Key result
Prasugrel's active metabolite (R-138727) yielded concentration-dependent inhibition of platelet aggregation and completely inhibited P2Y12 receptor binding at 30 micromol/L.
Why the study?
Does the active metabolite of prasugrel effectively inhibit platelet P2Y12 receptors and downstream procoagulant/pro-inflammatory responses in blood from healthy volunteers?
Population
Blood taken from healthy volunteers
Comparison
Pre-incubation with R-138727 or cangrelor… vs Clopidogrel or baseline/vehicle
Design
Preclinical
Authors
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In vitro data show potent P2Y12 blockade by prasugrel metabolite; leaves open clinical translation and dosing optimization.
Does the active metabolite of prasugrel effectively inhibit platelet P2Y12 receptors and downstream procoagulant/pro-inflammatory responses in blood from healthy volunteers?
The active metabolite of prasugrel provides complete, concentration-dependent blockade of the P2Y12 receptor, effectively inhibiting platelet aggregation and pro-inflammatory responses.
Judge et al. (2008) studied Healthy volunteers. R-138727 (prasugrel active metabolite) vs. Cangrelor and clopidogrel was evaluated on Platelet aggregation, VASP phosphorylation, and P2Y12 receptor antagonism. Prasugrel's active metabolite (R-138727) yielded concentration-dependent inhibition of platelet aggregation and completely inhibited P2Y12 receptor binding at 30 micromol/L.
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