Key result
Common functional CYP genetic variants did not affect active drug metabolite levels, platelet inhibition, or cardiovascular event rates in persons treated with prasugrel.
Why the study?
Do functional CYP genetic variants affect the pharmacokinetic, pharmacodynamic, or clinical response to prasugrel in healthy subjects and patients with acute coronary syndromes?
Cohort (n=1,704)
Do functional CYP genetic variants affect the pharmacokinetic, pharmacodynamic, or clinical response to prasugrel in healthy subjects and patients with acute coronary syndromes?
Common functional CYP genetic variants do not affect the pharmacokinetic, pharmacodynamic, or clinical response to prasugrel, contrasting with the known genetic variability in response to clopidogrel.
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Supports CYP-independent prasugrel use without genotyping; leaves open prospective validation versus clopidogrel.
Mega et al. (2009) conducted a cohort in Acute coronary syndromes (n=1,704). Prasugrel vs. Carriers vs noncarriers of reduced-function CYP alleles was evaluated on Cardiovascular death, myocardial infarction, or stroke. Common functional CYP genetic variants did not affect active drug metabolite levels, platelet inhibition, or cardiovascular event rates in persons treated with prasugrel.
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