Key result
A low affinity for Cox-1 and a high degree of Cox-2 selectivity confers a low potential to block aspirin inhibition of platelet Cox-1, with ibuprofen being the most potent antagonist and etoricoxib the least.
Why the study?
Do coxibs with high Cox-2 selectivity interfere less with aspirin's inactivation of platelet Cox-1 compared to ibuprofen?
Population
Purified enzyme and calcium ionophore-activated human platelets
Comparison
Ibuprofen and various coxibs vs Aspirin alone
Design
Preclinical
Authors
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High Cox-2 selectivity may minimize aspirin interference in animals; leaves open clinical translation and requires human trials.
Do coxibs with high Cox-2 selectivity interfere less with aspirin's inactivation of platelet Cox-1 compared to ibuprofen?
A high degree of Cox-2 selectivity in NSAIDs/coxibs confers a low potential to block aspirin's antiplatelet effect, providing a mechanistic basis for clinical observations.
Ouellet et al. (2001) studied Healthy volunteers (blood donors for in vitro assays). Ibuprofen and coxibs (celecoxib, valdecoxib, rofecoxib, etoricoxib) vs. Aspirin alone was evaluated on Antagonism of aspirin inhibition of platelet Cox-1 (EC50). A low affinity for Cox-1 and a high degree of Cox-2 selectivity confers a low potential to block aspirin inhibition of platelet Cox-1, with ibuprofen being the most potent antagonist and etoricoxib the least.
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