Pharmacogenomic variability, particularly in CYP2C19 and P-glycoprotein, significantly affects clopidogrel metabolism, highlighting a need for further research on risk stratification and tailored therapy.
May warrant pharmacogenomic consideration with clopidogrel; leaves optimal risk stratification and adjustment unresolved.
The thienopyridine antiplatelet agent clopidogrel is an effective drug for the prevention of vascular events. However, data has accumulated over time to suggest it is prone to significant interpatient variability. While there are several factors that contribute to this, one of the most important is variability in forming the active metabolite necessary for clopidogrel function. Several enzymes are involved in formation of this metabolite, and two, CYP2C19 and P-glycoprotein, appear to have alleles that both occur frequently in the population and have a clinically significant impact. Patients carrying these alleles can be identified, but it remains to be determined if this information is necessary or sufficient for risk stratification. Furthermore, if patients with high-risk alleles are identified, it is unclear how treatment should be adjusted.
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Chris M. Terpening (2010) studied this question.
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