphane significantly suppressed the expression of MDR1 and CYP3A mRNAs induced by atorvastatin lactone, lovastatin acid, and lovastatin lactone, comparable to the control level, and moderately inhibited that by cerivastatin acid, fluvastatin acid and simvastatin lactone. Atorvastatin lactone 88-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 19429419-5 2009 Sulforaphane significantly suppressed the expression of MDR1 and CYP3A mRNAs induced by atorvastatin lactone, lovastatin acid, and lovastatin lactone, comparable to the control level, and moderately inhibited that by cerivastatin acid, fluvastatin acid and simvastatin lactone. mevinolinic acid 110-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 19429419-5 2009 Sulforaphane significantly suppressed the expression of MDR1 and CYP3A mRNAs induced by atorvastatin lactone, lovastatin acid, and lovastatin lactone, comparable to the control level, and moderately inhibited that by cerivastatin acid, fluvastatin acid and simvastatin lactone. Lovastatin 131-149 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 19429419-5 2009 Sulforaphane significantly suppressed the expression of MDR1 and CYP3A mRNAs induced by atorvastatin lactone, lovastatin acid, and lovastatin lactone, comparable to the control level, and moderately inhibited that by cerivastatin acid, fluvastatin acid and simvastatin lactone. cerivastatin 217-234 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-70 19417737-0 2009 Bufalin inhibits CYP3A4 activity in vitro and in vivo. bufalin 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 19417737-2 2009 METHODS: Recombinant human CYP3A4 was incubated with bufalin in vitro. bufalin 53-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-33 19417737-3 2009 Bufalin was administered ig and iv to Wistar rats to further estimate its impact on CYP3A4, and midazolam was given to index the activity of CYP3A4. bufalin 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 19417737-5 2009 Bufalin affected CYP3A4 activity with increases in AUC(0-t) and t(1/2), and decreases in CL and the formation of 1-hydroxy-midazolam after ig or iv administration of midazolam (P<0.05). bufalin 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 19417737-8 2009 The likelihood of an interaction between bufalin and the CYP3A4-metabolized drugs in human might not be negated. bufalin 41-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 19358519-9 2009 The formation of GSH was only observed with the incubation of CYP3A4. Glutathione 17-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 19011599-3 2009 Retroviral transfer of CYP3A4 increased 9L gliosarcoma cell chemosensitivity to MMDX 120-fold (IC(50)=0.2 nM in 9L/3A4 cells). methoxy-morpholinyl-doxorubicin 80-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 19011599-4 2009 In CHO cells, overexpression of P450 reductase in combination with CYP3A4 enhanced chemosensitivity to MMDX, and to ifosfamide, another CYP3A4 prodrug, 11- to 23-fold compared with CYP3A4 expression alone. CAV protocol 3-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 19011599-4 2009 In CHO cells, overexpression of P450 reductase in combination with CYP3A4 enhanced chemosensitivity to MMDX, and to ifosfamide, another CYP3A4 prodrug, 11- to 23-fold compared with CYP3A4 expression alone. methoxy-morpholinyl-doxorubicin 103-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 19011599-4 2009 In CHO cells, overexpression of P450 reductase in combination with CYP3A4 enhanced chemosensitivity to MMDX, and to ifosfamide, another CYP3A4 prodrug, 11- to 23-fold compared with CYP3A4 expression alone. Ifosfamide 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 19011599-4 2009 In CHO cells, overexpression of P450 reductase in combination with CYP3A4 enhanced chemosensitivity to MMDX, and to ifosfamide, another CYP3A4 prodrug, 11- to 23-fold compared with CYP3A4 expression alone. Ifosfamide 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 19011599-4 2009 In CHO cells, overexpression of P450 reductase in combination with CYP3A4 enhanced chemosensitivity to MMDX, and to ifosfamide, another CYP3A4 prodrug, 11- to 23-fold compared with CYP3A4 expression alone. Ifosfamide 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 19011599-12 2009 These studies demonstrate that human CYP3A4 has strong potential for MMDX prodrug-activation therapy and suggest that endogenous tumor cell expression of CYP3A4, and not hepatic CYP3A4 activity, is a key determinant of responsiveness to MMDX therapy in cancer patients in vivo. methoxy-morpholinyl-doxorubicin 69-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 19011599-12 2009 These studies demonstrate that human CYP3A4 has strong potential for MMDX prodrug-activation therapy and suggest that endogenous tumor cell expression of CYP3A4, and not hepatic CYP3A4 activity, is a key determinant of responsiveness to MMDX therapy in cancer patients in vivo. methoxy-morpholinyl-doxorubicin 69-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 19011599-12 2009 These studies demonstrate that human CYP3A4 has strong potential for MMDX prodrug-activation therapy and suggest that endogenous tumor cell expression of CYP3A4, and not hepatic CYP3A4 activity, is a key determinant of responsiveness to MMDX therapy in cancer patients in vivo. methoxy-morpholinyl-doxorubicin 69-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 18752284-2 2009 Cytochrome P450 3A (CYP3A) including CYP3A5 are involved in the metabolism of amlodipine and it was reported that polymorphic CYP3A5 genotype modulates the plasma levels of amlodipine and thus affect its pharmacokinetics. Amlodipine 78-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-18 18752284-2 2009 Cytochrome P450 3A (CYP3A) including CYP3A5 are involved in the metabolism of amlodipine and it was reported that polymorphic CYP3A5 genotype modulates the plasma levels of amlodipine and thus affect its pharmacokinetics. Amlodipine 78-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-25 18752284-2 2009 Cytochrome P450 3A (CYP3A) including CYP3A5 are involved in the metabolism of amlodipine and it was reported that polymorphic CYP3A5 genotype modulates the plasma levels of amlodipine and thus affect its pharmacokinetics. Amlodipine 173-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-18 18752284-2 2009 Cytochrome P450 3A (CYP3A) including CYP3A5 are involved in the metabolism of amlodipine and it was reported that polymorphic CYP3A5 genotype modulates the plasma levels of amlodipine and thus affect its pharmacokinetics. Amlodipine 173-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-25 19358519-10 2009 In addition, the level of these GSH conjugates in human microsomes was reduced upon the addition of a CYP3A4 inhibitor ketoconazole. Glutathione 32-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 19358519-10 2009 In addition, the level of these GSH conjugates in human microsomes was reduced upon the addition of a CYP3A4 inhibitor ketoconazole. Ketoconazole 119-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 19358519-12 2009 These studies suggest that the CYP3A4 mediated quinone methide formation was associated with dauricine bioactivation. quinone 47-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 19358519-12 2009 These studies suggest that the CYP3A4 mediated quinone methide formation was associated with dauricine bioactivation. dauricine 93-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 19411315-6 2009 Because ixabepilone exposure is greater in patients with hepatic impairment and those receiving concomitant strong cytochrome P-450 CYP3A4 inhibitors, dose adjustments and restrictions are recommended according to the degree of hepatic impairment, whether ixabepilone is administered alone or in combination with capecitabine, and whether a strong CYP3A4 inhibitor is being coadministered. ixabepilone 8-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 19232844-2 2009 Methadone clearance and the drug interactions have been attributed to CYP3A4, but actual mechanisms of methadone clearance and the nelfinavir interaction are unknown. Methadone 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 19232844-4 2009 CYP3A4/5 and transporters were assessed using alfentanil and fexofenadine, respectively. Alfentanil 46-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 19232844-4 2009 CYP3A4/5 and transporters were assessed using alfentanil and fexofenadine, respectively. fexofenadine 61-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 19246723-8 2009 However, the major oxidative metabolic pathway for clopidogrel by which the reactive intermediate is formed is CYP3A4. Clopidogrel 51-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 111-117 19411315-6 2009 Because ixabepilone exposure is greater in patients with hepatic impairment and those receiving concomitant strong cytochrome P-450 CYP3A4 inhibitors, dose adjustments and restrictions are recommended according to the degree of hepatic impairment, whether ixabepilone is administered alone or in combination with capecitabine, and whether a strong CYP3A4 inhibitor is being coadministered. ixabepilone 8-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 348-354 19420891-5 2009 These results suggest that the administration of antibiotics with activity against LCA-producing bacteria can also cause a decrease in the LCA level in humans, which may lower CYP3A4 expression. Lithocholic Acid 83-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 19420891-5 2009 These results suggest that the administration of antibiotics with activity against LCA-producing bacteria can also cause a decrease in the LCA level in humans, which may lower CYP3A4 expression. Lithocholic Acid 139-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 19343062-1 2009 AIM: To evaluate the potential drug-drug interactions between bifendate and cyclosporine, a substrate of CYP3A4, in relation to different CYP3A4*18B genotype groups. bifendate 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 19384171-2 2009 We have determined the genotypic frequencies of the CYP3A and ATP-binding cassette sub-family B member 1 (ABCB1) genes, which encode the CYP3A and P-gp proteins, respectively, in Korean organ transplant recipients and donors, and have assessed the influence of CYP3A and ABCB1 polymorphisms on tacrolimus concentrations. Tacrolimus 294-304 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-57 19384171-2 2009 We have determined the genotypic frequencies of the CYP3A and ATP-binding cassette sub-family B member 1 (ABCB1) genes, which encode the CYP3A and P-gp proteins, respectively, in Korean organ transplant recipients and donors, and have assessed the influence of CYP3A and ABCB1 polymorphisms on tacrolimus concentrations. Tacrolimus 294-304 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-142 19384171-2 2009 We have determined the genotypic frequencies of the CYP3A and ATP-binding cassette sub-family B member 1 (ABCB1) genes, which encode the CYP3A and P-gp proteins, respectively, in Korean organ transplant recipients and donors, and have assessed the influence of CYP3A and ABCB1 polymorphisms on tacrolimus concentrations. Tacrolimus 294-304 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-142 18950609-12 2009 Results with the isoform-selective inhibitors suggest that the isoforms inhibited by ketoconazole (mainly CYP3A4) and diethyldithiocarbamate (mainly CYP2A6, and CYP2E1), but not the isoforms inhibited by furafylline (mainly CYP1A2), sulfaphenazole (mainly CYP2C9) and quinidine (mainly CYP2D6) are involved in the metabolic activation of AFB1. Ketoconazole 85-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 18950609-12 2009 Results with the isoform-selective inhibitors suggest that the isoforms inhibited by ketoconazole (mainly CYP3A4) and diethyldithiocarbamate (mainly CYP2A6, and CYP2E1), but not the isoforms inhibited by furafylline (mainly CYP1A2), sulfaphenazole (mainly CYP2C9) and quinidine (mainly CYP2D6) are involved in the metabolic activation of AFB1. furafylline 204-215 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 18950609-12 2009 Results with the isoform-selective inhibitors suggest that the isoforms inhibited by ketoconazole (mainly CYP3A4) and diethyldithiocarbamate (mainly CYP2A6, and CYP2E1), but not the isoforms inhibited by furafylline (mainly CYP1A2), sulfaphenazole (mainly CYP2C9) and quinidine (mainly CYP2D6) are involved in the metabolic activation of AFB1. Sulfaphenazole 233-247 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 18950609-12 2009 Results with the isoform-selective inhibitors suggest that the isoforms inhibited by ketoconazole (mainly CYP3A4) and diethyldithiocarbamate (mainly CYP2A6, and CYP2E1), but not the isoforms inhibited by furafylline (mainly CYP1A2), sulfaphenazole (mainly CYP2C9) and quinidine (mainly CYP2D6) are involved in the metabolic activation of AFB1. Quinidine 268-277 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 18950609-12 2009 Results with the isoform-selective inhibitors suggest that the isoforms inhibited by ketoconazole (mainly CYP3A4) and diethyldithiocarbamate (mainly CYP2A6, and CYP2E1), but not the isoforms inhibited by furafylline (mainly CYP1A2), sulfaphenazole (mainly CYP2C9) and quinidine (mainly CYP2D6) are involved in the metabolic activation of AFB1. Aflatoxin B1 338-342 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 19144646-6 2009 The chromatin immunoprecipitation (ChIP) assay showed that PRMT1 was recruited to the regulatory region of the PXR target gene cytochrome P450 3A4 (CYP3A4), with a concomitant methylation of arginine 3 of histone H4, in response to the PXR agonist rifampicin. Rifampin 248-258 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 19253920-2 2009 Previous studies have suggested that some statins may inhibit the antiplatelet effects of clopidogrel via competitive metabolism of its activating enzyme cytochrome P450 3A4 (CYP3A4). Clopidogrel 90-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-173 19253920-2 2009 Previous studies have suggested that some statins may inhibit the antiplatelet effects of clopidogrel via competitive metabolism of its activating enzyme cytochrome P450 3A4 (CYP3A4). Clopidogrel 90-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 19253920-11 2009 CONCLUSIONS: In this PCI cohort, the association of clopidogrel with CYP3A4-metabolized statins did not demonstrate an increased early risk of adverse cardiovascular events, although a small risk could not be completely excluded. Clopidogrel 52-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 19384171-0 2009 Tacrolimus concentrations in relation to CYP3A and ABCB1 polymorphisms among solid organ transplant recipients in Korea. Tacrolimus 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-46 19384171-1 2009 BACKGROUND: Cytochrome P450 3A (CYP3A) and the drug transporter P-glycoprotein (P-gp) affect the bioavailability of tacrolimus, the most commonly used immunosuppressive agent in organ transplant recipients. Tacrolimus 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-30 19384171-1 2009 BACKGROUND: Cytochrome P450 3A (CYP3A) and the drug transporter P-glycoprotein (P-gp) affect the bioavailability of tacrolimus, the most commonly used immunosuppressive agent in organ transplant recipients. Tacrolimus 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-37 19448787-9 2009 CONCLUSION: The inhibitory effects of BZP and TFMPP observed in this study are of potential significance to clinical practice because CYP2D6, CYP1A2, and CYP3A4 are involved in the metabolism of many commonly used drugs. 1-benzylpiperazine 38-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 19448787-9 2009 CONCLUSION: The inhibitory effects of BZP and TFMPP observed in this study are of potential significance to clinical practice because CYP2D6, CYP1A2, and CYP3A4 are involved in the metabolism of many commonly used drugs. 1-(3-trifluoromethylphenyl)piperazine 46-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 19022234-6 2009 By co-treatment with specific inhibitors for cytochrome P450 (CYP) 2C and CYP3A - the major phase I enzymes involved in liver xenobiotic metabolism - we could confirm the prominent role of CYP3A in the bioactivation of troglitazone as well as the role of CYP3A and CYP2C in the activation of diclofenac. Troglitazone 219-231 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-79 19022234-6 2009 By co-treatment with specific inhibitors for cytochrome P450 (CYP) 2C and CYP3A - the major phase I enzymes involved in liver xenobiotic metabolism - we could confirm the prominent role of CYP3A in the bioactivation of troglitazone as well as the role of CYP3A and CYP2C in the activation of diclofenac. Troglitazone 219-231 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-194 19022234-6 2009 By co-treatment with specific inhibitors for cytochrome P450 (CYP) 2C and CYP3A - the major phase I enzymes involved in liver xenobiotic metabolism - we could confirm the prominent role of CYP3A in the bioactivation of troglitazone as well as the role of CYP3A and CYP2C in the activation of diclofenac. Troglitazone 219-231 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-194 19022234-6 2009 By co-treatment with specific inhibitors for cytochrome P450 (CYP) 2C and CYP3A - the major phase I enzymes involved in liver xenobiotic metabolism - we could confirm the prominent role of CYP3A in the bioactivation of troglitazone as well as the role of CYP3A and CYP2C in the activation of diclofenac. Diclofenac 292-302 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-79 19022234-6 2009 By co-treatment with specific inhibitors for cytochrome P450 (CYP) 2C and CYP3A - the major phase I enzymes involved in liver xenobiotic metabolism - we could confirm the prominent role of CYP3A in the bioactivation of troglitazone as well as the role of CYP3A and CYP2C in the activation of diclofenac. Diclofenac 292-302 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-194 19022234-6 2009 By co-treatment with specific inhibitors for cytochrome P450 (CYP) 2C and CYP3A - the major phase I enzymes involved in liver xenobiotic metabolism - we could confirm the prominent role of CYP3A in the bioactivation of troglitazone as well as the role of CYP3A and CYP2C in the activation of diclofenac. Diclofenac 292-302 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-194 19144646-6 2009 The chromatin immunoprecipitation (ChIP) assay showed that PRMT1 was recruited to the regulatory region of the PXR target gene cytochrome P450 3A4 (CYP3A4), with a concomitant methylation of arginine 3 of histone H4, in response to the PXR agonist rifampicin. arginine 3 191-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-146 19144646-6 2009 The chromatin immunoprecipitation (ChIP) assay showed that PRMT1 was recruited to the regulatory region of the PXR target gene cytochrome P450 3A4 (CYP3A4), with a concomitant methylation of arginine 3 of histone H4, in response to the PXR agonist rifampicin. arginine 3 191-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 19144646-6 2009 The chromatin immunoprecipitation (ChIP) assay showed that PRMT1 was recruited to the regulatory region of the PXR target gene cytochrome P450 3A4 (CYP3A4), with a concomitant methylation of arginine 3 of histone H4, in response to the PXR agonist rifampicin. Rifampin 248-258 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-146 19343062-1 2009 AIM: To evaluate the potential drug-drug interactions between bifendate and cyclosporine, a substrate of CYP3A4, in relation to different CYP3A4*18B genotype groups. bifendate 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 19343062-1 2009 AIM: To evaluate the potential drug-drug interactions between bifendate and cyclosporine, a substrate of CYP3A4, in relation to different CYP3A4*18B genotype groups. Cyclosporine 76-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 19343062-1 2009 AIM: To evaluate the potential drug-drug interactions between bifendate and cyclosporine, a substrate of CYP3A4, in relation to different CYP3A4*18B genotype groups. Cyclosporine 76-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 19343062-7 2009 The oral clearance of cyclosporine was altered in all the subjects, with substantial increases by 10.2%+/-4.4% (P=0.004) in CYP3A4*1/*1 subjects, 14.0%+/-12.0% (P=0.048) in CYP3A4*1/*18B subjects, and 32.4%+/-21.7% (P=0.013) in CYP3A4*18B/*18B subjects. Cyclosporine 22-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 124-130 19343062-7 2009 The oral clearance of cyclosporine was altered in all the subjects, with substantial increases by 10.2%+/-4.4% (P=0.004) in CYP3A4*1/*1 subjects, 14.0%+/-12.0% (P=0.048) in CYP3A4*1/*18B subjects, and 32.4%+/-21.7% (P=0.013) in CYP3A4*18B/*18B subjects. Cyclosporine 22-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 19343062-7 2009 The oral clearance of cyclosporine was altered in all the subjects, with substantial increases by 10.2%+/-4.4% (P=0.004) in CYP3A4*1/*1 subjects, 14.0%+/-12.0% (P=0.048) in CYP3A4*1/*18B subjects, and 32.4%+/-21.7% (P=0.013) in CYP3A4*18B/*18B subjects. Cyclosporine 22-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 173-179 19343062-8 2009 CONCLUSION: These results suggest that bifendate decreases the plasma concentration of cyclosporine in a CYP3A4 genotype-dependent manner. bifendate 39-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 19343062-8 2009 CONCLUSION: These results suggest that bifendate decreases the plasma concentration of cyclosporine in a CYP3A4 genotype-dependent manner. Cyclosporine 87-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-111 19258444-2 2009 Following administration, sunitinib is metabolized by cytochrome P450 3A4 to an active metabolite (SU12662). Sunitinib 26-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-73 19336903-11 2009 In conclusion, the basal structure and the substituents of flavonoids are important in the inhibitory effects of flavonoids on CYP3A activity. Flavonoids 59-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 19336903-11 2009 In conclusion, the basal structure and the substituents of flavonoids are important in the inhibitory effects of flavonoids on CYP3A activity. Flavonoids 113-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-132 19336906-4 2009 On the other hand, pranlukast reversibly inhibited CYP2C8 and/or 2C9, and CYP3A4, with K(i) values of 3.9 and 4.1 micromol/l, respectively. pranlukast 19-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 19336903-4 2009 In this study, we investigated the inhibitory potentials on cytochrome P450 (CYP) 3A activity of 23 flavonoids using human liver microsomes, and tried to identify the molecular features that cause the inhibition of CYP3A. Flavonoids 100-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 215-220 19336903-5 2009 The activity of testosterone 6beta-hydroxylate was evaluated to quantify CYP3A activity. testosterone 6beta-hydroxylate 16-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 19336903-6 2009 We analyzed Quantification Theory I, in which extreme values of the inhibitory effects of CYP3A activity were tested with flavonoids supplied at a level of 10 microM. Flavonoids 122-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 19336903-9 2009 On the other hand, flavones with the basal structure and hydroxylation at positions 7 and 4" showed significantly increased inhibitory effects on CYP3A activity. Flavones 19-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-151 19258444-2 2009 Following administration, sunitinib is metabolized by cytochrome P450 3A4 to an active metabolite (SU12662). SU 12662 99-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-73 19158313-0 2009 Human pregnane X receptor activation and CYP3A4/CYP2B6 induction by 2,3-oxidosqualene:lanosterol cyclase inhibition. 2,3-oxidosqualene 68-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 19371315-1 2009 AIMS: To characterize the impact of potent CYP3A4 inhibition and induction on lapatinib pharmacokinetics. Lapatinib 78-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 19371315-9 2009 CONCLUSIONS: Systemic exposure to lapatinib was significantly altered by potent inhibition and induction of CYP3A4. Lapatinib 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 19371318-1 2009 AIMS: Midazolam (MDZ) is a benzodiazepine used as a CYP3A4 probe in clinical and in vitro studies. Midazolam 6-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 19371318-1 2009 AIMS: Midazolam (MDZ) is a benzodiazepine used as a CYP3A4 probe in clinical and in vitro studies. Midazolam 17-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 19371318-1 2009 AIMS: Midazolam (MDZ) is a benzodiazepine used as a CYP3A4 probe in clinical and in vitro studies. Benzodiazepines 27-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 19144769-2 2009 Racemic, (R)- and (S)-fluoxetine are potent reversible inhibitors of CYP2D6, and the racemate has been shown to be a mechanism-based inhibitor of CYP3A4. (r)- and 9-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 146-152 18654747-7 2009 Cytochrome P450 3A4 (CYP3A4) activity was determined by an erythromycin breath test (EBT) prior to diflomotecan administration in cycles 1 and 2. Erythromycin 59-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 18654747-7 2009 Cytochrome P450 3A4 (CYP3A4) activity was determined by an erythromycin breath test (EBT) prior to diflomotecan administration in cycles 1 and 2. Erythromycin 59-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 18654747-7 2009 Cytochrome P450 3A4 (CYP3A4) activity was determined by an erythromycin breath test (EBT) prior to diflomotecan administration in cycles 1 and 2. ebt 85-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 18654747-7 2009 Cytochrome P450 3A4 (CYP3A4) activity was determined by an erythromycin breath test (EBT) prior to diflomotecan administration in cycles 1 and 2. ebt 85-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 18654747-7 2009 Cytochrome P450 3A4 (CYP3A4) activity was determined by an erythromycin breath test (EBT) prior to diflomotecan administration in cycles 1 and 2. diflomotecan 99-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-19 18654747-7 2009 Cytochrome P450 3A4 (CYP3A4) activity was determined by an erythromycin breath test (EBT) prior to diflomotecan administration in cycles 1 and 2. diflomotecan 99-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 19158314-0 2009 CYP3A4-mediated ester cleavage as the major metabolic pathway of the oral taxane 3"-tert-butyl-3"-N-tert-butyloxycarbonyl-4-deacetyl-3"-dephenyl-3"-N-debenzoyl-4-O-methoxycarbonyl-paclitaxel (BMS-275183). Esters 16-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 19158314-0 2009 CYP3A4-mediated ester cleavage as the major metabolic pathway of the oral taxane 3"-tert-butyl-3"-N-tert-butyloxycarbonyl-4-deacetyl-3"-dephenyl-3"-N-debenzoyl-4-O-methoxycarbonyl-paclitaxel (BMS-275183). BMS-275183 192-202 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 19601875-3 2009 Glutathione and cyanide did not inhibit the enzymes at concentrations up to 10 mM; however methoxylamine did show inhibition, with IC(50) values of 0.53 mM for CYP1A2, 4.12 mM for CYP2C9, 2.04 mM for CYP2C19, 9.72 mM for CYP2D6, and 1.26 and >10 mM for CYP3A4/5 (for testosterone and midazolam, respectively, as substrates). methoxyamine 91-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 256-262 19158314-8 2009 These results showed that BMS-275183 is metabolized by CYP3A4 to yield baccatin through oxidation of side-chain t-butyl groups. Baccatin 71-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 19168709-13 2009 It seems that the potential for drug-drug interactions of RU486 may not be limited only to CYP3A4 and should also be evaluated for drugs metabolized primarily by CYP2B6, such as bupropion and efavirenz. Mifepristone 58-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 19356389-11 2009 CONCLUSIONS: Co-administration of erythromycin (a moderate CYP3A4 inhibitor) and roflumilast does not require dose adjustment of roflumilast. Erythromycin 34-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 19346885-7 2009 As posaconazole is an inhibitor of the isoenzyme CYP3A4, interactions with drugs that are metabolized via this pathway, such as vincristine, can be anticipated. posaconazole 3-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 19346885-7 2009 As posaconazole is an inhibitor of the isoenzyme CYP3A4, interactions with drugs that are metabolized via this pathway, such as vincristine, can be anticipated. Vincristine 128-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 19158361-3 2009 To address this issue, we examined in more detail the CYP3A4-UGT2B7 association by means of immunoprecipitation, overlay assay, and cross-linking involving 1-ethyl-3-[3-(dimethylamino)propyl]carbodiimide. Ethyldimethylaminopropyl Carbodiimide 156-203 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 19246722-2 2009 Ketoconazole interaction studies are frequently performed to determine a given compound"s sensitivity to CYP3A metabolism. Ketoconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-110 19307938-8 2009 The plasma concentration of midazolam at 4 hours was also estimated as another phenotyping index for CYP3A4 activity. Midazolam 28-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 19034627-4 2009 RESULTS: In human primary hepatocytes, real-time PCR analysis showed induction of CYP2B6, CYP3A4, UGT1A1, MDR1, and MRP2 by EGb 761, ginkgolide A (GA) and ginkgolide B (GB), but not by bilobalide (BB) or the flavonoids (quercetin, kaempferol and tamarixetin) of GBE. BDBM50323769 124-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 19142178-1 2009 Aripiprazole, a relatively new antipsychotic drug, is metabolized by cytochrome P450 3A4 (CYP3A4) and CYP2D6 to an active metabolite, dehydroaripiprazole. Aripiprazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-88 19142178-1 2009 Aripiprazole, a relatively new antipsychotic drug, is metabolized by cytochrome P450 3A4 (CYP3A4) and CYP2D6 to an active metabolite, dehydroaripiprazole. Aripiprazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 19142178-1 2009 Aripiprazole, a relatively new antipsychotic drug, is metabolized by cytochrome P450 3A4 (CYP3A4) and CYP2D6 to an active metabolite, dehydroaripiprazole. dehydroaripiprazole 134-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-88 19142178-1 2009 Aripiprazole, a relatively new antipsychotic drug, is metabolized by cytochrome P450 3A4 (CYP3A4) and CYP2D6 to an active metabolite, dehydroaripiprazole. dehydroaripiprazole 134-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 19142178-7 2009 Coadministration of a CYP3A4 inducer resulted in approximately 60% lower mean C:D ratios of aripiprazole, dehydroaripiprazole, and the sum of aripiprazole and dehydroaripiprazole (P < 0.05, P < 0.01, and P < 0.01, respectively). Aripiprazole 92-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 19350451-6 2009 In conclusion, both CYP3A4 and CYP2C8 play a major role in biotransformation of 7-epi-paclitaxel in human liver microsomes. 7-epipaclitaxel 80-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 19206087-0 2009 Rhabdomyolysis reports show interaction between simvastatin and CYP3A4 inhibitors. Simvastatin 48-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 19206087-1 2009 PURPOSE: To assess spontaneous reports of rhabdomyolysis associated with simvastatin (SV) and pravastatin (PV) for evidence of CYP3A4 interaction. Simvastatin 73-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-133 19142178-7 2009 Coadministration of a CYP3A4 inducer resulted in approximately 60% lower mean C:D ratios of aripiprazole, dehydroaripiprazole, and the sum of aripiprazole and dehydroaripiprazole (P < 0.05, P < 0.01, and P < 0.01, respectively). dehydroaripiprazole 106-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 19142178-7 2009 Coadministration of a CYP3A4 inducer resulted in approximately 60% lower mean C:D ratios of aripiprazole, dehydroaripiprazole, and the sum of aripiprazole and dehydroaripiprazole (P < 0.05, P < 0.01, and P < 0.01, respectively). Aripiprazole 113-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 19142178-7 2009 Coadministration of a CYP3A4 inducer resulted in approximately 60% lower mean C:D ratios of aripiprazole, dehydroaripiprazole, and the sum of aripiprazole and dehydroaripiprazole (P < 0.05, P < 0.01, and P < 0.01, respectively). dehydroaripiprazole 159-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 19142178-11 2009 In conclusion, concurrent treatment with CYP3A4 inducers, CYP2D6 inhibitors, alimemazine, or lithium resulted in changes in the systemic exposure of aripiprazole between 40% and 60%. Aripiprazole 149-161 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 19376366-3 2009 The bioavailability of CsA and FK506 seems to be associated with the cytocrhome P450 IIIA (CYP3A) gene. Tacrolimus 31-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-96 19138736-0 2009 PXR-mediated induction of human CYP3A4 and mouse Cyp3a11 by the glucocorticoid budesonide. Budesonide 79-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 19189363-0 2009 Cooperative effects on radical recombination in CYP3A4-catalyzed oxidation of the radical clock beta-thujone. beta-thujone 96-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 19138736-6 2009 Induction experiments in human LS180 colon carcinoma cells showed an increased expression of CYP3A4 mRNA after budesonide treatment. Budesonide 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 19138736-7 2009 Transactivation assays revealed that budesonide activates the CYP3A4 promoter via the pregnane X receptor (PXR). Budesonide 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 19189363-2 2009 Progesterone, a well-documented CYP3A4 allosteric effector, was found to increase the yield of the unrearranged, C4-derived product of beta-thujone oxidation at the expense of the combined yields of all the rearranged C4-oxidized metabolites. beta-thujone 135-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 19138736-2 2009 Cytochrome P450 3A4 (CYP3A4) is an enzyme involved in the metabolism of numerous drugs, including budesonide. Budesonide 98-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 19189363-3 2009 The results demonstrate that the apparent radical recombination rate in the CYP3A4 hydroxylation of beta-thujone is accelerated by the progesterone heterotropic cooperativity. beta-thujone 100-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 19138736-3 2009 Since inhibition or induction of CYP3A4 is often the cause of drug-drug interactions we analyzed how budesonide affects the activity and expression of this enzyme. Budesonide 101-111 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 19189363-3 2009 The results demonstrate that the apparent radical recombination rate in the CYP3A4 hydroxylation of beta-thujone is accelerated by the progesterone heterotropic cooperativity. Progesterone 135-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 19414330-0 2009 Flexible structure of cytochrome P450: promiscuity of ligand binding in the CYP3A4 heme pocket. Heme 83-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 19414330-4 2009 Molecular features of the ligand accessible regions in CYP3A4 were analyzed and their molecular parameters (e.g. dipole moment, solvation free energy, electrostatic potential fields) were determined. dipole 113-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 19261952-3 2009 In theory, clarithromycin has the potential to alter vinorelbine"s pharmacokinetics by inhibiting CYP3A and/or P-glycoprotein; this may result in massive exposure to vinorelbine and severe toxicity. Vinorelbine 53-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 19261952-3 2009 In theory, clarithromycin has the potential to alter vinorelbine"s pharmacokinetics by inhibiting CYP3A and/or P-glycoprotein; this may result in massive exposure to vinorelbine and severe toxicity. Clarithromycin 11-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-103 19414330-5 2009 RESULTS: Three ligand accessible regions (region 1-3) were present in erythromycin-bound CYP3A4, and these dipole moments indicated the same features as ketoconazole- or metyrapone-bound CYP3A4 molecules. Erythromycin 70-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 19414330-5 2009 RESULTS: Three ligand accessible regions (region 1-3) were present in erythromycin-bound CYP3A4, and these dipole moments indicated the same features as ketoconazole- or metyrapone-bound CYP3A4 molecules. Erythromycin 70-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 19414330-5 2009 RESULTS: Three ligand accessible regions (region 1-3) were present in erythromycin-bound