(1) Analgesic effect: It is mainly through inhibiting the synthesis of prostaglandins and other substances that can make pain sensitive to mechanical or chemical stimulation (such as bradykinin, histamine), and is a peripheral analgesic. However, the possibility of central analgesia (possibly acting on the hypothalamus) cannot be ruled out. (2) Anti-inflammatory effect: The exact mechanism is still unclear. It may be due to the fact that this product acts on inflamed tissues and inhibits the synthesis of prostaglandins or other substances that can cause inflammatory reactions (such as histamine) to exert an anti-inflammatory effect. Inhibition of the release of lysosomal enzymes and leukocyte chemotaxis may also be related to it. (3) Antipyretic effect: It may act on the hypothalamic temperature regulation center to cause peripheral vasodilation, increased skin blood flow, sweating, and increased heat dissipation to exert an antipyretic effect. This central effect may be related to the inhibition of prostaglandin synthesis in the hypothalamus. (4) Anti-rheumatic effect: The anti-rheumatic mechanism of this product, in addition to antipyretic and analgesic effects, is mainly anti-inflammatory. (5) Inhibit platelet aggregation: It works by inhibiting platelet cyclooxygenase and reducing the production of prostaglandins.

This product is a drug that inhibits the synthesis of uric acid. Allopurinol and its metabolite oxypurinol can inhibit xanthine oxidase, preventing hypoxanthine and xanthine from being metabolized into uric acid, thereby reducing the production of uric acid. It reduces the uric acid content in the blood and urine to a level below the solubility, prevents uric acid from forming crystals and depositing in joints and other tissues, and also helps to redissolve uric acid crystals in the tissues of gout patients. Allopurinol also inhibits the synthesis of new purines in the body by acting on hypoxanthine-guanine phosphate nucleic acid convertase.

Anticonvulsant, anti-epileptic, anti-neuropathic pain, anti-manic-depressive, improve the symptoms of certain mental illnesses, and prevent central diabetes insipidus. Possible mechanisms include: 1. Use-dependent blocking of various Na channels of excitable cell membranes, so it can significantly inhibit the occurrence and spread of abnormal high-frequency discharges. 2. Inhibit T-type calcium channels. 3. Enhance the activity of central noradrenergic nerves. 4. Promote the secretion of antidiuretic hormone (ADH) or increase the sensitivity of effectors to ADH.

It can improve mental disorders by blocking postsynaptic dopamine receptors in the brain, inhibit the ascending activation system of the brainstem reticular formation, cause sedation, and inhibit the medulla chemoreceptor area to exert an antiemetic effect. This product has weak anti-adrenergic and anti-cholinergic effects, and has anti-depressant and anti-anxiety effects.

It can improve mental disorders by blocking postsynaptic dopamine receptors in the brain, inhibit the ascending activation system of the brainstem reticular formation, cause sedation, and inhibit the medulla chemoreceptor area to exert an antiemetic effect. This product has weak anti-adrenergic and anti-cholinergic effects, and has anti-depressant and anti-anxiety effects.