Renal excretion of drugs involves glomerular filtration, tubular secretion and reabsorption processes . Compounds whose renal clearance is greater than glomerular filtration clearance will be subject to renal tubular secretion and hence can interact with transporters expressed on renal epithelial cells. Most cationic organic compounds are substrates for the organic cation transporter (OCT) 2, multidrug and toxin extrusion transporter (MATE) 1, and MATE2-K . Their renal excretion in vivo is largely mediated by OCT2, which is expressed on the apical side of renal epithelial cells, and MATE1, MATE2-K which are expressed on the basolateral side . It has been clinically reported that concomitant use of drugs which are also inhibitors of OCT2, MATE1 and MATE2-K results in drug-drug interactions (DDI) with decreased renal excretion. For example, renal clearance of metformin, which is a substrate for OCT2, MATE1, and MATE-2K, was decreased in the co-administration of cimetidine and pyrimethamine, which are inhibitors of those transporters . Regarding the mechanism of the clinical DDI between cimetidine and metformin, it has been hypothesized mechanistically that MATE1 and MATE2-K play major roles for DDIs in the kidney because of the lower Ki values for MATE1 and MATE2-K than OCT2 . This was also supported by PBPK modeling . MATE1 that is significantly more highly expressed than MATE2-K, is considered to have the similar potency of transportability with MATE2-K, and we have limited information of specific substrates in MATE2-K, suggesting that MATE1 plays a major role in the renal DDI of drugs . The current DDI guidelines (of the United States 10 , Europe 11 and Japan ) list MATE1 as a transporter to be evaluated, suggesting MATE1 is a clinically relevant transporter in terms of clinical DDI risk assessment. Consequently, a predictive method to prospectively evaluate the inhibitory potential of MATE1 in the early drug discovery stages is desirable to evaluate new molecular entities with respect to this clinically relevant endpoint.