PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26857559-0 2016 A pharmacogenetic pilot study reveals MTHFR, DRD3, and MDR1 polymorphisms as biomarker candidates for slow atorvastatin metabolizers. Atorvastatin 107-119 ATP binding cassette subfamily B member 1 Homo sapiens 55-59 26857559-8 2016 Six gene polymorphisms were found to have a significant effect on ATV pharmacokinetics: MTHFR (rs1801133), DRD3 (rs6280), GSTM3 (rs1799735), TNFalpha (rs1800629), MDR1 (rs1045642), and SLCO1B1 (rs4149056). Atorvastatin 66-69 ATP binding cassette subfamily B member 1 Homo sapiens 163-167 26857559-9 2016 The combination of MTHFR, DRD3 and MDR1 polymorphisms associated with a slow ATV metabolizer phenotype. Atorvastatin 77-80 ATP binding cassette subfamily B member 1 Homo sapiens 35-39 23677857-0 2013 Do MDR1 and SLCO1B1 polymorphisms influence the therapeutic response to atorvastatin? Atorvastatin 72-84 ATP binding cassette subfamily B member 1 Homo sapiens 3-7 24414406-0 2015 The role of Multidrug Resistance-1 (MDR1) variants in response to atorvastatin among Jordanians. Atorvastatin 66-78 ATP binding cassette subfamily B member 1 Homo sapiens 12-34 24414406-0 2015 The role of Multidrug Resistance-1 (MDR1) variants in response to atorvastatin among Jordanians. Atorvastatin 66-78 ATP binding cassette subfamily B member 1 Homo sapiens 36-40 24414406-2 2015 The P-gp has wide substrate specificity for multiple medications including the lipid lowering drug, atorvastatin. Atorvastatin 100-112 ATP binding cassette subfamily B member 1 Homo sapiens 4-8 24414406-3 2015 In this study, we investigated the possible association between three common MDR1 gene polymorphisms (G2677T, C3435T, and C1236T), and the lipid lowering effect of atorvastatin among Jordanians. Atorvastatin 164-176 ATP binding cassette subfamily B member 1 Homo sapiens 77-81 24414406-9 2015 In conclusion, the MDR1 gene polymorphisms G2677T, and C3435T, but not C1236T were associated with the lipid lowering effect of atorvastatin among Jordanians. Atorvastatin 128-140 ATP binding cassette subfamily B member 1 Homo sapiens 19-23 24452746-3 2014 Atorvastatin is metabolized primarily by CYP3A4 and is a P-gp inhibitor. Atorvastatin 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 57-61 23677857-5 2013 OBJECTIVE: To examine the impact of polymorphisms of the multidrug resistance 1(MDR1) and solute carrier organic anion transporter 1B1 (SLCO1B1) genes on the therapeutic response to atorvastatin as well as the presence of gender-gene interaction. Atorvastatin 182-194 ATP binding cassette subfamily B member 1 Homo sapiens 80-84 21447733-8 2011 Results indicate that atorvastatin, fluvastatin, and rosuvastatin were transported by P-gp, BCRP, and MRP2. Atorvastatin 22-34 ATP binding cassette subfamily B member 1 Homo sapiens 86-90 23751277-6 2013 Atorvastatin increased the expression of both ABCB1 and ABCG2 by more than 2-fold (P < 0.05). Atorvastatin 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 46-51 23751277-9 2013 Here we show for the first time that atorvastatin treatment leads to increased expression of the membrane transporters SLCO2B1, ABCB1, and ABCG2 in human liver tissue, which potentially may counteract the efficacy of the treatment, and our findings may cast light on the mechanisms of clinical problems with adverse reactions and drug interactions in statin treatment. Atorvastatin 37-49 ATP binding cassette subfamily B member 1 Homo sapiens 128-133 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 ATP binding cassette subfamily B member 1 Homo sapiens 92-96 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 ATP binding cassette subfamily B member 1 Homo sapiens 142-146 23379020-0 2013 MDR1 and LPL genetic variants are associated with unfavorable outcome in stroke patients under atorvastatin treatment. Atorvastatin 95-107 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 22810051-0 2012 Genetic variation in