PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32415468-12 2020 CONCLUSION: CYP2B6 G516T and CYP3A4 *20,*22 polymorphisms could influence imatinib plasma concentrations and safety profile, after single-dose administration to healthy subjects. Imatinib Mesylate 74-82 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 32529309-5 2020 RESULTS: Curcumin demonstrated potent reversible inhibition of cytochrome P450 (CYP)3A4-mediated N-demethylation of imatinib and bosutinib and CYP2C8-mediated metabolism of imatinib with inhibitory constants (ki,u) of <=1.5 mumol. Imatinib Mesylate 116-124 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-87 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 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 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 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 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 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 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 26693810-8 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 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 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 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 24739665-6 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 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 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 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 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 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 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 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 23028140-6 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 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 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 22014153-8 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 22014153-9 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 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 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 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 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 22014153-5 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 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 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 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 17180388-0 2007 The effect of hydroxyurea on P-glycoprotein/BCRP-mediated transport and CYP3A metabolism of imatinib mesylate. Imatinib Mesylate 92-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-77 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 20054526-4 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 20054526-9 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 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 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 18094422-0 2007 Influence of CYP3A4 inhibition on the steady-state pharmacokinetics of imatinib. Imatinib Mesylate 71-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 13-19 18094422-1 2007 PURPOSE: To evaluate the effects of ritonavir, a potent inhibitor of CYP3A4, on the steady-state pharmacokinetics of imatinib. Imatinib Mesylate 117-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 69-75 18094422-7 2007 In vitro, imatinib was metabolized to the active metabolite CGP74588 by CYP3A4 and CYP3A5 and, to a lesser extent, by CYP2D6. Imatinib Mesylate 10-18 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 72-78 18094422-8 2007 Ritonavir (1 micromol/L) completely inhibited CYP3A4-mediated metabolism of imatinib to CGP74588 but inhibited metabolism in microsomes by only 50%. Imatinib Mesylate 76-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-52 18094422-9 2007 Imatinib significantly inhibited CYP3A4 activity in vitro. Imatinib Mesylate 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 33-39 17180388-3 2007 The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib. Imatinib Mesylate 131-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 303-321 17180388-3 2007 The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib. Imatinib Mesylate 131-139 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 323-328 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 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 16914578-16 2006 CYP3A4 inducers, such as EIAEDs, substantially decreased plasma exposure of imatinib and should be avoided in patients receiving imatinib for chronic myelogenous leukemia and gastrointestinal stromal tumors. Imatinib Mesylate 76-84 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 16914578-16 2006 CYP3A4 inducers, such as EIAEDs, substantially decreased plasma exposure of imatinib and should be avoided in patients receiving imatinib for chronic myelogenous leukemia and gastrointestinal stromal tumors. Imatinib Mesylate 129-137 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 12006504-11 2002 Cytochrome P-450 3A4 is the main enzyme responsible for imatinib metabolism. Imatinib Mesylate 56-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-20 16286749-6 2005 Imatinib is primarily metabolized by the cytochrome CYP3A4. Imatinib Mesylate 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58 16286749-7 2005 Voriconazole is a cytochrome CYP3A4 inhibitor and can lead to high plasma levels of imatinib. Imatinib Mesylate 84-92 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 29-35 15350151-5 2004 Drugs most prominently affected and contraindicated for concomitant use with St John"s wort are metabolised via both CYP3A4 and P-glycoprotein pathways, including HIV protease inhibitors, HIV non-nucleoside reverse transcriptase inhibitors (only CYP3A4), the immunosuppressants ciclosporin and tacrolimus, and the antineoplastic agents irinotecan and imatinib mesylate. Imatinib Mesylate 351-368 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 117-123 16890580-1 2006 OBJECTIVE: Our objective was to explore the relationships between imatinib pharmacokinetics and 9 allelic variants in 7 genes coding for adenosine triphosphate-binding cassette transporters (ABCB1 and ABCG2) and enzymes (cytochrome P450 [CYP] 2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) of putative relevance for imatinib. Imatinib Mesylate 66-74 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 265-271 16122278-10 2005 Imatinib is metabolised mainly by the cytochrome P450 (CYP) 3A4 or CYP3A5 and can competitively inhibit the metabolism of drugs that are CYP3A4 or CYP3A5 substrates. Imatinib Mesylate 0-8 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 137-143 15470331-2 2004 Because imatinib is predominantly metabolized by cytochrome P450 (CYP) 3A4, its pharmacokinetics may be altered when it is coadministered with drugs or herbs (eg, St John"s wort) that modulate CYP3A4 activity. Imatinib Mesylate 8-16 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 193-199 14605865-1 2004 OBJECTIVE: This study was carried out to investigate the influence of CYP3A induction with rifampicin on imatinib (Gleevec) exposure. Imatinib Mesylate 105-113 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-75 14605865-1 2004 OBJECTIVE: This study was carried out to investigate the influence of CYP3A induction with rifampicin on imatinib (Gleevec) exposure. Imatinib Mesylate 115-122 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 70-75 14612892-1 2003 The inhibition by imatinib of the cytochrome p450 3A4 isoenzyme may reduce the CYP3A4-mediated metabolic clearance of clinically important coadministered drugs. Imatinib Mesylate 18-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 34-53 14612892-1 2003 The inhibition by imatinib of the cytochrome p450 3A4 isoenzyme may reduce the CYP3A4-mediated metabolic clearance of clinically important coadministered drugs. Imatinib Mesylate 18-26 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 79-85 14612892-2 2003 The main purpose of this study was to evaluate the effect of the coadministration of imatinib on the pharmacokinetics of simvastatin, a probe CYP3A4 substrate. Imatinib Mesylate 85-93 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 14612892-11 2003 Caution is therefore required when administering imatinib with CYP3A4 substrates with a narrow therapeutic window. Imatinib Mesylate 49-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 63-69 34473615-6 2021 RESULTS: Imatinib exhibited the strongest inhibitory effect towards CYP3A, while the inhibitory potential of gefitinib and sunitinib were comparable to each other but weaker than imatinib. Imatinib Mesylate 9-17 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 34473615-6 2021 RESULTS: Imatinib exhibited the strongest inhibitory effect towards CYP3A, while the inhibitory potential of gefitinib and sunitinib were comparable to each other but weaker than imatinib. Imatinib Mesylate 179-187 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 68-73 34473615-12 2021 Therefore, caution should be taken when CYP3A-metabolizing drugs are co-administrated with imatinib, sunitinib, or gefitinib. Imatinib Mesylate 91-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 28261657-0 2016 Impact of CYP3A4*18 and CYP3A5*3 Polymorphisms on Imatinib Mesylate Response Among Chronic Myeloid Leukemia Patients in Malaysia. Imatinib Mesylate 50-67 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 10-16