It can enhance the level of glutathione (GSH) in the liver, significantly enhance the activities of glutamylcysteine synthetase (GCS), glutathione reductase (GSSG-R) and glutathione S-transferase (GSH-S-Tx), and reduce the activity of glutathione peroxidase (GSH-Px), thereby enhancing the vitality of liver cells, increasing bile secretion, and having a choleretic effect.

It is an orally effective specific angiotensin (AT) II receptor antagonist that selectively acts on the AT1 receptor subtype, with an affinity for the AT1 receptor 20,000 times stronger than that for the AT2 receptor. For most patients, a single oral dose produces a blood pressure lowering effect within 2 hours, reaches a peak effect within 4-6 hours, and the blood pressure lowering effect is maintained for more than 24 hours after taking the medicine. In long-term treatment, the maximum blood pressure lowering effect is achieved after 2-4 weeks of treatment and is maintained. The antihypertensive effect of valsartan is significantly enhanced when combined with hydrochlorothiazide. Sudden termination of valsartan treatment does not cause hypertension "rebound" or other side effects. Valsartan does not affect the fasting total cholesterol, triglyceride, blood sugar or uric acid levels of hypertensive patients. Valsartan has no inhibitory effect on ACE and is not likely to cause coughing. It has no effect on other hormone receptors or ion channels known to play an important role in cardiovascular regulation. Valsartan does not affect heart rate when lowering elevated blood pressure.

Inhibiting the co-transport of sodium and chloride ions and competing for chloride ion sites can affect electrolyte reabsorption, directly increase the excretion of sodium and chloride, and indirectly reduce plasma volume, thereby increasing plasma renin activity, aldosterone secretion and potassium excretion, and reducing serum potassium. Because the renin-aldosterone system is angiotensin II-dependent, the combined use of angiotensin II receptor antagonists can reduce potassium loss associated with thiazide diuretics.

It mainly acts on bronchial adrenergic receptors to relax smooth muscles.

This product is a long-acting tricyclic antihistamine that can relieve seasonal allergic rhinitis or non-nasal symptoms by selectively antagonizing peripheral H1 receptors.

The second generation of sulfonylurea hypoglycemic drugs has a strong effect, selectively acting on pancreatic islet b cells, promoting insulin secretion, and increasing insulin release after eating glucose, so that the production and output of glycogen are inhibited. Animal experiments and clinical use have proven that it can reduce platelet aggregation and adhesion, and help prevent and treat diabetic microangiopathy.