MDR1, LPL and eNOS genes and the response to atorvastatin treatment in ischemic stroke. Atorvastatin 66-78 ATP binding cassette subfamily B member 1 Homo sapiens 21-25 22810051-7 2012 A significant association of MDR1 and LPL gene variants with bad outcome in stroke patients on atorvastatin therapy was found. Atorvastatin 95-107 ATP binding cassette subfamily B member 1 Homo sapiens 29-33 22810051-10 2012 In conclusion the individuals with HindIII (-/-) genotype of LPL and CC genotype of MDR1 gene would benefit more from atorvastatin therapy. Atorvastatin 118-130 ATP binding cassette subfamily B member 1 Homo sapiens 84-88 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 ATP binding cassette subfamily B member 1 Homo sapiens 127-141 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 ATP binding cassette subfamily B member 1 Homo sapiens 71-76 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 ATP binding cassette subfamily B member 1 Homo sapiens 39-44 21351272-9 2010 By contrast, while atorvastatin inhibited substrate transport by purified P-gp in proteoliposomes, it had no effect on doxorubicin transport in MDR tumor cells. Atorvastatin 19-31 ATP binding cassette subfamily B member 1 Homo sapiens 74-78 21392722-0 2011 The C3435T polymorphism in ABCB1 influences atorvastatin efficacy and muscle symptoms in a high-risk vascular cohort. Atorvastatin 44-56 ATP binding cassette subfamily B member 1 Homo sapiens 27-32 21392722-1 2011 OBJECTIVE: The CC genotype of the C3435T polymorphism in ABCB1 is associated with increased P-glycoprotein expression, reduced low-density lipoprotein cholesterol (LDL-C) response to atorvastatin, and a reduced area-under-the-curve in pharmacokinetic studies. Atorvastatin 183-195 ATP binding cassette subfamily B member 1 Homo sapiens 57-62 21392722-12 2011 CONCLUSION: In patients treated with atorvastatin, the CC genotype at the C3435T polymorphism in ABCB1 is associated with reduced atorvastatin efficacy independently of cholesterol metabolism. Atorvastatin 37-49 ATP binding cassette subfamily B member 1 Homo sapiens 97-102 21392722-12 2011 CONCLUSION: In patients treated with atorvastatin, the CC genotype at the C3435T polymorphism in ABCB1 is associated with reduced atorvastatin efficacy independently of cholesterol metabolism. Atorvastatin 130-142 ATP binding cassette subfamily B member 1 Homo sapiens 97-102 20040338-0 2010 Effects of SLCO1B1 and ABCB1 genotypes on the pharmacokinetics of atorvastatin and 2-hydroxyatorvastatin in healthy Korean subjects. Atorvastatin 66-78 ATP binding cassette subfamily B member 1 Homo sapiens 23-28 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 ATP binding cassette subfamily B member 1 Homo sapiens 111-116 20040338-1 2010 OBJECTIVE: This study aimed to evaluate the effect of genetic polymorphisms of SLCO1B1 and ABCB1 on the pharmacokinetics of atorvastatin and its metabolites. Atorvastatin 124-136 ATP binding cassette subfamily B member 1 Homo sapiens 91-96 20040338-8 2010 For ABCB1 genotypes, the half-lives of atorvastatin, atorvastatin lactone, 2-hydroxyatorvastatin and 2-hydroxyatorvastatin lactone were significantly longer in c.2677TT-c.3435TT (n = 3) vs. c.2677GG-c.3435CC and c.2677GT-c.3435CT (n = 10), yielding p = 0.049, 0.007, 0.007 and 0.007, respectively. Atorvastatin 39-51 ATP binding cassette subfamily B member 1 Homo sapiens 4-9 19394420-0 2009 Decreased ABCB1 mRNA expression induced by atorvastatin results from enhanced mRNA degradation in HepG2 cells. Atorvastatin 43-55 ATP binding cassette subfamily B member 1 Homo sapiens 10-15 19802823-1 2010 PURPOSE: Simvastatin and atorvastatin are metabolized by the CYP3A4 enzyme and transported by the ABCB1 transporter. Atorvastatin 25-37 ATP binding cassette subfamily B member 1 Homo sapiens 98-103 19802823-2 2010 We studied whether the polymorphism CYP3A4*1B and the polymorphisms C1236T, G2677A/T and C3435T in the ABCB1 gene were associated with