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