PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26784938-0	2016	The MATE1 rs2289669 polymorphism affects the renal clearance of metformin following ranitidine treatment.	Ranitidine	84-94	solute carrier family 47 member 1	Homo sapiens	4-9	
31542894-2	2020	To evaluate whether organic cation transporter (OCT) 1, OCT2 and multidrug and toxin extrusion (MATE) 1 and MATE2-K are involved in pharmacokinetics, competitions with ranitidine, a probe inhibitor of the cation transporters, were evaluated in transfected HEK293 cells.	Ranitidine	168-178	solute carrier family 47 member 1	Homo sapiens	79-103	
31542894-4	2020	Ranitidine inhibited OCT1, OCT2, MATE1, and MATE2-K with half maximal inhibitory concentration values of 186 +- 25 microM, 482 +- 105 microM, 134 +- 37 microM, and 35 +- 11 microM, respectively.	Ranitidine	0-10	solute carrier family 47 member 1	Homo sapiens	33-38	
31542894-8	2020	The renal effects apparently result from inhibition of MATE1 and/or MATE2-K by ranitidine as predicted by in vitro to in vivo extrapolation.	Ranitidine	79-89	solute carrier family 47 member 1	Homo sapiens	55-60	
26784938-2	2016	The goal of this study was to determine the association between metformin"s pharmacokinetics and pharmacodynamics and the genetic variants of MATE1 (rs2289669) and OCT2 (rs316019) before and after treatment with the potential MATE inhibitor, ranitidine.	Ranitidine	242-252	solute carrier family 47 member 1	Homo sapiens	142-147	
26784938-5	2016	However, the renal clearance of metformin was significantly higher (15.2%) after ranitidine treatment in the MATE1 GG group compared with the MATE1 GA + AA group.	Ranitidine	81-91	solute carrier family 47 member 1	Homo sapiens	109-114	
26784938-6	2016	Only the effect of MATE1 on the renal clearance of metformin after ranitidine treatment was significant (b = -0.465, p <= 0.05) after including demographic data and the OCT2 genotype in the model.	Ranitidine	67-77	solute carrier family 47 member 1	Homo sapiens	19-24