a decrease of the prescribed dose or a switch to another cholesterol lowering drug during simvastatin and atorvastatin therapy. Atorvastatin 241-253 ATP binding cassette subfamily B member 1 Homo sapiens 103-108 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 ATP binding cassette subfamily B member 1 Homo sapiens 184-189 19543298-3 2009 In this study, the effects of atorvastatin and simvastatin on mRNA expression of efflux (ABCB1, ABCG2 and ABCC2) and uptake (SLCO1B1, SLCO2B1 and SLC22A1) drug transporters in Caco-2 and HepG2 cells were investigated. Atorvastatin 30-42 ATP binding cassette subfamily B member 1 Homo sapiens 89-94 19394420-1 2009 The mechanisms underlying atorvastatin supression of ABCB1 gene expression, at transcriptional and post-transcriptional levels of ABCB1 gene in HepG2 (human hepatocellular carcinoma) cells were investigated. Atorvastatin 26-38 ATP binding cassette subfamily B member 1 Homo sapiens 53-58 19394420-5 2009 Exposure to atorvastatin for 24h resulted in a dose-dependent decrease of ABCB1 mRNA and protein levels, which was not abolished by addition of farnesyl or geranylgeranyl pyrophosphate. Atorvastatin 12-24 ATP binding cassette subfamily B member 1 Homo sapiens 74-79 19394420-6 2009 After removing fetal bovine serum from the media, however, ABCB1 expression was decreased by 2-fold in either HepG2 cells treated and non-treated with atorvastatin. Atorvastatin 151-163 ATP binding cassette subfamily B member 1 Homo sapiens 59-64 19394420-10 2009 mRNA stability studies revealed that ABCB1 mRNA degradation was increased in 1, 10 and 20muM atorvastatin-treated versus control cells (half-lives of 2h versus 7h). Atorvastatin 93-105 ATP binding cassette subfamily B member 1 Homo sapiens 37-42 19394420-11 2009 Therefore, evidence is provided that decreased mRNA stability by atorvastatin treatment may explain the decrease in ABCB1 transcript levels. Atorvastatin 65-77 ATP binding cassette subfamily B member 1 Homo sapiens 116-121 19238649-0 2008 ABCB1 haplotypes differentially affect the pharmacokinetics of the acid and lactone forms of simvastatin and atorvastatin. Atorvastatin 109-121 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 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 ATP binding cassette subfamily B member 1 Homo sapiens 172-186 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 ATP binding cassette subfamily B member 1 Homo sapiens 188-191 18851956-0 2009 ABCB1 and ABCC1 expression in peripheral mononuclear cells is influenced by gene polymorphisms and atorvastatin treatment. Atorvastatin 99-111 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 18851956-1 2009 This study investigated the effects of atorvastatin on ABCB1 and ABCC1 mRNA expression on peripheral blood mononuclear cells (PBMC) and their relationship with gene polymorphisms and lowering-cholesterol response. Atorvastatin 39-51 ATP binding cassette subfamily B member 1 Homo sapiens 55-60 18851956-6 2009 After atorvastatin treatment, both ABCB1 and ABCC1 genes showed 50% reduction of the mRNA expression (p<0.05). Atorvastatin 6-18 ATP binding cassette subfamily B member 1 Homo sapiens 35-40 18851956-9 2009 ABCB1 substrates or inhibitors did not affect the baseline expression, while ABCB1 inhibitors reversed the effects of atorvastatin on both ABCB1 and ABCC1 transporters. Atorvastatin 118-130 ATP binding cassette subfamily B member 1 Homo sapiens 77-82 18851956-9 2009 ABCB1 substrates or inhibitors did not affect the baseline expression, while ABCB1 inhibitors reversed the effects of atorvastatin on both ABCB1 and ABCC1 transporters. Atorvastatin 118-130 ATP binding cassette subfamily B member 1 Homo sapiens 77-82 18851956-10 2009 In conclusion, ABCB1 and ABCC1 mRNA levels in PBMC are modulated by atorvastatin and ABCB1 G2677T/A polymorphism and ABCB1 baseline expression is related to differences in serum LDL cholesterol and apoB in response to atorvastatin. Atorvastatin 