It acts on the second step of folic acid anabolism and selectively inhibits the action of dihydrofolate reductase. When used in combination with sulfamethoxazole, it can double-block the bacterial folic acid metabolism and enhance the synergistic antibacterial effect.

It acts on dihydrofolate synthase, interfering with the first step of folic acid synthesis. When used in combination with trimethoprim, it can double-block the bacterial folic acid metabolism and enhance the synergistic antibacterial effect.

It acts on the second step of folic acid anabolism, selectively inhibits the action of dihydrofolate reductase, and when used in combination with sulfamethoxazole, the bacterial folic acid metabolism is doubly blocked, thereby enhancing the synergistic antibacterial effect and reducing drug-resistant strains.

It acts on dihydrofolate synthase, interfering with the first step of folic acid synthesis. When used in combination with trimethoprim, the bacterial folic acid metabolism is doubly blocked, thereby enhancing the synergistic antibacterial effect and reducing drug-resistant strains. In particular, the antibacterial effect on Escherichia coli, Haemophilus influenzae, and Staphylococcus aureus is significantly enhanced compared to a single drug.

It selectively inhibits the action of dihydrofolate reductase. When used in combination with sulfamethoxazole, it can double-block the bacterial folate metabolism, enhance the synergistic antibacterial effect, and reduce drug-resistant strains.

It acts on dihydrofolate synthase, interfering with the first step of folic acid synthesis. When used in combination with trimethoprim, it can doubly block the bacterial folic acid metabolism, enhance the synergistic antibacterial effect, and reduce drug-resistant strains.

It acts on the second step of folic acid anabolism and selectively inhibits the action of dihydrofolate reductase. When used in combination with sulfamethoxazole, the bacterial folic acid metabolism is doubly blocked, and the synergistic antibacterial effect is enhanced compared with a single drug, reducing the number of strains that are resistant to it.

It acts on dihydrofolate synthase, interfering with the first step of folic acid synthesis; when used in combination with trimethoprim, the bacterial folic acid metabolism is doubly blocked, and the synergistic antibacterial effect is enhanced compared to a single drug, reducing the number of strains that are resistant to it.

H2 receptor antagonist, significantly inhibits the basal and nocturnal gastric acid secretion in normal people and ulcer patients, as well as the gastric acid secretion caused by pentagastrin, histamine and meals; has a certain inhibitory effect on the secretion of pepsinogen; has a protective effect on experimental gastric mucosal damage and acute ulcers; has no effect on the secretion of gastrin and sex hormones.