This product is a mucolytic agent that can increase the secretion of serous glands in the respiratory mucosa and reduce the secretion of mucous glands, thereby reducing sputum viscosity, promoting the secretion of pulmonary surfactant, increasing bronchial ciliary movement, and making sputum easier to cough up.

This product has a broad-spectrum antibacterial effect and strong antibacterial effect. It has strong antibacterial activity against most Enterobacteriaceae, such as Escherichia coli, Klebsiella, Proteus, Salmonella, Shigella, and Gram-negative bacteria such as Haemophilus influenzae, Legionella pneumophila, and Neisseria gonorrhoeae. It also has antibacterial effects on Gram-positive bacteria such as Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes, and Mycoplasma pneumoniae and Chlamydia pneumoniae, but has poor effects on anaerobic bacteria and enterococci. Its mechanism of action is to inhibit the activity of bacterial DNA gyrase, prevent the synthesis and replication of bacterial DNA, and cause bacterial death.

Telmisartan is a specific angiotensin II receptor (ATⅠ type) antagonist. Telmisartan replaces angiotensin II receptors and binds to ATⅠ receptor subtypes with high affinity, 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 (including AT2 and other AT receptors with fewer characteristics), does not inhibit human plasma renin and ion channels, and does not inhibit angiotensin converting enzyme II. Administration of 80 mg of telmisartan to humans 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 of telmisartan, and the maximum antihypertensive effect can be obtained 4 weeks after the start of treatment, and can be maintained in long-term treatment. Sudden interruption of treatment will not cause rebound hypertension, and the incidence of dry cough is significantly lower than that of the angiotensin converting enzyme inhibitor treatment group.

Unspecified

In vivo, it competitively inhibits the rate-limiting enzyme hydroxymethylglutaryl coenzyme A reductase in the cholesterol synthesis process, reducing the synthesis of cholesterol and increasing the synthesis of low-density lipoprotein receptors. Its main site of action is in the liver, resulting in lower blood cholesterol and low-density lipoprotein cholesterol levels, thereby playing a role in the prevention and treatment of atherosclerosis and coronary heart disease. This product also reduces serum triglyceride levels and increases blood high-density lipoprotein levels.