68-80 ATP binding cassette subfamily B member 1 Homo sapiens 15-20 18851956-10 2009 In conclusion, ABCB1 and ABCC1 mRNA levels in PBMC are modulated by atorvastatin and ABCB1 G2677T/A polymorphism and ABCB1 baseline expression is related to differences in serum LDL cholesterol and apoB in response to atorvastatin. Atorvastatin 218-230 ATP binding cassette subfamily B member 1 Homo sapiens 15-20 18851956-10 2009 In conclusion, ABCB1 and ABCC1 mRNA levels in PBMC are modulated by atorvastatin and ABCB1 G2677T/A polymorphism and ABCB1 baseline expression is related to differences in serum LDL cholesterol and apoB in response to atorvastatin. Atorvastatin 218-230 ATP binding cassette subfamily B member 1 Homo sapiens 85-90 18851956-10 2009 In conclusion, ABCB1 and ABCC1 mRNA levels in PBMC are modulated by atorvastatin and ABCB1 G2677T/A polymorphism and ABCB1 baseline expression is related to differences in serum LDL cholesterol and apoB in response to atorvastatin. Atorvastatin 218-230 ATP binding cassette subfamily B member 1 Homo sapiens 85-90 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 ATP binding cassette subfamily B member 1 Homo sapiens 27-41 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 ATP binding cassette subfamily B member 1 Homo sapiens 43-47 18703021-7 2008 A number of Pgp substrates (quinidine, amprenavir, irinotecan, topotecan, atorvastatin and erythromycin) induced net digoxin secretion, as did the non-Pgp substrate artemisinin. Atorvastatin 74-86 ATP binding cassette subfamily B member 1 Homo sapiens 12-15 18703021-9 2008 Of the compounds that increased Pgp secretion, quinidine, topotecan, atorvastatin and amprenavir pre-exposure also elevated MDR1 mRNA levels, whereas erythromycin, irinotecan and artemisinin displayed no change in transcript levels. Atorvastatin 69-81 ATP binding cassette subfamily B member 1 Homo sapiens 32-35 18703021-9 2008 Of the compounds that increased Pgp secretion, quinidine, topotecan, atorvastatin and amprenavir pre-exposure also elevated MDR1 mRNA levels, whereas erythromycin, irinotecan and artemisinin displayed no change in transcript levels. Atorvastatin 69-81 ATP binding cassette subfamily B member 1 Homo sapiens 124-128 19238649-3 2008 The simvastatin acid AUC(0-12h) was 60% larger, the atorvastatin AUC(0-infinity) 55% larger, and the atorvastatin half-life 24% longer in subjects with the ABCB1 TTT/TTT genotype (n = 12) than in those with the CGC/CGC genotype (n = 12) (P < 0.05), but there were no differences between the two genotypes with respect to the pharmacokinetics of the lactones of these drugs. Atorvastatin 52-64 ATP binding cassette subfamily B member 1 Homo sapiens 156-161 19238649-3 2008 The simvastatin acid AUC(0-12h) was 60% larger, the atorvastatin AUC(0-infinity) 55% larger, and the atorvastatin half-life 24% longer in subjects with the ABCB1 TTT/TTT genotype (n = 12) than in those with the CGC/CGC genotype (n = 12) (P < 0.05), but there were no differences between the two genotypes with respect to the pharmacokinetics of the lactones of these drugs. Atorvastatin 101-113 ATP binding cassette subfamily B member 1 Homo sapiens 156-161 15497697-0 2004 Interactions of human P-glycoprotein with simvastatin, simvastatin acid, and atorvastatin. Atorvastatin 77-89 ATP binding cassette subfamily B member 1 Homo sapiens 22-36 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 ATP binding cassette subfamily B member 1 Homo sapiens 182-186 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 ATP binding cassette subfamily B member 1 Homo sapiens 113-117 16996216-0 2006 Down-regulation of ABCB1 transporter by atorvastatin in a human hepatoma cell line and in human peripheral blood mononuclear cells. Atorvastatin 40-52 ATP binding cassette subfamily B member 1 Homo sapiens 19-24 16996216-1 2006 PURPOSE: The effect of atorvastatin, an HMG-CoA reductase inhibitor, on expression and activity of the drug