CYP3A4, and these dipole moments indicated the same features as ketoconazole- or metyrapone-bound CYP3A4 molecules. dipole 107-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 19414330-5 2009 RESULTS: Three ligand accessible regions (region 1-3) were present in erythromycin-bound CYP3A4, and these dipole moments indicated the same features as ketoconazole- or metyrapone-bound CYP3A4 molecules. dipole 107-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 19414330-5 2009 RESULTS: Three ligand accessible regions (region 1-3) were present in erythromycin-bound CYP3A4, and these dipole moments indicated the same features as ketoconazole- or metyrapone-bound CYP3A4 molecules. Ketoconazole 153-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 19414330-5 2009 RESULTS: Three ligand accessible regions (region 1-3) were present in erythromycin-bound CYP3A4, and these dipole moments indicated the same features as ketoconazole- or metyrapone-bound CYP3A4 molecules. Ketoconazole 153-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 19414330-5 2009 RESULTS: Three ligand accessible regions (region 1-3) were present in erythromycin-bound CYP3A4, and these dipole moments indicated the same features as ketoconazole- or metyrapone-bound CYP3A4 molecules. Metyrapone 170-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 19381336-1 2009 OBJECTIVES: Rifampin is a potent inducer of the cytochrome P450 3A4 isoenzyme (CYP3A4) that metabolizes most protease inhibitor (PI) antiretrovirals. Rifampin 12-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-77 19381336-1 2009 OBJECTIVES: Rifampin is a potent inducer of the cytochrome P450 3A4 isoenzyme (CYP3A4) that metabolizes most protease inhibitor (PI) antiretrovirals. Rifampin 12-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 19381336-2 2009 This study was designed to evaluate the steady-state pharmacokinetics and tolerability of the coadministration of the PIs saquinavir and ritonavir (a CYP3A4 inhibitor used as a pharmacoenhancer of other PIs) and rifampin when coadministered in healthy HIV-negative volunteers. Monothiopyrophosphoric acid 118-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 19414330-5 2009 RESULTS: Three ligand accessible regions (region 1-3) were present in erythromycin-bound CYP3A4, and these dipole moments indicated the same features as ketoconazole- or metyrapone-bound CYP3A4 molecules. Metyrapone 170-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193 19381336-2 2009 This study was designed to evaluate the steady-state pharmacokinetics and tolerability of the coadministration of the PIs saquinavir and ritonavir (a CYP3A4 inhibitor used as a pharmacoenhancer of other PIs) and rifampin when coadministered in healthy HIV-negative volunteers. Saquinavir 122-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 19381336-2 2009 This study was designed to evaluate the steady-state pharmacokinetics and tolerability of the coadministration of the PIs saquinavir and ritonavir (a CYP3A4 inhibitor used as a pharmacoenhancer of other PIs) and rifampin when coadministered in healthy HIV-negative volunteers. Ritonavir 137-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-156 19414330-6 2009 In progesterone-bound CYP3A4, four candidate ligand accessible regions were observed and progesterone could be bound by two selected ligand accessible regions. Progesterone 3-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 19414330-7 2009 CONCLUSION: The heme pocket of CYP3A4 is very flexible and is able to interact with various types of substrate. Heme 16-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 19203724-2 2009 Safety of approved oral budesonide is based on high intestinal and hepatic extraction by cytochrome P450 3A (CYP3A) enzymes. Budesonide 24-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-107 19203724-2 2009 Safety of approved oral budesonide is based on high intestinal and hepatic extraction by cytochrome P450 3A (CYP3A) enzymes. Budesonide 24-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-114 19203724-6 2009 We assessed CYP3A-dependent metabolites in both healthy subjects and patients after buccal budesonide. Budesonide 91-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-17 19203724-8 2009 Reduced buccal CYP3A activity (lower inactivation of budesonide) in patients contributed to this remarkable difference. Budesonide 53-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-20 19203724-10 2009 We are the first to report the biotransformation of budesonide via CYP3A enzymes after buccal drug administration. Budesonide 52-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-72 19393849-14 2009 The in vitro studies confirmed the involvement of CYP3A in the metabolism of dalcetrapib-S-methyl. dalcetrapib 77-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 19393849-14 2009 The in vitro studies confirmed the involvement of CYP3A in the metabolism of dalcetrapib-S-methyl. methyl radical 89-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 19393849-15 2009 CONCLUSIONS: In this clinical study in healthy male volunteers, coadministration of dalcetrapib 600 mg with the CYP3A4 inhibitor ketoconazole was not associated with any significant changes in the pharmacokinetic parameters of the parent compound. Ketoconazole 129-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 19393849-16 2009 Coadministration of dalcetrapib 900 mg with ketoconazole was associated with significant decreases in the dalcetrapib C(max) and AUC, contrary to the increases that would be expected if dalcetrapib were a substrate for CYP3A4. dalcetrapib 20-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 19393849-16 2009 Coadministration of dalcetrapib 900 mg with ketoconazole was associated with significant decreases in the dalcetrapib C(max) and AUC, contrary to the increases that would be expected if dalcetrapib were a substrate for CYP3A4. Ketoconazole 44-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 219-225 19196220-2 2009 Posaconazole, an extended-spectrum triazole, is an inhibitor of the cytochrome P450 (CYP) isoenzyme CYP3A4, and sirolimus, an immunosuppressant, is a substrate of the enzyme. posaconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 19196220-2 2009 Posaconazole, an extended-spectrum triazole, is an inhibitor of the cytochrome P450 (CYP) isoenzyme CYP3A4, and sirolimus, an immunosuppressant, is a substrate of the enzyme. Triazoles 35-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 19196220-11 2009 These increases are consistent with CYP3A4 inhibition by posaconazole. posaconazole 57-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 19442086-6 2009 CYP2B6, CYP3A4 and CYP2C9 play a relevant role in the metabolism of ketamine. Ketamine 68-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14 18988262-3 2009 Our recent demonstration that the P450 enzymes CYP2D6 and CYP3A4 can function very well in biphasic solvent systems is one step towards overcoming this drawback, but is not practical when substrates or products are unstable in water, or with water-soluble products. Water 227-232 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 18988262-3 2009 Our recent demonstration that the P450 enzymes CYP2D6 and CYP3A4 can function very well in biphasic solvent systems is one step towards overcoming this drawback, but is not practical when substrates or products are unstable in water, or with water-soluble products. Water 242-247 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 19020497-0 2009 The CYP3A4*18 genotype in the cytochrome P450 3A4 gene, a rapid metabolizer of sex steroids, is associated with low bone mineral density. Steroids 83-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 19020497-0 2009 The CYP3A4*18 genotype in the cytochrome P450 3A4 gene, a rapid metabolizer of sex steroids, is associated with low bone mineral density. Steroids 83-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-49 19020497-4 2009 In vitro functional analyses indicate that CYP3A4*18 is a gain-of-function mutation in sex steroid metabolism, resulting in rapid oxidation of estrogens and testosterone; in vivo pharmacokinetics using midazolam (MDZ) verify the altered activity of the CYP3A4*18, showing lower metabolic turnover in the mutant than in the wild type. Steroids 91-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 19020497-4 2009 In vitro functional analyses indicate that CYP3A4*18 is a gain-of-function mutation in sex steroid metabolism, resulting in rapid oxidation of estrogens and testosterone; in vivo pharmacokinetics using midazolam (MDZ) verify the altered activity of the CYP3A4*18, showing lower metabolic turnover in the mutant than in the wild type. Testosterone 157-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 19020497-4 2009 In vitro functional analyses indicate that CYP3A4*18 is a gain-of-function mutation in sex steroid metabolism, resulting in rapid oxidation of estrogens and testosterone; in vivo pharmacokinetics using midazolam (MDZ) verify the altered activity of the CYP3A4*18, showing lower metabolic turnover in the mutant than in the wild type. Midazolam 202-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 19020497-4 2009 In vitro functional analyses indicate that CYP3A4*18 is a gain-of-function mutation in sex steroid metabolism, resulting in rapid oxidation of estrogens and testosterone; in vivo pharmacokinetics using midazolam (MDZ) verify the altered activity of the CYP3A4*18, showing lower metabolic turnover in the mutant than in the wild type. Midazolam 213-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 19020497-5 2009 Molecular modeling reveals the structural changes in the substrate recognition sites of CYP3A4*18 that can cause changes in enzymatic activity and that potentially account for the difference between the catalytic activities of estrogen and MDZ, depending on the genotype. Midazolam 240-243 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 19020497-6 2009 The results indicate that a genetic variation in the CYP3A4 gene--as a gain-of-function mutation in the metabolism of certain CYP3A substrates, including sex steroids--may predispose individuals to osteoporosis. Steroids 158-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 19020497-6 2009 The results indicate that a genetic variation in the CYP3A4 gene--as a gain-of-function mutation in the metabolism of certain CYP3A substrates, including sex steroids--may predispose individuals to osteoporosis. Steroids 158-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 19442086-4 2009 Among these, halothane is metabolized by cytochrome P450 (CYP) 2E1 and, to a lesser extent, by CYP3A4 and CYP2A6. Halothane 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-101 19114462-2 2009 However, a clinical study involving the CYP3A probe substrate midazolam and a different cranberry juice product showed no interaction. Midazolam 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 19074530-0 2009 Dehydrogenation of the indoline-containing drug 4-chloro-N-(2-methyl-1-indolinyl)-3-sulfamoylbenzamide (indapamide) by CYP3A4: correlation with in silico predictions. Indapamide 48-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 19074530-0 2009 Dehydrogenation of the indoline-containing drug 4-chloro-N-(2-methyl-1-indolinyl)-3-sulfamoylbenzamide (indapamide) by CYP3A4: correlation with in silico predictions. Indapamide 104-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 19074530-6 2009 Here we identified several indapamide metabolic pathways in vitro with human liver microsomes and recombinant CYP3A4 that include the dehydrogenation of indapamide to its corresponding indole form, and also hydroxylation and epoxidation metabolites, as characterized by liquid chromatography/mass spectrometry. Indapamide 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 19074530-6 2009 Here we identified several indapamide metabolic pathways in vitro with human liver microsomes and recombinant CYP3A4 that include the dehydrogenation of indapamide to its corresponding indole form, and also hydroxylation and epoxidation metabolites, as characterized by liquid chromatography/mass spectrometry. Indapamide 153-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 19074530-6 2009 Here we identified several indapamide metabolic pathways in vitro with human liver microsomes and recombinant CYP3A4 that include the dehydrogenation of indapamide to its corresponding indole form, and also hydroxylation and epoxidation metabolites, as characterized by liquid chromatography/mass spectrometry. indole 185-191 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 19074530-0 2009 Dehydrogenation of the indoline-containing drug 4-chloro-N-(2-methyl-1-indolinyl)-3-sulfamoylbenzamide (indapamide) by CYP3A4: correlation with in silico predictions. indoline 23-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 19074530-7 2009 Indapamide dehydrogenation efficiency (V(max)/K(m)=204 min/mM) by CYP3A4 was approximately 10-fold greater than that of indoline dehydrogenation. Indapamide 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 19114462-7 2009 The hexane- and chloroform-soluble fractions at 50 microg/ml were the most potent, inhibiting by 77 and 63%, respectively, suggesting that the CYP3A inhibitors reside largely in these more lipophilic fractions. Hexanes 4-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 19114462-7 2009 The hexane- and chloroform-soluble fractions at 50 microg/ml were the most potent, inhibiting by 77 and 63%, respectively, suggesting that the CYP3A inhibitors reside largely in these more lipophilic fractions. Chloroform 16-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 143-148 18836708-8 2009 CONCLUSIONS: Voriconazole inhibits the CYP3A-mediated N-demethylation of oxycodone, drastically increasing exposure to oral oxycodone. Voriconazole 13-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 18836708-8 2009 CONCLUSIONS: Voriconazole inhibits the CYP3A-mediated N-demethylation of oxycodone, drastically increasing exposure to oral oxycodone. Nitrogen 2-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 18836708-8 2009 CONCLUSIONS: Voriconazole inhibits the CYP3A-mediated N-demethylation of oxycodone, drastically increasing exposure to oral oxycodone. Oxycodone 73-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 18836708-8 2009 CONCLUSIONS: Voriconazole inhibits the CYP3A-mediated N-demethylation of oxycodone, drastically increasing exposure to oral oxycodone. Oxycodone 124-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 19029318-5 2009 In pilot experiments, voriconazole showed inhibition of CYP2B6, CYP2C9, CYP2C19, and CYP3A (half-maximal [50%] inhibitory concentrations, <6 microM); its effect on CYP1A2, CYP2A6, CYP2C8, and CYP2D6 was marginal (<25% inhibition at 100 microM voriconazole). Voriconazole 22-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-90 19337788-0 2009 Frequency of CYP3A4, CYP3A5, CYP2C9, and CYP2C19 variant alleles in patients receiving clopidogrel that experience repeat acute coronary syndrome. Clopidogrel 87-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 19337788-2 2009 This research evaluated the frequency of variant alleles in the genes coding for CYP3A4, CYP3A5, CYP2C9, and CYP2C19 enzymes in patients on clopidogrel therapy and experiencing repeat acute coronary syndrome (ACS) compared to a control group with a matching ethnic composition. Clopidogrel 140-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 19246732-0 2009 Quantitative evaluation of pharmacokinetic inhibition of CYP3A substrates by ketoconazole: a simulation study. Ketoconazole 77-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 19246732-1 2009 The US Food and Drug Administration draft drug interaction guidance recommends that 400 mg ketoconazole (KTZ) be administered once daily for several days (QD400) for maximal CYP3A inhibition. Ketoconazole 91-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-179 19246732-1 2009 The US Food and Drug Administration draft drug interaction guidance recommends that 400 mg ketoconazole (KTZ) be administered once daily for several days (QD400) for maximal CYP3A inhibition. Ketoconazole 105-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-179 19246734-0 2009 The need for multiple doses of 400 mg ketoconazole as a precipitant inhibitor of a CYP3A substrate in an in vivo drug-drug interaction study. Ketoconazole 38-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-88 19074998-5 2009 Introduction of a mutation into either an alpha or beta half-site of CYP3A4 reporter genes almost completely diminished the rifampicin-induced transcription. Rifampin 124-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 19183931-7 2009 CYP3A4 inducers can lower levels of cyclosporine or tacrolimus so much that transplant rejection occurs, and CYP3A4 inhibitors can increase their levels, leading to nephrotoxicity. Cyclosporine 36-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 19183931-7 2009 CYP3A4 inducers can lower levels of cyclosporine or tacrolimus so much that transplant rejection occurs, and CYP3A4 inhibitors can increase their levels, leading to nephrotoxicity. Tacrolimus 52-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 19183931-8 2009 Levels of the anticholinergic darifenacin can be increased so much by potent CYP3A4 inhibitors that this combination is contraindicated. darifenacin 30-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 19056199-1 2009 An amperometric drug metabolism biosensor consisting of cytochrome P450-3A4 (CYP3A4) encapsulated in a didodecyldimethylammonium bromide (DDAB) vesicular system on a Pt disk electrode was developed for the determination of indinavir, a protease inhibitor antiretroviral drug. didodecyldimethylammonium 103-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-75 19056199-1 2009 An amperometric drug metabolism biosensor consisting of cytochrome P450-3A4 (CYP3A4) encapsulated in a didodecyldimethylammonium bromide (DDAB) vesicular system on a Pt disk electrode was developed for the determination of indinavir, a protease inhibitor antiretroviral drug. didodecyldimethylammonium 103-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 19056199-1 2009 An amperometric drug metabolism biosensor consisting of cytochrome P450-3A4 (CYP3A4) encapsulated in a didodecyldimethylammonium bromide (DDAB) vesicular system on a Pt disk electrode was developed for the determination of indinavir, a protease inhibitor antiretroviral drug. didodecyldimethylammonium 138-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 19056199-1 2009 An amperometric drug metabolism biosensor consisting of cytochrome P450-3A4 (CYP3A4) encapsulated in a didodecyldimethylammonium bromide (DDAB) vesicular system on a Pt disk electrode was developed for the determination of indinavir, a protease inhibitor antiretroviral drug. Indinavir 223-232 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-75 19056199-1 2009 An amperometric drug metabolism biosensor consisting of cytochrome P450-3A4 (CYP3A4) encapsulated in a didodecyldimethylammonium bromide (DDAB) vesicular system on a Pt disk electrode was developed for the determination of indinavir, a protease inhibitor antiretroviral drug. Indinavir 223-232 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 19056199-2 2009 Cyclic, square wave and pulse voltammetric responses of the bioelectrode showed quasi-reversible electrochemistry of the Fe(3+)/Fe(2+) redox species of the heme thiolate CYP3A4 enzyme under aerobic and anaerobic conditions. ferric sulfate 121-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 19056199-2 2009 Cyclic, square wave and pulse voltammetric responses of the bioelectrode showed quasi-reversible electrochemistry of the Fe(3+)/Fe(2+) redox species of the heme thiolate CYP3A4 enzyme under aerobic and anaerobic conditions. ammonium ferrous sulfate 128-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 170-176 19070657-0 2009 CYP1A1 induction and CYP3A4 inhibition by the fungicide imazalil in the human intestinal Caco-2 cells-comparison with other conazole pesticides. enilconazole 56-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 19070657-7 2009 Moreover, IMA strongly inhibited the CYP3A4 activity in 1,25-vitamin D(3)-induced Caco-2 cells. enilconazole 10-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 19070657-7 2009 Moreover, IMA strongly inhibited the CYP3A4 activity in 1,25-vitamin D(3)-induced Caco-2 cells. 1,25-vitamin d 56-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 19070657-10 2009 Our results imply that coingestion of IMA-contaminated food and CYP3A4- or CYP1A1-metabolizable drugs or chemicals could lead to drug bioavailability modulation or toxicological interactions, with possible adverse effects for human health. enilconazole 38-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 19270151-1 2009 Protease inhibitors boosted with ritonavir can lead to drug-drug interactions, particularly with inhaled corticosteroids such as fluticasone, because of the potent inhibition of cytochrome P450-3A4 activity. Ritonavir 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-197 19270151-1 2009 Protease inhibitors boosted with ritonavir can lead to drug-drug interactions, particularly with inhaled corticosteroids such as fluticasone, because of the potent inhibition of cytochrome P450-3A4 activity. Fluticasone 129-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 178-197 19148864-2 2009 In this study, we investigated in vitro the effect of repeated administration of GFJ and its major constituents (the flavonoid naringin, its aglycone naringenin and the furanocoumarin bergamottin) on mRNA expression of MDR1 and CYP3A4 in LS180 cells. furanocoumarin bergamottin 169-195 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 19148864-5 2009 Of the tested constituents, only 10 microM bergamottin and 200 microM naringenin induced MDR1 mRNA levels 2.9- and 4.0-fold, respectively (P<0.01 for both), and CYP3A4 mRNA levels 3.2- and 15.6-fold (P<0.01 for both), respectively. bergamottin 43-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 19148864-5 2009 Of the tested constituents, only 10 microM bergamottin and 200 microM naringenin induced MDR1 mRNA levels 2.9- and 4.0-fold, respectively (P<0.01 for both), and CYP3A4 mRNA levels 3.2- and 15.6-fold (P<0.01 for both), respectively. naringenin 70-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 164-170 19280517-3 2009 Atorvastatin and verapamil have interesting clinical pharmacology attributes in that both agents are substrates and/or inhibitors of the dual cytochrome P450 (CYP) 3A4 and P-glycoprotein (Pgp) efflux transporter interplay. Atorvastatin 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-167 19280517-3 2009 Atorvastatin and verapamil have interesting clinical pharmacology attributes in that both agents are substrates and/or inhibitors of the dual cytochrome P450 (CYP) 3A4 and P-glycoprotein (Pgp) efflux transporter interplay. Verapamil 17-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-167 19095658-4 2009 Peptide mapping coupled with mass spectrometric analyses of CYP3A4 phosphorylated in vitro by protein kinase C (PKC) previously identified two target sites, Thr(264) and Ser(420). Threonine 157-160 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 19095658-4 2009 Peptide mapping coupled with mass spectrometric analyses of CYP3A4 phosphorylated in vitro by protein kinase C (PKC) previously identified two target sites, Thr(264) and Ser(420). Serine 170-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 19095658-10 2009 cAMP-dependent protein kinase A/PKC-mediated phosphorylation of CYP3A4wt but not its S478A/T264A/S420A mutant enhanced its ubiquitination in this system. Cyclic AMP 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 19095658-11 2009 Together, these findings indicate that phosphorylation of CYP3A4 Ser(478), Thr(264), and Ser(420) residues by cytosolic kinases is important both for its ubiquitination and proteasomal degradation and suggest a direct link between P450 phosphorylation, ubiquitination, and degradation. Serine 65-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 19095658-11 2009 Together, these findings indicate that phosphorylation of CYP3A4 Ser(478), Thr(264), and Ser(420) residues by cytosolic kinases is important both for its ubiquitination and proteasomal degradation and suggest a direct link between P450 phosphorylation, ubiquitination, and degradation. Threonine 75-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 19095658-11 2009 Together, these findings indicate that phosphorylation of CYP3A4 Ser(478), Thr(264), and Ser(420) residues by cytosolic kinases is important both for its ubiquitination and proteasomal degradation and suggest a direct link between P450 phosphorylation, ubiquitination, and degradation. Serine 89-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 19179259-3 2009 CASE SUMMARY: A 66-year-old man with diabetes, ischaemic heart disease and hypertension, on medication of CYP3A4 substrates amlodipine and alprazolam, maximal daily dose of SIM has been started for unknown cholesterol level. Amlodipine 124-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 19179259-3 2009 CASE SUMMARY: A 66-year-old man with diabetes, ischaemic heart disease and hypertension, on medication of CYP3A4 substrates amlodipine and alprazolam, maximal daily dose of SIM has been started for unknown cholesterol level. Cholesterol 206-217 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 19029318-5 2009 In pilot experiments, voriconazole showed inhibition of CYP2B6, CYP2C9, CYP2C19, and CYP3A (half-maximal [50%] inhibitory concentrations, <6 microM); its effect on CYP1A2, CYP2A6, CYP2C8, and CYP2D6 was marginal (<25% inhibition at 100 microM voriconazole). Voriconazole 249-261 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-90 19029318-7 2009 The inhibition of CYP3A by voriconazole was explained by noncompetitive (K(i) = 2.97 microM) and competitive (K(i) = 0.66 microM) modes of inhibition. Voriconazole 27-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-23 19029318-8 2009 Prediction of the in vivo interaction of voriconazole from these in vitro data suggests that voriconazole would substantially increase the exposure of drugs metabolized by CYP2B6, CYP2C9, CYP2C19, and CYP3A. Voriconazole 41-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-206 19022226-6 2009 At 10 microM PCEEA, CBP reduced metabolite formation by 61%, while inhibition of CYP3A4 by ketoconazole and inhibition of CYP2C9 by sulfaphenazole showed no inhibitory effect. Ketoconazole 91-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 19029318-8 2009 Prediction of the in vivo interaction of voriconazole from these in vitro data suggests that voriconazole would substantially increase the exposure of drugs metabolized by CYP2B6, CYP2C9, CYP2C19, and CYP3A. Voriconazole 93-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-206 19022227-0 2009 Effects of dexamethasone, administered for growth promoting purposes, upon the hepatic cytochrome P450 3A expression in the veal calf. Dexamethasone 11-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-105 19220274-3 2009 Simvastatin exhibits particularly high interaction potential due to substantial metabolism via cytochrome P450 3A4 (CYP3A4). Simvastatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-114 19022227-2 2009 In human liver, DEX is metabolized by cytochrome P450 3A (CYP3A); moreover, it is among those xenobiotics which induce CYP3A itself. Dexamethasone 16-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-56 19022227-2 2009 In human liver, DEX is metabolized by cytochrome P450 3A (CYP3A); moreover, it is among those xenobiotics which induce CYP3A itself. Dexamethasone 16-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 19022227-2 2009 In human liver, DEX is metabolized by cytochrome P450 3A (CYP3A); moreover, it is among those xenobiotics which induce CYP3A itself. Dexamethasone 16-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-124 19022227-4 2009 In cattle, DEX is used at low dosages as a growth promoter; besides, CYP3A is expressed in the liver. Dexamethasone 11-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 19143748-1 2009 The purpose of this study was to evaluate the role of sequence variants in the CYP2C8, ABCB1 and CYP3A4 genes and the CYP3A4 phenotype for the pharmacokinetics and toxicity of paclitaxel in ovarian cancer patients. Paclitaxel 176-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 19143748-1 2009 The purpose of this study was to evaluate the role of sequence variants in the CYP2C8, ABCB1 and CYP3A4 genes and the CYP3A4 phenotype for the pharmacokinetics and toxicity of paclitaxel in ovarian cancer patients. Paclitaxel 176-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 19220274-3 2009 Simvastatin exhibits particularly high interaction potential due to substantial metabolism via cytochrome P450 3A4 (CYP3A4). Simvastatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 19220274-15 2009 Considering the pronounced interaction potential of simvastatin with CYP3A4 inhibitors, a negative influence of the new policy on overall statin safety seems likely. Simvastatin 52-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 18509327-4 2009 However, the simultaneous presence of the CYP3A4*1B and CYP3A5*1A alleles was associated with a 64% increase in docetaxel clearance (P = 0.0015), independent of both sex and CYP3A activity (as determined using the erythromycin breath test). Docetaxel 112-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 18509327-4 2009 However, the simultaneous presence of the CYP3A4*1B and CYP3A5*1A alleles was associated with a 64% increase in docetaxel clearance (P = 0.0015), independent of both sex and CYP3A activity (as determined using the erythromycin breath test). Docetaxel 112-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 19302901-2 2009 Midazolam, a short-acting benzodiazepine, is metabolized by CYP3A4. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 19302901-2 2009 Midazolam, a short-acting benzodiazepine, is metabolized by CYP3A4. Benzodiazepines 26-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 18509327-4 2009 However, the simultaneous presence of the CYP3A4*1B and CYP3A5*1A alleles was associated with a 64% increase in docetaxel clearance (P = 0.0015), independent of both sex and CYP3A activity (as determined using the erythromycin breath test). Erythromycin 214-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 19302901-3 2009 Potential drug interactions can be expected in patients who are concurrently receiving inhibitors and substrates of CYP3A4 (eg, ketoconazole, posaconazole) and benzodiazepines (eg, midazolam). Ketoconazole 128-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 18509327-4 2009 However, the simultaneous presence of the CYP3A4*1B and CYP3A5*1A alleles was associated with a 64% increase in docetaxel clearance (P = 0.0015), independent of both sex and CYP3A activity (as determined using the erythromycin breath test). Erythromycin 214-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 19302901-3 2009 Potential drug interactions can be expected in patients who are concurrently receiving inhibitors and substrates of CYP3A4 (eg, ketoconazole, posaconazole) and benzodiazepines (eg, midazolam). posaconazole 142-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 19302901-3 2009 Potential drug interactions can be expected in patients who are concurrently receiving inhibitors and substrates of CYP3A4 (eg, ketoconazole, posaconazole) and benzodiazepines (eg, midazolam). Midazolam 181-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 19302901-21 2009 CONCLUSIONS: The results from this study in a small, all-white population of healthy volunteers suggest that posaconazole was a potent inhibitor of CYP3A4, but to a lesser extent than was ketoconazole. posaconazole 109-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 148-154 19197797-5 2009 Elvitegravir is predominantly metabolized via cytochrome P450 (CYP)3A4, along with minor pathways including glucuronidation via UGT1A1/3 and oxidative metabolism. elvitegravir 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-70 19302901-22 2009 Monitoring patients for adverse events, the need for dose adjustments, or both during coadministration with posaconazole may be warranted in patients being treated with benzodiazepines that are predominantly metabolized through CYP3A4 (eg, midazolam). posaconazole 108-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 19302901-22 2009 Monitoring patients for adverse events, the need for dose adjustments, or both during coadministration with posaconazole may be warranted in patients being treated with benzodiazepines that are predominantly metabolized through CYP3A4 (eg, midazolam). Benzodiazepines 169-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 19302901-22 2009 Monitoring patients for adverse events, the need for dose adjustments, or both during coadministration with posaconazole may be warranted in patients being treated with benzodiazepines that are predominantly metabolized through CYP3A4 (eg, midazolam). Midazolam 240-249 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 19022227-7 2009 In summary, DEX modulates cattle liver CYP3A at pre- and post-translational level. Dexamethasone 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-44 19197797-6 2009 Consequently, the coadministration of elvitegravir with the protease inhibitor ritonavir (a substantial CYP3A4 inhibitor) results in significantly enhanced bioavailability and a longer half-life than with elvitegravir alone, allowing for the once-daily dosing of elvitegravir. elvitegravir 38-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 19197797-6 2009 Consequently, the coadministration of elvitegravir with the protease inhibitor ritonavir (a substantial CYP3A4 inhibitor) results in significantly enhanced bioavailability and a longer half-life than with elvitegravir alone, allowing for the once-daily dosing of elvitegravir. Ritonavir 79-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 19022943-0 2009 Metabolism of quetiapine by CYP3A4 and CYP3A5 in presence or absence of cytochrome B5. Quetiapine Fumarate 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 18971317-9 2009 Rosuvastatin was found to increase human constitutive androstane receptor (hCAR)-mediated transcription of CYP3A4, CYP2C9, and CYP2B6 genes, predicting the consequent potential for drug interactions with several coadministered drugs. Rosuvastatin Calcium 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 18971317-10 2009 Activation of hCAR and hPXR by atorvastatin and the subsequent induction of not only CYP2B6 and CYP3A4 but also of CYP2C9 present an additional target by which atorvastatin, a widely used cholesterol-lowering drug, can modify the kinetics of numerous drugs. Atorvastatin 160-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 18971317-10 2009 Activation of hCAR and hPXR by atorvastatin and the subsequent induction of not only CYP2B6 and CYP3A4 but also of CYP2C9 present an additional target by which atorvastatin, a widely used cholesterol-lowering drug, can modify the kinetics of numerous drugs. Cholesterol 188-199 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 19005028-0 2009 Metabolic activation of benzodiazepines by CYP3A4. Benzodiazepines 24-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 19005028-4 2009 To clarify whether benzodiazepines are metabolically activated, 14 benzodiazepines were investigated for their cytotoxic effects on HepG2 cells treated with recombinant CYP3A4. Benzodiazepines 67-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 169-175 19005028-5 2009 By exposure to 100 microM flunitrazepam, nimetazepam, or nitrazepam, the cell viability in the presence of CYP3A4 decreased more than 25% compared with that of the control. Flunitrazepam 26-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 19005028-5 2009 By exposure to 100 microM flunitrazepam, nimetazepam, or nitrazepam, the cell viability in the presence of CYP3A4 decreased more than 25% compared with that of the control. nimetazepam 41-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 19005028-5 2009 By exposure to 100 microM flunitrazepam, nimetazepam, or nitrazepam, the cell viability in the presence of CYP3A4 decreased more than 25% compared with that of the control. Nitrazepam 29-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 19005028-6 2009 In contrast, in the case of other benzodiazepines, the changes in the cell viability between CYP3A4 and control Supersomes were less than 10%. Benzodiazepines 34-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 19005028-7 2009 These results suggested that nitrobenzodiazepines such as flunitrazepam, nimetazepam, and nitrazepam were metabolically activated by CYP3A4, which resulted in cytotoxicity. nitrobenzodiazepines 29-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 19005028-7 2009 These results suggested that nitrobenzodiazepines such as flunitrazepam, nimetazepam, and nitrazepam were metabolically activated by CYP3A4, which resulted in cytotoxicity. Flunitrazepam 58-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 19022943-1 2009 The antipsychotic drug quetiapine is extensively metabolized by CYP3A4, but little is known about the possible influence of the polymorphic enzyme CYP3A5. Quetiapine Fumarate 23-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-70 19005028-7 2009 These results suggested that nitrobenzodiazepines such as flunitrazepam, nimetazepam, and nitrazepam were metabolically activated by CYP3A4, which resulted in cytotoxicity. nimetazepam 73-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 19005028-7 2009 These results suggested that nitrobenzodiazepines such as flunitrazepam, nimetazepam, and nitrazepam were metabolically activated by CYP3A4, which resulted in cytotoxicity. Nitrazepam 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 19022943-2 2009 This in vitro study investigated the relative importance of CYP3A4 and CYP3A5 in the metabolism of quetiapine and compared the metabolic pattern by the two enzymes, in the presence or absence of cytochrome b(5). Quetiapine Fumarate 99-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 19005028-10 2009 Therefore, the presence of a nitro group in the side chain of benzodiazepines may play a crucial role in the metabolic activation by CYP3A4. nitro 29-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 19022943-3 2009 Intrinsic clearance (CL(int)) of quetiapine was determined by the substrate depletion approach in CYP3A4 and CYP3A5 insect cell microsomes with or without coexpressed cytochrome b(5). Quetiapine Fumarate 33-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 19005028-10 2009 Therefore, the presence of a nitro group in the side chain of benzodiazepines may play a crucial role in the metabolic activation by CYP3A4. Benzodiazepines 62-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 19005028-11 2009 The present study suggested that metabolic activation by CYP3A4 was one of the mechanisms of liver injury by nitrobenzodiazepines. nitrobenzodiazepines 109-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 19022943-4 2009 Formation of the metabolites quetiapine sulfoxide, N-desalkylquetiapine, O-desalkylquetiapine, and 7-hydroxyquetiapine by CYP3A4 and CYP3A5 were compared in the different microsomal preparations. Quetiapine Sulfoxide 29-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 19022943-4 2009 Formation of the metabolites quetiapine sulfoxide, N-desalkylquetiapine, O-desalkylquetiapine, and 7-hydroxyquetiapine by CYP3A4 and CYP3A5 were compared in the different microsomal preparations. 