This product is a thromboxane (TX) synthase inhibitor, which can inhibit the generation of thromboxane A2 (TXA2) from prostaglandin H2 (PGH2), and promote the transfer of PGH2 derived from platelets to endothelial cells. Endothelial cells are used to synthesize PGI2, thereby improving the abnormal balance between TXA2 and prostaglandin PGI2. Theoretically, it can inhibit platelet aggregation and vasodilation. This product can improve movement disorders in the acute stage of cerebral thrombosis, improve circulatory disorders in the acute stage of cerebral ischemia, and improve abnormal energy metabolism during cerebral ischemia. Animal experiments have shown that intravenous administration can reduce plasma TXB2 levels, increase the ratio of 6-Keto-PGF1a/TXB2, inhibit platelet aggregation caused by different inducers, and prevent cerebral infarction caused by middle cerebral artery occlusion in rats. The half-maximal inhibitory concentration IC50 of this product for human platelet aggregation is low, at 4nM. Experiments using autologous blood injected into the subarachnoid hemorrhage model showed that continuous intravenous injection of this product has the effects of inhibiting blood TXB2 concentration and cerebral vasoconstriction.

This product is a thromboxane (TX) synthase inhibitor, which can inhibit the generation of thromboxane A2 (TXA2) from prostaglandin H2 (PGH2), and promote the transfer of PGH2 derived from platelets to endothelial cells. Endothelial cells are used to synthesize PGI2, thereby improving the abnormal balance between TXA2 and prostaglandin PGI2. Theoretically, it can inhibit platelet aggregation and vasodilation. This product can improve movement disorders in the acute stage of cerebral thrombosis, improve circulatory disorders in the acute stage of cerebral ischemia, and improve abnormal energy metabolism during cerebral ischemia. Animal experiments have shown that intravenous administration can reduce plasma TXB2 levels, increase the ratio of 6-Keto-PGF1a/TXB2, inhibit platelet aggregation caused by different inducers, and prevent cerebral infarction caused by middle cerebral artery occlusion in rats. The half-maximal inhibitory concentration IC50 of this product for human platelet aggregation is low, at 4nM. Experiments using autologous blood injected into the subarachnoid hemorrhage model showed that continuous intravenous injection of this product has the effects of inhibiting blood TXB2 concentration and cerebral vasoconstriction.

Antibacterial effect

No specific information provided