PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30690726-0	2019	Physiologically Based Pharmacokinetic Modeling Approach to Predict Drug-Drug Interactions With Ethionamide Involving Impact of Genetic Polymorphism on FMO3.	Ethionamide	95-106	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	151-155	
30690726-7	2019	Compared to the wild type, recombinant Lys158 -FMO3 and Gly308 -FMO3 variants significantly decreased the intrinsic clearance of ethionamide by 2% and 24%, respectively.	Ethionamide	129-140	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	64-68	
30690726-8	2019	Two prevalent functional variants of FMO3 were predicted to affect ethionamide disposition, with mean ratios of Cmax and AUC of up to 1.5 and 1.7, respectively, in comparison with the wild type.	Ethionamide	67-78	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	37-41	
30690726-9	2019	In comparing single ethionamide administration with the wild type, simulations of the combined effects of comedications and FMO3 genetic polymorphism estimated that the Cmax and AUC ratios of ethionamide increased up to 1.7 and 2.0, respectively.	Ethionamide	20-31	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	124-128	
30690726-9	2019	In comparing single ethionamide administration with the wild type, simulations of the combined effects of comedications and FMO3 genetic polymorphism estimated that the Cmax and AUC ratios of ethionamide increased up to 1.7 and 2.0, respectively.	Ethionamide	192-203	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	124-128	
30690726-10	2019	These findings suggested that FMO3-mediated drug-drug interaction and genetic polymorphism could be important determinants of interindividual heterogeneity in ethionamide disposition that need to be considered comprehensively to optimize the personalized dosing of ethionamide.	Ethionamide	159-170	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	30-34	
30690726-10	2019	These findings suggested that FMO3-mediated drug-drug interaction and genetic polymorphism could be important determinants of interindividual heterogeneity in ethionamide disposition that need to be considered comprehensively to optimize the personalized dosing of ethionamide.	Ethionamide	265-276	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	30-34	
30690726-2	2019	We previously reported the major contribution of flavin-containing monooxygenase 3 (FMO3) in the reductive elimination pathway of ethionamide.	Ethionamide	130-141	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	49-82	
30690726-2	2019	We previously reported the major contribution of flavin-containing monooxygenase 3 (FMO3) in the reductive elimination pathway of ethionamide.	Ethionamide	130-141	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	84-88	
30690726-4	2019	The drug-drug interaction leading to methimazole affecting the disposition of ethionamide mediated by FMO3 was then quantitated using a bottom-up approach with a physiologically based pharmacokinetic framework.	Ethionamide	78-89	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	102-106	
30690726-7	2019	Compared to the wild type, recombinant Lys158 -FMO3 and Gly308 -FMO3 variants significantly decreased the intrinsic clearance of ethionamide by 2% and 24%, respectively.	Ethionamide	129-140	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	47-51	
29878384-0	2018	Development of a Physiologically Based Pharmacokinetic Model of Ethionamide in the Pediatric Population by Integrating Flavin-Containing Monooxygenase 3 Maturational Changes Over Time.	Ethionamide	64-75	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	119-152	
29878384-5	2018	We hypothesized that the age-dependent changes in ethionamide elimination were predominantly a result of the progressive increases in the expression and metabolic capacity of FMO3 during childhood.	Ethionamide	50-61	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	175-179	
29878384-7	2018	Thus, a good prediction PBPK model was validated successfully both in adults and children and applied to demonstrate the critical contribution of FMO3 in the mechanistic elimination pathway of ethionamide.	Ethionamide	193-204	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	146-150	
28819071-1	2017	Hepatic flavin-containing mono-oxygenase 3 (FMO3) metabolizes a broad array of nucleophilic heteroatom (e.g., N or S)-containing xenobiotics (e.g., amphetamine, sulindac, benzydamine, ranitidine, tamoxifen, nicotine, and ethionamide), as well as endogenous compounds (e.g., catecholamine and trimethylamine).	Ethionamide	221-232	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	0-42	
28819071-1	2017	Hepatic flavin-containing mono-oxygenase 3 (FMO3) metabolizes a broad array of nucleophilic heteroatom (e.g., N or S)-containing xenobiotics (e.g., amphetamine, sulindac, benzydamine, ranitidine, tamoxifen, nicotine, and ethionamide), as well as endogenous compounds (e.g., catecholamine and trimethylamine).	Ethionamide	221-232	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	44-48	
18930751-0	2008	Metabolism of the anti-tuberculosis drug ethionamide by mouse and human FMO1, FMO2 and FMO3 and mouse and human lung microsomes.	Ethionamide	41-52	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	87-91