Key result
Selective activation of EP2 or EP4 by agonists AE1-259 and AE1-329 potently inhibited U-46619-induced platelet aggregation, with AE1-329 showing an IC50 of 2.3 nM in human platelets.
Population
Platelets prepared from wild-type mice, EP2-/- mice, EP4-/- mice, and human platelets
Comparison
Selective activation of EP2 or EP4 using… vs Wild-type vs knockout platelets; presence vs…
Design
Preclinical
Authors
Loading...
EP4 agonists merit preclinical exploration as antiplatelet agents; leaves open translation to human efficacy and safety trials.
Selective activation of EP2 or EP4 receptors inhibits platelet aggregation, suggesting EP4 agonists may serve as novel anti-platelet agents.
Yuhki et al. (2010) studied this question. Selective activation of EP2 or EP4 (AE1-259 and AE1-329) vs. Wild-type platelets / EP2-/- and EP4-/- platelets was evaluated on Inhibition of U-46619-induced platelet aggregation. Selective activation of EP2 or EP4 by agonists AE1-259 and AE1-329 potently inhibited U-46619-induced platelet aggregation, with AE1-329 showing an IC50 of 2.3 nM in human platelets.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: