Clopidogrel 是抗血小板治療中的利器，服用後須先經CYP2C19 等酵素轉化成活性代謝物以發揮藥效。臨床上影響clopidogrel 藥效的原因包括血小板基礎活性高、出現藥物– 藥物交互作用、服藥順從性不佳及遺傳變異。遺傳變異影響clopidogrel的代謝，CYP2C19 的等位基因若出現減效基因如CYP2C19*2，則使用clopidogrel時會因代謝較差而影響臨床療效，此時考慮改換其他抗血小板製劑如prasugrel 會是建議的替代做法。
 

Clopidogrel is key to antiplatelet therapy, but it must be converted to an active metabolite by CYP2C19 and other enzymes to exert its drug action. In clinical settings, the factors that may influence the therapeutic efficacy of clopidogrel include high basal platelet activity, drug-drug interactions, poor medication compliance, and genetic variation. Genetic variation impacts the metabolism of clopidogrel. If defective alleles of CYP2C19 (e.g., CYP2C19*2) are present, poor metabolism of clopidogrel will result and affect its clinical efficacy. In such cases, the recommended alternative is switching to other antiplatelet agents such as prasugrel.