Key result
Aspirin prodrugs effectively inhibited human platelet aggregation in platelet-rich plasma via butyrylcholinesterase activation, with a NO-releasing prodrug showing potent dual inhibitory effects.
Why the study?
Do aspirin prodrugs effectively inhibit human platelet aggregation compared to conventional aspirin?
Population
Human platelets (platelet-rich plasma and washed platelets)
Comparison
Aspirin and prodrugs of aspirin, including… vs Conventional aspirin
Design
Preclinical
Authors
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Aspirin prodrugs may inhibit platelet aggregation via esterases; hypothesis-generating for clinical alternatives pending human trials.
Do aspirin prodrugs effectively inhibit human platelet aggregation compared to conventional aspirin?
Aspirin prodrugs, including NO-releasing variants, effectively inhibit human platelet aggregation via esterase-dependent mechanisms, suggesting potential as alternatives to conventional aspirin.
Harmon et al. (2011) studied Platelet aggregation. Aspirin prodrugs (including ST0702 and Compound 4) vs. Aspirin was evaluated on Human platelet aggregation stimulated by ADP and collagen and associated receptor expression. Aspirin prodrugs effectively inhibited human platelet aggregation in platelet-rich plasma via butyrylcholinesterase activation, with a NO-releasing prodrug showing potent dual inhibitory effects.
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