PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25936586-3 2015 CTXA reversibly inhibited the CYP1A2-catalyzed phenacetin O-deethylation, CYP2C8-catalyzed paclitaxel 6-hydroxylation, and CYP2C9-catalyzed diclofenac 4"-hydroxylation with half-maximal inhibitory concentration (IC50) values of 3.9, 4.7, and 2.9 microM, respectively. Diclofenac 140-150 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 30-36 29027194-2 2018 The aim of this study was to characterize the pediatric predictive performance of the PBPK approach for 10 drugs extensively metabolized by CYP1A2 (theophylline), CYP2C8 (desloratidine, montelukast), CYP2C9 (diclofenac), CYP2C19 (esomeprazole, lansoprazole), CYP2D6 (tramadol), and CYP3A4 (itraconazole, ondansetron, sufentanil). Diclofenac 208-218 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 140-146 20877236-4 2010 Eupatilin and jaceosidin potently inhibited CYP1A2-catalyzed phenacetin O-deethylation with 50% inhibitory concentration (IC(50)) values of 9.4 microM and 5.3 microM, respectively, and CYP2C9-catalyzed diclofenac 4-hydroxylation with IC(50) values of 4.1 microM and 10.2 microM, respectively. Diclofenac 202-212 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 44-50 23777257-0 2014 Drug interactions of diclofenac and its oxidative metabolite with human liver microsomal cytochrome P450 1A2-dependent drug oxidation. Diclofenac 21-31 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 89-108 23777257-2 2014 The purpose of this study was to investigate the inhibitory effects of diclofenac on human cytochrome P450 1A2-, 2C19- and 3A4-mediated drug oxidations and to evaluate the drug interaction potential of diclofenac and 4"-hydroxydiclofenac. Diclofenac 71-81 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 91-110 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). Diclofenac 82-92 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 186-192 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. Diclofenac 183-193 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 79-85 12781337-5 2003 The results indicated that there was approximately one order of magnitude of interindividual variation in the expression of CYP1A2 and UGT2B7, activity of the enzymes toward DMXAA, and inhibition potency (IC(50)) by diclofenac, cyproheptadine, and alpha-naphthoflavone. Diclofenac 216-226 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 124-130 17542019-2 2007 Probe substrates were phenacetin, diclofenac, S-mephenytoin, and dextromethorphan for CYP1A2, CYP2C9, CYP2C19, and CYP2D6, respectively. Diclofenac 34-44 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 86-92 16049126-4 2005 Phenacetin, diclofenac, S-mephenytoin, bufuralol, and midazolam are used as substrates for CYP1A2, 2C9, 2C19, 2D6, and 3A4, and the assay differentiates between reversible and irreversible inhibition. Diclofenac 12-22 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 91-97 15618695-7 2002 In contrast, the inhibitory effects of phenacetin, diclofenac, S-mephenytoin, dextromethorphan, bufuralol and terfenadine, typical substrates for CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4, respectively, on each recombinant CYP activity decreased after preincubation. Diclofenac 51-61 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 146-152