It inhibits bacterial protein synthesis by hindering the bacterial transpeptidation process. It has antibacterial effects on a variety of Gram-positive aerobic bacteria, Gram-negative aerobic bacteria, anaerobic bacteria, sexually transmitted disease microorganisms and other microorganisms. The mechanism of action is the same as that of erythromycin, mainly binding to the 50S subunit of the bacterial ribosome to inhibit RNA-dependent protein synthesis.

By hindering the bacterial transpeptidation process and inhibiting bacterial protein synthesis, it has antibacterial effects on a variety of Gram-positive aerobic bacteria, Gram-negative aerobic bacteria, anaerobic bacteria, sexually transmitted disease microorganisms and other microorganisms. The mechanism of action is the same as that of erythromycin, mainly binding to the 50S subunit of the bacterial ribosome to inhibit RNA-dependent protein synthesis.

Telmisartan is a specific angiotensin II receptor (ATⅠ type) antagonist. Telmisartan replaces angiotensin II receptors and binds to ATⅠ receptor subtypes with high affinity. It has no agonist effect at any site, selectively binds to ATⅠ receptors, and the binding effect is long-lasting. Telmisartan has no affinity for other receptors, does not inhibit human plasma renin, does not block ion channels, and does not inhibit angiotensin converting enzyme Ⅱ. Administration of 80 mg of telmisartan can almost completely inhibit the increase in blood pressure caused by angiotensin Ⅱ, and the inhibitory effect lasts for more than 24 hours. The antihypertensive effect gradually becomes obvious within 3 hours after the first dose, and the maximum antihypertensive effect can be obtained and maintained 4 weeks after the start of treatment. If treatment is suddenly interrupted, blood pressure gradually returns to the pre-treatment level, and rebound hypertension does not occur. In clinical trials, the incidence of dry cough in the telmisartan treatment group was significantly lower than that in the angiotensin converting enzyme inhibitor treatment group.

In two clinical studies, it was found that simvastatin can moderately enhance the anticoagulant effect of bean-scented anticoagulants. Prothrombin time should be checked frequently before early anticoagulant therapy and simvastatin use in adults to determine whether there is a significant change in prothrombin time. When patients taking bean-scented derivatives have a stable prothrombin time, it is recommended to continue monitoring prothrombin time for a fixed period of time. If the dose of simvastatin is changed, the above procedure should be followed. In patients not taking anticoagulants, simvastatin treatment has never been reported to affect bleeding or prothrombin time.

This product is a methylhydroxyglutaryl coenzyme A (HMG-COA) reductase inhibitor, which inhibits the synthesis of endogenous cholesterol and is a blood lipid regulator. Literature data show that it can reduce the cholesterol (TC) content in the serum, liver, and aorta of hyperlipidemia rabbits, and reduce the levels of very low density lipoprotein cholesterol (VLDL-C) and low density lipoprotein cholesterol (LDL-C).