transporter ABCB1 in HepG2 cells and peripheral blood mononuclear cells (PBMCs) was examined. Atorvastatin 23-35 ATP binding cassette subfamily B member 1 Homo sapiens 120-125 16996216-3 2006 Expression of ABCB1 mRNA and ABCB1 activity were examined in atorvastatin-treated and control cells and PBMCs using real-time PCR and Rhodamine 123 efflux assay. Atorvastatin 61-73 ATP binding cassette subfamily B member 1 Homo sapiens 14-19 16996216-5 2006 Atorvastatin at 10 and 20 microM up-regulated ABCB1 expression resulting in a significant 1.4-fold increase of the protein levels. Atorvastatin 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 46-51 16996216-6 2006 Treatment of HepG2 cells with 20 microM atorvastatin caused a 60% reduction on mRNA expression (p<0.05) and a 41% decrease in ABCB1-mediated efflux of Rhodamine123 (p<0.01) by flow cytometry. Atorvastatin 40-52 ATP binding cassette subfamily B member 1 Homo sapiens 129-134 16996216-9 2006 Atorvastatin leads to decreased ABCB1 function and modulates ABCB1 synthesis in HepG2 cells and in PBMCs. Atorvastatin 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 32-37 16996216-9 2006 Atorvastatin leads to decreased ABCB1 function and modulates ABCB1 synthesis in HepG2 cells and in PBMCs. Atorvastatin 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 61-66 16996216-10 2006 ABCB1 plays a role in cellular protection as well as in secretion and/or disposition, therefore, inhibition of ABCB1 synthesis may increase the atorvastatin efficacy, leading to a more pronounced reduction of plasma cholesterol. Atorvastatin 144-156 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 16996216-10 2006 ABCB1 plays a role in cellular protection as well as in secretion and/or disposition, therefore, inhibition of ABCB1 synthesis may increase the atorvastatin efficacy, leading to a more pronounced reduction of plasma cholesterol. Atorvastatin 144-156 ATP binding cassette subfamily B member 1 Homo sapiens 111-116 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 ATP binding cassette subfamily B member 1 Homo sapiens 81-95 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 ATP binding cassette subfamily B member 1 Homo sapiens 97-101 16103896-5 2005 The only significant associations with LDL-C lowering were found with apoE2 in which carriers of the rare allele who took atorvastatin lowered their LDL-C by 3.5% more than those homozygous for the common allele and with rs2032582 (S893A in ABCB1) in which the two groups of homozygotes differed by 3% in LDL-C lowering. Atorvastatin 122-134 ATP binding cassette subfamily B member 1 Homo sapiens 241-246 15497697-1 2004 PURPOSE: In this study, P-glycoprotein (P-gp) mediated efflux of simvastatin (SV), simvastatin acid (SVA), and atorvastatin (AVA) and inhibition of P-gp by SV, SVA, and AVA were evaluated to assess the role of P-gp in drug interactions. Atorvastatin 111-123 ATP binding cassette subfamily B member 1 Homo sapiens 24-38 15497697-1 2004 PURPOSE: In this study, P-glycoprotein (P-gp) mediated efflux of simvastatin (SV), simvastatin acid (SVA), and atorvastatin (AVA) and inhibition of P-gp by SV, SVA, and AVA were evaluated to assess the role of P-gp in drug interactions. Atorvastatin 111-123 ATP binding cassette subfamily B member 1 Homo sapiens 40-44 15497697-1 2004 PURPOSE: In this study, P-glycoprotein (P-gp) mediated efflux of simvastatin (SV), simvastatin acid (SVA), and atorvastatin (AVA) and inhibition of P-gp by SV, SVA, and AVA were evaluated to assess the role of P-gp in drug interactions. Atorvastatin 111-123 ATP binding cassette subfamily B member 1 Homo sapiens 148-152 15497697-1 2004 PURPOSE: In this study, P-glycoprotein (P-gp) mediated efflux of simvastatin (SV), simvastatin acid (SVA), and atorvastatin (AVA) and inhibition of P-gp by SV, SVA, and AVA were evaluated to assess the role of P-gp in drug interactions. Atorvastatin 111-123 ATP binding cassette subfamily B member 