The effect of CYP2C19 polymorphism on the pharmacokinetics and pharmacodynamics of clopidogrel: A possible mechanism for clopidogrel resistance
- Authors
- Kim, K. A.; Park, P. W.; Hong, S. J.; Park, J-Y
- Issue Date
- 8월-2008
- Publisher
- WILEY
- Citation
- CLINICAL PHARMACOLOGY & THERAPEUTICS, v.84, no.2, pp.236 - 242
- Indexed
- SCIE
SCOPUS
- Journal Title
- CLINICAL PHARMACOLOGY & THERAPEUTICS
- Volume
- 84
- Number
- 2
- Start Page
- 236
- End Page
- 242
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/122889
- DOI
- 10.1038/clpt.2008.20
- ISSN
- 0009-9236
- Abstract
- We evaluated the effect of the CYP2C19 genotype on the pharmacokinetics and pharmacodynamcis of clopidogrel. Twenty-four subjects were divided into three groups on the basis of their CYP2C19 genotype: homozygous extensive metabolizers (homoEMs, n = 8), heterozygous EMs (heteroEMs, n = 8), and poor metabolizers (PMs, n = 8). After a single 300-mg loading dose of clopidogrel on day 1, followed by a 75-mg daily maintenance dose from days 2 to 7, we measured the plasma levels of clopidogrel and assessed the antiplatelet effect as pharmacodynamics. The mean clopidogrel area under the curve (AUC) for PMs was 1.8- and 2.9-fold higher than that for heteroEMs and homoEMs, respectively (P = 0.013). The mean peak plasma concentration in PMs was 1.8- and 4.7-fold higher than that of heteroEMs and homoEMs, respectively (P = 0.008). PMs exhibited a significantly lower antiplatelet effect than heteroEMs or homoEMs (P < 0.001). From these findings it is clear that the CYP2C19 genotype affects the plasma levels of clopidogrel and modulates the antiplatelet effect of clopidogrel.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
- College of Medicine > Department of Medical Science > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.