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Abstract
It has been suggested that genetic polymorphisms in drug transporters as well as drug-metabolizing enzymes are associated with interindividual differences in drug disposition, efficacy, and toxicity and in disease. Organic anion and cation transporters are expressed in the selective or multiple tissues such as small intestine, liver and kidney, and mediate the transport of many clinically useful drugs. Polymorphisms of drug transporter genes have recently been identified and demonstrated to have functional significance for transporter activity and expression. For example, genetic variants in the OATP-C (SLC21A6) gene are associated with alterations in pravastatin and rifampin uptake into liver. In addition, homozygotes for OCTN2 (SLC22A5) mutant alleles cause systemic carnitine deficiency because of a disruption of carnitine reabsorption in the kidney. Since a growing number of preclinical and clinical studies have demonstrated that the polymorphisms of various drug transporter genes may be responsible for overall outcomes of pharmacokinetics and pharmacotherapy of certain drugs, further understanding of the physiology and biochemistry of drug transporters with respect to genetic variations will be important to establish individualized pharmacotherapy with clinically used drugs.
Keywords: anion and cation transporters, genetic polymorphisms, clinically useful drugs, pharmacokinetics, pharmacodynamics