Pub. Date : 2017
PMID : 29236753
13 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
1 | Ranitidine was reported to be a substrate of the organic cation transporters OCT1 and OCT2. | Ranitidine | solute carrier family 22 member 1 | Homo sapiens |
2 | 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 | solute carrier family 22 member 1 | Homo sapiens |
3 | 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 | solute carrier family 22 member 1 | Homo sapiens |
4 | Ranitidine was transported by wild-type OCT1 with a Km of 62.9 muM and a vmax of 1125 pmol/min/mg protein. | Ranitidine | solute carrier family 22 member 1 | Homo sapiens |
5 | Alleles OCT1*5, *6, *12, and *13 completely lacked ranitidine uptake. | Ranitidine | solute carrier family 22 member 1 | Homo sapiens |
6 | 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 | solute carrier family 22 member 1 | Homo sapiens |
7 | 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 | solute carrier family 22 member 1 | Homo sapiens |
8 | Ranitidine inhibited the OCT1-mediated uptake of metformin and morphine at clinically relevant concentrations. | Ranitidine | solute carrier family 22 member 1 | Homo sapiens |
9 | 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 | solute carrier family 22 member 1 | Homo sapiens |
10 | 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 | solute carrier family 22 member 1 | Homo sapiens |
11 | 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 | solute carrier family 22 member 1 | Homo sapiens |
12 | 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 | solute carrier family 22 member 1 | Homo sapiens |
13 | The effects of the frequent OCT1 polymorphisms on ranitidine pharmacokinetics in humans remain to be analyzed. | Ranitidine | solute carrier family 22 member 1 | Homo sapiens |