7-Hydroxy Quetiapine 99-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 19022943-5 2009 CL(int) of quetiapine by CYP3A5 was less than 35% relative to CYP3A4. Quetiapine Fumarate 11-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 19022943-7 2009 Metabolism of quetiapine by CYP3A5 revealed a different metabolic pattern compared with CYP3A4. Quetiapine Fumarate 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 19022943-10 2009 However, a different metabolic pattern by CYP3A5 compared with CYP3A4 could possibly result in different pharmacological and/or toxicological effects of quetiapine in patients expressing CYP3A5. Quetiapine Fumarate 153-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 19255936-9 2009 Slow acting inhibitors (such as verapamil/CYP3A4 or S-fluoxetine/CYP2C19) showed an increase in IC(50) shift between 10 and 30 min suggesting a longer maximum pre-incubation time with wider spacing of time points for K(I)/k(inact). Verapamil 32-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 19203567-1 2009 UNLABELLED: Phenotyping intestinal and hepatic cytochrome P450 (CYP) 3A activity with oral midazolam can be limited by midazolam-induced central nervous system (CNS) side effects. Midazolam 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-71 19203567-1 2009 UNLABELLED: Phenotyping intestinal and hepatic cytochrome P450 (CYP) 3A activity with oral midazolam can be limited by midazolam-induced central nervous system (CNS) side effects. Midazolam 119-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-71 19203567-2 2009 Determining methods to minimize CNS side effects optimizes use of midazolam as a CYP3A probe. Midazolam 66-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-86 19203567-4 2009 flumazenil on midazolam apparent oral clearance (a surrogate marker of CYP3A activity). Flumazenil 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-76 19203567-18 2009 flumazenil can be used in conjunction with oral midazolam for CYP3A phenotyping. Flumazenil 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 19203567-18 2009 flumazenil can be used in conjunction with oral midazolam for CYP3A phenotyping. Midazolam 48-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 19182847-2 2009 Moreover, the 1 mg overnight dexamethasone suppression test was positive and the midnight serum cortisol level was slightly increased, probably as a result of carbamazepine-induced activity of CYP3A4 and increased levels of cortisol binding globulin. Carbamazepine 159-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 193-199 19033450-1 2009 In vitro data on the metabolism of the antifungal voriconazole suggest that its pharmacokinetics might be influenced by the activity of CYP2C19, CYP2C9, and CYP3A. Voriconazole 50-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 157-162 19017849-8 2009 Metabolite determinations of the dimethyl-ifosfamide analogs were performed using liquid chromatography and tandem mass spectrometry after in vitro biotransformation by drug-induced rat liver microsomes and human microsomes expressing the main CYP3A4 and minor CYP2B6 enzymes. dimethyl-ifosfamide 33-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 244-250 19255936-9 2009 Slow acting inhibitors (such as verapamil/CYP3A4 or S-fluoxetine/CYP2C19) showed an increase in IC(50) shift between 10 and 30 min suggesting a longer maximum pre-incubation time with wider spacing of time points for K(I)/k(inact). Fluoxetine 52-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 19255940-0 2009 Functional characterization of CYP3A4.16: catalytic activities toward midazolam and carbamazepine. Midazolam 70-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 19255940-0 2009 Functional characterization of CYP3A4.16: catalytic activities toward midazolam and carbamazepine. Carbamazepine 84-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 19255940-6 2009 When midazolam was used as a substrate, K(m) and V(max) for 1"-hydroxylation in CYP3A4.16 were significantly higher and lower, respectively, than those in the wild-type, resulting in a 50% decrease in intrinsic clearance (V(max)/K(m)) of the variant. Midazolam 5-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 18805405-0 2009 PXR-mediated transcriptional activation of CYP3A4 by cryptotanshinone and tanshinone IIA. cryptotanshinone 53-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 18805405-0 2009 PXR-mediated transcriptional activation of CYP3A4 by cryptotanshinone and tanshinone IIA. tanshinone 74-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 18805405-6 2009 Our observations showed that Danshen ethanol extract could activate human PXR and induce the CYP3A4 reporter construct in HepG2 cells. danshen ethanol 29-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 20230761-7 2009 A drug-drug interaction study with itraconazole confirmed in vitro metabolic results implicating CYP3A enzymes as the major contributors to in vivo oxidative metabolism. Itraconazole 35-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-102 18805405-7 2009 Tanshinone IIA and cryptotanshinone were identified as efficacious PXR agonists, and cryptotanshinone activated the CYP3A4 promoter more strongly than tanshinone IIA. cryptotanshinone 85-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 116-122 18805405-8 2009 Furthermore, CAR and GR were also involved in the induction of CYP3A4 expression by tanshinones, though their roles seemed not as important as PXR. tanshinone 84-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 18805405-9 2009 Treatment of LS174T cells with cryptotanshinone or tanshinone IIA resulted in a significant increase of CYP3A4 mRNA, which was consistent with the results from the reporter gene assay. cryptotanshinone 31-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 18805405-9 2009 Treatment of LS174T cells with cryptotanshinone or tanshinone IIA resulted in a significant increase of CYP3A4 mRNA, which was consistent with the results from the reporter gene assay. tanshinone 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 18805405-10 2009 Collectively, activation of PXR and the resultant CYP3A4 induction mediated by cryptotanshinone and tanshinone IIA provide a molecular mechanism for previously observed CYP3A induction by Danshen extracts, and our findings also suggest that caution should be taken when Danshen products are used in combination with therapeutic drugs metabolized by CYP3A4. cryptotanshinone 79-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 18805405-10 2009 Collectively, activation of PXR and the resultant CYP3A4 induction mediated by cryptotanshinone and tanshinone IIA provide a molecular mechanism for previously observed CYP3A induction by Danshen extracts, and our findings also suggest that caution should be taken when Danshen products are used in combination with therapeutic drugs metabolized by CYP3A4. cryptotanshinone 79-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 18805405-10 2009 Collectively, activation of PXR and the resultant CYP3A4 induction mediated by cryptotanshinone and tanshinone IIA provide a molecular mechanism for previously observed CYP3A induction by Danshen extracts, and our findings also suggest that caution should be taken when Danshen products are used in combination with therapeutic drugs metabolized by CYP3A4. cryptotanshinone 79-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 349-355 18983865-6 2009 The strong and overlapping inductive role of phenobarbital strengthens the participation of CYP2B6 and CYP3A in diazepam N-demethylation and CYP3A in temazepam formation. Phenobarbital 45-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 18983865-6 2009 The strong and overlapping inductive role of phenobarbital strengthens the participation of CYP2B6 and CYP3A in diazepam N-demethylation and CYP3A in temazepam formation. Phenobarbital 45-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-146 18983865-6 2009 The strong and overlapping inductive role of phenobarbital strengthens the participation of CYP2B6 and CYP3A in diazepam N-demethylation and CYP3A in temazepam formation. Diazepam 112-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-108 18983865-6 2009 The strong and overlapping inductive role of phenobarbital strengthens the participation of CYP2B6 and CYP3A in diazepam N-demethylation and CYP3A in temazepam formation. Temazepam 150-159 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-146 18983865-7 2009 Aroclor 1254 preferentially generated temazepam due to the interaction with CYP3A and potentially CYP2C19. Chlorodiphenyl (54% Chlorine) 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 18983865-7 2009 Aroclor 1254 preferentially generated temazepam due to the interaction with CYP3A and potentially CYP2C19. Temazepam 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 19076156-0 2009 Polymorphisms of drug-metabolizing enzymes (GST, CYP2B6 and CYP3A) affect the pharmacokinetics of thiotepa and tepa. Thiotepa 98-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 19076156-0 2009 Polymorphisms of drug-metabolizing enzymes (GST, CYP2B6 and CYP3A) affect the pharmacokinetics of thiotepa and tepa. Triethylenephosphoramide 102-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 19006545-0 2009 4beta-hydroxycholesterol as an endogenous marker for CYP3A4/5 activity. cholest-5-ene-3,4-diol 0-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 19076156-5 2009 The purpose of this study was to evaluate effects of known allelic variants in CYP2B6, CYP3A4, CYP3A5, GSTA1 and GSTP1 genes on pharmacokinetics of thiotepa and tepa. Thiotepa 148-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 19006545-2 2009 AIMS: The oxysterol 4beta-hydroxycholesterol has been suggested as a marker for CYP3A4/5 activity. oxysterol 4beta-hydroxycholesterol 10-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 19006545-3 2009 We have previously shown that plasma 4beta-hydroxycholesterol continues to increase for several weeks after maximal induction of CYP3A4/5 by carbamazepine at the dose given. cholest-5-ene-3,4-diol 37-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 19006545-3 2009 We have previously shown that plasma 4beta-hydroxycholesterol continues to increase for several weeks after maximal induction of CYP3A4/5 by carbamazepine at the dose given. Carbamazepine 141-154 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 19006545-4 2009 In the present study we aimed to determine the time course of the decrease in plasma 4beta-hydroxycholesterol after termination of induction of CYP3A4/5 by rifampicin. cholest-5-ene-3,4-diol 85-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 19076156-5 2009 The purpose of this study was to evaluate effects of known allelic variants in CYP2B6, CYP3A4, CYP3A5, GSTA1 and GSTP1 genes on pharmacokinetics of thiotepa and tepa. Triethylenephosphoramide 152-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 19006545-4 2009 In the present study we aimed to determine the time course of the decrease in plasma 4beta-hydroxycholesterol after termination of induction of CYP3A4/5 by rifampicin. Rifampin 156-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 144-150 19067473-3 2009 As with lansoprazole, dexlansoprazole is metabolized mainly by CYP3A and CYP2C19. Lansoprazole 8-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 19006545-14 2009 CONCLUSIONS: After termination of induction of CYP3A4/5, plasma 4beta-hydroxycholesterol levels decreased slowly during 8 weeks. cholest-5-ene-3,4-diol 64-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-53 19133059-0 2009 Contribution of the activities of CYP3A, CYP2D6, CYP1A2 and other potential covariates to the disposition of methadone in patients undergoing methadone maintenance treatment. Methadone 109-118 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-39 19133059-7 2009 RESULTS: Between 61 and 68% of the overall variation in total plasma trough concentrations of (RS)-, (R)- and (S)-methadone was explained by methadone dose, duration of addiction before starting MMT, CYP3A activity and illicit morphine use. Methadone 110-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-205 19133059-7 2009 RESULTS: Between 61 and 68% of the overall variation in total plasma trough concentrations of (RS)-, (R)- and (S)-methadone was explained by methadone dose, duration of addiction before starting MMT, CYP3A activity and illicit morphine use. Methadone 114-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-205 19133059-8 2009 CYP3A activity explained 22, 16, 15 and 23% of the variation in unbound (R)-, unbound (S)-, total (RS)- and total (S)-methadone clearances, respectively. Methadone 118-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 19133059-10 2009 CONCLUSIONS: CYP3A activity has a modest influence on methadone disposition. Methadone 54-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-18 19289993-1 2009 BACKGROUND: Tacrolimus is a substrate of cytochrome P-450 (CYP) 3A enzyme and of the drug transporter ABCB1. Tacrolimus 12-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-66 19067473-3 2009 As with lansoprazole, dexlansoprazole is metabolized mainly by CYP3A and CYP2C19. Dexlansoprazole 22-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-68 19151423-3 2009 As ciprofloxacin is a weak inhibitor of CYP3A4, it is very likely that other mechanisms involving the ATP-binding cassette drug efflux transporter family played a role in this drug interaction. Ciprofloxacin 3-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 19566112-5 2009 Solifenacin is eliminated mainly through hepatic metabolism via cytochrome P450 (CYP) 3A4, with about only 7% (3-13%) of the dose being excreted unchanged in the urine. Solifenacin Succinate 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-89 19067731-8 2009 Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes. Aspirin 45-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 19067731-8 2009 Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes. Clopidogrel 57-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 19071883-9 2009 In addition to the clinical pharmacokinetic analysis, the ability of mipomersen sodium to inhibit the major CYP isoform enzymes (namely CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4) was evaluated in cryo-preserved human hepatocytes in vitro. Sodium 80-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 19725591-8 2009 Etravirine has the potential for interactions by inducing CYP3A and inhibiting CYP2C9 and 2C19; it is a mild inhibitor of P-glycoprotein but not a substrate. etravirine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-63 19743887-6 2009 METHODS: A matrix table was composed by stratifying two basic parameters of the prediction: the contribution ratio of CYP3A4 to the oral clearance of substrates (CR), and the inhibition ratio of inhibitors (IR). Chromium 162-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 19499965-0 2009 Management of metabolic cytochrome P450 3A4 drug-drug interaction between everolimus and azole antifungals in a renal transplant patient. Everolimus 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-43 19499965-0 2009 Management of metabolic cytochrome P450 3A4 drug-drug interaction between everolimus and azole antifungals in a renal transplant patient. Azoles 89-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-43 19499965-3 2009 We observed pharmacokinetic drug interactions between both voriconazole and posaconazole, and everolimus cytochrome P450 3A4 metabolism, resulting in 7.5- and 3.8-fold increase, respectively, in everolimus blood trough concentrations. Everolimus 94-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-124 18815591-0 2009 Dose-response of ritonavir on hepatic CYP3A activity and elvitegravir oral exposure. Ritonavir 17-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-43 18815591-1 2009 Ritonavir, a potent inhibitor of cytochrome P450 isoform 3A (CYP3A) activity, is frequently used to boost the effects of protease inhibitors at doses of 100-400 mg per day; however, human data regarding the optimal dose required for boosting are limited. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-59 18815591-1 2009 Ritonavir, a potent inhibitor of cytochrome P450 isoform 3A (CYP3A) activity, is frequently used to boost the effects of protease inhibitors at doses of 100-400 mg per day; however, human data regarding the optimal dose required for boosting are limited. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-66 18815591-2 2009 This study systematically evaluated the ritonavir dose-response relationship on presystemic and systemic CYP3A metabolism using the human immunodeficiency virus integrase inhibitor elvitegravir and midazolam as probe substrates. Ritonavir 40-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-110 18815591-4 2009 The 20-mg dose of ritonavir substantially reduced CYP3A-mediated clearance (CL), as evidenced by a 66% reduction in midazolam CL that plateaued to 17% of baseline activity at a 100-mg dose. Ritonavir 18-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-55 18815591-6 2009 These data provide a critical understanding of ritonavir"s dose-response relationship for inhibition of CYP3A activity in humans. Ritonavir 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-109 19566112-11 2009 Exposure to solifenacin is increased about 1.2-fold in elderly subjects and about 2-fold in subjects with moderate hepatic and severe renal impairment, as well as by coadministration of the potent CYP3A4 inhibitor ketoconazole 200 mg/day. Solifenacin Succinate 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 19566112-11 2009 Exposure to solifenacin is increased about 1.2-fold in elderly subjects and about 2-fold in subjects with moderate hepatic and severe renal impairment, as well as by coadministration of the potent CYP3A4 inhibitor ketoconazole 200 mg/day. Ketoconazole 214-226 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 197-203 20110052-1 2009 BACKGROUND: The proteasome inhibitor bortezomib undergoes oxidative biotransformation via multiple cytochrome P450 (CYP) enzymes, with CYP3A4 identified as a partial, yet potentially important, contributor based on in vitro drug metabolism studies. Bortezomib 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 19566113-13 2009 Dose adjustments of cinacalcet may be necessary, and parathyroid hormone (PTH) and serum calcium concentrations should be closely monitored if a patient initiates or discontinues therapy with a strong CYP3A4 inhibitor (e.g. ketoconazole, erythromycin, itraconazole). Ketoconazole 224-236 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-207 20110052-12 2009 CONCLUSION: Concomitant administration of the CYP3A inhibitor ketoconazole with bortezomib resulted in a mean increase of 35% in bortezomib exposure. Ketoconazole 62-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-51 19228077-9 2009 Metabolism of sorafenib occurs primarily in the liver and is mediated via cytochrome P450 (CYP) 3A4 and uridine diphosphate glucuronosyltransferase 1A9. Sorafenib 14-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-99 20110052-12 2009 CONCLUSION: Concomitant administration of the CYP3A inhibitor ketoconazole with bortezomib resulted in a mean increase of 35% in bortezomib exposure. Bortezomib 80-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-51 20110052-12 2009 CONCLUSION: Concomitant administration of the CYP3A inhibitor ketoconazole with bortezomib resulted in a mean increase of 35% in bortezomib exposure. Bortezomib 129-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-51 20110053-2 2009 Nilotinib is metabolized in the liver via oxidation and hydroxylation pathways, mediated primarily by the cytochrome P450 3A4 isozyme. nilotinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-125 18845661-11 2009 Consequently, ketamine-caused cytoskeletal interruption led to suppression of CYP3A4 expression and its metabolizing activity. Ketamine 14-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 19323590-19 2009 Darunavir is primarily metabolized by the hepatic cytochrome P450 (CYP) enzymes, primarily CYP3A. Darunavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-96 19323590-20 2009 The "boosting" dose of ritonavir acts an an inhibitor of CYP3A, thereby increasing darunavir bioavailability. Ritonavir 23-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 19323590-20 2009 The "boosting" dose of ritonavir acts an an inhibitor of CYP3A, thereby increasing darunavir bioavailability. Darunavir 83-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 19323590-21 2009 Drug interactions can result when darunavir is coadministered with other drugs that are inducers or inhibitors of, or act as substrates for, CYP3A. Darunavir 34-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-146 19353999-6 2009 Aliquots of the extract were tested for their ability to inhibit the metabolism of the human CYP3A4 probe quinine, using an in vitro liver microsomal technique. Quinine 106-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 19353999-8 2009 Formation of quinine"s metabolite 3-hydroxyquinine, generated by the CYP3A4-mediated reaction, was measured by HPLC. Quinine 13-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 19353999-8 2009 Formation of quinine"s metabolite 3-hydroxyquinine, generated by the CYP3A4-mediated reaction, was measured by HPLC. 3-hydroxyquinidine 34-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 19353999-11 2009 Among the supplements tested, GTE produced the most pronounced inhibition of CYP3A4, which ranged from 5.6% by Nature"s Resource to 89.9% by Natrol GTE product. gte 30-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 19353999-11 2009 Among the supplements tested, GTE produced the most pronounced inhibition of CYP3A4, which ranged from 5.6% by Nature"s Resource to 89.9% by Natrol GTE product. natrol gte 141-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 19353999-13 2009 This study suggests that GTE use may cause significant interactions with drugs metabolized by CYP3A4. gte 25-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 19353999-14 2009 However, the effect on CYP3A4 varied among different brands of GTE, possibly due to variations in their content of the herbal product"s active ingredients. gte 63-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 19356113-0 2009 Utility of Nicotiana tabacum cell suspension cultures expressing human CYP1A1, CYP1A2 and CYP3A4 to study the oxidative metabolism of the herbicide 14C-fluometuron. Carbon-14 148-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 19571438-0 2009 Different enzyme kinetics of midazolam in recombinant CYP3A4 microsomes from human and insect sources. Midazolam 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 19571438-2 2009 The aim of this study was to compare midazolam enzyme kinetics in recombinant expressed CYP3A4 microsomes from human and insect cells. Midazolam 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 19571438-3 2009 The amounts of 1"- hydroxymidazolam and 4-hydroxymidazolam formed in CYP3A4 microsomes from transfected human liver epithelial cells (T5-3A4 microsomes) and baculovirus-infected insect cells (with and without coexpressed cytochrome b(5)) were analysed by LC-MS. 1-hydroxymethylmidazolam 15-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 19571438-3 2009 The amounts of 1"- hydroxymidazolam and 4-hydroxymidazolam formed in CYP3A4 microsomes from transfected human liver epithelial cells (T5-3A4 microsomes) and baculovirus-infected insect cells (with and without coexpressed cytochrome b(5)) were analysed by LC-MS. 4-hydroxymidazolam 40-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 19571438-8 2009 The different enzyme kinetics of midazolam observed in recombinant CYP3A4 microsomes from human and insect sources, especially the substantially higher K(m) obtained in human microsomes compared to insect microsomes, should be further evaluated since it may have implications for correlations to in vivo situation. Midazolam 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 19728747-9 2009 Ciclosporin and tacrolimus have distinct pharmacokinetics, but both are metabolized by intestinal and hepatic CYP3A4/3A5 and transported across the cell membrane by P-glycoprotein. Cyclosporine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 19728747-9 2009 Ciclosporin and tacrolimus have distinct pharmacokinetics, but both are metabolized by intestinal and hepatic CYP3A4/3A5 and transported across the cell membrane by P-glycoprotein. Tacrolimus 16-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 19728747-14 2009 Proliferation signal inhibitors (PSIs) such as sirolimus and everolimus are substrates of CYP3A4 and P-glycoprotein and have a macrolide structure very similar to tacrolimus, which explains why common drug interactions with PSIs are comparable to those with calcineurin inhibitors. Sirolimus 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 19728747-14 2009 Proliferation signal inhibitors (PSIs) such as sirolimus and everolimus are substrates of CYP3A4 and P-glycoprotein and have a macrolide structure very similar to tacrolimus, which explains why common drug interactions with PSIs are comparable to those with calcineurin inhibitors. Everolimus 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 19881256-3 2009 Positive controls for CYP1A2 and CYP3A4 used beta-naphthoflavone (beta-NF) and rifampicin (Rif), respectively. beta-Naphthoflavone 45-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 20408500-2 2009 Inhibition of CYP1A2, CYP2E1, CYP2C19, CYP2C9, CYP2D6, and CYP3A4 by CGS was assessed using recombinant human enzymes incubated with CGS (up to 3 mM expressed as free base). cysteinylglycine 69-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 20408500-3 2009 Induction of CYP1A2, CYP2B6, CYP2C9, CYP2C19 and CYP3A4 by CGS (0.01, 0.3 and 3 mM) was evaluated in cryopreserved human hepatocytes, by determining CYP mRNA expression using quantitative RT-PCR. cysteinylglycine 59-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 18948380-10 2009 Human P450 isoforms that showed activity toward multiple pyrethroids were CYP2C8, CYP2C9, CYP2C19, and CYP3A4. Pyrethrins 57-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 19228077-12 2009 For example, sorafenib exposure was reduced by an average 37% with concomitant administration of the CYP3A4 inducer rifampicin (rifampin); sorafenib concentrations may also be decreased by other CYP3A4 inducers. Sorafenib 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 19228077-12 2009 For example, sorafenib exposure was reduced by an average 37% with concomitant administration of the CYP3A4 inducer rifampicin (rifampin); sorafenib concentrations may also be decreased by other CYP3A4 inducers. Sorafenib 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 19228077-12 2009 For example, sorafenib exposure was reduced by an average 37% with concomitant administration of the CYP3A4 inducer rifampicin (rifampin); sorafenib concentrations may also be decreased by other CYP3A4 inducers. Rifampin 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 19228077-12 2009 For example, sorafenib exposure was reduced by an average 37% with concomitant administration of the CYP3A4 inducer rifampicin (rifampin); sorafenib concentrations may also be decreased by other CYP3A4 inducers. Rifampin 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 19228077-12 2009 For example, sorafenib exposure was reduced by an average 37% with concomitant administration of the CYP3A4 inducer rifampicin (rifampin); sorafenib concentrations may also be decreased by other CYP3A4 inducers. Rifampin 128-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 19228077-12 2009 For example, sorafenib exposure was reduced by an average 37% with concomitant administration of the CYP3A4 inducer rifampicin (rifampin); sorafenib concentrations may also be decreased by other CYP3A4 inducers. Rifampin 128-136 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 19228077-12 2009 For example, sorafenib exposure was reduced by an average 37% with concomitant administration of the CYP3A4 inducer rifampicin (rifampin); sorafenib concentrations may also be decreased by other CYP3A4 inducers. Sorafenib 139-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-107 19228077-12 2009 For example, sorafenib exposure was reduced by an average 37% with concomitant administration of the CYP3A4 inducer rifampicin (rifampin); sorafenib concentrations may also be decreased by other CYP3A4 inducers. Sorafenib 139-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 195-201 19077665-0 2009 Inhibition of CYP3A4 expression by ketoconazole is mediated by the disruption of pregnane X receptor, steroid receptor coactivator-1, and hepatocyte nuclear factor 4alpha interaction. Ketoconazole 35-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 18957504-8 2009 RESULTS: Compared to P450c21, the Vmax/Km for 21-hydroxylation of progesterone by CYP2C19 and CYP3A4 were 17 and 10%, respectively. Progesterone 66-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 18957504-12 2009 CONCLUSIONS: CYP2C19 and CYP3A4 can 21-hydroxylate progesterone but not 17OHP, possibly ameliorating mineralocorticoid deficiency, but not glucocorticoid deficiency. 21-hydroxylate progesterone 36-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 18957504-12 2009 CONCLUSIONS: CYP2C19 and CYP3A4 can 21-hydroxylate progesterone but not 17OHP, possibly ameliorating mineralocorticoid deficiency, but not glucocorticoid deficiency. 