This product is a sulfonamide antibiotic. When used in combination with trimethoprim, it can double block bacterial folate metabolism and enhance the synergistic antibacterial effect, especially the antibacterial effect on Escherichia coli, Haemophilus influenzae, and Staphylococcus aureus is significantly enhanced compared with a single drug.

This product is a sulfonamide antibiotic. When used in combination with sulfamethoxazole, it can double block bacterial folate metabolism, enhance synergistic antibacterial effects, and reduce the emergence of drug-resistant strains.

1. Pharmacology This product is a sulfonamide antibacterial drug, a compound preparation of sulfamethoxazole (SMZ) and trimethoprim (TMP). It has good antibacterial effects on non-enzyme-producing Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, Escherichia coli, Klebsiella, Salmonella, Proteus, Morganella, Shigella and other Enterobacteriaceae, Neisseria gonorrhoeae, Neisseria meningitidis, and Haemophilus influenzae. In particular, the antibacterial effect on Escherichia coli, Haemophilus influenzae, and Staphylococcus aureus is significantly enhanced compared with SMZ alone. In addition, it also has good antimicrobial activity against Chlamydia trachomatis, Nocardia asteroides, protozoa, and Toxoplasma in vitro. The mechanism of action of this product is: SMZ acts on the action of dihydrofolate reductase, and the combination of the two can double-block the folic acid metabolism of bacteria. The synergistic antibacterial effect of this product is enhanced compared with a single drug, and the number of drug-resistant strains is reduced. However, in recent years, bacterial resistance to this drug has also been on the rise.

This product is a quinolone antibacterial drug, which has antibacterial effects on Gram-negative bacteria, such as Escherichia coli, Klebsiella pneumoniae, Enterobacter aerogenes, Proteus mirabilis, Serratia, Salmonella typhi, Shigella, Pseudomonas aeruginosa, etc. This product acts on bacterial DNA gyrase, interfering with the synthesis of bacterial DNA, thereby causing bacterial death.

By inhibiting the early synthesis of bacterial cell walls, bacterial cell wall synthesis is inhibited, leading to their death

Interfere with bacterial folic acid metabolism, selectively inhibit the activity of bacterial dihydrofolate reductase, prevent dihydrofolate from being reduced to tetrahydrofolate, and prevent the synthesis of bacterial nucleic acids and proteins

By inhibiting the early synthesis of bacterial cell walls, bacterial cell wall synthesis is inhibited, leading to their death

Interfere with bacterial folic acid metabolism, selectively inhibit the activity of bacterial dihydrofolate reductase, prevent dihydrofolate from being reduced to tetrahydrofolate, and prevent the synthesis of bacterial nucleic acids and proteins

1. Stimulate the pancreatic beta cells to secrete insulin, the prerequisite is that the pancreatic beta cells still have a certain ability to synthesize and secrete insulin; 2. By increasing the level of portal vein insulin or directly acting on the liver, inhibiting liver glycogenolysis and gluconeogenesis, the liver produces and outputs less glucose; 3. It may also increase the sensitivity of extra-pancreatic tissues to insulin and the utilization of sugar (probably mainly through post-receptor effects). Therefore, the overall effect is to lower fasting blood sugar and postprandial blood sugar.