This drug is a central antitussive drug that can inhibit the cough center in the medulla oblongata to produce an antitussive effect. Its antitussive effect is equal to or slightly stronger than that of codeine. The general therapeutic dose does not inhibit breathing, and long-term use is non-addictive and non-tolerant.

This product is a broad-spectrum semi-synthetic cephalosporin antibiotic. Its activity against penicillinase-producing Staphylococcus aureus, group A hemolytic streptococci, viridans streptococci and Staphylococcus epidermidis is the same as that of cefadroxil, and its antibacterial effect against non-enzyme-producing Staphylococcus aureus and pneumococci is 2 to 4 times stronger than that of cefadroxil. Its activity against Gram-negative bacilli, including Escherichia coli and Klebsiella pneumoniae, is stronger than that of cefadroxil, and is similar to that of cefadroxil. Its activity against Proteus mirabilis, Salmonella and Shigella is stronger than that of cefadroxil. 2.9 to 8 mg/L of this product can inhibit all Haemophilus influenzae, including strains resistant to ampicillin. Moraxella catarrhalis and Neisseria gonorrhoeae are very sensitive to this product. Indole-positive Proteus, Serratia, Acinetobacter and Pseudomonas aeruginosa are all resistant to this product. The mechanism of action of this product is to inhibit the synthesis of bacterial cell walls.

This product is a broad-spectrum semi-synthetic cephalosporin antibiotic. Its activity against penicillinase-producing Staphylococcus aureus, group A hemolytic streptococci, viridans streptococci and Staphylococcus epidermidis is the same as that of cefadroxil, and its antibacterial effect against non-enzyme-producing Staphylococcus aureus and pneumococci is 2 to 4 times stronger than that of cefadroxil. Its activity against Gram-negative bacilli, including Escherichia coli and Klebsiella pneumoniae, is stronger than that of cefadroxil, and is similar to that of cefadroxil. Its activity against Proteus mirabilis, Salmonella and Shigella is stronger than that of cefadroxil. 2.9 to 8 mg/L of this product can inhibit all Haemophilus influenzae, including strains resistant to ampicillin. Moraxella catarrhalis and Neisseria gonorrhoeae are very sensitive to this product. Indole-positive Proteus, Serratia, Acinetobacter and Pseudomonas aeruginosa are all resistant to this product. The mechanism of action of this product is to inhibit the synthesis of bacterial cell walls.

Extract from the above information

Telmisartan is a specific angiotensin II receptor (ATⅠ type) antagonist. Telmisartan replaces angiotensin II receptors and binds to ATⅠ receptor subtypes (known angiotensin II action sites) with high affinity. Telmisartan has no agonist effect at any site on the ATⅠ receptor site. Telmisartan 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). The functions of the above other receptors are not yet known, and the excessive receptor stimulation effect that may be caused by the increase in angiotensin II levels caused by telmisartan is also unknown. Telmisartan does not inhibit human plasma renin or block ion channels. Telmisartan does not inhibit angiotensin converting enzyme II, which can also degrade bradykinin and cause adverse reactions. In humans, administration of 80 mg of telmisartan can almost completely inhibit the increase in blood pressure caused by angiotensin II. The inhibitory effect lasts for 24 hours and can still be measured after 48 hours. The antihypertensive effect gradually becomes apparent within 3 hours after the first dose of telmisartan. The maximum antihypertensive effect can be achieved 4 weeks after the start of treatment and can be maintained in long-term treatment. If telmisartan treatment is suddenly interrupted, blood pressure gradually returns to pre-treatment levels after a few days without rebound hypertension. In a clinical trial directly comparing two antihypertensive drugs, the incidence of dry cough in the telmisartan treatment group was significantly lower than that in the angiotensin-converting enzyme inhibitor treatment group.