17-alpha-Hydroxyprogesterone 72-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 19004846-8 2009 Furthermore, anacetrapib appears to be a moderately sensitive substrate of CYP3A. anacetrapib 13-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-80 20027145-9 2009 Among recombinant rat and human CYP enzymes tested in this study, rat CYP3A2 and human CYP3A4/5, followed by CYP1A1 of both organisms were the most effective enzymes converting 3-ABA. 3-aminobenzanthrone 177-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-95 19077665-4 2009 We therefore focused on the role of PXR-HNF4alpha interaction in the transcriptional regulation of CYP3A4 under rifampin-mediated ketoconazole inhibition. Ketoconazole 130-142 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 19077665-6 2009 Here, we report that HNF4alpha plays a critical role in CYP3A4 promoter activation, and the interaction between PXR and HNF4alpha, which is closely related to the expression of CYP3A4, might be involved in ketoconazole-mediated inhibition of CYP3A4 gene expression. Ketoconazole 206-218 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 19077665-6 2009 Here, we report that HNF4alpha plays a critical role in CYP3A4 promoter activation, and the interaction between PXR and HNF4alpha, which is closely related to the expression of CYP3A4, might be involved in ketoconazole-mediated inhibition of CYP3A4 gene expression. Ketoconazole 206-218 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 18762932-1 2009 OBJECTIVE: Induction of CYP3A by St. John"s wort (SJW) products with high hyperforin content is well described. hyperforin 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 18762932-2 2009 Since CYP3A induction is mediated by hyperforin in a concentration-dependent manner, and SJW preparations differ significantly in hyperforin content, the aim of the study was to evaluate the effect of an SJW powder with low hyperforin content on CYP3A function. hyperforin 37-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-11 18777173-4 2009 CONCLUSIONS: Miconazole oral gel and oral voriconazole produced comparable increase in the exposure to etoricoxib, presumably via CYP3A inhibition. Miconazole 13-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-135 18777173-4 2009 CONCLUSIONS: Miconazole oral gel and oral voriconazole produced comparable increase in the exposure to etoricoxib, presumably via CYP3A inhibition. Voriconazole 42-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-135 18777173-4 2009 CONCLUSIONS: Miconazole oral gel and oral voriconazole produced comparable increase in the exposure to etoricoxib, presumably via CYP3A inhibition. Etoricoxib 103-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 130-135 19202563-3 2009 Clotrimazole, rifampin, ritonavir, phenytoin, and phenobarbital induced CYP2C9 consistent with previous findings for CYP3A4. Clotrimazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 19202563-3 2009 Clotrimazole, rifampin, ritonavir, phenytoin, and phenobarbital induced CYP2C9 consistent with previous findings for CYP3A4. Rifampin 14-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 19202563-3 2009 Clotrimazole, rifampin, ritonavir, phenytoin, and phenobarbital induced CYP2C9 consistent with previous findings for CYP3A4. Ritonavir 24-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 19202563-3 2009 Clotrimazole, rifampin, ritonavir, phenytoin, and phenobarbital induced CYP2C9 consistent with previous findings for CYP3A4. Phenytoin 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 19202563-3 2009 Clotrimazole, rifampin, ritonavir, phenytoin, and phenobarbital induced CYP2C9 consistent with previous findings for CYP3A4. Phenobarbital 50-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 19004846-0 2009 Assessment of the CYP3A-mediated drug interaction potential of anacetrapib, a potent cholesteryl ester transfer protein (CETP) inhibitor, in healthy volunteers. anacetrapib 63-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-23 19004846-1 2009 In this study, midazolam was used as a probe-sensitive CYP3A substrate to investigate the effect of anacetrapib on CYP3A activity, and ketoconazole was used as a probe-inhibitor to investigate the effect of potent CYP3A inhibition on the pharmacokinetics of anacetrapib, a novel cholesteryl ester transfer protein inhibitor in development for the treatment of dyslipidemia. Midazolam 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 19077665-6 2009 Here, we report that HNF4alpha plays a critical role in CYP3A4 promoter activation, and the interaction between PXR and HNF4alpha, which is closely related to the expression of CYP3A4, might be involved in ketoconazole-mediated inhibition of CYP3A4 gene expression. Ketoconazole 206-218 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 177-183 19077665-1 2009 BACKGROUND: Earlier studies have shown that ketoconazole inhibits CYP3A4 expression through pregnane X receptor (PXR)-mediated transcription and coactivator interaction. Ketoconazole 44-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 19077665-3 2009 It was recently reported that hepatocyte nuclear receptor 4alpha (HNF4alpha), a master regulator of several nuclear receptors, associates with PXR thus regulates the expression of CYP3A4 under rifampin treatment. Rifampin 193-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 19077665-4 2009 We therefore focused on the role of PXR-HNF4alpha interaction in the transcriptional regulation of CYP3A4 under rifampin-mediated ketoconazole inhibition. Rifampin 112-120 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 19088019-3 2008 Other tamoxifen-related genetic variants of CYP3A4, CYP3A5, and sulfotransferase1A1 (SULT1A1) are also briefly reviewed here. Tamoxifen 6-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 19219743-7 2009 In addition, intestinal microsomes metabolized eperisone to M3 and M4 via CYP2J2- and CYP3A4-mediated reactions, which are supposed to contribute to presystemic metabolism of eperisone. eperisone 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 19219743-7 2009 In addition, intestinal microsomes metabolized eperisone to M3 and M4 via CYP2J2- and CYP3A4-mediated reactions, which are supposed to contribute to presystemic metabolism of eperisone. eperisone 175-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 19219744-4 2009 This method was used to determine the bioactivation of acetaminophen at two concentrations: 50 microM therapeutic and 1 mM toxic by using nine human recombinant CYP enzymes: CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4; and with different microsomes from experimental animals. Acetaminophen 55-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 243-249 19219744-5 2009 At the toxic concentration the formation of NAPQI-glutathione was highest with CYP3A4 followed by CYP2E1, CYP1A2, and CYP2D6. napqi-glutathione 44-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 19219744-9 2009 This study suggests that CYP3A4 is the major CYP enzyme form catalysing acetaminophen oxidation to NAPQI in human liver. Acetaminophen 72-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 19219744-9 2009 This study suggests that CYP3A4 is the major CYP enzyme form catalysing acetaminophen oxidation to NAPQI in human liver. N-acetyl-4-benzoquinoneimine 99-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 19012403-1 2008 Furanocoumarins (FCs) in the human diet irreversibly inhibit human cytochrome P450 3A4 (CYP 3A4) and are responsible for the "grapefruit/drug""interaction phenomenon. Furocoumarins 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-86 19012403-1 2008 Furanocoumarins (FCs) in the human diet irreversibly inhibit human cytochrome P450 3A4 (CYP 3A4) and are responsible for the "grapefruit/drug""interaction phenomenon. Furocoumarins 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-95 19088049-2 2008 The effect of smoking on the pharmacokinetics of imatinib, which is metabolized by CYP3A4 and partly by CYP1A2, is unknown. Imatinib Mesylate 49-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 18799803-3 2008 SKF525A and its metabolite and primary amine analog all inhibited CYP2B6-, CYP2C9-, CYP2C19-, CYP2D6-, and CYP3A-selective reactions to varying degrees but had little effect on CYP1A2, CYP2A6, and CYP2E1 reactions. Proadifen 0-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-112 18799805-9 2008 By using TgCYP3A4/hPXR mice, human PXR-CYP3A4-mediated rifampicin-protease inhibitor interactions were recapitulated, as the metabolic stability of amprenavir, nelfinavir, and saquinavir decreased 52, 53, and 99%, respectively, in the liver microsomes of TgCYP3A4/hPXR mice pretreated with rifampicin. Rifampin 55-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 19185782-2 2008 The main pharmacokinetic characteristics of rivaroxaban are a bioavailability of approximately 80-100%, a maximum concentration obtained in 2 to 4 hours, a terminal half-life of elimination of 7 to 11 hours, a renal elimination for 1/3 for the active hepatic metabolism from the cytochrome P450 (3A4) for the other 2/3. Rivaroxaban 44-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 279-299 19149415-5 2008 Triacetyloleandomycin, a specific inhibitor of human CYP3A4, inhibited the metabolism of lovastatin in pig and human liver microsomes. Troleandomycin 0-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 19149415-5 2008 Triacetyloleandomycin, a specific inhibitor of human CYP3A4, inhibited the metabolism of lovastatin in pig and human liver microsomes. Lovastatin 89-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 18799803-3 2008 SKF525A and its metabolite and primary amine analog all inhibited CYP2B6-, CYP2C9-, CYP2C19-, CYP2D6-, and CYP3A-selective reactions to varying degrees but had little effect on CYP1A2, CYP2A6, and CYP2E1 reactions. Amines 39-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-112 18809730-2 2008 CYP1A2 is generally considered to be the major enzyme involved in the biotransformation of CLZ to its N-demethylated (norCLZ) and N-oxygenated (CLZ N-oxide) metabolites in liver, but several studies have also implicated CYP3A4. Clozapine 91-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 220-226 18799803-4 2008 Only the inhibition of CYP3A showed major enhancement when the inhibitors were preincubated with NADPH-fortified microsomes, and the extent of metabolic intermediate (MI) complex formation approximated typical CYP3A content. NADP 97-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-28 18809730-5 2008 In contrast, the activity of CYP3A4 alone was correlated with the susceptibility of CLZ N-oxide formation to inhibition by these agents. clozapine N-oxide 84-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 18809730-7 2008 In vivo assessment of CYP1A2 and CYP3A4 activities, perhaps by phenotyping approaches, could assist the optimization of CLZ dosage and minimize pharmacokinetic interactions with coadministered drugs. Clozapine 120-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 19356104-4 2008 Therefore, the methadone-maintenance-treatment outcome should be evaluated when patients are treated with drugs which are supposed to induce CYP3A4 and CYP2B6 isoforms. Methadone 15-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 141-147 18799805-6 2008 In TgCYP3A4/hPXR mice, CYP3A4 was strongly induced by rifampicin, a human-specific PXR ligand, but not by pregnenolone 16alpha-carbonitrile, a rodent-specific PXR ligand. Rifampin 54-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 5-11 20116610-9 2008 ATV is a weak competitive inhibitor of CYP3A4 and a strong inhibitor of uridine diphosphate-glucuronosyltransferase 1A1, which is the cause of the frequent high plasma bilirubin after its administration and of its pharmacological interactions. Atazanavir Sulfate 0-3 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 18679666-8 2008 CONCLUSION: The present data permit us to conclude that the apparent clearance of lidocaine and MEGX was reduced in diabetic patients compared to normal women, suggesting that GDM inhibits the CYP1A2/CYP3A4 isoforms responsible for the metabolism of this drug and its metabolite. Lidocaine 82-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 18679666-8 2008 CONCLUSION: The present data permit us to conclude that the apparent clearance of lidocaine and MEGX was reduced in diabetic patients compared to normal women, suggesting that GDM inhibits the CYP1A2/CYP3A4 isoforms responsible for the metabolism of this drug and its metabolite. monoethylglycinexylidide 96-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 200-206 19186349-1 2008 PURPOSE: Ritonavir is a powerful inhibitor of cytochrome P450 3A (CYP3A) that metabolizes many antiretrovirals. Ritonavir 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-64 19186349-1 2008 PURPOSE: Ritonavir is a powerful inhibitor of cytochrome P450 3A (CYP3A) that metabolizes many antiretrovirals. Ritonavir 9-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 19186349-4 2008 RESULTS: CYP3A activity was expressed as oral clearance of the midazolam probe. Midazolam 63-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-14 19186349-7 2008 CYP3A activity in subjects on ritonavir and with CVH was further reduced to 4% of controls (no CVH, R+ 2.1 +/- 0.8 vs. R+, CVH+ 1.0 +/- 0.4 mL/min/kg, P < 0.006). Ritonavir 30-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 19186349-8 2008 CONCLUSIONS: Ritonavir markedly decreases CYP3A activity. Ritonavir 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-47 19186349-9 2008 In the presence of CVH, ritonavir-based therapy further reduces CYP3A activity by half. cvh 19-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 19186349-9 2008 In the presence of CVH, ritonavir-based therapy further reduces CYP3A activity by half. Ritonavir 24-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 19186349-10 2008 Coinfection with CVH impairs CYP3A activity in the presence of the CYP3A inhibitor ritonavir. Ritonavir 83-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-72 19337422-8 2008 In addition, tolvaptan is metabolized by the CYP3A4 system; thus physicians should be aware of the potential for increased interactions with other medications. Tolvaptan 13-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 21291779-11 2008 Further studies are also needed to determine whether concomitant administration of a non-CYP3A4-metabolized statin (such as fluvastatin, pravastatin, or rosuvastatin) with a CYP3A4 inhibitor, may reduce adverse event rates in routine clinical practice. Fluvastatin 124-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 21291779-11 2008 Further studies are also needed to determine whether concomitant administration of a non-CYP3A4-metabolized statin (such as fluvastatin, pravastatin, or rosuvastatin) with a CYP3A4 inhibitor, may reduce adverse event rates in routine clinical practice. Fluvastatin 124-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 21291779-11 2008 Further studies are also needed to determine whether concomitant administration of a non-CYP3A4-metabolized statin (such as fluvastatin, pravastatin, or rosuvastatin) with a CYP3A4 inhibitor, may reduce adverse event rates in routine clinical practice. Pravastatin 137-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 19130187-14 2008 CONCLUSION: The optimal sparse design enabled the estimation of CL/F of a CYP3A4 substrate and inhibitor when co-administered together and to show the interaction leading to the same conclusion as the full empirical design. Fluorine 67-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 18976719-1 2008 OBJECTIVES: It has been reported that telithromycin is primarily metabolized via hepatic CYP3A4 and 3A1/2 in humans and rats, respectively, and that the protein expression of hepatic CYP3A subfamily significantly decreased (59.1% decrease) in 24-h KPLPS rats (lipopolysaccharide derived from Klebsiella pneumoniae; the protein expression was measured 24h after KPLPS administration) compared with that in control rats, but restored to that in control rats in 96-h KPLPS rats. telithromycin 38-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-105 18978522-1 2008 Cyclosporine is a substrate of cytochrome P450 (CYP) 3A and of the transporter ABCB1, for which polymorphisms have been described. Cyclosporine 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-55 18978522-6 2008 CYP3A4 rs4646437C>T influenced cyclosporine kinetics, the T carriers requiring higher cyclosporine dose. Cyclosporine 34-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18978522-6 2008 CYP3A4 rs4646437C>T influenced cyclosporine kinetics, the T carriers requiring higher cyclosporine dose. Cyclosporine 89-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18978522-8 2008 In conclusion, CYP3A4, CYP3A5, and CYP3A7 polymorphisms affect cyclosporine metabolism, and therefore, their genotyping could be useful, in association with therapeutic drug monitoring, to prospectively optimize cyclosporine prescription in transplant recipients. Cyclosporine 63-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 18978522-8 2008 In conclusion, CYP3A4, CYP3A5, and CYP3A7 polymorphisms affect cyclosporine metabolism, and therefore, their genotyping could be useful, in association with therapeutic drug monitoring, to prospectively optimize cyclosporine prescription in transplant recipients. Cyclosporine 212-224 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 18978522-9 2008 The administration of a CYP3A genotype-dependent cyclosporine starting dose should therefore be tested prospectively in a randomized controlled clinical trial to assess whether it leads to an improvement of the patients outcome after transplantation, with adequate immunosuppression and decreased toxicity. Cyclosporine 49-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 18784074-5 2008 Here we report that inhibition of cyclin-dependent kinases (Cdks) by kenpaullone and roscovitine (two small molecule inhibitors of Cdks that we identified in a screen for compounds that activate hPXR) leads to activation of hPXR-mediated CYP3A4 gene expression in HepG2 human liver carcinoma cells. kenpaullone 69-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 238-244 18989830-4 2008 CYP3A4 mRNA and activity were induced by the prototypical pregnane X receptor (PXR) ligands, rifampicin (E(max) = 36- and 6-fold, respectively, and EC(50) = 4 microM) and phenobarbital (E(max) = 12- and 4-fold, respectively, and EC(50) = 205 microM). Rifampin 93-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18989830-4 2008 CYP3A4 mRNA and activity were induced by the prototypical pregnane X receptor (PXR) ligands, rifampicin (E(max) = 36- and 6-fold, respectively, and EC(50) = 4 microM) and phenobarbital (E(max) = 12- and 4-fold, respectively, and EC(50) = 205 microM). Phenobarbital 171-184 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18980315-2 2008 Here, in the first single-molecule (SM) fluorescence studies of CYPs, we use total internal reflection fluorescence microscopy to measure residence times of the fluorescent dye Nile Red in CYP3A4 incorporated in surface-immobilized lipid Nanodiscs, with and without the effector alpha-naphthoflavone. nile red 177-185 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 189-195 18706998-1 2008 The CYP3A4 substrate budesonide was used to investigate gut wall first-pass metabolism in jejunum, ileum and colon of eight healthy men. Budesonide 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 18706998-9 2008 The data are in accordance with the well-known CYP3A activity in the small intestine, evidently capable of metabolising at least half the absorbed dose of budesonide. Budesonide 155-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 47-52 18982531-6 2008 The results demonstrate that CYP3A4 and CYP2C19 could be involved in the metabolism of triptolide in human liver, and that CYP3A4 was the primary isoform responsible for its hydroxylation. triptolide 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 18982531-6 2008 The results demonstrate that CYP3A4 and CYP2C19 could be involved in the metabolism of triptolide in human liver, and that CYP3A4 was the primary isoform responsible for its hydroxylation. triptolide 87-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 18784074-5 2008 Here we report that inhibition of cyclin-dependent kinases (Cdks) by kenpaullone and roscovitine (two small molecule inhibitors of Cdks that we identified in a screen for compounds that activate hPXR) leads to activation of hPXR-mediated CYP3A4 gene expression in HepG2 human liver carcinoma cells. Roscovitine 85-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 238-244 19007592-1 2008 OBJECTIVES: Because of the known CYP3A4 inhibition by calcium-channel blockers (CCBs), we hypothesized that there might be a drug-drug interaction between clopidogrel and dihydropyridines in patients with coronary artery disease. Clopidogrel 155-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 19005401-1 2008 BACKGROUND: Bioavailability of tacrolimus (Tac) and cyclosporine is determined by cytochrome P450IIIA and by P-glycoprotein encoded by the CYP3A4/CYP3A5 and ABCB1 genes. Tacrolimus 31-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 19005401-1 2008 BACKGROUND: Bioavailability of tacrolimus (Tac) and cyclosporine is determined by cytochrome P450IIIA and by P-glycoprotein encoded by the CYP3A4/CYP3A5 and ABCB1 genes. Cyclosporine 52-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 18794387-2 2008 In agreement with in vitro evidence, these data suggest that chloramphenicol is a rather significant inhibitor of hepatic CYP3A4 and/or CYP2C19. Chloramphenicol 61-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 18812562-11 2008 The interaction is due to the inhibition of CYP3A4-mediated everolimus clearance. Everolimus 60-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 18812562-14 2008 According to the different inhibitory potency of CYP3A4 activity, the reduction should be lower during fluconazole than during voriconazole cotreatment. Fluconazole 103-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 18812562-14 2008 According to the different inhibitory potency of CYP3A4 activity, the reduction should be lower during fluconazole than during voriconazole cotreatment. Voriconazole 127-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 19007592-1 2008 OBJECTIVES: Because of the known CYP3A4 inhibition by calcium-channel blockers (CCBs), we hypothesized that there might be a drug-drug interaction between clopidogrel and dihydropyridines in patients with coronary artery disease. Dihydropyridines 171-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 19007592-2 2008 BACKGROUND: Clopidogrel is activated by CYP3A4, which also metabolizes CCBs of the dihydropyridine class. Clopidogrel 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 19007592-2 2008 BACKGROUND: Clopidogrel is activated by CYP3A4, which also metabolizes CCBs of the dihydropyridine class. 1,4-dihydropyridine 83-98 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 19025521-4 2008 The aim of this study was to evaluate whether itraconazole, which is a potent inhibitor of P-glycoprotein and CYP3A4, would change the pharmacokinetics or the pharmacodynamics of oral morphine. Itraconazole 46-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 19025521-4 2008 The aim of this study was to evaluate whether itraconazole, which is a potent inhibitor of P-glycoprotein and CYP3A4, would change the pharmacokinetics or the pharmacodynamics of oral morphine. Morphine 184-192 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 18687804-10 2008 In contrast, (+)-phenylahistin mainly produced P3 in human microsomes and CYP3A human expressed P450s. phenylahistin 13-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-79 19011672-2 2008 In humans, CITA is metabolized to demethylcitalopram (DCITA) by CYP2C19, CYP2D6, and CYP3A and to didemethylcitalopram by CYP2D6. Citalopram 11-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-90 19011672-2 2008 In humans, CITA is metabolized to demethylcitalopram (DCITA) by CYP2C19, CYP2D6, and CYP3A and to didemethylcitalopram by CYP2D6. demethylcitalopram 34-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-90 19011672-2 2008 In humans, CITA is metabolized to demethylcitalopram (DCITA) by CYP2C19, CYP2D6, and CYP3A and to didemethylcitalopram by CYP2D6. demethylcitalopram 54-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-90 18669585-4 2008 Midazolam (MDZ), testosterone (TST), and nifedipine (NIF) were used to assess the catalytic activities of the CYP3A4 wild type (CYP3A4.1) and its variants. Nifedipine 41-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 18669585-4 2008 Midazolam (MDZ), testosterone (TST), and nifedipine (NIF) were used to assess the catalytic activities of the CYP3A4 wild type (CYP3A4.1) and its variants. Nifedipine 53-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 18669585-8 2008 In summary, CYP3A4.2 and CYP3A4.16 exhibited significantly lower activity for MDZ, TST, and NIF oxidations than CYP3A4.1. Midazolam 78-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 18669585-8 2008 In summary, CYP3A4.2 and CYP3A4.16 exhibited significantly lower activity for MDZ, TST, and NIF oxidations than CYP3A4.1. Midazolam 78-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 18669585-8 2008 In summary, CYP3A4.2 and CYP3A4.16 exhibited significantly lower activity for MDZ, TST, and NIF oxidations than CYP3A4.1. Midazolam 78-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-31 18694908-9 2008 In vitro studies using human subcellular fractions suggested that the initial metabolism of torcetrapib proceeds via CYP3A-mediated decarbamoylation. torcetrapib 92-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-122 18636247-1 2008 OBJECTIVE: The objective of this study was to retrospectively evaluate the effects of MDR1, CYP3A4*18B, and CYP3A5*3 genetic polymorphisms on cyclosporine A (CsA) pharmacokinetics in Chinese renal transplant patients during the first month after transplantation. Cyclosporine 142-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 18636247-10 2008 Patients with CYP3A4*18B alleles may require higher doses of CsA to reach the target levels. Cyclosporine 61-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 18661126-0 2008 Dual drug interactions via P-glycoprotein (P-gp)/ cytochrome P450 (CYP3A4) interplay: recent case study of oral atorvastatin and verapamil. Atorvastatin 112-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 18608282-10 2008 Cyclosporine co-administration increases colchicine toxicity by a dual mechanism: cyclosporine inhibits P-glycoprotein resulting in increased intracellular colchicine concentrations and decreased hepatic and renal excretion of the drug and cyclosporine interacts with CYP3A4 to decreases the hepatic elimination of colchicine. Cyclosporine 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 268-274 18608282-10 2008 Cyclosporine co-administration increases colchicine toxicity by a dual mechanism: cyclosporine inhibits P-glycoprotein resulting in increased intracellular colchicine concentrations and decreased hepatic and renal excretion of the drug and cyclosporine interacts with CYP3A4 to decreases the hepatic elimination of colchicine. Cyclosporine 82-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 268-274 18661126-0 2008 Dual drug interactions via P-glycoprotein (P-gp)/ cytochrome P450 (CYP3A4) interplay: recent case study of oral atorvastatin and verapamil. Verapamil 129-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 18784280-4 2008 Coadministration with aliskiren resulted in changes of <30% in AUC(tau) and C(max,ss) of digoxin, atorvastatin, o-hydroxy-atorvastatin, and rho-hydroxy-atorvastatin, indicating no clinically significant interaction with P-glycoprotein or CYP3A4 substrates. aliskiren 22-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 241-247 18784280-5 2008 Aliskiren AUC(tau) was significantly increased by coadministration with atorvastatin (by 47%, P < .001) or ketoconazole (by 76%, P < .001) through mechanisms most likely involving transporters such as P-glycoprotein and organic anion-transporting peptide and possibly through metabolic pathways such as CYP3A4 in the gut wall. Atorvastatin 72-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 309-315 18784280-5 2008 Aliskiren AUC(tau) was significantly increased by coadministration with atorvastatin (by 47%, P < .001) or ketoconazole (by 76%, P < .001) through mechanisms most likely involving transporters such as P-glycoprotein and organic anion-transporting peptide and possibly through metabolic pathways such as CYP3A4 in the gut wall. Ketoconazole 110-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 309-315 18623043-1 2008 Clindamycin is an antimicrobial agent metabolized by CYP3A4. Clindamycin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59 18846481-5 2008 Also determined was the effect of CYP3A4 inhibitors and non-inhibitors on nifedipine hydroxylation. Nifedipine 74-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 18846481-8 2008 HepG2-GS-3A4 selectively metabolized substrates of CYP3A4 (diazepam, nordiazepam, lidocaine, atorvastatin, and nifedipine) to a greater degree than control. Diazepam 59-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 18846481-8 2008 HepG2-GS-3A4 selectively metabolized substrates of CYP3A4 (diazepam, nordiazepam, lidocaine, atorvastatin, and nifedipine) to a greater degree than control. Nordazepam 69-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 18846481-8 2008 HepG2-GS-3A4 selectively metabolized substrates of CYP3A4 (diazepam, nordiazepam, lidocaine, atorvastatin, and nifedipine) to a greater degree than control. Lidocaine 82-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 18846481-8 2008 HepG2-GS-3A4 selectively metabolized substrates of CYP3A4 (diazepam, nordiazepam, lidocaine, atorvastatin, and nifedipine) to a greater degree than control. Atorvastatin 93-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 18846481-8 2008 HepG2-GS-3A4 selectively metabolized substrates of CYP3A4 (diazepam, nordiazepam, lidocaine, atorvastatin, and nifedipine) to a greater degree than control. Nifedipine 111-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 18647303-8 2008 Using recombinant CYP3A4, N-dealkylation was characterized by a K(m) of 13 microM and a V(max) of 3 pmol pmol(-1) CYP min(-1). Nitrogen 26-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 18537963-9 2008 CONCLUSIONS: Saliva appears to be a suitable matrix for non-invasive CYP3A phenotyping using midazolam as a probe drug, but sensitive analytical methods are required. Midazolam 93-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-74 19238656-6 2008 Acute ritonavir inhibits first-pass CYP3A > 96%. Ritonavir 6-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 19238656-7 2008 Chronic ritonavir inhibits hepatic CYP3A (> 70%) and first-pass CYP3A (> 90%). Ritonavir 8-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-40 19238656-1 2008 Ritonavir effects on CYP3A and P-glycoprotein activities. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-26 19238656-7 2008 Chronic ritonavir inhibits hepatic CYP3A (> 70%) and first-pass CYP3A (> 90%). Ritonavir 8-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-72 19238656-2 2008 Ritonavir diminishes methadone plasma concentrations, an effect attributed to CYP3A induction, but the actual mechanisms are unknown. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 19238656-9 2008 Steady-state compared with acute ritonavir caused mild apparent induction of P-gp and hepatic CYP3A, but net inhibition still predominated. Ritonavir 33-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-99 19238656-2 2008 Ritonavir diminishes methadone plasma concentrations, an effect attributed to CYP3A induction, but the actual mechanisms are unknown. Methadone 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 19238656-10 2008 Ritonavir inhibited both intestinal and hepatic CYP3A and drug transport. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-53 19238656-3 2008 We determined short-term (2-day) and steady-state (2-week) ritonavir effects on intestinal and hepatic CYP3A4/5 (probed with intravenous (IV) and oral alfentanil (ALF) and with miosis) and P-glycoprotein (P-gp) (fexofenadine), and on methadone pharmacokinetics and pharmacodynamics in healthy volunteers. Ritonavir 59-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 103-109 19238656-11 2008 ALF miosis noninvasively determined CYP3A inhibition by ritonavir. Ritonavir 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-41 18645035-3 2008 Using a panel of eight inhibitors, we show that at least four molecules of the widely used CYP3A4 substrate 7-benzyloxyquinoline can bind simultaneously to the enzyme. 7-benzyloxyquinoline 108-128 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-97 18583509-6 2008 Of the recombinant P450 enzymes tested, only CYP3A4 catalyzed 3-dehydrocholic acid formation. 7,12-dihydroxy-3-oxocholanic acid 62-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 18645036-0 2008 Role of vitamin D receptor in the lithocholic acid-mediated CYP3A induction in vitro and in vivo. Lithocholic Acid 34-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 18645036-1 2008 Lipophilic bile acids are suggested to be involved in the endogenous expression of CYP3A4 in human and experimental animals as ligands of nuclear receptors. Bile Acids and Salts 11-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-89 18583509-8 2008 Among the human recombinant P450 enzymes examined, CYP3A4 exhibited the highest rates of formation for 7alpha-hydroxy-3-oxo-5beta-cholan-24-oic acid and gamma-muricholic acid from chenodeoxycholic acid. 7alpha-Hydroxy-3-oxo-5beta-cholan-24-oic Acid 103-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 18583509-8 2008 Among the human recombinant P450 enzymes examined, CYP3A4 exhibited the highest rates of formation for 7alpha-hydroxy-3-oxo-5beta-cholan-24-oic acid and gamma-muricholic acid from chenodeoxycholic acid. muricholic acid 153-174 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 18645036-2 2008 To verify the nuclear receptor specificity, the bile acid-mediated induction of CYP3A4 has been studied in vitro and in vivo in the present study. Bile Acids and Salts 48-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 18583509-8 2008 Among the human recombinant P450 enzymes examined, CYP3A4 exhibited the highest rates of formation for 7alpha-hydroxy-3-oxo-5beta-cholan-24-oic acid and gamma-muricholic acid from chenodeoxycholic acid. Chenodeoxycholic Acid 180-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 51-57 18645036-3 2008 Lithocholic acid (LCA) strongly enhanced the activities of the CYP3A4 reporter gene, which contained multiple nuclear receptor binding elements, in both HepG2 and LS174T cells. Lithocholic Acid 0-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 18583509-11 2008 This study highlights a major role for CYP3A4 and suggests a possible route for the elimination of these two bile acids. Bile Acids and Salts 109-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 18645036-3 2008 Lithocholic acid (LCA) strongly enhanced the activities of the CYP3A4 reporter gene, which contained multiple nuclear receptor binding elements, in both HepG2 and LS174T cells. Lithocholic Acid 18-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 18645036-4 2008 The introduction of small interfering RNA for human vitamin D receptor (VDR), but not for human pregnane X receptor, reduced the LCA-induced activation of the reporter gene in these cells, suggesting the major role of VDR in the LCA induction of CYP3A4. Lithocholic Acid 129-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 246-252 18645036-4 2008 The introduction of small interfering RNA for human vitamin D receptor (VDR), but not for human pregnane X receptor, reduced the LCA-induced activation of the reporter gene in these cells, suggesting the major role of VDR in the LCA induction of CYP3A4. Lithocholic Acid 229-232 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 246-252 18645036-5 2008 Consistently, oral administration of LCA (100 mg/kg/day for 3 days) increased Cyp3a protein levels in the intestine but not in the liver, where a negligible level of VDR mRNA is detected. Lithocholic Acid 37-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-83 18653741-4 2008 The turnover of 1 was NADPH-dependent and was completely inhibited by ketoconazole and quercetin in the CYP3A4/5 and CYP2C8 incubations, respectively. NADP 22-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 19195459-2 2008 This drug is primarily metabolized by the liver through the cytochrome P450 3A4 (CYP3A4) isozyme and consequently coadministration with low doses of ritonavir markedly increases exposure and allows both daily doses and pill burden to be reduced. Ritonavir 149-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-79 19195459-2 2008 This drug is primarily metabolized by the liver through the cytochrome P450 3A4 (CYP3A4) isozyme and consequently coadministration with low doses of ritonavir markedly increases exposure and allows both daily doses and pill burden to be reduced. Ritonavir 149-158 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 19195459-3 2008 Both darunavir and ritonavir act as inhibitors and substrates of CYP3A4 and may therefore present pharmacological interactions with a large number of drugs commonly used in HIV-infected patients. Darunavir 5-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 19195459-3 2008 Both darunavir and ritonavir act as inhibitors and substrates of CYP3A4 and may therefore present pharmacological interactions with a large number of drugs commonly used in HIV-infected patients. Ritonavir 19-28 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 18653741-4 2008 The turnover of 1 was NADPH-dependent and was completely inhibited by ketoconazole and quercetin in the CYP3A4/5 and CYP2C8 incubations, respectively. Ketoconazole 70-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 18653741-4 2008 The turnover of 1 was NADPH-dependent and was completely inhibited by ketoconazole and quercetin in the CYP3A4/5 and CYP2C8 incubations, respectively. Quercetin 87-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 18650247-1 2008 Vincristine is metabolized to one primary metabolite, M1, by cDNA-expressed CYP3A4 and CYP3A5 and by CYP3A enzymes in human liver microsomes. Vincristine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 19230594-3 2008 The formation of AS2036313-00, and YM-394111 or YM-394112 were mediated by CYP2D6 and CYP3A4, respectively, which was elucidated by using a bank of human liver microsomes and recombinant CYP enzymes in combination with the utilization of typical substrates and inhibitors. as2036313 17-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 19230594-3 2008 The formation of AS2036313-00, and YM-394111 or YM-394112 were mediated by CYP2D6 and CYP3A4, respectively, which was elucidated by using a bank of human liver microsomes and recombinant CYP enzymes in combination with the utilization of typical substrates and inhibitors. ym-394111 35-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 19230594-3 2008 The formation of AS2036313-00, and YM-394111 or YM-394112 were mediated by CYP2D6 and CYP3A4, respectively, which was elucidated by using a bank of human liver microsomes and recombinant CYP enzymes in combination with the utilization of typical substrates and inhibitors. ym-394112 48-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 18650247-1 2008 Vincristine is metabolized to one primary metabolite, M1, by cDNA-expressed CYP3A4 and CYP3A5 and by CYP3A enzymes in human liver microsomes. Vincristine 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 18671948-1 2008 We recently demonstrated that nemorubicin (MMDX), an investigational antitumor drug, is converted to an active metabolite, PNU-159682, by human liver cytochrome P450 (CYP) 3A4. nemorubicin 30-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-175 18704002-2 2008 The aim of this study was to examine the influence of the CYP3A4, CYP3A5, and MDR1 single nucleotide polymorphisms on changes in tacrolimus exposure and dosing in renal allograft recipients treated with fluconazole. Tacrolimus 129-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 18671948-1 2008 We recently demonstrated that nemorubicin (MMDX), an investigational antitumor drug, is converted to an active metabolite, PNU-159682, by human liver cytochrome P450 (CYP) 3A4. N-neopentyl-N-nitrosourea 123-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-175 18671948-1 2008 We recently demonstrated that nemorubicin (MMDX), an investigational antitumor drug, is converted to an active metabolite, PNU-159682, by human liver cytochrome P450 (CYP) 3A4. methoxy-morpholinyl-doxorubicin 43-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-175 18647599-2 2008 The extent of CYP3A4 induction (measured as RIF ratio in comparison to rifampicin) and EC50 was obtained from the dose-response curve. Rifampin 71-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 18954002-1 2008 A multiconformational study of substrates of cytochrome P450 3A4 has been carried out within the BiS/MC algorithm. Bismuth 97-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-64 18647599-7 2008 Flutamide and haloperidol were further demonstrated to cause CYP3A4 induction in human cryopreserved hepatocytes based on testosterone 6beta-hydroxylation activity. Flutamide 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 18647599-7 2008 Flutamide and haloperidol were further demonstrated to cause CYP3A4 induction in human cryopreserved hepatocytes based on testosterone 6beta-hydroxylation activity. Haloperidol 14-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 18647599-7 2008 Flutamide and haloperidol were further demonstrated to cause CYP3A4 induction in human cryopreserved hepatocytes based on testosterone 6beta-hydroxylation activity. Testosterone 122-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 18954002-1 2008 A multiconformational study of substrates of cytochrome P450 3A4 has been carried out within the BiS/MC algorithm. Methylcholanthrene 101-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-64 18781906-2 2008 CYP3A4 enzyme-inducing antiepileptic drugs (EIAEDs) like carbamazepine, phenytoin, and oxcarbazepine--as well as non-EIAEDs like valproic acid, levetiracetam, and lamotrigine--are frequently used in patients with GBM. Carbamazepine 57-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18662288-11 2008 The OR for potentially arrhythmogenic CYP3A4 inhibitors was 3.79 (1.76, 8.15) in cisapride users and 3.47 (2.06, 5.83) in PPI users. Cisapride 81-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 18662288-13 2008 Although use of potentially arrhythmogenic CYP3A4 inhibitors was associated with an increased risk, this appears to be due to a direct effect of the drugs themselves rather than an interaction with cisapride. Cisapride 198-207 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 18431572-8 2008 In human liver microsomal preparations, eribulin suppressed the activities of CYP3A4-mediated testosterone and midazolam hydroxylation with an apparent K (i) of approximately 20 microM. Testosterone 94-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 18619640-13 2008 In addition to the dioxin-like actions, the BDE47 sample enhanced Cyp2B and Cyp3A expression suggesting that commercial PBDE mixtures, which also often contain brominated furans, may disturb cellular homeostasis at multiple levels. Halogenated Diphenyl Ethers 120-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-81 18781906-3 2008 Since CYP3A4 is the major isozyme involved in the metabolism of imatinib, we investigated the influence of EIAEDs on imatinib pharmacokinetics (pk). Imatinib Mesylate 64-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 18556438-8 2008 Collectively, multiple in vitro experiments showed that dasatinib was predominately metabolized by CYP3A4. Dasatinib 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 18573861-10 2008 Furthermore, studies with expressed enzymes showed that 17-OHPC is metabolized exclusively by CYP3A4 and CYP3A5. 