PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 33222380-0 2021 Pharmacoenhancement of Low Crizotinib Plasma Concentrations in Patients with Anaplastic Lymphoma Kinase-Positive Non-Small Cell Lung Cancer using the CYP3A Inhibitor Cobicistat. Crizotinib 27-37 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 150-155 33222380-3 2021 We investigated whether the CYP3A inhibitor cobicistat increases Cmin,ss of the CYP3A substrate crizotinib in patients with low exposure. Crizotinib 96-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 28-33 33222380-3 2021 We investigated whether the CYP3A inhibitor cobicistat increases Cmin,ss of the CYP3A substrate crizotinib in patients with low exposure. Crizotinib 96-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 80-85 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 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. 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. 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 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 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 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 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 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 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