1 Homo sapiens 148-152 15497697-1 2004 PURPOSE: In this study, P-glycoprotein (P-gp) mediated efflux of simvastatin (SV), simvastatin acid (SVA), and atorvastatin (AVA) and inhibition of P-gp by SV, SVA, and AVA were evaluated to assess the role of P-gp in drug interactions. Atorvastatin 125-128 ATP binding cassette subfamily B member 1 Homo sapiens 40-44 15497697-1 2004 PURPOSE: In this study, P-glycoprotein (P-gp) mediated efflux of simvastatin (SV), simvastatin acid (SVA), and atorvastatin (AVA) and inhibition of P-gp by SV, SVA, and AVA were evaluated to assess the role of P-gp in drug interactions. Atorvastatin 125-128 ATP binding cassette subfamily B member 1 Homo sapiens 148-152 15497697-1 2004 PURPOSE: In this study, P-glycoprotein (P-gp) mediated efflux of simvastatin (SV), simvastatin acid (SVA), and atorvastatin (AVA) and inhibition of P-gp by SV, SVA, and AVA were evaluated to assess the role of P-gp in drug interactions. Atorvastatin 125-128 ATP binding cassette subfamily B member 1 Homo sapiens 148-152 34403130-5 2022 We find that variants in drug transporter genes (SLCO1B1 and ABCB1) positively impacted atorvastatin and simvastatin response, whereas variants in genes of drug metabolizing enzymes (CYP3A5) decreased response. Atorvastatin 88-100 ATP binding cassette subfamily B member 1 Homo sapiens 61-66 15081455-0 2004 Polymorphisms in the multidrug resistance-1 (MDR1) gene influence the response to atorvastatin treatment in a gender-specific manner. Atorvastatin 82-94 ATP binding cassette subfamily B member 1 Homo sapiens 21-43 15081455-0 2004 Polymorphisms in the multidrug resistance-1 (MDR1) gene influence the response to atorvastatin treatment in a gender-specific manner. Atorvastatin 82-94 ATP binding cassette subfamily B member 1 Homo sapiens 45-49 15081455-1 2004 To test the hypothesis that variations in the multidrug resistance-1 gene influence the response to statin treatment, 2 prevalent polymorphisms (G2677T/A and C3435T) were examined in 344 hypercholesterolemic patients treated with atorvastatin (10 mg). Atorvastatin 230-242 ATP binding cassette subfamily B member 1 Homo sapiens 46-68 10631627-0 2000 Atorvastatin coadministration may increase digoxin concentrations by inhibition of intestinal P-glycoprotein-mediated secretion. Atorvastatin 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 94-108 10631627-7 2000 Since atorvastatin is a CYP3A4 substrate and many CYP3A4 substrates are also substrates for P-glycoprotein transport, the influence of atorvastatin and its metabolites on P-glycoprotein-mediated digoxin transport in monolayers of the human colon carcinoma (Caco-2) cell line was investigated. Atorvastatin 6-18 ATP binding cassette subfamily B member 1 Homo sapiens 171-185 10631627-9 2000 Atorvastatin (100 microM) inhibited digoxin secretion (transport from the basolateral to apical aspect of the monolayer) by 58%, equivalent to the extent of inhibition observed with verapamil, a known inhibitor of P-glycoprotein transport. Atorvastatin 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 214-228 12773066-12 2003 The pharmacokinetic profiles of these agents suggest that a possible contribution to this reaction was P-glycoprotein (PGP) inhibition by esomeprazole altering atorvastatin"s normally significant first-pass clearance. Atorvastatin 160-172 ATP binding cassette subfamily B member 1 Homo sapiens 103-117 12773066-12 2003 The pharmacokinetic profiles of these agents suggest that a possible contribution to this reaction was P-glycoprotein (PGP) inhibition by esomeprazole altering atorvastatin"s normally significant first-pass clearance. Atorvastatin 160-172 ATP binding cassette subfamily B member 1 Homo sapiens 119-122 12773066-13 2003 CONCLUSIONS: PGP drug interactions with atorvastatin and other hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) may be associated with unreported risks for RML. Atorvastatin 40-52 ATP binding cassette