Key result
The effects of cangrelor, ticagrelor, and prasugrel on platelet function are mediated mainly through P2Y12 receptors and not through other G-protein-coupled receptors.
Population
In vitro platelet model
Comparison
P2Y12 antagonists vs Selective IP, EP4 and A2A agonists
Design
Preclinical
Authors
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Supports P2Y12 selectivity in animal platelets; leaves open human receptor specificity and clinical relevance.
The inhibitory effects of cangrelor, ticagrelor, and prasugrel on platelet function are mediated primarily through P2Y12 receptors without significant interaction with other G-protein-coupled receptors.
Glenn et al. (2010) studied this question. P2Y12 antagonists (cangrelor, ticagrelor, prasugrel active metabolite) vs. Selective IP, EP4 and A2A agonists was evaluated on Platelet aggregation and phosphorylation of vasodilator-stimulated phosphoprotein (VASP). The effects of cangrelor, ticagrelor, and prasugrel on platelet function are mediated mainly through P2Y12 receptors and not through other G-protein-coupled receptors.
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