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The Study on Association of Calcium Channel SNPs with Adverse Drug Reaction of Calcium Channel Blocker in Korean

  • Chung, Myeon-Woo (National Institute of Toxicological Research, Korea Food and Drug Administration) ;
  • Bang, Sy-Rie (National Institute of Toxicological Research, Korea Food and Drug Administration) ;
  • Jin, Sun-Kyung (National Institute of Toxicological Research, Korea Food and Drug Administration) ;
  • Woo, Sun-Wook (National Institute of Toxicological Research, Korea Food and Drug Administration) ;
  • Lee, Yoon-Jung (National Institute of Toxicological Research, Korea Food and Drug Administration) ;
  • Kim, Young-Sik (College of Medicine, University of Ulsan) ;
  • Lee, Jong-Keuk (College of Medicine, University of Ulsan) ;
  • Lee, Sung-Ho (Department of Thoracic & Cardiovascular Surgery, Anam Hospital, Korea University) ;
  • Roh, Jae-Sook (National Institute of Toxicological Research, Korea Food and Drug Administration) ;
  • Chung, Hye-Joo (National Institute of Toxicological Research, Korea Food and Drug Administration)
  • Published : 2007.09.30

Abstract

Rapid advances in pharmacogenomic research have provided important information to improve drug selection, to maximize drug efficacy, and to minimize drug adverse reaction. The SNPs that are the most abundant type of genetic variants have been proven as valid biomarkers to give information on the prediction of pharmacokinetic/pharmacodynamic properties of drugs based on genotype. In order to elucidate a correlation between SNPs of calcium channel encoding gene and adverse reactions of calcium channel blockers, we investigated SNPs in CACNA1C gene known as a binding site of calcium channel blocker. 96 patients with hypertension who had taken or are taking an antihypertensive drug, 1,4-dihydropyridine (DHP) were included for analysis. These patients were composed of 47 patients with adverse drug reactions (ADR) such as edema from calcium channel blockers and 49 patients without ADR as a control group. The exons encoding the drug binding sites were amplified by PCR using specific primers, and SNPs were analyzed by direct sequencing. We found that there was no SNP in the exons encoding DHP binding site, but four novel SNPs in the exon-intron junction region. However, four novel SNPs were not associated with the ADR of calcium channel blockers. In conclusion, this study showed that ADR from calcium channel blockers may not be caused by SNPs of the binding sites of calcium channel blockers in CACNA1C gene.

Keywords

References

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