The antithrombotic drug clopidogrel, widely prescribed after heart attacks, is a prodrug and must be metabolically activated. The efficiency of this activation step varies among individuals and is thought to account for clopidogrel's variable clinical efficacy, a major drawback to its use. Heleen Bouman et al. provide biochemical, clinical and epidemiological evidence to show that a common polymorphism in the gene encoding paraoxonase-1 is largely responsible for this variability. Paraoxonase-1 genotyping might identify those individuals unlikely to benefit from clopidogrel treatment.
- Heleen J Bouman
- Edgar Schömig
- Dirk Taubert
