PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
23413279-0	2013	The effect of CYP2C19 polymorphism on the safety, tolerability, and pharmacokinetics of tivantinib (ARQ 197): results from a phase I trial in advanced solid tumors.	ARQ 197	88-98	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21	
24169346-0	2013	CYP2C19 genotype-based phase I studies of a c-Met inhibitor tivantinib in combination with erlotinib, in advanced/metastatic non-small cell lung cancer.	ARQ 197	60-70	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7	
24169346-2	2013	Polymorphisms of CYP2C19, the key metabolic enzyme for tivantinib, should be addressed to translate the previous Western study to Asian population, because higher incidence of poor metabolisers (PMs) is reported in Asian population.	ARQ 197	55-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24	
24169346-11	2013	CONCLUSION: Two doses of tivantinib in combination with erlotinib were recommended based on CYP2C19 genotype: 360 mg BID for EMs and 240 mg BID for PMs.	ARQ 197	25-35	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	92-99	
25711511-1	2015	A c-Met inhibitor tivantinib is a candidate anticancer agent for patients with hepatocellular carcinoma (HCC), and CYP2C19 is the key metabolic enzyme for tivantinib.	ARQ 197	155-165	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	115-122	
23413279-1	2013	BACKGROUND: Tivantinib (formerly ARQ 197) is a selective inhibitor of c-Met mainly metabolized by CYP2C19.	ARQ 197	12-22	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	98-105	
27991432-5	2016	The concommitant use of omeprazole/esomeprazole, therefore, could have critical clinical relevance in individualizing medications metabolized primarily by CYP2C19 such as PPI, clopidogrel, phenytoin, cyclophosphamide, thalidomide, citalopram, clonazepam, diazepam, proguanil, tivantinib etc.	ARQ 197	276-286	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	155-162	
26899628-13	2016	The stereoselective hydroxylation by CYP2C19 and substrate stereoselectivity of ADH4-catalyzed oxidation in the in vitro metabolism of tivantinib was discovered.	ARQ 197	135-145	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	37-44	
26899628-0	2016	Stereoselective hydroxylation by CYP2C19 and oxidation by ADH4 in the in vitro metabolism of tivantinib.	ARQ 197	93-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40	
26899628-5	2016	The primary isoforms involved in the elimination of tivantinib were CYP2C19 and CYP3A4/5.	ARQ 197	52-62	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-75	
26899628-12	2016	In conclusion, CYP2C19, CYP3A4/5, UGT1A9 and ADH4 were the primary drug metabolizing enzymes involved in the in vitro metabolism of tivantinib and its metabolites.	ARQ 197	132-142	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	15-22