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June 28, 2010

Prasugrel as a Potential Cancer Promoter: Review of the Unpublished Data

Author Affiliations

Author Affiliations: Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle (Dr Floyd); and HeartDrug Research Laboratories, Johns Hopkins University, Towson, Maryland (Dr Serebruany).

Arch Intern Med. 2010;170(12):1078-1080. doi:10.1001/archinternmed.2010.154

On July 10, 2009, the US Food and Drug Administration (FDA) approved prasugrel for use in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention based on the results of the Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis in Myocardial Infarction 38 (TRITON–TIMI 38), a multicenter randomized clinical trial of 13 608 patients that showed a 19% relative risk reduction in the composite end point of nonfatal myocardial infarction, nonfatal stroke, and cardiovascular death with prasugrel compared with clopidogrel.1,2 Like other thienopyridines, prasugrel irreversibly inhibits platelet activation and aggregation through a P2Y12-receptor dependent mechanism. However, based on conventional aggregation studies, the approved daily dose of prasugrel (10 mg) appears to be 2.5 to 2.7 times more potent than the standard 75-mg daily dose of clopidogrel, and a 50% increase in life-threatening hemorrhage and a 4-fold increase in fatal hemorrhage were observed in TRITON-TIMI 38.2,3

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