Key result
GR32191 potently and specifically antagonized U-46619-induced human platelet aggregation in whole blood with a pA2 of 8.23, demonstrating its efficacy as a thromboxane A2 receptor blocker.
Authors
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Supports preclinical development of thromboxane antagonists; leaves open clinical translation for antiplatelet therapy.
Effect estimate: pA2 8.23 (95% CI 7.90-8.56)
Lumley et al. (1989) studied In vitro platelet aggregation and smooth muscle contraction. GR32191 vs. Vehicle / Control was evaluated on Antagonism of U-46619-induced human platelet aggregation in whole blood (pA2) (pA2 8.23, 95% CI 7.90-8.56). GR32191 potently and specifically antagonized U-46619-induced human platelet aggregation in whole blood with a pA2 of 8.23, demonstrating its efficacy as a thromboxane A2 receptor blocker.
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