subfamily B member 1 Homo sapiens 13-16 10751037-0 2000 Atorvastatin transport in the Caco-2 cell model: contributions of P-glycoprotein and the proton-monocarboxylic acid co-transporter. Atorvastatin 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 66-80 10751037-5 2000 Cyclosporin A (20 microM) was present in the uptake media to block potential P-glycoprotein-mediated atorvastatin efflux. Atorvastatin 101-113 ATP binding cassette subfamily B member 1 Homo sapiens 77-91 10751037-8 2000 The B-to-A permeability of atorvastatin was significantly reduced by cyclosporin A (10 microM), verapamil (100 microM), and a P-glycoprotein specific monoclonal antibody, UIC2(10 microg/ml) (43%, 25%, and 13%, respectively). Atorvastatin 27-39 ATP binding cassette subfamily B member 1 Homo sapiens 126-140 10751037-17 2000 CONCLUSION: This study demonstrated that atorvastatin was secreted across the apical surface of Caco-2 cell monolayers via P-glycoprotein-mediated efflux and transported across the apical membrane in the absorptive direction via a H(+)-monocarboxylic acid cotransporter (MCT). Atorvastatin 41-53 ATP binding cassette subfamily B member 1 Homo sapiens 123-137 10751037-18 2000 In addition, this study provided the first evidence that negatively charged compounds, such as atorvastatin, can be a substrate for P-glycoprotein. Atorvastatin 95-107 ATP binding cassette subfamily B member 1 Homo sapiens 132-146 34162690-5 2021 In our study, apically expressed breast cancer resistance protein (BCRP) and P-glycoprotein (P-gp) transported atorvastatin, fluvastatin, pitavastatin, and rosuvastatin. Atorvastatin 111-123 ATP binding cassette subfamily B member 1 Homo sapiens 77-91 34162690-5 2021 In our study, apically expressed breast cancer resistance protein (BCRP) and P-glycoprotein (P-gp) transported atorvastatin, fluvastatin, pitavastatin, and rosuvastatin. Atorvastatin 111-123 ATP binding cassette subfamily B member 1 Homo sapiens 93-97 34162690-9 2021 For atorvastatin, the corresponding values for P-gp-mediated efflux were 32-73% and 56%, respectively. Atorvastatin 4-16 ATP binding cassette subfamily B member 1 Homo sapiens 47-51 34162690-11 2021 These data indicate that BCRP may play an important role in limiting the intestinal absorption and facilitating the biliary excretion of rosuvastatin and that P-gp may restrict the intestinal absorption and mediate the biliary excretion of atorvastatin. Atorvastatin 240-252 ATP binding cassette subfamily B member 1 Homo sapiens 159-163 33459228-7 2021 The statins like Simvastatin, Lovastatin, and Atorvastatin are substrates of CYP3A4 enzyme and P-glycoprotein and their concomitant use with the drugs inhibiting or inducing them would result in changes in plasma concentrations and toxicity/efficacy. Atorvastatin 46-58 ATP binding cassette subfamily B member 1 Homo sapiens 95-109 28833323-0 2018 Transporter genes ABCG2 rs2231142 and ABCB1 rs1128503 polymorphisms and atorvastatin response in Chilean subjects. Atorvastatin 72-84 ATP binding cassette subfamily B member 1 Homo sapiens 38-43 32275773-6 2020 Cancer patients treated with paclitaxel and P-gp inhibitors had a 2.4-fold (95% confidence interval (CI): 1.3-4.3) increased risk of peripheral neuropathy-induced dose modification, a 4.7-fold (95% CI: 1.9-11.9) increased risk for patients treated with strong P-gp inhibitors and a 7.0-fold (95% CI: 2.3-21.5) increased risk in patients treated with atorvastatin. Atorvastatin 350-362 ATP binding cassette subfamily B member 1 Homo sapiens 44-48 31574240-0 2020 Association of ABCB1 polymorphisms with lipid homeostasis and liver injury response to atorvastatin in the Chinese population. Atorvastatin 87-99 ATP binding cassette subfamily B member 1 Homo sapiens 15-20 31084979-7 2019 The most frequent interactions were amiodarone-statin for CYP3A4 and atorvastatin-verapamil-diltiazem for P-gp. Atorvastatin 69-81 ATP binding cassette subfamily B member 1 Homo