17 alpha-Hydroxyprogesterone Caproate 56-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 18559486-9 2008 Stimulation with 3-methylcholanthrene and rifampicin markedly increased CYP1A1/2 or CYP3A4 activities, which could be selectively inhibited by nifedipine, verapamil, ketoconazole, and quercetin. Methylcholanthrene 17-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 18559486-9 2008 Stimulation with 3-methylcholanthrene and rifampicin markedly increased CYP1A1/2 or CYP3A4 activities, which could be selectively inhibited by nifedipine, verapamil, ketoconazole, and quercetin. Rifampin 42-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 18559486-9 2008 Stimulation with 3-methylcholanthrene and rifampicin markedly increased CYP1A1/2 or CYP3A4 activities, which could be selectively inhibited by nifedipine, verapamil, ketoconazole, and quercetin. Nifedipine 143-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 18573861-12 2008 In summary, this study shows that 17-OHPC is metabolized by CYP3A. 17 alpha-Hydroxyprogesterone Caproate 34-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-65 18559486-9 2008 Stimulation with 3-methylcholanthrene and rifampicin markedly increased CYP1A1/2 or CYP3A4 activities, which could be selectively inhibited by nifedipine, verapamil, ketoconazole, and quercetin. Verapamil 155-164 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 18559486-9 2008 Stimulation with 3-methylcholanthrene and rifampicin markedly increased CYP1A1/2 or CYP3A4 activities, which could be selectively inhibited by nifedipine, verapamil, ketoconazole, and quercetin. Ketoconazole 166-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 18559486-9 2008 Stimulation with 3-methylcholanthrene and rifampicin markedly increased CYP1A1/2 or CYP3A4 activities, which could be selectively inhibited by nifedipine, verapamil, ketoconazole, and quercetin. Quercetin 184-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 18573861-13 2008 Because CYP3A is involved in the oxidative metabolism of numerous commonly used drugs, 17-OHPC may be involved in clinically relevant metabolic drug interactions with coadministered CYP3A inhibitors or inducers. 17 alpha-Hydroxyprogesterone Caproate 87-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-13 18573861-8 2008 Metabolism of 17-OHPC was significantly inhibited by the CYP3A4 inhibitors ketoconazole and troleandomycin in HLM and FHH. 17 alpha-Hydroxyprogesterone Caproate 14-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 18573861-13 2008 Because CYP3A is involved in the oxidative metabolism of numerous commonly used drugs, 17-OHPC may be involved in clinically relevant metabolic drug interactions with coadministered CYP3A inhibitors or inducers. 17 alpha-Hydroxyprogesterone Caproate 87-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 182-187 18573861-8 2008 Metabolism of 17-OHPC was significantly inhibited by the CYP3A4 inhibitors ketoconazole and troleandomycin in HLM and FHH. Ketoconazole 75-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 18803184-1 2008 An electrophoretically mediated microanalysis method for the determination of CYP3A4 activity using testosterone and nifedipine as substrates was developed. Testosterone 100-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 18573861-8 2008 Metabolism of 17-OHPC was significantly inhibited by the CYP3A4 inhibitors ketoconazole and troleandomycin in HLM and FHH. Troleandomycin 92-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 18573861-9 2008 Metabolism of 17-OHPC was significantly greater in FHH treated with the CYP3A inducers, rifampin and phenobarbital. 17 alpha-Hydroxyprogesterone Caproate 14-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-77 18803184-1 2008 An electrophoretically mediated microanalysis method for the determination of CYP3A4 activity using testosterone and nifedipine as substrates was developed. Nifedipine 117-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 18803184-3 2008 The CYP3A4 activity was determined by quantitation of the reactant cofactor, NADPH. NADP 77-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 18803184-7 2008 Using the Lineweaver-Burk equation, the Michaelis constants (K(m)) for the oxidation of testosterone and nifedipine by CYP3A4 were calculated to be 58.6+/-8.3 and 19.1+/-2.4 microM, respectively, which are consistent with off-line assay and previously reported values. Testosterone 88-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 18803184-7 2008 Using the Lineweaver-Burk equation, the Michaelis constants (K(m)) for the oxidation of testosterone and nifedipine by CYP3A4 were calculated to be 58.6+/-8.3 and 19.1+/-2.4 microM, respectively, which are consistent with off-line assay and previously reported values. Nifedipine 105-115 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 119-125 18528690-0 2008 CYP3A4*1G polymorphism is associated with lipid-lowering efficacy of atorvastatin but not of simvastatin. Atorvastatin 69-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18528690-8 2008 The CYP3A4*1G polymorphism had a gene-dose-dependent effect on percentage reduction in serum TC (P < 0.01). Technetium 93-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 18528690-10 2008 CONCLUSIONS: Carrying CYP3A4*1G increase the lipid-lowering efficacy of atorvastatin and may have no significant effect on simvastatin treatment. Atorvastatin 72-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 18581106-11 2008 CONCLUSIONS: Orthogonal regression analysis between midazolam clearance and log of the plasma concentrations of the omeprazole/omeprazole sulfone ratio (R = -0.7544, P < 0.05) suggests that both midazolam and omeprazole can be used as markers of CYP3A activity in the population investigated. Midazolam 52-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 249-254 18633604-7 2008 The CYP7A1, CYP27A1, CYP46A1 and CYP3A4 enzymes generate major oxysterols that enter the circulation. oxysterols 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 18581106-11 2008 CONCLUSIONS: Orthogonal regression analysis between midazolam clearance and log of the plasma concentrations of the omeprazole/omeprazole sulfone ratio (R = -0.7544, P < 0.05) suggests that both midazolam and omeprazole can be used as markers of CYP3A activity in the population investigated. Omeprazole 116-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 249-254 18581106-11 2008 CONCLUSIONS: Orthogonal regression analysis between midazolam clearance and log of the plasma concentrations of the omeprazole/omeprazole sulfone ratio (R = -0.7544, P < 0.05) suggests that both midazolam and omeprazole can be used as markers of CYP3A activity in the population investigated. omeprazole sulfone 127-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 249-254 18997493-9 2008 This is because sildenafil, vardenafil, and tadalafil are metabolized mainly via the CYP3A4 pathway. Sildenafil Citrate 16-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 21218106-4 2008 The aim of this study was to evaluate the efficiency of different in vitro systems containing individual enzymes of the mixed-function monooxygenase system to oxidize two model substrates of CYP3A enzymes, exogenous and endogenous compounds, alpha-naphtoflavone (alpha-NF) and testosterone, respectively. alpha-naphthoflavone 242-261 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-196 21218106-4 2008 The aim of this study was to evaluate the efficiency of different in vitro systems containing individual enzymes of the mixed-function monooxygenase system to oxidize two model substrates of CYP3A enzymes, exogenous and endogenous compounds, alpha-naphtoflavone (alpha-NF) and testosterone, respectively. alpha-nf 263-271 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-196 21218106-4 2008 The aim of this study was to evaluate the efficiency of different in vitro systems containing individual enzymes of the mixed-function monooxygenase system to oxidize two model substrates of CYP3A enzymes, exogenous and endogenous compounds, alpha-naphtoflavone (alpha-NF) and testosterone, respectively. Testosterone 277-289 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-196 21218106-7 2008 The results presented in this study demonstrate the suitability of the supersomal CYP3A4 systems for studies investigating oxidation of testosterone and alpha-NF in vitro. Testosterone 136-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 18997493-9 2008 This is because sildenafil, vardenafil, and tadalafil are metabolized mainly via the CYP3A4 pathway. Vardenafil Dihydrochloride 28-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 18997493-9 2008 This is because sildenafil, vardenafil, and tadalafil are metabolized mainly via the CYP3A4 pathway. Tadalafil 44-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 85-91 18556719-1 2008 Aprepitant (AP) is a known inhibitor of cytochrome P450 3A4 which may affect tacrolimus metabolism. Tacrolimus 77-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-59 18516595-11 2008 Inhibition assays demonstrated that tilidine and nortilidine can also inhibit CYP3A4, CYP2C19, CYP2D6, ABCB1, but not ABCG2, whereas inhibition of CYP2D6 and possibly also of CYP3A4 might be clinically relevant. nortilidine 49-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 18516595-12 2008 By calculating the metabolic clearance based on the in vitro and published in vivo data, CYP3A4 and CYP2C19 were identified as the main elimination routes of tilidine. Tilidine 158-166 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 18516595-0 2008 In vitro metabolism of the opioid tilidine and interaction of tilidine and nortilidine with CYP3A4, CYP2C19, and CYP2D6. Tilidine 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 18516595-13 2008 In vivo, drug-drug interactions of tilidine with CYP3A4 or CYP2C19 inhibitors are to be anticipated, whereas substrates of CYP2C19, ABCB1, or ABCG2 will presumably not be influenced by tilidine or nortilidine. Tilidine 35-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-55 18516595-0 2008 In vitro metabolism of the opioid tilidine and interaction of tilidine and nortilidine with CYP3A4, CYP2C19, and CYP2D6. nortilidine 75-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 92-98 18516595-10 2008 Investigations with recombinant CYP3A4 and CYP2C19 confirmed that the demethylation of tilidine occurs via these two CYPs. Tilidine 87-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 18516595-11 2008 Inhibition assays demonstrated that tilidine and nortilidine can also inhibit CYP3A4, CYP2C19, CYP2D6, ABCB1, but not ABCG2, whereas inhibition of CYP2D6 and possibly also of CYP3A4 might be clinically relevant. Tilidine 36-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 18516595-11 2008 Inhibition assays demonstrated that tilidine and nortilidine can also inhibit CYP3A4, CYP2C19, CYP2D6, ABCB1, but not ABCG2, whereas inhibition of CYP2D6 and possibly also of CYP3A4 might be clinically relevant. Tilidine 36-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-181 18516595-11 2008 Inhibition assays demonstrated that tilidine and nortilidine can also inhibit CYP3A4, CYP2C19, CYP2D6, ABCB1, but not ABCG2, whereas inhibition of CYP2D6 and possibly also of CYP3A4 might be clinically relevant. nortilidine 49-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-84 18602459-7 2008 mRNA of Cyp1A2 and Cyp3A4 was not expressed neither at the basal level, nor after naphthalene treatment, while treatment with 1,4-naphthoquinone induced expression of both enzymes in both genders, with Cyp1A2 being expressed four times more than Cyp3A4. 1,4-naphthoquinone 126-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 246-252 19066408-6 2008 Aliskiren is slightly metabolized (20%) by CYP3A4. aliskiren 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 17992531-0 2008 Impact of CYP3A4 haplotypes on irinotecan pharmacokinetics in Japanese cancer patients. Irinotecan 31-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16 18720283-4 2008 Two metabolites of atorvastatin, para- and ortho-hydroxyatorvastatin, were produced by human liver microsomes and human recombinant CYP3A enzymes, and the enzyme kinetic pattern exhibited substrate inhibition. Atorvastatin 19-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-137 18720283-4 2008 Two metabolites of atorvastatin, para- and ortho-hydroxyatorvastatin, were produced by human liver microsomes and human recombinant CYP3A enzymes, and the enzyme kinetic pattern exhibited substrate inhibition. para- and ortho-hydroxyatorvastatin 33-68 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-137 18720283-5 2008 The intrinsic clearance (CL(int)) rates of para- and ortho-hydroxyatorvastatin by CYP3A4 were 2.4- and 5.0-fold of the respective CL(int) rates of CYP3A5, indicating that CYP3A4 is the major P450 isoform responsible for atorvastatin metabolism. hydroxyatorvastatin 59-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 18720283-5 2008 The intrinsic clearance (CL(int)) rates of para- and ortho-hydroxyatorvastatin by CYP3A4 were 2.4- and 5.0-fold of the respective CL(int) rates of CYP3A5, indicating that CYP3A4 is the major P450 isoform responsible for atorvastatin metabolism. hydroxyatorvastatin 59-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 18720283-5 2008 The intrinsic clearance (CL(int)) rates of para- and ortho-hydroxyatorvastatin by CYP3A4 were 2.4- and 5.0-fold of the respective CL(int) rates of CYP3A5, indicating that CYP3A4 is the major P450 isoform responsible for atorvastatin metabolism. Atorvastatin 66-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-88 18720283-5 2008 The intrinsic clearance (CL(int)) rates of para- and ortho-hydroxyatorvastatin by CYP3A4 were 2.4- and 5.0-fold of the respective CL(int) rates of CYP3A5, indicating that CYP3A4 is the major P450 isoform responsible for atorvastatin metabolism. Atorvastatin 66-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 18720283-6 2008 These results suggest that atorvastatin is preferentially metabolized by CYP3A4 rather than by CYP3A5, and thus the genetic CYP3A5 polymorphism might not be an important factor in the inter-individual variation of atorvastatin disposition and pharmacodynamics in human. Atorvastatin 27-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 18667310-1 2008 A novel series of potent zwitterionic uracil GnRH antagonists were discovered that showed reduced liability for CYP3A4 enzyme inhibition. Uracil 38-44 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 17922273-0 2008 Effect of medical castration on CYP3A4 enzyme activity using the erythromycin breath test. Erythromycin 65-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 17922273-4 2008 CYP3A4 activity was determined using the erythromycin breath test (EBT) in each patient prior to their beginning with an LHRH-agonist (leuprolide or goserelin). Erythromycin 41-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 17922273-4 2008 CYP3A4 activity was determined using the erythromycin breath test (EBT) in each patient prior to their beginning with an LHRH-agonist (leuprolide or goserelin). ebt 67-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 17992531-1 2008 BACKGROUND AND PURPOSE: Cytochrome P450 3A4 (CYP3A4) converts an anticancer prodrug, irinotecan, to inactive metabolites such as APC. Irinotecan 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-43 17992531-1 2008 BACKGROUND AND PURPOSE: Cytochrome P450 3A4 (CYP3A4) converts an anticancer prodrug, irinotecan, to inactive metabolites such as APC. Irinotecan 85-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 17992531-2 2008 However, the contribution of CYP3A4 genetic polymorphisms to irinotecan pharmacokinetics (PK) and pharmacodynamics (PD) is not fully elucidated. Irinotecan 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 17992531-7 2008 RESULTS: Area under the concentration-time curve ratios of APC/irinotecan, an in vivo parameter for CYP3A4 activity, were significantly higher in females than in males. Irinotecan 63-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 17992531-12 2008 CONCLUSION: This study suggested that CYP3A4*16B was associated with decreased metabolism of irinotecan to APC. Irinotecan 93-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 38-44 17992531-3 2008 In paclitaxel-administered cancer patients, an association of CYP3A4*16B harboring the low activity allele *16 [554C > G (Thr185Ser)] has been shown with altered metabolite/paclitaxel area under the plasma concentration-time curve (AUC) ratios, suggesting a possible impact of *16B on the PK of other drugs. Paclitaxel 3-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 17992531-3 2008 In paclitaxel-administered cancer patients, an association of CYP3A4*16B harboring the low activity allele *16 [554C > G (Thr185Ser)] has been shown with altered metabolite/paclitaxel area under the plasma concentration-time curve (AUC) ratios, suggesting a possible impact of *16B on the PK of other drugs. Paclitaxel 176-186 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-68 17992531-4 2008 In this study, the effects of CYP3A4 haplotypes including *16B on irinotecan PK/PD were investigated in irinotecan-administered patients. Irinotecan 66-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 17992531-5 2008 METHODS: The CYP3A4 genotypes for 177 Japanese cancer patients who received irinotecan were defined in terms of 4 major haplotypes, i.e., *1A (wild type), *1G (IVS10 + 12G > A), *16B [554C > G (Thr185Ser) and IVS10 + 12G > A], and *18B [878T > C (Leu293Pro) and IVS10 + 12G > A]. Irinotecan 76-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 17992531-6 2008 Associations of CYP3A4 genotypes with irinotecan PK and severe toxicities (grade 3 diarrhea and grade 3 or 4 neutropenia) were investigated. Irinotecan 38-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22 18288078-1 2008 The objectives of the study were to evaluate the effects of pregnancy on CYP3A and P-glycoprotein (P-gp) activities, as measured by disposition of midazolam and digoxin, respectively. Midazolam 147-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 18288078-1 2008 The objectives of the study were to evaluate the effects of pregnancy on CYP3A and P-glycoprotein (P-gp) activities, as measured by disposition of midazolam and digoxin, respectively. Digoxin 161-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-78 18474675-2 2008 Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A). Clopidogrel 41-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 338-343 18803986-8 2008 Lapatinib is metabolized primarily by the cytochrome P450 3A4 isozyme, with 1 metabolite remaining active against EGFR but not HER2. Lapatinib 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-61 18463198-6 2008 Studies with a panel of cDNA-expressed enzymes revealed that CYP2C19 and CYP3A4 were high (S50 = 30 microM) and low (S50 = 203 microM) affinity enzymes, respectively, for 2,3-diOHCBZ formation and suggested that CYP3A4, but not CYP2C19, might be inactivated by a metabolite formed from 3-OHCBZ. 2,3-diohcbz 171-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 18463198-6 2008 Studies with a panel of cDNA-expressed enzymes revealed that CYP2C19 and CYP3A4 were high (S50 = 30 microM) and low (S50 = 203 microM) affinity enzymes, respectively, for 2,3-diOHCBZ formation and suggested that CYP3A4, but not CYP2C19, might be inactivated by a metabolite formed from 3-OHCBZ. 2,3-diohcbz 171-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 212-218 18463198-6 2008 Studies with a panel of cDNA-expressed enzymes revealed that CYP2C19 and CYP3A4 were high (S50 = 30 microM) and low (S50 = 203 microM) affinity enzymes, respectively, for 2,3-diOHCBZ formation and suggested that CYP3A4, but not CYP2C19, might be inactivated by a metabolite formed from 3-OHCBZ. 3-hydroxycarbamazepine 286-293 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 18474675-2 2008 Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A). Ticlopidine 54-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 338-343 18463198-6 2008 Studies with a panel of cDNA-expressed enzymes revealed that CYP2C19 and CYP3A4 were high (S50 = 30 microM) and low (S50 = 203 microM) affinity enzymes, respectively, for 2,3-diOHCBZ formation and suggested that CYP3A4, but not CYP2C19, might be inactivated by a metabolite formed from 3-OHCBZ. 3-hydroxycarbamazepine 286-293 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 212-218 18463198-7 2008 Subsequent experiments demonstrated that preincubation of 3-OHCBZ with human liver microsomes or recombinant CYP3A4 led to decreased CYP3A4 activity, which was both preincubation time- and concentration-dependent, but not inhibited by inclusion of glutathione or N-acetylcysteine. 3-hydroxycarbamazepine 58-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 18474675-2 2008 Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A). triethylenethiophoramide 71-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 338-343 18463198-7 2008 Subsequent experiments demonstrated that preincubation of 3-OHCBZ with human liver microsomes or recombinant CYP3A4 led to decreased CYP3A4 activity, which was both preincubation time- and concentration-dependent, but not inhibited by inclusion of glutathione or N-acetylcysteine. 3-hydroxycarbamazepine 58-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 18463198-7 2008 Subsequent experiments demonstrated that preincubation of 3-OHCBZ with human liver microsomes or recombinant CYP3A4 led to decreased CYP3A4 activity, which was both preincubation time- and concentration-dependent, but not inhibited by inclusion of glutathione or N-acetylcysteine. Glutathione 248-259 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 18463198-7 2008 Subsequent experiments demonstrated that preincubation of 3-OHCBZ with human liver microsomes or recombinant CYP3A4 led to decreased CYP3A4 activity, which was both preincubation time- and concentration-dependent, but not inhibited by inclusion of glutathione or N-acetylcysteine. Glutathione 248-259 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 18480186-0 2008 Curcuminoids inhibit multiple human cytochromes P450, UDP-glucuronosyltransferase, and sulfotransferase enzymes, whereas piperine is a relatively selective CYP3A4 inhibitor. piperine 121-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 18463198-7 2008 Subsequent experiments demonstrated that preincubation of 3-OHCBZ with human liver microsomes or recombinant CYP3A4 led to decreased CYP3A4 activity, which was both preincubation time- and concentration-dependent, but not inhibited by inclusion of glutathione or N-acetylcysteine. Acetylcysteine 263-279 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 18463198-7 2008 Subsequent experiments demonstrated that preincubation of 3-OHCBZ with human liver microsomes or recombinant CYP3A4 led to decreased CYP3A4 activity, which was both preincubation time- and concentration-dependent, but not inhibited by inclusion of glutathione or N-acetylcysteine. Acetylcysteine 263-279 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 18463198-8 2008 CYP3A4, CYP3A5, CYP3A7, CYP2C19, and CYP1A2 converted [14C]3-OHCBZ into protein-reactive metabolites, but CYP3A4 was the most catalytically active enzyme. [14c]3-ohcbz 54-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18463198-8 2008 CYP3A4, CYP3A5, CYP3A7, CYP2C19, and CYP1A2 converted [14C]3-OHCBZ into protein-reactive metabolites, but CYP3A4 was the most catalytically active enzyme. [14c]3-ohcbz 54-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 18463198-9 2008 The results of this study suggest that CYP3A4-dependent secondary oxidation of 3-OHCBZ represents a potential carbamazepine bioactivation pathway via formation of reactive metabolites capable of inactivating CYP3A4, potentially generating a neoantigen that may play a role in the etiology of carbamazepine-induced idiosyncratic toxicity. 3-hydroxycarbamazepine 79-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 18463198-9 2008 The results of this study suggest that CYP3A4-dependent secondary oxidation of 3-OHCBZ represents a potential carbamazepine bioactivation pathway via formation of reactive metabolites capable of inactivating CYP3A4, potentially generating a neoantigen that may play a role in the etiology of carbamazepine-induced idiosyncratic toxicity. 3-hydroxycarbamazepine 79-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 208-214 18463198-9 2008 The results of this study suggest that CYP3A4-dependent secondary oxidation of 3-OHCBZ represents a potential carbamazepine bioactivation pathway via formation of reactive metabolites capable of inactivating CYP3A4, potentially generating a neoantigen that may play a role in the etiology of carbamazepine-induced idiosyncratic toxicity. Carbamazepine 110-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 18480186-3 2008 The curcuminoid extract inhibited SULT > CYP2C19 > CYP2B6 > UGT > CYP2C9 > CYP3A activities with IC(50) values ranging from 0.99 +/- 0.04 to 25.3 +/- 1.3 microM, whereas CYP2D6, CYP1A2, and CYP2E1 activities were less affected (IC(50) values > 60 microM). curcuminoid 4-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-95 18463198-9 2008 The results of this study suggest that CYP3A4-dependent secondary oxidation of 3-OHCBZ represents a potential carbamazepine bioactivation pathway via formation of reactive metabolites capable of inactivating CYP3A4, potentially generating a neoantigen that may play a role in the etiology of carbamazepine-induced idiosyncratic toxicity. Carbamazepine 110-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 208-214 18463198-9 2008 The results of this study suggest that CYP3A4-dependent secondary oxidation of 3-OHCBZ represents a potential carbamazepine bioactivation pathway via formation of reactive metabolites capable of inactivating CYP3A4, potentially generating a neoantigen that may play a role in the etiology of carbamazepine-induced idiosyncratic toxicity. Carbamazepine 292-305 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-45 18480186-4 2008 Inhibition of CYP3A activity by curcuminoid extract was consistent with competitive inhibition (K(i) = 11.0 +/- 1.3 microM), whereas inhibition of both CYP2C9 and CYP2C19 activities were consistent with mixed competitive-noncompetitive inhibition (10.6 +/- 1.1 and 7.8 +/- 0.9 microM, respectively). curcuminoid 32-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-19 18463198-9 2008 The results of this study suggest that CYP3A4-dependent secondary oxidation of 3-OHCBZ represents a potential carbamazepine bioactivation pathway via formation of reactive metabolites capable of inactivating CYP3A4, potentially generating a neoantigen that may play a role in the etiology of carbamazepine-induced idiosyncratic toxicity. Carbamazepine 292-305 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 208-214 18480186-5 2008 Piperine was a relatively selective noncompetitive inhibitor of CYP3A (IC(50) 5.5 +/- 0.7 microM, K(i) = 5.4 +/- 0.3 microM) with less effect on other enzymes evaluated (IC(50) > 29 microM). piperine 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 18490434-0 2008 The influence of CYP3A5 genotype on dexamethasone induction of CYP3A activity in African Americans. Dexamethasone 36-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-22 18480186-6 2008 Curcuminoid extract and piperine inhibited recombinant CYP3A4 much more potently (by >5-fold) than CYP3A5. curcuminoid 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 18490434-3 2008 We have previously noted a correlation between basal CYP3A activity and the inductive effects of dexamethasone using the erythromycin breath test (ERBT). Dexamethasone 97-110 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 18480186-6 2008 Curcuminoid extract and piperine inhibited recombinant CYP3A4 much more potently (by >5-fold) than CYP3A5. piperine 24-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-61 18490434-3 2008 We have previously noted a correlation between basal CYP3A activity and the inductive effects of dexamethasone using the erythromycin breath test (ERBT). Erythromycin 121-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-58 18480186-10 2008 administered curcuminoid/piperine combination is most likely to inhibit CYP3A, CYP2C9, UGT, and SULT metabolism within the intestinal mucosa. curcuminoid 13-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-77 18480186-10 2008 administered curcuminoid/piperine combination is most likely to inhibit CYP3A, CYP2C9, UGT, and SULT metabolism within the intestinal mucosa. piperine 25-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-77 18448569-2 2008 Pactimibe has two equally dominant clearance pathways forming R-125528 by CYP3A4 and M-1 by CYP2D6 in vitro. pactimibe 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 18505790-6 2008 CYP3A4 activity was significantly increased by rifampin (9.7-fold), nafcillin and dicloxacillin (5.9-fold), and weakly induced (2-fold) by tetracycline, sufisoxazole, troleandomycin, and clindamycin. Rifampin 47-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18505790-6 2008 CYP3A4 activity was significantly increased by rifampin (9.7-fold), nafcillin and dicloxacillin (5.9-fold), and weakly induced (2-fold) by tetracycline, sufisoxazole, troleandomycin, and clindamycin. Nafcillin 68-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18505790-6 2008 CYP3A4 activity was significantly increased by rifampin (9.7-fold), nafcillin and dicloxacillin (5.9-fold), and weakly induced (2-fold) by tetracycline, sufisoxazole, troleandomycin, and clindamycin. Dicloxacillin 82-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18505790-6 2008 CYP3A4 activity was significantly increased by rifampin (9.7-fold), nafcillin and dicloxacillin (5.9-fold), and weakly induced (2-fold) by tetracycline, sufisoxazole, troleandomycin, and clindamycin. Tetracycline 139-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18505790-6 2008 CYP3A4 activity was significantly increased by rifampin (9.7-fold), nafcillin and dicloxacillin (5.9-fold), and weakly induced (2-fold) by tetracycline, sufisoxazole, troleandomycin, and clindamycin. sufisoxazole 153-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18505790-6 2008 CYP3A4 activity was significantly increased by rifampin (9.7-fold), nafcillin and dicloxacillin (5.9-fold), and weakly induced (2-fold) by tetracycline, sufisoxazole, troleandomycin, and clindamycin. Troleandomycin 167-181 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18505790-6 2008 CYP3A4 activity was significantly increased by rifampin (9.7-fold), nafcillin and dicloxacillin (5.9-fold), and weakly induced (2-fold) by tetracycline, sufisoxazole, troleandomycin, and clindamycin. Clindamycin 187-198 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18505790-9 2008 In summary, nafcillin, dicloxacillin, cephradine, tetracycline, sulfixoxazole, erythromycin, clindamycin, and griseofulvin exhibit a clear propensity to induce CYP3A4 and warrant further clinical investigation. Nafcillin 12-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 18505790-9 2008 In summary, nafcillin, dicloxacillin, cephradine, tetracycline, sulfixoxazole, erythromycin, clindamycin, and griseofulvin exhibit a clear propensity to induce CYP3A4 and warrant further clinical investigation. Dicloxacillin 23-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 18505790-9 2008 In summary, nafcillin, dicloxacillin, cephradine, tetracycline, sulfixoxazole, erythromycin, clindamycin, and griseofulvin exhibit a clear propensity to induce CYP3A4 and warrant further clinical investigation. Cephradine 38-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 18505790-9 2008 In summary, nafcillin, dicloxacillin, cephradine, tetracycline, sulfixoxazole, erythromycin, clindamycin, and griseofulvin exhibit a clear propensity to induce CYP3A4 and warrant further clinical investigation. Tetracycline 50-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 18505790-9 2008 In summary, nafcillin, dicloxacillin, cephradine, tetracycline, sulfixoxazole, erythromycin, clindamycin, and griseofulvin exhibit a clear propensity to induce CYP3A4 and warrant further clinical investigation. sulfixoxazole 64-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 18505790-9 2008 In summary, nafcillin, dicloxacillin, cephradine, tetracycline, sulfixoxazole, erythromycin, clindamycin, and griseofulvin exhibit a clear propensity to induce CYP3A4 and warrant further clinical investigation. Erythromycin 79-91 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 18505790-9 2008 In summary, nafcillin, dicloxacillin, cephradine, tetracycline, sulfixoxazole, erythromycin, clindamycin, and griseofulvin exhibit a clear propensity to induce CYP3A4 and warrant further clinical investigation. Clindamycin 93-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 18505790-9 2008 In summary, nafcillin, dicloxacillin, cephradine, tetracycline, sulfixoxazole, erythromycin, clindamycin, and griseofulvin exhibit a clear propensity to induce CYP3A4 and warrant further clinical investigation. Griseofulvin 110-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 19356088-2 2008 Itraconazole (ITZ) functions as an inhibitor of both the P-gp and CYP3A and is used as a fungistatic/fungicidal agent in human and veterinary medicine. Itraconazole 