Telmisartan is an oral specific non-peptide angiotensin II receptor (AT1 type) antagonist. Telmisartan selectively binds to the AT1 receptor site with high affinity, persistently antagonizes angiotensin II, and causes a decrease in blood aldosterone levels, thereby reducing blood pressure. Telmisartan does not inhibit human plasma renin, nor does it block ion channels, nor does it inhibit angiotensin converting enzyme (kinase II), nor does it affect the degradation of bradykinin by the enzyme, so there will be no adverse reactions caused by the enhanced effect of bradykinin. For patients with hypertension, telmisartan can reduce systolic and diastolic blood pressure without affecting heart rate. Rebound hypertension does not occur after discontinuation of telmisartan.

By antagonizing HMG-CoA reductase, it hinders the biosynthesis of cholesterol in the liver, promotes the expression of liver LDL receptors and the entry of LDL from the blood into the liver, and lowers total cholesterol; reduces the secretion of VLDL into the blood, lowers plasma triglycerides; inhibits blood lipid accumulation and intimal thickening; promotes LDL receptor expression and reduces VLDL secretion.

By antagonizing HMG-CoA reductase, it hinders the cholesterol synthesis in the liver, promotes the expression of low-density lipoprotein (LDL) receptors in the liver and the entry of LDL from the blood into the liver, thereby lowering total cholesterol; it continuously inhibits the biosynthesis of cholesterol in the liver, reduces the secretion of very low-density lipoprotein (VLDL) into the blood, and lowers triglycerides in plasma.

This product is a hypoglycemic drug. The main effect of insulin is to lower blood sugar, and it also affects protein and fat metabolism, including the following effects: 1. Inhibit liver glycogenolysis and gluconeogenesis, and reduce liver output of glucose; 2. Promote liver uptake of glucose and synthesis of liver glycogen; 3. Promote muscle and adipose tissue to take up glucose and amino acids, promote protein and fat synthesis and storage; 4. Promote the liver to produce very low density lipoprotein and activate lipoprotein lipase, promote the decomposition of very low density lipoprotein; 5. Inhibit the decomposition of fat and protein in fat and muscle, inhibit the production of ketone bodies and promote the use of ketone bodies by surrounding tissues.