This product is a dibenzodiazepine antipsychotic. It has a strong blocking effect on the 5-hydroxytryptamine (5-HT2A) receptor and dopamine (DA1) receptor in the brain, and also has a blocking effect on the dopamine (DA4) receptor, and a weaker blocking effect on the dopamine (DA2) receptor. In addition, it also has anticholinergic (M1), antihistamine (H1) and anti-α-adrenaline receptor effects. Extrapyramidal reactions are rare, and generally do not cause an increase in blood prolactin. It can directly inhibit the ascending activation system of the brainstem reticular formation and has a strong sedative and hypnotic effect.

It can relax vascular smooth muscle and cause vasodilation. Its most important function is to dilate veins to reduce venous blood return, and also dilate systemic arteries and main coronary arteries, thereby reducing the preload and postload of the heart and promoting oxygen supply. It can also improve blood supply to ischemic areas by promoting the redistribution of myocardial blood flow and play an anti-myocardial ischemia effect.

Diclofenac sodium is a non-steroidal anti-inflammatory analgesic derived from phenylacetic acid. Its mechanism of action is to inhibit the activity of cyclooxygenase, thereby blocking the conversion of arachidonic acid to prostaglandins. At the same time, it can also promote the combination of arachidonic acid and triglycerides, reduce the concentration of free arachidonic acid in cells, and indirectly inhibit the synthesis of leukotrienes. Diclofenac sodium is a stronger non-steroidal anti-inflammatory drug. Its inhibitory effect on prostaglandin synthesis is stronger than that of aspirin and indomethacin.

Diclofenac sodium is a non-steroidal anti-inflammatory analgesic derived from phenylacetic acid. Its mechanism of action is to inhibit the activity of cyclooxygenase, thereby blocking the conversion of arachidonic acid to prostaglandins. At the same time, it can also promote the combination of arachidonic acid and triglycerides, reduce the concentration of free arachidonic acid in cells, and indirectly inhibit the synthesis of leukotrienes. Diclofenac sodium is a stronger non-steroidal anti-inflammatory drug. Its inhibitory effect on prostaglandin synthesis is stronger than that of aspirin and indomethacin.

Calcium channel blockers can inhibit the transmembrane calcium ion influx of myocardial and vascular smooth muscle without changing the blood calcium concentration; they have a high degree of vascular selectivity, dilate coronary vascular smooth muscle, reduce peripheral vascular resistance to lower blood pressure, increase cardiac ejection fraction and cardiac output; temporarily increase urinary sodium excretion; block slow calcium channels without affecting fast sodium channels; in animal experiments, they dilate coronary arteries and increase local myocardial blood flow without affecting atrioventricular conduction.