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 19356088-2 2008 Itraconazole (ITZ) functions as an inhibitor of both the P-gp and CYP3A and is used as a fungistatic/fungicidal agent in human and veterinary medicine. Itraconazole 14-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-71 19356092-0 2008 Effects of enzyme sources on midazolam 1"-hydroxylation activity catalyzed by recombinant cytochrome P450 3A4 in combination with NADPH-cytochrome P450 reductase. Midazolam 29-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-109 19356092-1 2008 The influence of the enzyme source such as phospholipid and expression ratio of NADPH-cytochrome P450 reductase on midazolam 1"-hydroxylation activity of cytochrome P450 3A4 was investigated in reconstituted systems and in membranes using bicistronic expressions. Phospholipids 43-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-173 19356092-1 2008 The influence of the enzyme source such as phospholipid and expression ratio of NADPH-cytochrome P450 reductase on midazolam 1"-hydroxylation activity of cytochrome P450 3A4 was investigated in reconstituted systems and in membranes using bicistronic expressions. Midazolam 115-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-173 18458892-0 2008 CYP3A induction and inhibition by different antiretroviral regimens reflected by changes in plasma 4beta-hydroxycholesterol levels. cholest-5-ene-3,4-diol 99-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5 18458892-1 2008 OBJECTIVE AND METHODS: A member of the major human cytochrome P450 superfamily of hemoproteins, CYP3A4/5, converts cholesterol into 4beta-hydroxycholesterol. Cholesterol 115-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 18458892-1 2008 OBJECTIVE AND METHODS: A member of the major human cytochrome P450 superfamily of hemoproteins, CYP3A4/5, converts cholesterol into 4beta-hydroxycholesterol. cholest-5-ene-3,4-diol 132-156 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 18458892-3 2008 Efavirenz is an inducer of CYP3A, whereas the ritonavir-boosted regimens are net inhibitors of CYP3A. efavirenz 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 27-32 18458892-3 2008 Efavirenz is an inducer of CYP3A, whereas the ritonavir-boosted regimens are net inhibitors of CYP3A. Ritonavir 46-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 95-100 18458892-7 2008 CONCLUSION: Changes in plasma 4beta-hydroxycholesterol following the initiation of efavirenz- or atazanavir/ritonavir-based antiretroviral therapy reflected the respective net increase and decrease of CYP3A activity of these regimens. cholest-5-ene-3,4-diol 30-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-206 18458892-7 2008 CONCLUSION: Changes in plasma 4beta-hydroxycholesterol following the initiation of efavirenz- or atazanavir/ritonavir-based antiretroviral therapy reflected the respective net increase and decrease of CYP3A activity of these regimens. efavirenz 83-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-206 18458892-7 2008 CONCLUSION: Changes in plasma 4beta-hydroxycholesterol following the initiation of efavirenz- or atazanavir/ritonavir-based antiretroviral therapy reflected the respective net increase and decrease of CYP3A activity of these regimens. Atazanavir Sulfate 97-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-206 18458892-7 2008 CONCLUSION: Changes in plasma 4beta-hydroxycholesterol following the initiation of efavirenz- or atazanavir/ritonavir-based antiretroviral therapy reflected the respective net increase and decrease of CYP3A activity of these regimens. Ritonavir 108-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-206 18662109-7 2008 Etravirine is an inducer of CYP3A4 and a weak inhibitor of CYP2C9, CYP2C19 and P-glycoprotein. etravirine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 18448569-2 2008 Pactimibe has two equally dominant clearance pathways forming R-125528 by CYP3A4 and M-1 by CYP2D6 in vitro. R-125528 62-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-80 18819885-3 2008 After 15 min of culture, the substrates (testosterone for CYP3A4 and phenacetin for CYP1A2) were added and incubated for another 20 min. Testosterone 41-53 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 18819885-6 2008 The IC(50) of ketoconazole for CYP3A4 was 0. Ketoconazole 14-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 18819885-11 2008 CONCLUSION: In the range of maximum clinical blood concentration, ketoconazole can inhibit the activity of CYP3A4, but not that of CYP1A2, in the hepatic microsomes in healthy adults. Ketoconazole 66-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 18819885-8 2008 Both the quantity of 6-testosterone and the relative activity of CYP3A4 were reduced gradually with the increment of ketoconazole concentration. Ketoconazole 117-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 18538745-3 2008 Stimulation of dopaminergic receptors in the pituitary, a target for the tuberoinfundibular pathway, by dopamine (a D(1)/D(2) receptor agonist) administered intraperitoneally caused a significant increase in the activities and protein levels of CYP2B, CYP2C11 and CYP3A, a substantial increase in the blood plasma level of growth hormone (GH) and a significant decrease in triiodothyronine (T(3)) level. Dopamine 15-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 264-269 18433425-13 2008 These data suggest that CYP2D6 and CYP3A4 genotypes which determine the metabolism of yohimbine may influence its sympathetic and gastrointestinal effects. Yohimbine 86-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 18628990-3 2008 Herein, we first evaluated the inhibitory effects of fifteen ginsenosides and sapogenins on human CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4 enzymes by using commercially available fluorescent probes. Sapogenins 78-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 18628990-3 2008 Herein, we first evaluated the inhibitory effects of fifteen ginsenosides and sapogenins on human CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4 enzymes by using commercially available fluorescent probes. Ginsenosides 61-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-140 18628990-5 2008 Moreover, substrate-dependent phenomena were found in ginsenosides" effects on CYP3A4 when another fluorescent probe was used, and were further confirmed in tests with conventional drug probes and human liver microsomes. Ginsenosides 54-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 18455890-1 2008 Lopinavir (LVR) is extensively metabolized by CYP3A4 and is prevented from entering the cells by membrane efflux pumps such as P-gp and MRP2. Lopinavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 18572407-0 2008 Balancing oral exposure with Cyp3A4 inhibition in benzimidazole-based IGF-IR inhibitors. benzimidazole 50-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 18572407-1 2008 3-(Benzimidazol-2-yl)-pyridine-2-one-based ATP competitive inhibitors of Insulin-like Growth Factor 1 Kinase (IGF-IR) were optimized for reduced Cyp3A4 inhibition and improved oral exposure. 3-(benzimidazol-2-yl)-pyridine-2-one 0-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 18572407-1 2008 3-(Benzimidazol-2-yl)-pyridine-2-one-based ATP competitive inhibitors of Insulin-like Growth Factor 1 Kinase (IGF-IR) were optimized for reduced Cyp3A4 inhibition and improved oral exposure. Adenosine Triphosphate 43-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 18455890-1 2008 Lopinavir (LVR) is extensively metabolized by CYP3A4 and is prevented from entering the cells by membrane efflux pumps such as P-gp and MRP2. Lopinavir 11-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 17909805-1 2008 PURPOSE: The aims were to determine the maximum tolerable dose (MTD) of docetaxel with CYP3A inhibition by ketoconazole, and to correlate the pharmacokinetics of docetaxel with midazolam phenotyping of CYP3A activity. Docetaxel 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 17909805-1 2008 PURPOSE: The aims were to determine the maximum tolerable dose (MTD) of docetaxel with CYP3A inhibition by ketoconazole, and to correlate the pharmacokinetics of docetaxel with midazolam phenotyping of CYP3A activity. Docetaxel 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 202-207 17909805-1 2008 PURPOSE: The aims were to determine the maximum tolerable dose (MTD) of docetaxel with CYP3A inhibition by ketoconazole, and to correlate the pharmacokinetics of docetaxel with midazolam phenotyping of CYP3A activity. Ketoconazole 107-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-92 17909805-1 2008 PURPOSE: The aims were to determine the maximum tolerable dose (MTD) of docetaxel with CYP3A inhibition by ketoconazole, and to correlate the pharmacokinetics of docetaxel with midazolam phenotyping of CYP3A activity. Docetaxel 162-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 202-207 17971810-0 2008 Pharmacodynamics of carbamazepine-mediated induction of CYP3A4, CYP1A2, and Pgp as assessed by probe substrates midazolam, caffeine, and digoxin. Carbamazepine 20-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 17971810-1 2008 The aim of this study was to develop a model describing the carbamazepine autoinduction and the carbamazepine-mediated induction of CYP3A4, CYP1A2, and P-glycoprotein. Carbamazepine 96-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 132-138 18183034-0 2008 Effect of an antiretroviral regimen containing ritonavir boosted lopinavir on intestinal and hepatic CYP3A, CYP2D6 and P-glycoprotein in HIV-infected patients. Ritonavir 47-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 18183034-1 2008 This study aimed to quantify the inhibition of cytochrome P450 (CYP3A), CYP2D6, and P-glycoprotein in human immunodeficiency virus (HIV)-infected patients receiving an antiretroviral therapy (ART) containing ritonavir boosted lopinavir, and to identify factors influencing ritonavir and lopinavir pharmacokinetics. Lopinavir 287-296 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 18183034-0 2008 Effect of an antiretroviral regimen containing ritonavir boosted lopinavir on intestinal and hepatic CYP3A, CYP2D6 and P-glycoprotein in HIV-infected patients. Lopinavir 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 101-106 18183034-4 2008 Oral midazolam clearance (overall CYP3A activity) decreased to 0.19-fold (90% confidence interval (CI), 0.15-0.23), hepatic midazolam clearance and intestinal midazolam availability changed to 0.24-fold (0.20-0.29) and 1.12-fold (1.00-1.26), respectively. Midazolam 5-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-39 18183034-8 2008 In conclusion, CYP3A, CYP2D6, and P-glycoprotein are profoundly inhibited in patients receiving ritonavir boosted lopinavir. Ritonavir 96-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-20 18183034-8 2008 In conclusion, CYP3A, CYP2D6, and P-glycoprotein are profoundly inhibited in patients receiving ritonavir boosted lopinavir. Lopinavir 114-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-20 18183036-1 2008 The relationship between cytochrome P4503A4 (CYP3A4) activity and docetaxel clearance in patients with varying degrees of liver function (LF) was evaluated. Docetaxel 66-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 25-43 18183036-1 2008 The relationship between cytochrome P4503A4 (CYP3A4) activity and docetaxel clearance in patients with varying degrees of liver function (LF) was evaluated. Docetaxel 66-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 18183036-3 2008 Baseline CYP3A activity was assessed using the erythromycin breath test (ERMBT). Erythromycin 47-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 9-14 18183034-1 2008 This study aimed to quantify the inhibition of cytochrome P450 (CYP3A), CYP2D6, and P-glycoprotein in human immunodeficiency virus (HIV)-infected patients receiving an antiretroviral therapy (ART) containing ritonavir boosted lopinavir, and to identify factors influencing ritonavir and lopinavir pharmacokinetics. Ritonavir 208-217 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 18183034-1 2008 This study aimed to quantify the inhibition of cytochrome P450 (CYP3A), CYP2D6, and P-glycoprotein in human immunodeficiency virus (HIV)-infected patients receiving an antiretroviral therapy (ART) containing ritonavir boosted lopinavir, and to identify factors influencing ritonavir and lopinavir pharmacokinetics. Lopinavir 226-235 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 18183034-1 2008 This study aimed to quantify the inhibition of cytochrome P450 (CYP3A), CYP2D6, and P-glycoprotein in human immunodeficiency virus (HIV)-infected patients receiving an antiretroviral therapy (ART) containing ritonavir boosted lopinavir, and to identify factors influencing ritonavir and lopinavir pharmacokinetics. Ritonavir 273-282 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 64-69 18691982-11 2008 Fluoxetine and paroxetine are potent inhibitors of CYP2D6, fluvoxamine markedly inhibits CYP1A2 and CYP2C19, and nefazodone is a substantial inhibitor of CYP3A4. Fluoxetine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 18322448-1 2008 Budesonide treatment of chronic inflammatory bowel disease commonly leads to non-response or adverse reactions, possibly because of alterations in efflux transport mediated by the ABCB1 gene product P-glycoprotein or metabolism by CYP3A isoenzymes. Budesonide 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 231-236 18322448-6 2008 However, intestinal CYP3A4 expression was shown to correlate directly with partial metabolic clearances of 16-hydroxy-prednisolone (r(2) = 0.30; P = 0.010) and 6-hydroxy-budesonide (r(2) = 0.25; P = 0.016), but inversely with budesonide AUC(0-24 h) (r(2) = 0.18; P = 0.040). 16-hydroxyprednisolone 107-130 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 18322448-6 2008 However, intestinal CYP3A4 expression was shown to correlate directly with partial metabolic clearances of 16-hydroxy-prednisolone (r(2) = 0.30; P = 0.010) and 6-hydroxy-budesonide (r(2) = 0.25; P = 0.016), but inversely with budesonide AUC(0-24 h) (r(2) = 0.18; P = 0.040). 6-hydroxybudesonide 160-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 18322448-6 2008 However, intestinal CYP3A4 expression was shown to correlate directly with partial metabolic clearances of 16-hydroxy-prednisolone (r(2) = 0.30; P = 0.010) and 6-hydroxy-budesonide (r(2) = 0.25; P = 0.016), but inversely with budesonide AUC(0-24 h) (r(2) = 0.18; P = 0.040). Budesonide 170-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 18322448-8 2008 This study suggests that intestinal CYP3A4 expression has an impact on budesonide pharmacokinetics. Budesonide 71-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 36-42 18691982-11 2008 Fluoxetine and paroxetine are potent inhibitors of CYP2D6, fluvoxamine markedly inhibits CYP1A2 and CYP2C19, and nefazodone is a substantial inhibitor of CYP3A4. Paroxetine 15-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 18691982-11 2008 Fluoxetine and paroxetine are potent inhibitors of CYP2D6, fluvoxamine markedly inhibits CYP1A2 and CYP2C19, and nefazodone is a substantial inhibitor of CYP3A4. nefazodone 113-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 154-160 18691984-15 2008 CONCLUSION: In this study, use of medications that are potential inhibitors of CYP2D6 and CYP3A4 appeared to be associated with an increased risk of nonpersistence with risperidone, particularly while patients were still new to treatment. Risperidone 169-180 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 18385292-8 2008 The P450 probe substrates indicate a decrease in CYP1A2, CYP2B6, CYP2C9, and CYP3A4 activities in HepaRG cells 1 day after removal of DMSO from the medium. Dimethyl Sulfoxide 134-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 18385293-7 2008 Among the spices that showed inhibitory effect on MDZ metabolism in HLM, only AMD showed a preincubation time-dependent inhibitory effect on MDZ metabolism in HLM, suggesting the AMD as an irreversible CYP3A4 inhibitor. Midazolam 141-144 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 202-208 18381488-3 2008 Whereas ketoconazole is often used to study the worst-case scenario for clinical pharmacokinetic drug-drug interactions (DDIs) for drugs that are primarily metabolized by CYP3A4, fluconazole is considered to be a moderate inhibitor of CYP3A4, providing assessment of the moderate-case scenario of CYP3A-based DDIs. Ketoconazole 8-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 171-177 18381488-3 2008 Whereas ketoconazole is often used to study the worst-case scenario for clinical pharmacokinetic drug-drug interactions (DDIs) for drugs that are primarily metabolized by CYP3A4, fluconazole is considered to be a moderate inhibitor of CYP3A4, providing assessment of the moderate-case scenario of CYP3A-based DDIs. Fluconazole 179-190 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 235-241 18411403-4 2008 Our results show that CYP3A4 and CYP2D6 are the two P450s most affected by mibefradil, Ro40-5966, and NNC55-0396. Mibefradil 75-85 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 22-28 18381489-11 2008 Augmentation of the new data set with the one generated previously produced broader a database that provided further support for the wider applicability of this approach using ketoconazole as a potent CYP3A inhibitor. Ketoconazole 176-188 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 201-206 18411402-9 2008 Studies using recombinant P450s suggested that the major P450 isozymes involved in the bioactivation of flutamide and its metabolites were CYP1A2, CYP3A4, and CYP2C19. Flutamide 104-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-153 18411403-10 2008 Our results suggest that NNC55-0396 could be a more favorable T-type Ca(2+) antagonist than its parent compound, mibefradil, which was withdrawn from the market because of strong inhibition of CYP3A4. NNC 55-0396 25-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 193-199 18411403-0 2008 The mibefradil derivative NNC55-0396, a specific T-type calcium channel antagonist, exhibits less CYP3A4 inhibition than mibefradil. Mibefradil 4-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 18420779-0 2008 Comparative analysis of CYP3A heteroactivation by steroid hormones and flavonoids in different in vitro systems and potential in vivo implications. Steroids 50-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 18411403-0 2008 The mibefradil derivative NNC55-0396, a specific T-type calcium channel antagonist, exhibits less CYP3A4 inhibition than mibefradil. NNC 55-0396 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 98-104 18420779-0 2008 Comparative analysis of CYP3A heteroactivation by steroid hormones and flavonoids in different in vitro systems and potential in vivo implications. Flavonoids 71-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 18420779-1 2008 A systematic analysis of the heteroactivation of CYP3A-mediated carbamazepine 10,11-epoxidation has been investigated in three different in vitro systems, namely recombinant CYP3A4 and CYP3A5, human liver microsomes (HLMs) and cryopreserved human hepatocytes. Carbamazepine 64-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 49-54 18576910-7 2008 Warfarin has two enantiomers, R-and S-warfarin, which are substrates primarily of cytochrome P450 (CYP) 3A4 (R-warfarin), CYP1A2 (R-warfarin), and CYP2C9 (S-warfarin). Warfarin 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-107 18806899-4 2008 Desvenlafaxine has linear pharmacokinetics, low protein binding, a half-life of approximately 10 hours and is metabolized primarily via glucuronidation, and to a minor extent through CYP3A4. Desvenlafaxine Succinate 0-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 183-189 18576910-7 2008 Warfarin has two enantiomers, R-and S-warfarin, which are substrates primarily of cytochrome P450 (CYP) 3A4 (R-warfarin), CYP1A2 (R-warfarin), and CYP2C9 (S-warfarin). Ranolazine 30-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-107 18576910-7 2008 Warfarin has two enantiomers, R-and S-warfarin, which are substrates primarily of cytochrome P450 (CYP) 3A4 (R-warfarin), CYP1A2 (R-warfarin), and CYP2C9 (S-warfarin). Warfarin 38-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-107 18576910-7 2008 Warfarin has two enantiomers, R-and S-warfarin, which are substrates primarily of cytochrome P450 (CYP) 3A4 (R-warfarin), CYP1A2 (R-warfarin), and CYP2C9 (S-warfarin). Warfarin 109-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-107 18576910-7 2008 Warfarin has two enantiomers, R-and S-warfarin, which are substrates primarily of cytochrome P450 (CYP) 3A4 (R-warfarin), CYP1A2 (R-warfarin), and CYP2C9 (S-warfarin). Sulfur 36-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-107 18576910-7 2008 Warfarin has two enantiomers, R-and S-warfarin, which are substrates primarily of cytochrome P450 (CYP) 3A4 (R-warfarin), CYP1A2 (R-warfarin), and CYP2C9 (S-warfarin). Warfarin 111-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 82-107 18576910-9 2008 The increased warfarin doses required in these two patients may have been caused by induction of CYP3A4 by nevirapine, CYP2C9 by nelfinavir, or CYP2C9 by lopinavir-ritonavir. Warfarin 14-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 18213452-0 2008 Pharmacokinetics of the CYP 3A substrate simvastatin following administration of delayed versus immediate release oral dosage forms. Simvastatin 41-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-30 18213452-2 2008 MATERIALS AND METHODS: To target drug release and to assess regional gastrointestinal absorption of the CYP 3A substrate simvastatin from the distal parts of the intestine, delayed release film coated tableted oral dosage forms were developed. Simvastatin 121-132 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 18576910-9 2008 The increased warfarin doses required in these two patients may have been caused by induction of CYP3A4 by nevirapine, CYP2C9 by nelfinavir, or CYP2C9 by lopinavir-ritonavir. Nevirapine 107-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 18576910-9 2008 The increased warfarin doses required in these two patients may have been caused by induction of CYP3A4 by nevirapine, CYP2C9 by nelfinavir, or CYP2C9 by lopinavir-ritonavir. Nelfinavir 129-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 18576910-9 2008 The increased warfarin doses required in these two patients may have been caused by induction of CYP3A4 by nevirapine, CYP2C9 by nelfinavir, or CYP2C9 by lopinavir-ritonavir. Ritonavir 164-173 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 18462715-7 2008 Our results revealed that 18alpha-GL led to the enhancement of the hypoglycemic effect of glibenclamide by inhibiting the activity of CYP3A; on the other hand, 18alpha-GL protected the pancreatic islet beta cells and liver from damage in diabetes which suggested that 18alpha-GL might be beneficial as an adjuvant drug of glibenclamide in a proper dose, especially to the diabetic patients associated with liver dysfunction. 18alpha-gl 26-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-139 18562244-6 2008 The results showed that human recombinant CYP1A1 enzyme was much more active than CYP1A2 and CYP3A4 in the genotoxic activation of PBTA-4, PBTA-6, PBTA-7, and PBTA-8. pbta-4 131-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 18562244-6 2008 The results showed that human recombinant CYP1A1 enzyme was much more active than CYP1A2 and CYP3A4 in the genotoxic activation of PBTA-4, PBTA-6, PBTA-7, and PBTA-8. 2-(2-(acetylamino)-4-(N-(2-cyanoethyl)ethylamino)-5-methoxyphenyl)-5-amino-7-bromo-4-chloro-2H-benzotriazole 131-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 18562244-6 2008 The results showed that human recombinant CYP1A1 enzyme was much more active than CYP1A2 and CYP3A4 in the genotoxic activation of PBTA-4, PBTA-6, PBTA-7, and PBTA-8. PBTA-7 147-153 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 18562244-6 2008 The results showed that human recombinant CYP1A1 enzyme was much more active than CYP1A2 and CYP3A4 in the genotoxic activation of PBTA-4, PBTA-6, PBTA-7, and PBTA-8. PBTA-8 159-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 18468591-5 2008 Additionally, infected hepatocytes retain the capacity for CYP3A4 induction in response to treatment with phenobarbital, a uniquely sensitive indicator of hepatic differentiation status. Phenobarbital 106-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 18462715-7 2008 Our results revealed that 18alpha-GL led to the enhancement of the hypoglycemic effect of glibenclamide by inhibiting the activity of CYP3A; on the other hand, 18alpha-GL protected the pancreatic islet beta cells and liver from damage in diabetes which suggested that 18alpha-GL might be beneficial as an adjuvant drug of glibenclamide in a proper dose, especially to the diabetic patients associated with liver dysfunction. Glyburide 90-103 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 134-139 18395506-5 2008 Here, equilibrium binding studies, including "reverse titrations" spanning low ratios of CYP3A4/Nile Red, indicate two binding sites for Nile Red with a contribution to the "red emission" greater than can be accounted for by free Nile Red. nile red 96-104 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 18545703-7 2008 In the present study we show that recombinant CYP3A43 metabolizes ALP to both alpha-OHALP and 4-hydroxy alprazolam (4-OHALP) while CYP3A4 metabolizes ALP predominantly to its inactive metabolite, 4-OHALP. alpha-ohalp 78-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 18545703-7 2008 In the present study we show that recombinant CYP3A43 metabolizes ALP to both alpha-OHALP and 4-hydroxy alprazolam (4-OHALP) while CYP3A4 metabolizes ALP predominantly to its inactive metabolite, 4-OHALP. 4-hydroxyalprazolam 94-114 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 18545703-7 2008 In the present study we show that recombinant CYP3A43 metabolizes ALP to both alpha-OHALP and 4-hydroxy alprazolam (4-OHALP) while CYP3A4 metabolizes ALP predominantly to its inactive metabolite, 4-OHALP. 4-ohalp 116-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 18545703-7 2008 In the present study we show that recombinant CYP3A43 metabolizes ALP to both alpha-OHALP and 4-hydroxy alprazolam (4-OHALP) while CYP3A4 metabolizes ALP predominantly to its inactive metabolite, 4-OHALP. 4-ohalp 196-203 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 18458675-3 2008 Because temsirolimus and its primary metabolite, sirolimus, are metabolised by the cytochrome P450 3A4 pathway (CYP3A4), the potential exists for pharmacokinetic (PK) drug interactions with the numerous agents that modulate CYP3A4 isozyme activity. temsirolimus 8-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-102 18458675-3 2008 Because temsirolimus and its primary metabolite, sirolimus, are metabolised by the cytochrome P450 3A4 pathway (CYP3A4), the potential exists for pharmacokinetic (PK) drug interactions with the numerous agents that modulate CYP3A4 isozyme activity. temsirolimus 8-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 18458675-3 2008 Because temsirolimus and its primary metabolite, sirolimus, are metabolised by the cytochrome P450 3A4 pathway (CYP3A4), the potential exists for pharmacokinetic (PK) drug interactions with the numerous agents that modulate CYP3A4 isozyme activity. temsirolimus 8-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 224-230 18458675-3 2008 Because temsirolimus and its primary metabolite, sirolimus, are metabolised by the cytochrome P450 3A4 pathway (CYP3A4), the potential exists for pharmacokinetic (PK) drug interactions with the numerous agents that modulate CYP3A4 isozyme activity. Sirolimus 11-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-102 18458675-3 2008 Because temsirolimus and its primary metabolite, sirolimus, are metabolised by the cytochrome P450 3A4 pathway (CYP3A4), the potential exists for pharmacokinetic (PK) drug interactions with the numerous agents that modulate CYP3A4 isozyme activity. Sirolimus 11-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 18458675-3 2008 Because temsirolimus and its primary metabolite, sirolimus, are metabolised by the cytochrome P450 3A4 pathway (CYP3A4), the potential exists for pharmacokinetic (PK) drug interactions with the numerous agents that modulate CYP3A4 isozyme activity. Sirolimus 11-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 224-230 18458675-11 2008 temsirolimus, concomitant treatment with agents that have strong CYP3A4 inhibition potential should be avoided. temsirolimus 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-71 18395506-5 2008 Here, equilibrium binding studies, including "reverse titrations" spanning low ratios of CYP3A4/Nile Red, indicate two binding sites for Nile Red with a contribution to the "red emission" greater than can be accounted for by free Nile Red. nile red 137-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 18395506-5 2008 Here, equilibrium binding studies, including "reverse titrations" spanning low ratios of CYP3A4/Nile Red, indicate two binding sites for Nile Red with a contribution to the "red emission" greater than can be accounted for by free Nile Red. nile red 137-145 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 18395506-7 2008 In addition, the red spectral component, with an apparent K(D)=2.2muM, is selectively eliminated by titration with the known allosteric effectors of CYP3A4, alpha-napthoflavone and testosterone. alpha-napthoflavone 157-176 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 18395506-7 2008 In addition, the red spectral component, with an apparent K(D)=2.2muM, is selectively eliminated by titration with the known allosteric effectors of CYP3A4, alpha-napthoflavone and testosterone. Testosterone 181-193 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 149-155 18395506-9 2008 Together these data indicate that a second Nile Red site competes with other effectors of CYP3A4 at a site that results in Nile Red emission at 660nm. nile red 43-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 18395506-9 2008 Together these data indicate that a second Nile Red site competes with other effectors of CYP3A4 at a site that results in Nile Red emission at 660nm. nile red 123-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 18400206-0 2008 Retinoids induce cytochrome P450 3A4 through RXR/VDR-mediated pathway. Retinoids 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-36 18400206-1 2008 A panel of retinoids and carotenoids was screened as potential inducers of CYP3A4 through the RXR/VDR-mediated signaling pathway. Retinoids 11-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 18400206-7 2008 A direct role of retinoid-mediated CYP3A4 induction through RXRalpha/VDR was proved by the results that 9-cis-retinal, 9-cis-RA, and all-trans-RA recruited RXRalpha and VDR to CYP3A4 regulatory region pER6 (proximal everted repeat with a 6-nucleotide spacer) and dXREM (distal xenobiotic-responsive enhancer module). Retinoids 17-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-182 18400206-1 2008 A panel of retinoids and carotenoids was screened as potential inducers of CYP3A4 through the RXR/VDR-mediated signaling pathway. Carotenoids 25-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-81 18400206-8 2008 Thus, using various approaches, we have unequivocally demonstrated that retinoids transactivate RXR/VDR heterodimers and RXR homodimers and induce CYP3A expression at mRNA as well as enzyme activity levels in both liver and intestinal cells. Retinoids 72-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 147-152 18400206-9 2008 It is possible that retinoids might alter endobiotic metabolism through CYP3A4 induction in vivo. Retinoids 20-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 18400206-2 2008 Transient transfection assays revealed that 3 out of 12 retinoids screened transactivated RXRalpha/VDR and induced CYP3A4 reporter activity. Retinoids 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 115-121 18400206-6 2008 Moreover, retinoids induced CYP3A4 enzyme activity in HepG2 human hepatoma and Caco-2 human colorectal adenocarcinoma cells. Retinoids 10-19 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-34 18400206-7 2008 A direct role of retinoid-mediated CYP3A4 induction through RXRalpha/VDR was proved by the results that 9-cis-retinal, 9-cis-RA, and all-trans-RA recruited RXRalpha and VDR to CYP3A4 regulatory region pER6 (proximal everted repeat with a 6-nucleotide spacer) and dXREM (distal xenobiotic-responsive enhancer module). Retinoids 17-25 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 18520073-8 2008 These results suggested that cytochrome P450 (CYP) 2D6 and CYP1A2 are involved in the stereoselective oxidation of carvedilol in the liver, that CYP3A4 is involved in intestinal oxidation, and that glucuronidation in the liver and intestine is at least partly responsible for stereoselective presystemic clearance. Carvedilol 115-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 18442910-1 2008 Incorporation of a carboxylic acid into a series of uracil derivatives as hGnRH-R antagonists resulted in a significant reduction of CYP3A4 inhibitory activity. Carboxylic Acids 19-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 18442910-1 2008 Incorporation of a carboxylic acid into a series of uracil derivatives as hGnRH-R antagonists resulted in a significant reduction of CYP3A4 inhibitory activity. Uracil 52-58 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 18332078-5 2008 By using an optimized induction assay for Fa2N-4 cells, CYP3A4 induction by rifampicin, the prototypical PXR activator, increased from 1.5- to 7-fold at the level of functional activity. Rifampin 76-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 18537577-2 2008 Clozapine is metabolized primarily by CYP1A2, with additional contributions by CYP2C19, CYP2D6 and CYP3A4. Clozapine 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 18537577-3 2008 Risperidone is metabolized primarily by CYP2D6 and to a lesser extent by CYP3A4; the 9-hydroxy metabolite of risperidone (paliperidone) is now marketed as an antipsychotic in its own right. Risperidone 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 73-79 18537577-4 2008 Olanzapine is metabolized primarily by direct glucuronidation and CYP1A2 and to a lesser extent by CYP2D6 and CYP3A4. Olanzapine 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 18537577-5 2008 Quetiapine is metabolized by CYP3A4, as is ziprasidone, although in the latter case aldehyde oxidase is the enzyme responsible for most of the metabolism. Quetiapine Fumarate 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 18537577-6 2008 CYP2D6 and CYP3A4 are important in the metabolism of aripiprazole, and CYP-catalyzed metabolism of paliperidone and amisulpride appears to be minor. Aripiprazole 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 18332078-8 2008 CYP3A4 and CYP2B6 induction in Fa2N-4 cells were also low for phenytoin, phenobarbital, and efavirenz, which are dual activators of PXR/CAR. Phenytoin 62-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18332086-5 2008 CYP3A4 activity (1"-hydroxymidazolam formation) was increased (2-fold) by rifampin (10 microM) but was reduced by the PIs (1.5- to 7-fold). 