Competitively blocks the binding of histamine to H2 receptors. Inhibits gastric acid, 5 to 12 times more potent than cimetidine in terms of molarity. A potent H2 receptor blocker

It has anti-thrombotic effect. 1. It inhibits the uptake of adenosine by platelets, epithelial cells and erythrocytes. The inhibitory effect is dose-dependent at therapeutic concentrations. The local adenosine concentration increases, acts on the A2 receptor of platelets, stimulates adenylate cyclase, increases cyclic adenosine monophosphate (cAMP) in platelets, and thus inhibits platelet aggregation; 2. It inhibits phosphodiesterase (PDE) in various tissues. The therapeutic concentration inhibits cyclic guanosine monophosphate phosphodiesterase (cGMP-PDE), and enhances the increase in cGMP concentration caused by endothelial relaxing factor (EDRF); 3. It inhibits the formation of thromboxane A2 (TXA2), which is a strong agonist of platelet activity; 4. It enhances the effect of endogenous PGI2 and has a dilating effect on blood vessels. Dipyridamole administered intraduodenally to dogs produces a dose-related decrease in systemic and coronary vascular resistance, a decrease in systemic blood pressure and an increase in coronary blood flow. The same hemodynamic effect is observed in humans. However, acute intravenous administration can reduce local myocardial perfusion in the distal part of the stenotic coronary artery.

It selectively inhibits succinate dehydrogenase in the muscles of the worm, affects the anaerobic metabolism of the worm muscles, and reduces energy production; it depolarizes the nerve muscles, causing the worm muscles to continue to contract and paralyze; its cholinergic effect is beneficial to the excretion of the worm; it may have an inhibitory effect on the microtubule structure of the worm; it has immune regulation and immune excitation functions.

It selectively inhibits succinate dehydrogenase in the muscles of the worm, affects the anaerobic metabolism of the muscles of the worm, and reduces energy production; it depolarizes the nerve muscles, causing continuous muscle contraction and paralysis, and its cholinergic effect helps the worm to be expelled; it may inhibit the microtubule structure of the worm; it has immunomodulatory and immune enhancement functions.

This product has anti-inflammatory, antipyretic and analgesic effects. Its mechanism of action is to reduce the synthesis of prostaglandins by inhibiting cyclooxygenase. It stops the formation of pain nerve impulses in inflammatory tissues and inhibits inflammatory reactions, including inhibiting the chemotaxis of leukocytes and the release of lysosomal enzymes. As for the antipyretic effect, it acts on the hypothalamic temperature regulation center, causing peripheral vasodilation and sweating, which increases heat dissipation. This central antipyretic effect may also be related to the inhibition of prostaglandin synthesis in the hypothalamus.