sapiens 106-110 31298164-0 2019 Association of SLCO1B1 and ABCB1 Genetic Variants with Atorvastatin-induced Myopathy in Patients with Acute Ischemic Stroke. Atorvastatin 55-67 ATP binding cassette subfamily B member 1 Homo sapiens 27-32 28833323-3 2018 We aimed to investigate the influence of two single nucleotide polymorphisms (SNP) (ABCB1 rs1128503 and ABCG2 rs2231142) in the ABC transporter genes on response to short-term low-dose atorvastatin in Chilean hypercholesterolaemic patients. Atorvastatin 185-197 ATP binding cassette subfamily B member 1 Homo sapiens 84-89 27575876-0 2016 Atorvastatin attenuation of ABCB1 expression is mediated by microRNA miR-491-3p in Caco-2 cells. Atorvastatin 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 28-33 27238935-0 2017 Association of ABCB1 (C3435T) and ABCC1 (G2012T) Polymorphisms with Clinical Response to Atorvastatin in Iranian Patients with Primary Hyperlipidemia. Atorvastatin 89-101 ATP binding cassette subfamily B member 1 Homo sapiens 15-20 27238935-3 2017 This study investigated the association of ABCB1 (C3435T) and ABCC1 (G2012T) polymorphisms with clinical response to atorvastatin in Iranian primary hyperlipidemic patients. Atorvastatin 117-129 ATP binding cassette subfamily B member 1 Homo sapiens 43-48 27575876-1 2016 AIM: Atorvastatin, a HMG-CoA reductase inhibitor, used in the treatment of hypercholesterolemia, has been previously shown to regulate ABCB1 expression in vivo and in vitro. Atorvastatin 5-17 ATP binding cassette subfamily B member 1 Homo sapiens 135-140 27575876-3 2016 METHODS: Expression of microRNAs and ABCB1 mRNA was examined in atorvastatin-treated and control cells using real-time PCR. Atorvastatin 64-76 ATP binding cassette subfamily B member 1 Homo sapiens 37-42 27575876-9 2016 Finally, functional analysis revealed that treatment with miR-491-3p inhibitor could reverses atorvastatin attenuation of ABCB1 (Pg-p) protein levels. Atorvastatin 94-106 ATP binding cassette subfamily B member 1 Homo sapiens 122-127 27575876-10 2016 CONCLUSION: Our results suggest atorvastatin control ABCB1 expression via miR-491-3p in Caco-2 cells. Atorvastatin 32-44 ATP binding cassette subfamily B member 1 Homo sapiens 53-58 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 ATP binding cassette subfamily B member 1 Homo sapiens 74-79 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 ATP binding cassette subfamily B member 1 Homo sapiens 168-173 27296832-0 2016 ABCB1 polymorphism is associated with atorvastatin-induced liver injury in Japanese population. Atorvastatin 38-50 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 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 ATP binding cassette subfamily B member 1 Homo sapiens 239-244 27296832-3 2016 The cytotoxicity test demonstrated that IC50 value of atorvastatin to inhibit the growth and/or viability of Flp-In-293/ABCB1 (2677G) cells was 5.44 +- 0.10 mM, which was significantly lower than those in Flp-In-293/ABCB1 (2677 T) (6.02 +- 0.07 mM) and Flp-In-293/ABCB1 (2677A) cells (5.95 +- 0.08 mM). Atorvastatin 54-66 ATP binding cassette subfamily B member 1 Homo sapiens 120-125 27296832-3 2016 The cytotoxicity test demonstrated that IC50 value of atorvastatin to inhibit the growth and/or viability of Flp-In-293/ABCB1 (2677G) cells was 5.44 +- 0.10 mM, which was significantly lower than those in Flp-In-293/ABCB1 (2677 T) (6.02 +- 0.07 mM) and Flp-In-293/ABCB1 (2677A) cells (5.95 +- 0.08 mM). Atorvastatin 54-66 ATP binding cassette subfamily B member 1 Homo sapiens 216-221 27296832-3 2016 The cytotoxicity test demonstrated that IC50 value of atorvastatin to inhibit the growth and/or viability of Flp-In-293/ABCB1 (2677G) cells was 5.44 +- 0.10 mM, which was significantly lower than those in Flp-In-293/ABCB1 (2677 T) (6.02 +- 0.07 mM) and Flp-In-293/ABCB1 (2677A) cells (5.95 +- 0.08 mM). Atorvastatin 54-66 ATP binding cassette subfamily B member 1 Homo sapiens 216-221