1-hydroxymethylmidazolam 17-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18332078-8 2008 CYP3A4 and CYP2B6 induction in Fa2N-4 cells were also low for phenytoin, phenobarbital, and efavirenz, which are dual activators of PXR/CAR. Phenobarbital 73-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18332086-5 2008 CYP3A4 activity (1"-hydroxymidazolam formation) was increased (2-fold) by rifampin (10 microM) but was reduced by the PIs (1.5- to 7-fold). Rifampin 74-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18332086-8 2008 Furthermore, in a PXR-knockdown stable LS180 cell line, induction of CYP3A4 and MDR1 mRNA after treatment with PIs and rifampin was significantly reduced (1.4- to 5-fold) compared with that in PXR nonsilenced cells. Rifampin 119-127 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 18332078-8 2008 CYP3A4 and CYP2B6 induction in Fa2N-4 cells were also low for phenytoin, phenobarbital, and efavirenz, which are dual activators of PXR/CAR. efavirenz 92-101 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18332078-10 2008 The EC(50) value for rifampicin-mediated CYP3A4 induction was 10-fold higher than that in human hepatocytes. Rifampin 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 18362161-4 2008 In vitro studies have shown that CYP2C19, CYP3A4, and to a lesser extent CYP2C9 contribute to the oxidative metabolism of voriconazole. Voriconazole 122-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 18347083-7 2008 Moreover, using the comet assay, a dose-dependent DNA damage was observed after a 3-h treatment of differentiated HepaRG cells with 1 to 5 microM aflatoxin B(1) in the absence of any cell damage, and this DNA damaging effect was strongly reduced in the presence of ketoconazole, a CYP3A4 inhibitor. Aflatoxin B1 146-157 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 281-287 18308836-2 2008 We investigated the contributions of the CYP3A4 and CYP3A5 isoforms to the metabolism of the phosphodiesterase type 5 inhibitors (PDE5Is) sildenafil, udenafil, and vardenafil. Sildenafil Citrate 138-148 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 41-47 18308836-4 2008 Recombinant CYP3A4 and CYP3A5 both produced N-desalkyl metabolites of sildenafil, udenafil, and vardenafil. Sildenafil Citrate 70-80 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 18308836-4 2008 Recombinant CYP3A4 and CYP3A5 both produced N-desalkyl metabolites of sildenafil, udenafil, and vardenafil. udenafil 82-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 18308836-4 2008 Recombinant CYP3A4 and CYP3A5 both produced N-desalkyl metabolites of sildenafil, udenafil, and vardenafil. Vardenafil Dihydrochloride 96-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 12-18 18214455-1 2008 OBJECTIVE: Omeprazole is metabolized by the two cytochrome P450 isoforms, CYP3A (sulfoxidation) and CYP2C 19 (hydroxydation). Omeprazole 11-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 74-79 17998150-0 2008 Metabolic stereoselectivity of cytochrome P450 3A4 towards deoxypodophyllotoxin: In silico predictions and experimental validation. deoxypodophyllotoxin 59-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-50 18385991-1 2008 OBJECTIVE: Clopidogrel is activated by cytochrome P450 3A (CYP3A) to generate an active metabolite that inhibits adenosine diphosphate (ADP)-induced platelet aggregation through irreversible binding to the platelet P2Y12 receptor. Clopidogrel 11-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-57 17998150-1 2008 Deoxypodophyllotoxin is stereoselectively converted into epipodophyllotoxin by recombinant human cytochrome P450 3A4 (CYP3A4). deoxypodophyllotoxin 0-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-116 17998150-1 2008 Deoxypodophyllotoxin is stereoselectively converted into epipodophyllotoxin by recombinant human cytochrome P450 3A4 (CYP3A4). deoxypodophyllotoxin 0-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 17998150-1 2008 Deoxypodophyllotoxin is stereoselectively converted into epipodophyllotoxin by recombinant human cytochrome P450 3A4 (CYP3A4). Podophyllotoxin 57-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-116 17998150-1 2008 Deoxypodophyllotoxin is stereoselectively converted into epipodophyllotoxin by recombinant human cytochrome P450 3A4 (CYP3A4). Podophyllotoxin 57-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-124 17998150-2 2008 Further kinetic analysis revealed that the Michaelis-Menten K(m) and V(max) for hydroxylation of deoxypodophyllotoxin by CYP3A4 at C7 position were 1.93 microM and 1.48 nmol/min/nmol, respectively. deoxypodophyllotoxin 97-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 18385991-1 2008 OBJECTIVE: Clopidogrel is activated by cytochrome P450 3A (CYP3A) to generate an active metabolite that inhibits adenosine diphosphate (ADP)-induced platelet aggregation through irreversible binding to the platelet P2Y12 receptor. Clopidogrel 11-22 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 17998150-3 2008 Deoxypodophyllotoxin was subjected to automated docking analysis in order to get better knowledge of the interaction between the CYP3A4 enzyme and the substrate, using the PatchDock algorithm with distance constraints. deoxypodophyllotoxin 0-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-135 17998150-5 2008 The docking results are consistent with the experimental data for the bioconversion of deoxypodophyllotoxin into epipodophyllotoxin by CYP3A4. deoxypodophyllotoxin 87-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 18385991-1 2008 OBJECTIVE: Clopidogrel is activated by cytochrome P450 3A (CYP3A) to generate an active metabolite that inhibits adenosine diphosphate (ADP)-induced platelet aggregation through irreversible binding to the platelet P2Y12 receptor. Adenosine Diphosphate 113-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-57 17998150-5 2008 The docking results are consistent with the experimental data for the bioconversion of deoxypodophyllotoxin into epipodophyllotoxin by CYP3A4. Podophyllotoxin 113-131 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 135-141 18385991-1 2008 OBJECTIVE: Clopidogrel is activated by cytochrome P450 3A (CYP3A) to generate an active metabolite that inhibits adenosine diphosphate (ADP)-induced platelet aggregation through irreversible binding to the platelet P2Y12 receptor. Adenosine Diphosphate 113-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 18385991-1 2008 OBJECTIVE: Clopidogrel is activated by cytochrome P450 3A (CYP3A) to generate an active metabolite that inhibits adenosine diphosphate (ADP)-induced platelet aggregation through irreversible binding to the platelet P2Y12 receptor. Adenosine Diphosphate 136-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 39-57 18385991-1 2008 OBJECTIVE: Clopidogrel is activated by cytochrome P450 3A (CYP3A) to generate an active metabolite that inhibits adenosine diphosphate (ADP)-induced platelet aggregation through irreversible binding to the platelet P2Y12 receptor. Adenosine Diphosphate 136-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-64 18334598-5 2008 Similar to results in primary hepatocytes, the inhibition of the proteasome with N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal (MG132) suppresses CYP3A4 protein levels. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 124-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 18535361-6 2008 For example,the antibiotic rifampicin, one of the strongest inducers of the human gene CYP3A4, was the strongest inducer of the worm ortholog CYP13A7. Rifampin 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 18334598-8 2008 When the HepG2 cells were treated with cycloheximide, a general inhibitor of protein synthesis, the loss of CYP3A4 protein was accelerated by cotreatment with either proteasome or NF-kappaB inhibitors. Cycloheximide 39-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 108-114 18496126-6 2008 Furthermore, we have found statistically significant association of sites under adaptive evolution and Gotoh"s substrate recognition sites in rat and rabbit CYP2C (5%), human CYP3A and rat CYP2D (10%). gotoh 103-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-180 18493655-4 2008 In support of this idea, we found that adding FKBP blocks binding of FK506 to the common cytochrome P(450) enzyme CYP3A4 in vitro. Tacrolimus 69-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 114-120 18157519-1 2008 Animal and in vitro studies suggest that ursodeoxycholic acid (UDCA) can induce cytochrome P450 3A (CYP3A) expression and enhance its activities. Ursodeoxycholic Acid 41-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-98 18157519-1 2008 Animal and in vitro studies suggest that ursodeoxycholic acid (UDCA) can induce cytochrome P450 3A (CYP3A) expression and enhance its activities. Ursodeoxycholic Acid 41-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-105 18157519-4 2008 The aim of this study was to investigate the effects of UDCA on the intestinal and hepatic CYP3A activities by administration of midazolam (MDZ), as a specific probe for CYP3A activity, in humans. Midazolam 129-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-96 18157519-4 2008 The aim of this study was to investigate the effects of UDCA on the intestinal and hepatic CYP3A activities by administration of midazolam (MDZ), as a specific probe for CYP3A activity, in humans. Midazolam 140-143 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 91-96 18322939-11 2008 Fipronil can inhibit testosterone metabolism by CYP3A4 and is an effective inducer of CYP isoforms in human hepatocytes. fipronil 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 18322939-11 2008 Fipronil can inhibit testosterone metabolism by CYP3A4 and is an effective inducer of CYP isoforms in human hepatocytes. Testosterone 21-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-54 18496131-10 2008 CONCLUSION: This study indicates that the presently evaluated variant alleles in the CYP2B6, CYP2C9, CYP2C19, CYP3A4, CYP3A5, GSTA1, GSTP1, ALDH1A1 and ALDH3A1 genes do not explain the interindividual variability in cyclophosphamide and 4-hydroxycyclophosphamide pharmacokinetics and are, probably, not the cause of the observed variability in toxicity. Cyclophosphamide 216-232 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 18520601-9 2008 These differences may be the result of variability in affinity of itraconazole, OH-itraconazole, and CsA for the cytochrome P450 3A4 metabolic system and the occurrence of P-glycoprotein polymorphisms. Itraconazole 66-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-132 18496131-10 2008 CONCLUSION: This study indicates that the presently evaluated variant alleles in the CYP2B6, CYP2C9, CYP2C19, CYP3A4, CYP3A5, GSTA1, GSTP1, ALDH1A1 and ALDH3A1 genes do not explain the interindividual variability in cyclophosphamide and 4-hydroxycyclophosphamide pharmacokinetics and are, probably, not the cause of the observed variability in toxicity. hydroxycyclophosphamide 239-262 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 110-116 18518855-7 2008 In adults, genetic polymorphisms in the genes encoding the cyclosporine-metabolizing enzymes CYP3A4 and CYP3A5, as well as the ABCB1 gene, which encodes the efflux-pump P-glycoprotein, seem to have a limited effect, if any, on cyclosporine pharmacokinetics. Cyclosporine 59-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 18563665-0 2008 Mechanism-based inactivation of cytochrome P450 3A4 by methylenedioxyphenyl lignans from Acanthopanax chiisanensis. Lignans 76-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-51 18563665-1 2008 The purpose of this investigation is to characterize the inhibition of CYP3A4 by methylenedioxyphenyl lignans isolated from ACANTHOPANAX CHIISANENSIS. Lignans 102-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 71-77 18563665-3 2008 The inhibition of CYP3A4 activity by these lignans was suppressed in the presence of a competitive CYP3A4 substrate, ketoconazole. Lignans 43-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 18563665-3 2008 The inhibition of CYP3A4 activity by these lignans was suppressed in the presence of a competitive CYP3A4 substrate, ketoconazole. Lignans 43-50 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 18563665-3 2008 The inhibition of CYP3A4 activity by these lignans was suppressed in the presence of a competitive CYP3A4 substrate, ketoconazole. Ketoconazole 117-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 18-24 18563665-3 2008 The inhibition of CYP3A4 activity by these lignans was suppressed in the presence of a competitive CYP3A4 substrate, ketoconazole. Ketoconazole 117-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 18563665-6 2008 These results collectively demonstrate that savinin, helioxanthin and 3-(3"",4""-dimethoxybenzyl)-2-(3",4"-methylenedioxybenzyl)butyrolactone from A. CHIISANENSIS inactivate CYP3A4 in a mechanism-based mode. savinin 44-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 18563665-6 2008 These results collectively demonstrate that savinin, helioxanthin and 3-(3"",4""-dimethoxybenzyl)-2-(3",4"-methylenedioxybenzyl)butyrolactone from A. CHIISANENSIS inactivate CYP3A4 in a mechanism-based mode. helioxanthin 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 18563665-6 2008 These results collectively demonstrate that savinin, helioxanthin and 3-(3"",4""-dimethoxybenzyl)-2-(3",4"-methylenedioxybenzyl)butyrolactone from A. CHIISANENSIS inactivate CYP3A4 in a mechanism-based mode. 3-(3"",4""-dimethoxybenzyl)-2-(3",4"-methylenedioxybenzyl)butyrolactone 70-141 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 18332045-0 2008 Phthalate induction of CYP3A4 is dependent on glucocorticoid regulation of PXR expression. phthalic acid 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 18332045-6 2008 We suggest that the magnitude of CYP3A4 induction by phthalates is dependent on the expression of PXR and may be significantly higher in the presence of glucocorticoids. phthalic acid 53-63 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 18332045-7 2008 DEHP and MEHP induced PXR-mediated transcription of the CYP3A4 promoter in a dose-dependent fashion. Diethylhexyl Phthalate 0-4 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 18332045-7 2008 DEHP and MEHP induced PXR-mediated transcription of the CYP3A4 promoter in a dose-dependent fashion. mono-(2-ethylhexyl)phthalate 9-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 18332045-8 2008 Coexposure to phthalates and dexamethasone (Dex) resulted in enhanced CYP3A4 promoter activity; furthermore, this induction was abrogated by both the GR antagonist RU486 and GR small interfering ribonucleic acid. phthalic acid 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 18332045-8 2008 Coexposure to phthalates and dexamethasone (Dex) resulted in enhanced CYP3A4 promoter activity; furthermore, this induction was abrogated by both the GR antagonist RU486 and GR small interfering ribonucleic acid. Dexamethasone 29-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 18332045-8 2008 Coexposure to phthalates and dexamethasone (Dex) resulted in enhanced CYP3A4 promoter activity; furthermore, this induction was abrogated by both the GR antagonist RU486 and GR small interfering ribonucleic acid. Dexamethasone 44-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 18332045-8 2008 Coexposure to phthalates and dexamethasone (Dex) resulted in enhanced CYP3A4 promoter activity; furthermore, this induction was abrogated by both the GR antagonist RU486 and GR small interfering ribonucleic acid. Mifepristone 164-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 18332045-10 2008 CYP3A4 protein was highly induced by Dex and DEHP coadministration in human hepatocyte cultures. Dexamethasone 37-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18332045-11 2008 Finally, enhanced 6beta-hydroxytestosterone formation in Dex and phthalate cotreated human hepatocytes confirmed CYP3A4 enzyme induction. 6 beta-hydroxytestosterone 18-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 18332045-11 2008 Finally, enhanced 6beta-hydroxytestosterone formation in Dex and phthalate cotreated human hepatocytes confirmed CYP3A4 enzyme induction. Dexamethasone 57-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 18332045-11 2008 Finally, enhanced 6beta-hydroxytestosterone formation in Dex and phthalate cotreated human hepatocytes confirmed CYP3A4 enzyme induction. phthalic acid 65-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-119 18332045-12 2008 Concomitant exposure to glucocorticoids and phthalates resulting in enhanced metabolic activity of CYP3A4 may play a role in altered efficacy of pharmaceutical agents. phthalic acid 44-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 18570159-4 2008 Treatment of human hepatocytes for 72 h with 2-200 microM TB produced concentration-dependent increases in CYP1A2, CYP2B6 and CYP3A4 mRNA levels, whereas treatment with BHT increased CYP2B6 and CYP3A4 mRNA levels. Thiabendazole 58-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 126-132 18520601-9 2008 These differences may be the result of variability in affinity of itraconazole, OH-itraconazole, and CsA for the cytochrome P450 3A4 metabolic system and the occurrence of P-glycoprotein polymorphisms. oh-itraconazole 80-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 113-132 18589174-12 2008 Coadministration of DTZ may further optimize the TAC level through preferential P-gp binding and CYP3A4 inhibition. Diltiazem 20-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 18589198-4 2008 Oral and intravenous midazolam was used as the probe to measure hepatic and intestinal CYP3A4 activities at two different time points (phases one and two). Midazolam 21-30 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 18570159-11 2008 In summary, the results demonstrate that TB is a mixed inducer of CYP forms in human hepatocytes inducing CYP1A, CYP2B and CYP3A forms, whereas BHT is an inducer of CYP2B and CYP3A forms. Butylated Hydroxytoluene 144-147 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-180 18570159-4 2008 Treatment of human hepatocytes for 72 h with 2-200 microM TB produced concentration-dependent increases in CYP1A2, CYP2B6 and CYP3A4 mRNA levels, whereas treatment with BHT increased CYP2B6 and CYP3A4 mRNA levels. Thiabendazole 58-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 18570159-4 2008 Treatment of human hepatocytes for 72 h with 2-200 microM TB produced concentration-dependent increases in CYP1A2, CYP2B6 and CYP3A4 mRNA levels, whereas treatment with BHT increased CYP2B6 and CYP3A4 mRNA levels. Butylated Hydroxytoluene 169-172 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 194-200 18570159-5 2008 CYP1A2, CYP2B6 and CYP3A4 mRNA levels were induced around 48-, 21- and 9-fold, respectively, by 200 microM TB, with CYP2B6 and CYP 3A4 mRNA levels being induced around 12- and 7-fold, respectively, by 200 microM BHT. Thiabendazole 107-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 18570159-5 2008 CYP1A2, CYP2B6 and CYP3A4 mRNA levels were induced around 48-, 21- and 9-fold, respectively, by 200 microM TB, with CYP2B6 and CYP 3A4 mRNA levels being induced around 12- and 7-fold, respectively, by 200 microM BHT. Thiabendazole 107-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 127-134 18570159-9 2008 The treatment of human hepatocytes with TB also induced CYP1A-dependent 7-ethoxyresorufin O-deethylase activity, whereas BHT induced CYP3A-dependent testosterone 6beta-hydroxylase activity. Butylated Hydroxytoluene 121-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-138 18570159-11 2008 In summary, the results demonstrate that TB is a mixed inducer of CYP forms in human hepatocytes inducing CYP1A, CYP2B and CYP3A forms, whereas BHT is an inducer of CYP2B and CYP3A forms. Thiabendazole 41-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-128 18570159-11 2008 In summary, the results demonstrate that TB is a mixed inducer of CYP forms in human hepatocytes inducing CYP1A, CYP2B and CYP3A forms, whereas BHT is an inducer of CYP2B and CYP3A forms. Thiabendazole 41-43 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 175-180 18242899-1 2008 The aim of this work was to investigate the effects of pluronic F68 block copolymer on the P-gp-mediated transport of celiprolol (CEL) and CYP3A4-mediated formation of midazolam (MDZ) metabolite 1"-hydroxymidazolam. CHEMBL564199 64-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 18242899-1 2008 The aim of this work was to investigate the effects of pluronic F68 block copolymer on the P-gp-mediated transport of celiprolol (CEL) and CYP3A4-mediated formation of midazolam (MDZ) metabolite 1"-hydroxymidazolam. copolymer 74-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 18242899-1 2008 The aim of this work was to investigate the effects of pluronic F68 block copolymer on the P-gp-mediated transport of celiprolol (CEL) and CYP3A4-mediated formation of midazolam (MDZ) metabolite 1"-hydroxymidazolam. Midazolam 168-177 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 18242899-1 2008 The aim of this work was to investigate the effects of pluronic F68 block copolymer on the P-gp-mediated transport of celiprolol (CEL) and CYP3A4-mediated formation of midazolam (MDZ) metabolite 1"-hydroxymidazolam. Midazolam 179-182 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 18242899-1 2008 The aim of this work was to investigate the effects of pluronic F68 block copolymer on the P-gp-mediated transport of celiprolol (CEL) and CYP3A4-mediated formation of midazolam (MDZ) metabolite 1"-hydroxymidazolam. 1-hydroxymethylmidazolam 195-214 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 139-145 18242899-4 2008 Furthermore, CYP3A4-catalyzed formation of 1"-hydroxymidazolam was inhibited by pluronic F68 with IC(50) and K(i) values of 0.11 and 0.16 mg/ml, respectively. 1-hydroxymethylmidazolam 43-62 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 18242899-4 2008 Furthermore, CYP3A4-catalyzed formation of 1"-hydroxymidazolam was inhibited by pluronic F68 with IC(50) and K(i) values of 0.11 and 0.16 mg/ml, respectively. CHEMBL564199 89-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 18242899-5 2008 The results indicate that pluronic F68 is a potent in vitro inhibitor of both P-gp and CYP3A4, suggesting a potential for pluronic F68 to modify the pharmacokinetics of orally administered drugs that are P-gp and/or CYP3A4 substrates in vivo. Poloxamer 26-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 18242899-5 2008 The results indicate that pluronic F68 is a potent in vitro inhibitor of both P-gp and CYP3A4, suggesting a potential for pluronic F68 to modify the pharmacokinetics of orally administered drugs that are P-gp and/or CYP3A4 substrates in vivo. Poloxamer 26-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-222 18242899-5 2008 The results indicate that pluronic F68 is a potent in vitro inhibitor of both P-gp and CYP3A4, suggesting a potential for pluronic F68 to modify the pharmacokinetics of orally administered drugs that are P-gp and/or CYP3A4 substrates in vivo. CHEMBL564199 35-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 18242899-5 2008 The results indicate that pluronic F68 is a potent in vitro inhibitor of both P-gp and CYP3A4, suggesting a potential for pluronic F68 to modify the pharmacokinetics of orally administered drugs that are P-gp and/or CYP3A4 substrates in vivo. CHEMBL564199 35-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 216-222 18359012-5 2008 Formation of GSH conjugates was primarily catalyzed by heterologously expressed recombinant CYP2D6, CYP3A4, CYP3A5, and to a less extent, CYP1A2. Glutathione 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 18440347-1 2008 BACKGROUND: Clopidogrel is inactive in vitro and is metabolized by hepatic cytochrome P-450-3A4 to produce active metabolites. Clopidogrel 12-23 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 75-95 18440347-2 2008 Unlike pravastatin, atorvastatin is a statin that is subject to metabolism by cytochrome P-450-3A4, and drug-drug interactions with other potent inhibitors of this cytochrome system have been demonstrated. Atorvastatin 20-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 78-98 18372180-0 2008 An epoxidation mechanism of carbamazepine by CYP3A4. Carbamazepine 28-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 18285471-1 2008 Ritonavir is the most potent and efficacious inhibitor of cytochrome P4503A (CYP3A), and it is used accordingly for the pharmacoenhancement of other antiretrovirals. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 58-64 18285471-1 2008 Ritonavir is the most potent and efficacious inhibitor of cytochrome P4503A (CYP3A), and it is used accordingly for the pharmacoenhancement of other antiretrovirals. Ritonavir 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-82 18285477-2 2008 Since AMD070 is a substrate of cytochrome P450 3A4 and P-glycoprotein, both of which may be affected by ritonavir, we tested for a ritonavir effect on AMD070 pharmacokinetics. Ritonavir 131-140 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-50 18316526-2 2008 The main objective of this study was to assess the effects of oral ketoconazole, a potent inhibitor of the cytochrome P450 3A4 (CYP3A4) isoenzyme, on the pharmacokinetics of maribavir. Ketoconazole 67-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-126 18316526-2 2008 The main objective of this study was to assess the effects of oral ketoconazole, a potent inhibitor of the cytochrome P450 3A4 (CYP3A4) isoenzyme, on the pharmacokinetics of maribavir. Ketoconazole 67-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 18316526-2 2008 The main objective of this study was to assess the effects of oral ketoconazole, a potent inhibitor of the cytochrome P450 3A4 (CYP3A4) isoenzyme, on the pharmacokinetics of maribavir. maribavir 174-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-126 18316526-2 2008 The main objective of this study was to assess the effects of oral ketoconazole, a potent inhibitor of the cytochrome P450 3A4 (CYP3A4) isoenzyme, on the pharmacokinetics of maribavir. maribavir 174-183 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 18316526-8 2008 Based on the assumption of complete inhibition of CYP3A4 activity, CYP3A4 is responsible for 35% of the overall clearance of maribavir. maribavir 125-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 50-56 18316526-8 2008 Based on the assumption of complete inhibition of CYP3A4 activity, CYP3A4 is responsible for 35% of the overall clearance of maribavir. maribavir 125-134 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 18451520-7 2008 Extracts having relatively strong inhibitory effects for CYP3A4 tended to contain higher amounts of naringin, bergamottin and 6",7"-dihydroxybergamottin. naringin 100-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 18451520-7 2008 Extracts having relatively strong inhibitory effects for CYP3A4 tended to contain higher amounts of naringin, bergamottin and 6",7"-dihydroxybergamottin. bergamottin 110-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 18451520-7 2008 Extracts having relatively strong inhibitory effects for CYP3A4 tended to contain higher amounts of naringin, bergamottin and 6",7"-dihydroxybergamottin. 6',7'-dihydroxybergamottin 126-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-63 18372180-3 2008 To clarify the reason why CYP3A4 produces such an energetically unfavorable compound, the mechanism of epoxidation of CBZ by CYP3A4 was investigated by theoretical calculations. Carbamazepine 118-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 26-32 18372180-3 2008 To clarify the reason why CYP3A4 produces such an energetically unfavorable compound, the mechanism of epoxidation of CBZ by CYP3A4 was investigated by theoretical calculations. Carbamazepine 118-121 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 125-131 18372180-1 2008 Human CYP3A4 catalyzes the 10,11-epoxidation of carbamazepine (CBZ). Carbamazepine 48-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 18372180-1 2008 Human CYP3A4 catalyzes the 10,11-epoxidation of carbamazepine (CBZ). Carbamazepine 63-66 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 6-12 18279471-1 2008 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: CYP3A4 converts cholesterol into 4beta-hydroxycholesterol. Cholesterol 58-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 18373546-0 2008 Exploring QSARs for binding affinity of azoles with CYP2B and CYP3A enzymes using GFA and G/PLS techniques. Azoles 40-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 62-67 18319058-5 2008 The sulfoxidation metabolic index (measure of collective CYP3A activity) indicates that the CYP3A5*1/*1, (high-expressers), *1/*3, (low-expressers), and *3/*3 (no-expressers) groups have medium, lowest and highest activities on ilaprazole metabolism, inconsistent with genotype-based CYP3A5 enzymatic activity. ilaprazole 228-238 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 57-62 18407675-2 2008 The primary metabolite of PH-302 is a catechol ( 2) resulting from oxidative demethylenation of the methylenedioxyphenyl moiety by cytochrome P450 3A4. catechol 38-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 131-150 18451235-1 2008 PURPOSE: To determine if ixabepilone is a substrate for cytochrome P450 3A4 (CYP3A4) and if its metabolism by this cytochrome is clinically important, we did a clinical drug interaction study in humans using ketoconazole as an inhibitor of CYP3A4. ixabepilone 25-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-75 18451235-1 2008 PURPOSE: To determine if ixabepilone is a substrate for cytochrome P450 3A4 (CYP3A4) and if its metabolism by this cytochrome is clinically important, we did a clinical drug interaction study in humans using ketoconazole as an inhibitor of CYP3A4. ixabepilone 25-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 18451235-3 2008 Computational docking (CYP3A4) studies were done for epothilone B and ixabepilone. epothilone B 53-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 18451235-3 2008 Computational docking (CYP3A4) studies were done for epothilone B and ixabepilone. ixabepilone 70-81 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 18451235-4 2008 A follow-up clinical study was done in patients with cancer to determine if 400 mg/d ketoconazole (inhibitor of CYP3A4) altered the pharmacokinetics, drug-target interactions, and pharmacodynamics of ixabepilone. Ketoconazole 85-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 18451235-4 2008 A follow-up clinical study was done in patients with cancer to determine if 400 mg/d ketoconazole (inhibitor of CYP3A4) altered the pharmacokinetics, drug-target interactions, and pharmacodynamics of ixabepilone. ixabepilone 200-211 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118 18451235-5 2008 RESULTS: Molecular modeling and human microsomal studies predicted ixabepilone to be a good substrate for CYP3A4. ixabepilone 67-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 106-112 18451235-10 2008 CONCLUSIONS: Ixabepilone is a good CYP3A4 substrate in vitro; however, in humans, it is likely to be cleared by multiple mechanisms. ixabepilone 13-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 18451235-12 2008 Strong inhibitors of CYP3A4 should be used cautiously in the context of ixabepilone dosing. ixabepilone 72-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-27 18473749-3 2008 A recent study indicates that CYP3A4 undergoes dramatic conformational changes upon binding to ketoconazole or erythromycin with a differential but substantial (>80%) increase in the active site volume, providing a structural basis for ligand promiscuity of CYP3A4. Ketoconazole 95-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 18473749-3 2008 A recent study indicates that CYP3A4 undergoes dramatic conformational changes upon binding to ketoconazole or erythromycin with a differential but substantial (>80%) increase in the active site volume, providing a structural basis for ligand promiscuity of CYP3A4. Ketoconazole 95-107 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 261-267 18473749-3 2008 A recent study indicates that CYP3A4 undergoes dramatic conformational changes upon binding to ketoconazole or erythromycin with a differential but substantial (>80%) increase in the active site volume, providing a structural basis for ligand promiscuity of CYP3A4. Erythromycin 111-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 18473749-3 2008 A recent study indicates that CYP3A4 undergoes dramatic conformational changes upon binding to ketoconazole or erythromycin with a differential but substantial (>80%) increase in the active site volume, providing a structural basis for ligand promiscuity of CYP3A4. Erythromycin 111-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 261-267 18473749-9 2008 A small number of drugs such as rifampin, phenytoin and ritonavir are identified as inducers of CYP3A4. Rifampin 32-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 18473749-9 2008 A small number of drugs such as rifampin, phenytoin and ritonavir are identified as inducers of CYP3A4. Phenytoin 42-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 18473749-9 2008 A small number of drugs such as rifampin, phenytoin and ritonavir are identified as inducers of CYP3A4. Ritonavir 56-65 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 96-102 18238859-9 2008 In addition, in vitro experiments in human liver microsomes with cytochrome P450 (P450)-specific inhibitors revealed that CYP3A4 was the major enzyme responsible for the metabolism of TZB-30878. thiazolinobutazone 184-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 18256203-1 2008 Midazolam (MDZ) is one of the most commonly used in vivo and in vitro CYP3A4 probe substrates for drug-drug interactions (DDI) studies. Midazolam 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 18279471-1 2008 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: CYP3A4 converts cholesterol into 4beta-hydroxycholesterol. cholest-5-ene-3,4-diol 75-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 42-48 18256203-1 2008 Midazolam (MDZ) is one of the most commonly used in vivo and in vitro CYP3A4 probe substrates for drug-drug interactions (DDI) studies. Midazolam 11-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-76 18256203-2 2008 The major metabolic pathway of MDZ in humans consists of the CYP3A4-mediated 1"-hydroxylation followed by urinary excretion as 1"-O-glucuronide derivative. Midazolam 31-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 18279471-2 2008 We have suggested that 4beta-hydroxycholesterol could be used as a clinical marker for CYP3A4 activity aiding in dose adjustments. cholest-5-ene-3,4-diol 23-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 87-93 18256203-10 2008 The N-glucuronide derivative was found in human hepatocytes incubated under control conditions but also in the presence of the well known CYP3A4 inhibitor, ketoconazole. n-glucuronide 4-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 18279471-4 2008 WHAT THIS STUDY ADDS: The concentration of 4beta-hydroxycholesterol increases very slowly during CYP3A4/5 induction in paediatric patients. cholest-5-ene-3,4-diol 43-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 18256203-10 2008 The N-glucuronide derivative was found in human hepatocytes incubated under control conditions but also in the presence of the well known CYP3A4 inhibitor, ketoconazole. Ketoconazole 156-168 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-144 18279471-5 2008 Whereas induction of CYP3A4/5 was apparently complete within 1-2 weeks of carbamazepine treatment, plasma 4beta-hydroxycholesterol levels continued to increase until at least 8 weeks of treatment. Carbamazepine 74-87 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 21-29 18256203-11 2008 In the context of the in vitro study of CYP3A4-mediated DDI using MDZ and ketoconazole, direct MDZ N-glucuronidation may partly compensate the decrease in MDZ metabolic clearance caused by the addition of the inhibitor, thus potentially leading to underestimation, at least in vitro, of the extent of DDI. Midazolam 66-69 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 18256203-11 2008 In the context of the in vitro study of CYP3A4-mediated DDI using MDZ and ketoconazole, direct MDZ N-glucuronidation may partly compensate the decrease in MDZ metabolic clearance caused by the addition of the inhibitor, thus potentially leading to underestimation, at least in vitro, of the extent of DDI. Ketoconazole 74-86 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 18279471-14 2008 CONCLUSIONS: Carbamazepine treatment of paediatric patients with epilepsy resulted in an induction of CYP3A4/5 and a concomitant increase in plasma 4beta-hydroxycholesterol. Carbamazepine 13-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 102-108 18256203-11 2008 In the context of the in vitro study of CYP3A4-mediated DDI using MDZ and ketoconazole, direct MDZ N-glucuronidation may partly compensate the decrease in MDZ metabolic clearance caused by the addition of the inhibitor, thus potentially leading to underestimation, at least in vitro, of the extent of DDI. Nitrogen 99-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-46 18299335-0 2008 Role of human pregnane X receptor in tamoxifen- and 4-hydroxytamoxifen-mediated CYP3A4 induction in primary human hepatocytes and LS174T cells. Tamoxifen 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 18299335-0 2008 Role of human pregnane X receptor in tamoxifen- and 4-hydroxytamoxifen-mediated CYP3A4 induction in primary human hepatocytes and LS174T cells. hydroxytamoxifen 52-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 18299335-1 2008 Previously we observed that the antiestrogens tamoxifen and 4-hydroxytamoxifen (4OHT) induce CYP3A4 in primary human hepatocytes and activate human pregnane X receptor (PXR) in cell-based reporter assays. Tamoxifen 46-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 18299335-1 2008 Previously we observed that the antiestrogens tamoxifen and 4-hydroxytamoxifen (4OHT) induce CYP3A4 in primary human hepatocytes and activate human pregnane X receptor (PXR) in cell-based reporter assays. hydroxytamoxifen 60-78 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 18299335-1 2008 Previously we observed that the antiestrogens tamoxifen and 4-hydroxytamoxifen (4OHT) induce CYP3A4 in primary human hepatocytes and activate human pregnane X receptor (PXR) in cell-based reporter assays. 