Valsartan 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. Valsartan reduces elevated blood pressure without affecting heart rate. 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 maintains a blood pressure-lowering effect for more than 24 hours after taking the drug. The maximum blood pressure-lowering effect is achieved after 2-4 weeks of treatment, and the effect is maintained during long-term treatment.

Valsartan 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. Valsartan does not have any partial agonist activity on the AT1 receptor, does not affect the heart rate, and reduces elevated blood pressure. Valsartan has no inhibitory effect on ACE, does not cause retention of bradykinin or substance P, and therefore does not cause coughing.

This product is a fully synthetic cholesterol-lowering drug, a hydroxymethylglutaryl coenzyme A reductase inhibitor that can convert HMG-CoA into 3-methyl-3,5-dihydroxyvaleric acid. The site of action of this product is in the liver, which has the effects of inhibiting the synthesis of endogenous cholesterol, reducing the cholesterol content in liver cells, stimulating the synthesis of low-density lipoprotein receptors, increasing the uptake of LDL particles and reducing the total cholesterol concentration in plasma. Based on the changes in the minimum lumen diameter before and after each patient, the percentage of stenosis diameter or the formation of new lesions, fluvastatin sodium significantly slowed the progression of coronary artery lesions.

Artificially synthesized HMG-CoA reductase inhibitor, it has a significant effect of lowering serum total cholesterol, LDL and serum TG. The cholesterol-lowering effect of this product can be enhanced when used in combination with cholestyramine. It is rapidly and completely absorbed after oral administration. It has a first-pass effect in the liver and is excreted through bile, with a half-life of about 4-7 hours.

Artificially synthesized HMG-CoA reductase inhibitor, it has a significant effect of lowering serum total cholesterol, LDL and serum TG. The cholesterol-lowering effect of this product can be enhanced when used in combination with cholestyramine. It is rapidly and completely absorbed after oral administration. It has a first-pass effect in the liver and is excreted through bile, with a half-life of about 4-7 hours.

This product is a prodrug, which becomes the active substance benazeprilat after hydrolysis, which can inhibit angiotensin converting enzyme (ACE), prevent the conversion of angiotensin I into angiotensin II, thereby reducing vasoconstriction and aldosterone production; inhibit kininase and reduce bradykinin degradation, which helps to improve the anti-hypertensive effect; generally lower the blood pressure of patients with hypertension at all stages; improve the hemodynamic performance of patients with congestive heart failure; delay the progression of chronic renal insufficiency and reduce proteinuria.