期刊
PHARMACOGENOMICS
卷 12, 期 7, 页码 1017-1037出版社
FUTURE MEDICINE LTD
DOI: 10.2217/PGS.11.44
关键词
aliskiren; cimetidine; digoxin; drug-drug interaction; drug transporter; fexofenadine; MATE1; OAT1; OAT3; OATP1B1; OCT2; P-gp; probenecid; rosuvastatin
资金
- German Cancer Aid (Deutsche Krebshilfe) [107854]
- DFG (Deutsche Forschungsgemeinschaft) [FR1298/5-1]
- DOKTOR ROBERT PFLEGER-STIFTUNG Bamberg
- AstraZeneca
- Bayer Schering Pharma
- Boehringer Ingelheim
- Merck KGaA
- Ferring
- Novartis
Drug-drug interactions are a serious clinical issue. An important mechanism underlying drug-drug interactions is induction or inhibition of drug transporters that mediate the cellular uptake and efflux of xenobiotics. Especially drug transporters of the small intestine, liver and kidney are major determinants of the pharmacokinetic profile of drugs. Transporter-mediated drug-drug interactions in these three organs can considerably influence the pharmacokinetics and clinical effects of drugs. In this article, we focus on probe drugs lacking significant metabolism to highlight mechanisms of interactions of selected intestinal, hepatic and renal drug transporters (e. g., organic anion transporting polypeptide [OATP] 1A2, OATP2B1, OATP1B1, OATP1B3, P-gp, organic anion transporter [OAT] 1, OAT3, breast cancer resistance protein [BCRP], organic cation transporter [OCT] 2 and multidrug and toxin extrusion protein [MATE] 1). Genotype-dependent drug-drug interactions are also discussed.
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