This drug belongs to Class 2A, i.e., a β1-receptor blocker without partial agonist activity (cardioselective β-receptor blocker). It has a selective blocking effect on β1-receptors, no PAA (partial agonist activity), and no membrane stabilizing effect. Its effect on blocking β-receptors is approximately equal to that of propranolol (PP), and its selectivity for β1-receptors is slightly inferior to that of atenolol. Metoprolol's effects on the heart, such as slowing heart rate, inhibiting cardiac contractility, reducing automaticity, and delaying atrioventricular conduction time, are similar to those of propranolol and atenolol (AT). Its effect on reducing elevated blood pressure and heart rate during exercise testing is also similar to that of PP and AT. Its contraction effect on vascular and bronchial smooth muscle is weaker than that of PP, so its effect on the respiratory tract is also smaller, but still stronger than that of AT. Metoprolol can also reduce plasma renin activity.

This product belongs to the aminoglycoside antibiotics. The antibacterial spectrum is similar to that of gentamicin. It has antibacterial effects on Gram-negative bacteria such as Escherichia coli, aerogenes, Klebsiella, Proteus mirabilis, some indole-positive Proteus, Pseudomonas aeruginosa, some Neisseria, some non-pigmented Serratia and Shigella; the antibacterial effect of this product on Pseudomonas aeruginosa is 3 to 5 times stronger than that of gentamicin, and Pseudomonas aeruginosa that is moderately sensitive to gentamicin is highly sensitive to this product. Among Gram-positive bacteria, Staphylococcus aureus (including b-lactamase-producing strains) is sensitive to this product; Streptococci (including Streptococcus pyogenes, Pneumococcus, Streptococcus faecalis, etc.) are all resistant to this product. Anaerobic bacteria (Bacteroides), Mycobacterium tuberculosis, Rickettsia, viruses and fungi are also resistant to this product. The mechanism of action of this product is to bind to the 30S subunit of the bacterial ribosome and inhibit the synthesis of bacterial proteins.

Pharmacological action not specified

Vitamin D2 must be converted by both the liver and kidneys to become biologically active vitamin D3, which regulates calcium and phosphorus metabolism. In this conversion process, only a portion of vitamin D2 is ultimately converted into vitamin D3. Therefore, the biological activity of vitamin D2 is far inferior to that of vitamin D3.

It must be converted by both the liver and kidneys to become biologically active vitamin D3, which plays a role in regulating calcium and phosphorus metabolism. In this conversion process, only a portion of vitamin D2 is ultimately converted into vitamin D3. Therefore, the biological activity of vitamin D2 is far inferior to that of vitamin D3.

Vitamin D2 must be converted by both the liver and kidneys to become biologically active vitamin D3, which regulates calcium and phosphorus metabolism. In this conversion process, only a portion of vitamin D2 is ultimately converted into vitamin D3. Therefore, the biological activity of vitamin D2 is far inferior to that of vitamin D3.

This product is first converted into 5-fluoro-2-deoxyuridine nucleotide in the body, which inhibits thymine nucleotide synthetase, blocking the conversion of deoxyuridine nucleotide into deoxythymine nucleotide, thereby inhibiting DNA biosynthesis. In addition, by preventing uracil and orotic acid from incorporating into RNA, the effect of inhibiting RNA synthesis is achieved. This product is a cell cycle-specific drug that mainly inhibits S-phase cells.