PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 22 member 1 Homo sapiens 20-54 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 22 member 1 Homo sapiens 21-25 17614008-5 2007 The [(3)H]-MPP uptake by hOCT1/rOct1 and hOCT3/rOct3 was inhibited by famotidine and ranitidine whereas that by hOCT2/rOct2 was not. Ranitidine 85-95 solute carrier family 22 member 1 Homo sapiens 25-30 29236753-2 2017 Ranitidine was reported to be a substrate of the organic cation transporters OCT1 and OCT2. Ranitidine 0-10 solute carrier family 22 member 1 Homo sapiens 77-81 29236753-7 2017 AIM: In this study we analyzed the effects of genetic polymorphisms in OCT1 and OCT2 on the uptake of ranitidine and on its potency to inhibit uptake of other drugs. Ranitidine 102-112 solute carrier family 22 member 1 Homo sapiens 71-75 29236753-8 2017 METHODS AND RESULTS: We characterized ranitidine uptake using HEK293 and CHO cells stably transfected to overexpress wild type OCT1, OCT2, or their naturally occurring allelic variants. Ranitidine 38-48 solute carrier family 22 member 1 Homo sapiens 127-131 29236753-9 2017 Ranitidine was transported by wild-type OCT1 with a Km of 62.9 muM and a vmax of 1125 pmol/min/mg protein. Ranitidine 0-10 solute carrier family 22 member 1 Homo sapiens 40-44 29236753-10 2017 Alleles OCT1*5, *6, *12, and *13 completely lacked ranitidine uptake. Ranitidine 51-61 solute carrier family 22 member 1 Homo sapiens 8-12 29236753-13 2017 The effects of OCT1 alleles on ranitidine uptake strongly correlated with the effects on morphine uptake suggesting common interaction mechanisms of both drugs with OCT1. Ranitidine 31-41 solute carrier family 22 member 1 Homo sapiens 15-19 29236753-13 2017 The effects of OCT1 alleles on ranitidine uptake strongly correlated with the effects on morphine uptake suggesting common interaction mechanisms of both drugs with OCT1. Ranitidine 31-41 solute carrier family 22 member 1 Homo sapiens 165-169 29236753-14 2017 Ranitidine inhibited the OCT1-mediated uptake of metformin and morphine at clinically relevant concentrations. Ranitidine 0-10 solute carrier family 22 member 1 Homo sapiens 25-29 29236753-17 2017 CONCLUSIONS: We confirmed ranitidine as an OCT1 substrate and demonstrated that common genetic polymorphisms in OCT1 strongly affect ranitidine uptake and modulate ranitidine"s potential to cause drug-drug interactions. Ranitidine 26-36 solute carrier family 22 member 1 Homo sapiens 43-47 29236753-17 2017 CONCLUSIONS: We confirmed ranitidine as an OCT1 substrate and demonstrated that common genetic polymorphisms in OCT1 strongly affect ranitidine uptake and modulate ranitidine"s potential to cause drug-drug interactions. Ranitidine 26-36 solute carrier family 22 member 1 Homo sapiens 112-116 29236753-17 2017 CONCLUSIONS: We confirmed ranitidine as an OCT1 substrate and demonstrated that common genetic polymorphisms in OCT1 strongly affect ranitidine uptake and modulate ranitidine"s potential to cause drug-drug interactions. Ranitidine 133-143 solute carrier family 22 member 1 Homo sapiens 112-116 29236753-17 2017 CONCLUSIONS: We confirmed ranitidine as an OCT1 substrate and demonstrated that common genetic polymorphisms in OCT1 strongly affect ranitidine uptake and modulate ranitidine"s potential to cause drug-drug interactions. Ranitidine 133-143 solute carrier family 22 member 1 Homo sapiens 112-116 29236753-18 2017 The effects of the frequent OCT1 polymorphisms on ranitidine pharmacokinetics in humans remain to be analyzed. Ranitidine 50-60 solute carrier family 22 member 1 Homo sapiens 28-32 18971316-8 2009 Ranitidine, an hOCT1 inhibitor, reversed this hOCT1-mediated potentiation of cytotoxicity. Ranitidine 0-10 solute carrier family 22 member 1 Homo sapiens 15-20 18971316-8 2009 Ranitidine, an hOCT1 inhibitor, reversed this hOCT1-mediated potentiation of cytotoxicity. Ranitidine 0-10 solute carrier family 22 member 1 Homo sapiens 46-51 16141367-0 2005 Differential substrate and inhibitory activities of ranitidine and famotidine toward human organic cation transporter 1 (hOCT1; SLC22A1), hOCT2 (SLC22A2), and hOCT3 (SLC22A3). Ranitidine 52-62 solute carrier family 22 member 1 Homo sapiens 91-119 16141367-0 2005 Differential substrate and inhibitory activities of ranitidine and famotidine toward human organic cation transporter 1 (hOCT1; SLC22A1), hOCT2 (SLC22A2), and hOCT3 (SLC22A3). Ranitidine 52-62 solute carrier family 22 member 1 Homo sapiens 121-126 16141367-0 2005 Differential substrate and inhibitory activities of ranitidine and famotidine toward human organic cation transporter 1 (hOCT1; SLC22A1), hOCT2 (SLC22A2), and hOCT3 (SLC22A3). Ranitidine 52-62 solute carrier family 22 member 1 Homo sapiens 128-135 16141367-3 2005 Inhibition and substrate specificity of hOCT1, hOCT2, and hOCT3 for ranitidine and famotidine were elucidated in cRNA-injected Xenopus laevis oocytes. Ranitidine 68-78 solute carrier family 22 member 1 Homo sapiens 40-45 16141367-4 2005 Ranitidine and famotidine exhibited similarly potent inhibition of [3H]1-methyl-4-phenyl pyridinium uptake into hOCT1-expressing (IC50= 33 and 28 microM, respectively) and hOCT2-expressing oocytes (IC50= 76 and 114 microM, respectively). Ranitidine 0-10 solute carrier family 22 member 1 Homo sapiens 112-117 16141367-6 2005 [3H]Ranitidine uptake was stimulated by hOCT1 (Km= 70 +/- 9 microM) and to a much smaller extent by hOCT2. Ranitidine 4-14 solute carrier family 22 member 1 Homo sapiens 40-45 16141367-9 2005 Thus, hOCT1, which is expressed in the intestine and liver, is likely to play a major role in the intestinal absorption and hepatic disposition of ranitidine and famotidine in humans, whereas hOCT2, the major isoform present in the kidney, may play only a minor role in their renal elimination. Ranitidine 147-157 solute carrier family 22 member 1 Homo sapiens 6-11