Iron is a component of hemoglobin in red blood cells. When iron is deficient, the amount of hemoglobin synthesized by red blood cells decreases, causing the red blood cells to become smaller and their oxygen-carrying capacity to decrease, resulting in iron-deficiency anemia. Oral administration of this product can supplement iron and correct iron-deficiency anemia.

A selective β1-adrenergic receptor blocker with no membrane stabilizing effect and endogenous sympathomimetic activity. However, it does not inhibit the bronchodilator effect of isoproterenol. Its mechanism of lowering blood pressure and reducing myocardial oxygen consumption is the same as that of propranolol. Large-scale clinical trials have confirmed that atenolol can reduce the mortality rate of acute myocardial infarction within 0 to 7 days. The therapeutic dose has no significant inhibition on myocardial contractility.

A selective β1-adrenergic receptor blocker with no membrane stabilizing effect and endogenous sympathomimetic activity. However, it does not inhibit the bronchodilator effect of isoproterenol. Its mechanism of lowering blood pressure and reducing myocardial oxygen consumption is the same as that of propranolol. Large-scale clinical trials have confirmed that atenolol can reduce the mortality rate of acute myocardial infarction within 0 to 7 days. The therapeutic dose has no significant inhibition on myocardial contractility.

It has a direct relaxing effect on vascular smooth muscle, reducing peripheral resistance and lowering blood pressure. It has an antispasmodic effect on gastrointestinal smooth muscle.

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 transferase. The blood uric acid concentration begins to decrease 24 hours after oral administration of this product, and the decrease is most obvious in 2 to 4 weeks.