Key result
The synthetic prostaglandin analog 9,11-azoprosta-5,13-dienoic acid potently inhibited human platelet thromboxane synthetase and antagonized platelet aggregation induced by PGH2 or arachidonic acid.
Why the study?
Does 9,11-azoprosta-5,13-dienoic acid inhibit thromboxane synthetase and prevent aggregation in human platelets?
Population
Human platelets
Design
Preclinical
Authors
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May inhibit platelet aggregation via thromboxane synthetase blockade in vitro; leaves open clinical antithrombotic utility.
Does 9,11-azoprosta-5,13-dienoic acid inhibit thromboxane synthetase and prevent aggregation in human platelets?
The study provides mechanistic evidence that PGH2 must be converted to thromboxane A2 to induce human platelet aggregation, using a novel thromboxane synthetase inhibitor.
Gorman et al. (1977) studied this question. 9,11-azoprosta-5,13-dienoic acid (azo analog I) was evaluated on Inhibition of human platelet thromboxane synthetase and platelet aggregation. The synthetic prostaglandin analog 9,11-azoprosta-5,13-dienoic acid potently inhibited human platelet thromboxane synthetase and antagonized platelet aggregation induced by PGH2 or arachidonic acid.
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