4,17 beta-dihydroxy-4-androstene-3-one 80-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 93-99 18299335-3 2008 First, we observed that transfection of the primary cultures of human hepatocytes with PXR-specific small interfering RNA reduced the PXR mRNA expression and the extent of CYP3A4 induction by tamoxifen and 4OHT by 50%. Tamoxifen 192-201 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 18299335-3 2008 First, we observed that transfection of the primary cultures of human hepatocytes with PXR-specific small interfering RNA reduced the PXR mRNA expression and the extent of CYP3A4 induction by tamoxifen and 4OHT by 50%. 4,17 beta-dihydroxy-4-androstene-3-one 206-210 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-178 18299335-9 2008 Collectively, our findings suggest that the CYP3A4 induction by tamoxifen and 4OHT is primarily mediated by PXR but the overall stoichiometry of other nuclear receptors and transcription cofactors also contributes to the extent of the inductive effect. Tamoxifen 64-73 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 44-50 18193210-1 2008 AIM: It has been reported that verapamil and atorvastatin are inhibitors of both P-glycoprotein (P-gp) and microsomal cytochrome P450 (CYP) 3A4, and verapamil is a substrate of both P-gp and CYP3A4. Atorvastatin 45-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-143 18193210-1 2008 AIM: It has been reported that verapamil and atorvastatin are inhibitors of both P-glycoprotein (P-gp) and microsomal cytochrome P450 (CYP) 3A4, and verapamil is a substrate of both P-gp and CYP3A4. Verapamil 31-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 118-143 18193210-1 2008 AIM: It has been reported that verapamil and atorvastatin are inhibitors of both P-glycoprotein (P-gp) and microsomal cytochrome P450 (CYP) 3A4, and verapamil is a substrate of both P-gp and CYP3A4. Atorvastatin 45-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-197 18193210-1 2008 AIM: It has been reported that verapamil and atorvastatin are inhibitors of both P-glycoprotein (P-gp) and microsomal cytochrome P450 (CYP) 3A4, and verapamil is a substrate of both P-gp and CYP3A4. Verapamil 31-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 191-197 18193210-8 2008 CONCLUSION: The above data suggest that atorvastatin could inhibit the absorption of verapamil via inhibition of P-gp and/or the metabolism of verapamil by CYP3A4 in humans. Atorvastatin 40-52 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 18193210-8 2008 CONCLUSION: The above data suggest that atorvastatin could inhibit the absorption of verapamil via inhibition of P-gp and/or the metabolism of verapamil by CYP3A4 in humans. Verapamil 85-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 18193210-8 2008 CONCLUSION: The above data suggest that atorvastatin could inhibit the absorption of verapamil via inhibition of P-gp and/or the metabolism of verapamil by CYP3A4 in humans. Verapamil 143-152 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 156-162 18305126-3 2008 Tadalafil is mainly metabolized by cytochrome P450 (CYP) 3A4, and as bosentan induces CYP2C9 and CYP3A4, a pharmacokinetic interaction is possible between these agents. Bosentan 69-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 97-103 18356043-2 2008 Screening with well-established chemical inhibitors showed that the formation of norethindrone was potently inhibited by CYP3A4 inhibitor ketoconazole (IC(50)=0.02 microM) and with CYP2C9 inhibitor sulphaphenazole (IC(50)=2.13 microM); the further biotransformation of norethindrone was strongly inhibited by ketoconazole (IC(50)=0.09 microM). Norethindrone 81-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 18319360-2 2008 CYP3A4 and ABCC2, the major variables in pharmacokinetics of propiverine, are less expressed in the colon. propiverine 61-72 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18319360-5 2008 Serum and urine propiverine levels were measured repeatedly following oral administration on day 7 for up to 72 hours and correlated to duodenal expression of CYP3A4, ABCB1, and ABCC2. propiverine 16-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-165 18356043-6 2008 Norethindrone hydroxylation correlated significantly with model reactions of CYP2C19 and CYP3A4. Norethindrone 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 18356043-2 2008 Screening with well-established chemical inhibitors showed that the formation of norethindrone was potently inhibited by CYP3A4 inhibitor ketoconazole (IC(50)=0.02 microM) and with CYP2C9 inhibitor sulphaphenazole (IC(50)=2.13 microM); the further biotransformation of norethindrone was strongly inhibited by ketoconazole (IC(50)=0.09 microM). Ketoconazole 138-150 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 18356043-8 2008 The CYP3A4-Ab reduced norethindrone hydroxylation by 96%. Norethindrone 22-35 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 4-10 18356043-2 2008 Screening with well-established chemical inhibitors showed that the formation of norethindrone was potently inhibited by CYP3A4 inhibitor ketoconazole (IC(50)=0.02 microM) and with CYP2C9 inhibitor sulphaphenazole (IC(50)=2.13 microM); the further biotransformation of norethindrone was strongly inhibited by ketoconazole (IC(50)=0.09 microM). Norethindrone 269-282 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 18356043-10 2008 In conclusion, CYP2C9, CYP2C19 and CYP3A4 are the primary cytochromes in the bioactivation of lynestrenol in vitro, while CYP3A4 catalyses the further metabolism of norethindrone. Lynestrenol 94-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 18356043-2 2008 Screening with well-established chemical inhibitors showed that the formation of norethindrone was potently inhibited by CYP3A4 inhibitor ketoconazole (IC(50)=0.02 microM) and with CYP2C9 inhibitor sulphaphenazole (IC(50)=2.13 microM); the further biotransformation of norethindrone was strongly inhibited by ketoconazole (IC(50)=0.09 microM). Ketoconazole 309-321 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-127 18356043-10 2008 In conclusion, CYP2C9, CYP2C19 and CYP3A4 are the primary cytochromes in the bioactivation of lynestrenol in vitro, while CYP3A4 catalyses the further metabolism of norethindrone. Lynestrenol 94-105 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 18356043-10 2008 In conclusion, CYP2C9, CYP2C19 and CYP3A4 are the primary cytochromes in the bioactivation of lynestrenol in vitro, while CYP3A4 catalyses the further metabolism of norethindrone. Norethindrone 165-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 35-41 18356043-4 2008 Lynestrenol bioactivation was mainly catalysed by recombinant human CYP2C9, CYP2C19 and CYP3A4; rCYP3A4 was responsible for the hydroxylation of norethindrone. Lynestrenol 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-94 18356043-10 2008 In conclusion, CYP2C9, CYP2C19 and CYP3A4 are the primary cytochromes in the bioactivation of lynestrenol in vitro, while CYP3A4 catalyses the further metabolism of norethindrone. Norethindrone 165-178 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 122-128 18490798-2 2008 Drugs interacting with colchicine metabolism through CYP(3)A(4) and P-glycoprotein can accelerate accumulation and toxicity. Colchicine 23-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-63 17922881-1 2008 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: * Nelfinavir is an HIV protease inhibitor, substrate of the transporter P-glycoprotein and metabolized via CYP2C19, CYP3A4 and CYP3A5 enzymes. Nelfinavir 44-54 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 158-164 18328680-6 2008 PB induced CYP3A4, 3A5, 2B6 and 2A6, UGT1A1 and all transporters. Phenobarbital 0-2 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17 18328680-8 2008 Enzyme activity of CYP3A4, measured by testosterone metabolism, was increased after 24h by RIF. Testosterone 39-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 18328680-8 2008 Enzyme activity of CYP3A4, measured by testosterone metabolism, was increased after 24h by RIF. Rifampin 91-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 19-25 18248513-6 2008 Both of naringenin and elacridar separately enhanced the sensitivity for CPT-11 and SN-38 in KYN-2 cells abundantly expressing BCRP, CYP3A4/5 and UGT1A1, but not in KYN-1 cells expressing lower levels. naringenin 8-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 18248513-6 2008 Both of naringenin and elacridar separately enhanced the sensitivity for CPT-11 and SN-38 in KYN-2 cells abundantly expressing BCRP, CYP3A4/5 and UGT1A1, but not in KYN-1 cells expressing lower levels. Irinotecan 84-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 18333863-27 2008 CONCLUSIONS: Potent CYP3A4 inhibitors, including ketoconazole and protease inhibitors (except TPV/r), increase maraviroc exposure. Ketoconazole 49-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 20-26 18294327-1 2008 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: * Voriconazole, a broad-spectrum antifungal drug, is a substrate and inhibitor of CYP2C19 and CYP3A4 isozymes. Voriconazole 44-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142 18294327-2 2008 * Ethinyl oestradiol and norethindrone, components of the combination oral contraceptive drug Ortho-Novum 1/35, also are substrates of cytochrome P450 CYP2C19 and CYP3A4 isozymes. Ethinyl Estradiol 2-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 18294327-2 2008 * Ethinyl oestradiol and norethindrone, components of the combination oral contraceptive drug Ortho-Novum 1/35, also are substrates of cytochrome P450 CYP2C19 and CYP3A4 isozymes. Norethindrone 25-38 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 163-169 18333864-28 2008 CONCLUSION: As expected with a CYP3A4 substrate, maraviroc exposure (C(max) and AUC(12)) was significantly reduced by the known CYP3A4 inducers, rifampicin and EFV, by approximately 70% and 50%, respectively. efavirenz 160-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 31-37 18333864-28 2008 CONCLUSION: As expected with a CYP3A4 substrate, maraviroc exposure (C(max) and AUC(12)) was significantly reduced by the known CYP3A4 inducers, rifampicin and EFV, by approximately 70% and 50%, respectively. efavirenz 160-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 18311908-4 2008 In this study, the structural characteristics of nitrogen-containing compounds, which bind to the iron atom in two CYP isoforms (CYP2C9 and CYP3A4), were investigated. Nitrogen 49-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 18096694-5 2008 We found that coumestrol was able to suppress the effects of PXR agonists on the expression of the known PXR target genes, CYP3A4 and CYP2B6, in primary human hepatocytes as well as inhibit metabolism of tribromoethanol in humanized PXR mice. Coumestrol 14-24 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 123-129 18311908-4 2008 In this study, the structural characteristics of nitrogen-containing compounds, which bind to the iron atom in two CYP isoforms (CYP2C9 and CYP3A4), were investigated. Iron 98-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 140-146 18191104-0 2008 Flavonoids diosmetin and luteolin inhibit midazolam metabolism by human liver microsomes and recombinant CYP 3A4 and CYP3A5 enzymes. Flavonoids 0-10 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-112 18340561-3 2008 In the current study, the metabolite kinetics of a series of CYP3A4 substrates (benzodiazepines) in fresh human hepatocytes from five donors, via a major UK supplier, were investigated and compared with those previously reported (by the authors" laboratory) for cryopreserved human hepatocytes and hepatic microsomes. Benzodiazepines 80-95 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 61-67 18191104-0 2008 Flavonoids diosmetin and luteolin inhibit midazolam metabolism by human liver microsomes and recombinant CYP 3A4 and CYP3A5 enzymes. diosmetin 11-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-112 18191104-0 2008 Flavonoids diosmetin and luteolin inhibit midazolam metabolism by human liver microsomes and recombinant CYP 3A4 and CYP3A5 enzymes. Midazolam 42-51 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 105-112 18191104-1 2008 We evaluated the effects of increasing concentrations of the flavonoids salvigenin, diosmetin and luteolin on the in vitro metabolism of midazolam (MDZ), a probe substrate for cytochrome P450 (CYP) 3A enzymes, which is converted into 1"-hydroxy-midazolam (1"-OH-MDZ) and 4-hydroxy-midazolam (4-OH-MDZ) by human liver microsomes. Flavonoids 61-71 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-200 18191104-1 2008 We evaluated the effects of increasing concentrations of the flavonoids salvigenin, diosmetin and luteolin on the in vitro metabolism of midazolam (MDZ), a probe substrate for cytochrome P450 (CYP) 3A enzymes, which is converted into 1"-hydroxy-midazolam (1"-OH-MDZ) and 4-hydroxy-midazolam (4-OH-MDZ) by human liver microsomes. salvigenin 72-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-200 18191104-1 2008 We evaluated the effects of increasing concentrations of the flavonoids salvigenin, diosmetin and luteolin on the in vitro metabolism of midazolam (MDZ), a probe substrate for cytochrome P450 (CYP) 3A enzymes, which is converted into 1"-hydroxy-midazolam (1"-OH-MDZ) and 4-hydroxy-midazolam (4-OH-MDZ) by human liver microsomes. Midazolam 137-146 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-200 18191104-1 2008 We evaluated the effects of increasing concentrations of the flavonoids salvigenin, diosmetin and luteolin on the in vitro metabolism of midazolam (MDZ), a probe substrate for cytochrome P450 (CYP) 3A enzymes, which is converted into 1"-hydroxy-midazolam (1"-OH-MDZ) and 4-hydroxy-midazolam (4-OH-MDZ) by human liver microsomes. Midazolam 148-151 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-200 18191104-1 2008 We evaluated the effects of increasing concentrations of the flavonoids salvigenin, diosmetin and luteolin on the in vitro metabolism of midazolam (MDZ), a probe substrate for cytochrome P450 (CYP) 3A enzymes, which is converted into 1"-hydroxy-midazolam (1"-OH-MDZ) and 4-hydroxy-midazolam (4-OH-MDZ) by human liver microsomes. 1-hydroxymethylmidazolam 234-254 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 176-200 18191104-3 2008 Both diosmetin and luteolin decreased 1"-OH-MDZ formation by human recombinant CYP3A4, but not CYP3A5, whereas they decreased 4-OH-MDZ formation by both recombinant enzymes. diosmetin 5-14 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 18191104-3 2008 Both diosmetin and luteolin decreased 1"-OH-MDZ formation by human recombinant CYP3A4, but not CYP3A5, whereas they decreased 4-OH-MDZ formation by both recombinant enzymes. Luteolin 19-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 18191104-3 2008 Both diosmetin and luteolin decreased 1"-OH-MDZ formation by human recombinant CYP3A4, but not CYP3A5, whereas they decreased 4-OH-MDZ formation by both recombinant enzymes. 1"-oh-mdz 38-47 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 18191104-7 2008 The results of the study may be of clinical relevance since they suggest that luteolin and diosmetin may cause pharmacokinetic interactions with co-administered drugs metabolized via CYP3A. diosmetin 91-100 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 183-188 18206979-0 2008 Effect of glutathione on homo- and heterotropic cooperativity in cytochrome P450 3A4. Glutathione 10-21 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 65-84 18206979-1 2008 Glutathione (GSH) exerted a profound effect on the oxidation of 7-benzyloxy-4-(trifluoromethyl)coumarin (BFC) and 7-benzyloxyquinoline (BQ) by human liver microsomes as well as by CYP3A4-containing insect cell microsomes (Baculosomes). Glutathione 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 18206979-1 2008 Glutathione (GSH) exerted a profound effect on the oxidation of 7-benzyloxy-4-(trifluoromethyl)coumarin (BFC) and 7-benzyloxyquinoline (BQ) by human liver microsomes as well as by CYP3A4-containing insect cell microsomes (Baculosomes). Glutathione 13-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 18206979-1 2008 Glutathione (GSH) exerted a profound effect on the oxidation of 7-benzyloxy-4-(trifluoromethyl)coumarin (BFC) and 7-benzyloxyquinoline (BQ) by human liver microsomes as well as by CYP3A4-containing insect cell microsomes (Baculosomes). 7-benzyloxy-4-trifluoromethylcoumarin 105-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 18206979-1 2008 Glutathione (GSH) exerted a profound effect on the oxidation of 7-benzyloxy-4-(trifluoromethyl)coumarin (BFC) and 7-benzyloxyquinoline (BQ) by human liver microsomes as well as by CYP3A4-containing insect cell microsomes (Baculosomes). 7-benzyloxyquinoline 136-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 180-186 18206979-3 2008 Addition of GSH also increased the amplitude of the 1-PB induced spin shift with purified CYP3A4 and abolished the cooperativity of 1-PB or BFC binding. Glutathione 12-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 18206979-3 2008 Addition of GSH also increased the amplitude of the 1-PB induced spin shift with purified CYP3A4 and abolished the cooperativity of 1-PB or BFC binding. 1-pb 52-56 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 90-96 18206979-4 2008 Changes in fluorescence of 6-bromoacetyl-2-dimethylaminonaphthalene attached to the cysteine-depleted mutant CYP3A4(C58,C64) suggest a GSH-induced conformational changes in proximity of alpha-helix A. 6-bromoacetyl-2-dimethylaminonaphthalene 27-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 18206979-4 2008 Changes in fluorescence of 6-bromoacetyl-2-dimethylaminonaphthalene attached to the cysteine-depleted mutant CYP3A4(C58,C64) suggest a GSH-induced conformational changes in proximity of alpha-helix A. Cysteine 84-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 18206979-4 2008 Changes in fluorescence of 6-bromoacetyl-2-dimethylaminonaphthalene attached to the cysteine-depleted mutant CYP3A4(C58,C64) suggest a GSH-induced conformational changes in proximity of alpha-helix A. Glutathione 135-138 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 109-115 18206979-5 2008 Importantly, the K(S) value for formation of the GSH complex and the concentrations in which GSH decreases CYP3A4 cooperativity are consistent with the physiological concentrations of GSH in hepatocytes. Glutathione 93-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 18206979-5 2008 Importantly, the K(S) value for formation of the GSH complex and the concentrations in which GSH decreases CYP3A4 cooperativity are consistent with the physiological concentrations of GSH in hepatocytes. Glutathione 93-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 107-113 18206979-6 2008 Therefore, the allosteric effect of GSH on CYP3A4 may play an important role in regulation of microsomal monooxygenase activity in vivo. Glutathione 36-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 43-49 18292673-10 2008 RESULTS: At clinical concentrations, methadone enantiomer N-demethylation by recombinant CYPs 2B6, 3A4, and 2C19 was S > R, S = R, and S << R. Greater stereoselective metabolism (S > R) occurred in livers expressing high levels of CYP2B6 compared with CYP3A4. Nitrogen 58-59 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 264-270 18164204-4 2008 Further modification resulted in the discovery of 2-hydroxymethylimidazo[1,2-a]pyridine 2e (FXa IC(50)=0.0090 microM), which was found to be a selective and orally bioavailable FXa inhibitor with reduced CYP3A4 inhibition. 2-hydroxymethylimidazo[1,2-a]pyridine 2e 50-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 204-210 18292673-2 2008 Initial in vitro studies attributed methadone metabolism to cytochrome P4503A4 (CYP3A4). Methadone 36-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-78 18189136-1 2008 Furanocoumarins (FCs) in grapefruit are involved in the "grapefruit/drug interactions" in humans, in which the FCs inhibit the intestinal cytochrome P450 3A4 (CYP 3A4) activity responsible for metabolizing certain prescribed medications. Furocoumarins 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-157 18292673-2 2008 Initial in vitro studies attributed methadone metabolism to cytochrome P4503A4 (CYP3A4). Methadone 36-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-86 18292673-3 2008 CYP3A4 was also assumed responsible for methadone clearance in vivo. Methadone 40-49 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18292673-10 2008 RESULTS: At clinical concentrations, methadone enantiomer N-demethylation by recombinant CYPs 2B6, 3A4, and 2C19 was S > R, S = R, and S << R. Greater stereoselective metabolism (S > R) occurred in livers expressing high levels of CYP2B6 compared with CYP3A4. Methadone 37-46 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 264-270 18086551-0 2008 Kinetics of electron transfer in the complex of cytochrome P450 3A4 with the flavin domain of cytochrome P450BM-3 as evidence of functional heterogeneity of the heme protein. 4,6-dinitro-o-cresol 77-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 48-67 18189136-1 2008 Furanocoumarins (FCs) in grapefruit are involved in the "grapefruit/drug interactions" in humans, in which the FCs inhibit the intestinal cytochrome P450 3A4 (CYP 3A4) activity responsible for metabolizing certain prescribed medications. Furocoumarins 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-166 18086551-1 2008 We used a rapid scanning stop-flow technique to study the kinetics of reduction of cytochrome P450 3A4 (CYP3A4) by the flavin domain of cytochrome P450-BM3 (BMR), which was shown to form a stoichiometric complex (K(D)=0.48 microM) with CYP3A4. 4,6-dinitro-o-cresol 119-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 83-102 18189136-1 2008 Furanocoumarins (FCs) in grapefruit are involved in the "grapefruit/drug interactions" in humans, in which the FCs inhibit the intestinal cytochrome P450 3A4 (CYP 3A4) activity responsible for metabolizing certain prescribed medications. Furocoumarins 17-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-157 18086551-1 2008 We used a rapid scanning stop-flow technique to study the kinetics of reduction of cytochrome P450 3A4 (CYP3A4) by the flavin domain of cytochrome P450-BM3 (BMR), which was shown to form a stoichiometric complex (K(D)=0.48 microM) with CYP3A4. 4,6-dinitro-o-cresol 119-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-110 18189136-1 2008 Furanocoumarins (FCs) in grapefruit are involved in the "grapefruit/drug interactions" in humans, in which the FCs inhibit the intestinal cytochrome P450 3A4 (CYP 3A4) activity responsible for metabolizing certain prescribed medications. Furocoumarins 17-20 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 159-166 18086551-1 2008 We used a rapid scanning stop-flow technique to study the kinetics of reduction of cytochrome P450 3A4 (CYP3A4) by the flavin domain of cytochrome P450-BM3 (BMR), which was shown to form a stoichiometric complex (K(D)=0.48 microM) with CYP3A4. 4,6-dinitro-o-cresol 119-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 236-242 18096676-6 2008 Incubation of CYP3A4 Supersomes with (3)H-CBZ resulted in its irreversible binding to CYP3A4 protein with a stoichiometry of 1.58 +/- 0.15 pmol (3)H-CBZ bound/pmol CYP3A4. (3)h-cbz 37-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 18188833-6 2008 CYP3A4 isozyme showed the broadest metabolic capacity, whereas CYP1A1, CYP1B1 and FMO3 isozymes biotransformed imatinib with a high intrinsic clearance. Imatinib Mesylate 111-119 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18431272-13 2008 CONCLUSIONS: Some catecholamines can induce an inflammatory response and exacerbate the hepatic dysfunction observed during sepsis, favoring the idea that catecholamines could alter the biotransformation of drugs metabolized by CYP3A4 and that alternative vasoactive agents, such as vasopressin, merit further investigation in septic shock patients. Catecholamines 18-32 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 18431272-13 2008 CONCLUSIONS: Some catecholamines can induce an inflammatory response and exacerbate the hepatic dysfunction observed during sepsis, favoring the idea that catecholamines could alter the biotransformation of drugs metabolized by CYP3A4 and that alternative vasoactive agents, such as vasopressin, merit further investigation in septic shock patients. Catecholamines 155-169 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 228-234 18094037-8 2008 In proximal jejunum, rifampicin (RIF) [pregnane X receptor (PXR) ligand] induced CYP3A4 (5.2-fold), CYP2B6 (2-fold), UGT1A6 (2.2-fold), and multidrug resistance-1 (MDR1)/ABCB1 mRNA (2.7-fold), whereas 6beta-hydroxytestosterone formation (CYP3A4) increased 2-fold. Rifampin 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 18094037-10 2008 Dexamethasone (glucocorticoid receptor and PXR ligand) induced CYP3A4 mRNA (3.5-fold) and activity (5-fold) in proximal jejunum. Dexamethasone 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 18094037-8 2008 In proximal jejunum, rifampicin (RIF) [pregnane X receptor (PXR) ligand] induced CYP3A4 (5.2-fold), CYP2B6 (2-fold), UGT1A6 (2.2-fold), and multidrug resistance-1 (MDR1)/ABCB1 mRNA (2.7-fold), whereas 6beta-hydroxytestosterone formation (CYP3A4) increased 2-fold. Rifampin 21-31 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 238-244 18094037-8 2008 In proximal jejunum, rifampicin (RIF) [pregnane X receptor (PXR) ligand] induced CYP3A4 (5.2-fold), CYP2B6 (2-fold), UGT1A6 (2.2-fold), and multidrug resistance-1 (MDR1)/ABCB1 mRNA (2.7-fold), whereas 6beta-hydroxytestosterone formation (CYP3A4) increased 2-fold. Rifampin 33-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 81-87 18094037-8 2008 In proximal jejunum, rifampicin (RIF) [pregnane X receptor (PXR) ligand] induced CYP3A4 (5.2-fold), CYP2B6 (2-fold), UGT1A6 (2.2-fold), and multidrug resistance-1 (MDR1)/ABCB1 mRNA (2.7-fold), whereas 6beta-hydroxytestosterone formation (CYP3A4) increased 2-fold. Rifampin 33-36 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 238-244 18096676-6 2008 Incubation of CYP3A4 Supersomes with (3)H-CBZ resulted in its irreversible binding to CYP3A4 protein with a stoichiometry of 1.58 +/- 0.15 pmol (3)H-CBZ bound/pmol CYP3A4. h-cbz 40-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 18096676-6 2008 Incubation of CYP3A4 Supersomes with (3)H-CBZ resulted in its irreversible binding to CYP3A4 protein with a stoichiometry of 1.58 +/- 0.15 pmol (3)H-CBZ bound/pmol CYP3A4. h-cbz 40-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 18094037-11 2008 Phenobarbital (constitutive androstane receptor activator) induced CYP3A4 (4.1-fold, only in jejunum), CYP2B6 (4.9-fold in colon and 2.3-fold in proximal jejunum), and MDR1/ABCB1 mRNA and CYP3A4 activity (2-fold only proximal jejunum). Phenobarbital 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 18096676-6 2008 Incubation of CYP3A4 Supersomes with (3)H-CBZ resulted in its irreversible binding to CYP3A4 protein with a stoichiometry of 1.58 +/- 0.15 pmol (3)H-CBZ bound/pmol CYP3A4. h-cbz 40-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 18096676-8 2008 Similar binding (1.0 +/- 0.4 pmol (3)H-CBZ bound/pmol CYP3A4) was observed after (3)H-CBZ incubation with functionally reconstituted, purified recombinant CYP3A4(His)(6). h-cbz 37-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 18094037-11 2008 Phenobarbital (constitutive androstane receptor activator) induced CYP3A4 (4.1-fold, only in jejunum), CYP2B6 (4.9-fold in colon and 2.3-fold in proximal jejunum), and MDR1/ABCB1 mRNA and CYP3A4 activity (2-fold only proximal jejunum). Phenobarbital 0-13 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 188-194 18096676-8 2008 Similar binding (1.0 +/- 0.4 pmol (3)H-CBZ bound/pmol CYP3A4) was observed after (3)H-CBZ incubation with functionally reconstituted, purified recombinant CYP3A4(His)(6). h-cbz 37-42 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 18096676-8 2008 Similar binding (1.0 +/- 0.4 pmol (3)H-CBZ bound/pmol CYP3A4) was observed after (3)H-CBZ incubation with functionally reconstituted, purified recombinant CYP3A4(His)(6). h-cbz 84-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 18096676-0 2008 CYP3A4-Mediated carbamazepine (CBZ) metabolism: formation of a covalent CBZ-CYP3A4 adduct and alteration of the enzyme kinetic profile. Carbamazepine 16-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18096676-8 2008 Similar binding (1.0 +/- 0.4 pmol (3)H-CBZ bound/pmol CYP3A4) was observed after (3)H-CBZ incubation with functionally reconstituted, purified recombinant CYP3A4(His)(6). h-cbz 84-89 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 18096676-0 2008 CYP3A4-Mediated carbamazepine (CBZ) metabolism: formation of a covalent CBZ-CYP3A4 adduct and alteration of the enzyme kinetic profile. Carbamazepine 16-29 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 18096676-8 2008 Similar binding (1.0 +/- 0.4 pmol (3)H-CBZ bound/pmol CYP3A4) was observed after (3)H-CBZ incubation with functionally reconstituted, purified recombinant CYP3A4(His)(6). Histidine 162-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 54-60 18096676-8 2008 Similar binding (1.0 +/- 0.4 pmol (3)H-CBZ bound/pmol CYP3A4) was observed after (3)H-CBZ incubation with functionally reconstituted, purified recombinant CYP3A4(His)(6). Histidine 162-165 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 155-161 18096676-0 2008 CYP3A4-Mediated carbamazepine (CBZ) metabolism: formation of a covalent CBZ-CYP3A4 adduct and alteration of the enzyme kinetic profile. Carbamazepine 31-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18096676-9 2008 The CBZ-modified CYP3A4 retained its functional activity albeit at a reduced level, but its testosterone 6beta-hydroxylase kinetics were altered from sigmoidal (a characteristic profile of substrate cooperativity) to near-hyperbolic (Michaelis-Menten) type, suggesting that CBZ may have modified CYP3A4 within its active site. Carbamazepine 4-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 18096676-0 2008 CYP3A4-Mediated carbamazepine (CBZ) metabolism: formation of a covalent CBZ-CYP3A4 adduct and alteration of the enzyme kinetic profile. Carbamazepine 31-34 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 18096676-9 2008 The CBZ-modified CYP3A4 retained its functional activity albeit at a reduced level, but its testosterone 6beta-hydroxylase kinetics were altered from sigmoidal (a characteristic profile of substrate cooperativity) to near-hyperbolic (Michaelis-Menten) type, suggesting that CBZ may have modified CYP3A4 within its active site. Carbamazepine 4-7 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 296-302 18096676-9 2008 The CBZ-modified CYP3A4 retained its functional activity albeit at a reduced level, but its testosterone 6beta-hydroxylase kinetics were altered from sigmoidal (a characteristic profile of substrate cooperativity) to near-hyperbolic (Michaelis-Menten) type, suggesting that CBZ may have modified CYP3A4 within its active site. Carbamazepine 274-277 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 17-23 18096676-0 2008 CYP3A4-Mediated carbamazepine (CBZ) metabolism: formation of a covalent CBZ-CYP3A4 adduct and alteration of the enzyme kinetic profile. Carbamazepine 72-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 18096676-0 2008 CYP3A4-Mediated carbamazepine (CBZ) metabolism: formation of a covalent CBZ-CYP3A4 adduct and alteration of the enzyme kinetic profile. Carbamazepine 72-75 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82 18096676-2 2008 Sera of CBZ-hypersensitive patients often contain anti-CYP3A antibodies, including those to a CYP3A23 K-helix peptide that is also modified during peroxidative CYP3A4 heme-fragmentation. Carbamazepine 8-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 18096676-2 2008 Sera of CBZ-hypersensitive patients often contain anti-CYP3A antibodies, including those to a CYP3A23 K-helix peptide that is also modified during peroxidative CYP3A4 heme-fragmentation. Carbamazepine 8-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 18096676-2 2008 Sera of CBZ-hypersensitive patients often contain anti-CYP3A antibodies, including those to a CYP3A23 K-helix peptide that is also modified during peroxidative CYP3A4 heme-fragmentation. Heme 167-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 55-60 18096676-2 2008 Sera of CBZ-hypersensitive patients often contain anti-CYP3A antibodies, including those to a CYP3A23 K-helix peptide that is also modified during peroxidative CYP3A4 heme-fragmentation. Heme 167-171 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 160-166 18096676-3 2008 We explored the possibility that cytochromes P450 (P450s) such as CYP3A4 bioactivate CBZ to reactive metabolite(s) that irreversibly modify the P450 protein. Carbamazepine 85-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 66-72 18096676-6 2008 Incubation of CYP3A4 Supersomes with (3)H-CBZ resulted in its irreversible binding to CYP3A4 protein with a stoichiometry of 1.58 +/- 0.15 pmol (3)H-CBZ bound/pmol CYP3A4. (3)h-cbz 37-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 14-20 18096676-6 2008 Incubation of CYP3A4 Supersomes with (3)H-CBZ resulted in its irreversible binding to CYP3A4 protein with a stoichiometry of 1.58 +/- 0.15 pmol (3)H-CBZ bound/pmol CYP3A4. (3)h-cbz 37-45 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-92 18290640-3 2008 We developed a new combined model, MLite, for the prediction of regioselectivity in the cytochrome P450 3A4 mediated metabolism. mlite 35-40 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 88-107 17999057-8 2008 All are eliminated by hepatic metabolism involving mainly CYP2C9 (celecoxib, lumiracoxib) and CYP3A4 (etoricoxib). Etoricoxib 102-112 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 18195053-2 2008 TMC125 is an inducer of CYP3A and an inhibitor of CYP2C. etravirine 0-6 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 24-29 21279172-3 2008 The concomitant use of either CYP3A4 inducer rifampicin or CYP3A4 inhibitor erythromycin may influence the results of MEGX test. Rifampin 45-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 30-36 21279172-3 2008 The concomitant use of either CYP3A4 inducer rifampicin or CYP3A4 inhibitor erythromycin may influence the results of MEGX test. Erythromycin 76-88 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 59-65 21279172-4 2008 Hence, the objective of this study was to evaluate the effect of a CYP3A4 inhibitor erythromycin and inducer rifampicin on the MEGX test. Erythromycin 84-96 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 67-73 18218784-5 2008 Plasma concentrations of imidafenacin and M-2, the major metabolite of imidafenacin metabolized by CYP3A4, were determined. imidafenacin 71-83 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 99-105 18218784-8 2008 In conclusion, itraconazole increases the plasma concentrations of imidafenacin by inhibiting CYP3A4. Itraconazole 15-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 18218784-8 2008 In conclusion, itraconazole increases the plasma concentrations of imidafenacin by inhibiting CYP3A4. imidafenacin 67-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 94-100 18218784-9 2008 Therefore, itraconazole or potent CYP3A4 inhibitors should be carefully added to imidafenacin drug regimens. imidafenacin 81-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-40 18725509-10 2008 In conclusion, CYP3A4 was the major P450 isoform involved in MPA hydroxylation, with 6beta, 2beta, and 1beta being the possible hydroxylation sites. 6beta 85-90 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 18725509-10 2008 In conclusion, CYP3A4 was the major P450 isoform involved in MPA hydroxylation, with 6beta, 2beta, and 1beta being the possible hydroxylation sites. 2beta 92-97 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21 18725509-10 2008 In conclusion, CYP3A4 was the major P450 isoform involved in MPA hydroxylation, with 6beta, 2beta, and 1beta being the possible hydroxylation sites. 1,2-Di(anthracen-9-yl)ethyne 103-108 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 15-21