Nateglinide is an amino acid derivative and an oral antidiabetic drug used to treat patients with type 2 diabetes. The action of nateglinide depends on the function of pancreatic beta cells. Nateglinide binds to the ATP-sensitive K channel receptor on the beta cell membrane and closes it, causing cell depolarization, calcium channel opening, calcium influx, stimulating insulin secretion, and lowering blood sugar. The insulin secretion-promoting effect of nateglinide depends on the glucose level. When the glucose level is low, the insulin secretion is weakened. Nateglinide has a high degree of tissue selectivity and has a low affinity for cardiac muscle and skeletal muscle.

Nateglinide is an amino acid derivative and an oral antidiabetic drug used to treat patients with type 2 diabetes. The action of nateglinide depends on the function of pancreatic beta cells. Nateglinide binds to the ATP-sensitive K channel receptor on the beta cell membrane and closes it, causing cell depolarization, calcium channel opening, calcium influx, stimulating insulin secretion, and lowering blood sugar. The insulin secretion-promoting effect of nateglinide depends on the glucose level. When the glucose level is low, the insulin secretion is weakened. Nateglinide has a high degree of tissue selectivity and has a low affinity for cardiac muscle and skeletal muscle.

This product is a nitroimidazole derivative that can inhibit the redox reaction of amoeba and break the nitrogen chain of the protozoa. In vitro tests have shown that when the drug concentration is 1~2mg/L, the histolytica amoeba can undergo morphological changes in 6~20 hours and all are killed within 24 hours. When the concentration is 0.2mg/L, the histolytica amoeba can be killed within 72 hours. This product has a strong effect of killing trichomonas, and its mechanism is unknown. Metronidazole has a killing effect on anaerobic microorganisms, and the metabolites generated when it is reduced in the human body also have anti-anaerobic effects, inhibiting the synthesis of bacterial deoxyribonucleic acid, thereby interfering with the growth and reproduction of bacteria, and ultimately causing bacterial death. It has a carcinogenic effect on some animals.

Trimethoprim (TMP) is an antibacterial agent, a lipophilic weak base, and its chemical structure belongs to the pyrimethamine class. It has antibacterial activity against Escherichia coli, Klebsiella, Proteus mirabilis, Salmonella, and Shigella, but has no obvious antibacterial effect on Streptococcus pneumoniae, Neisseria gonorrhoeae, and Neisseria meningitidis, and has no effect on Pseudomonas aeruginosa. The mechanism of action of this product is to interfere with bacterial folic acid metabolism. It mainly selectively inhibits the activity of bacterial dihydrofolate reductase, so that dihydrofolate cannot be reduced to tetrahydrofolate, and synthetic folic acid is the main component of nucleic acid biosynthesis. Therefore, this product prevents the synthesis of bacterial nucleic acids and proteins, and the binding of this product to bacterial dihydrofolate reductase is 50,000 to 60,000 times tighter than that to mammalian enzymes. The combination of this product and sulfonamides can double block the bacterial folic acid synthesis metabolism, have a synergistic effect, enhance the antibacterial activity of sulfonamides, and convert the antibacterial effect into a bactericidal effect, reducing the production of drug-resistant strains.

Trimethoprim (TMP) is an antibacterial agent, a lipophilic weak base, and its chemical structure belongs to the pyrimethamine class. It has antibacterial activity against Escherichia coli, Klebsiella, Proteus mirabilis, Salmonella, and Shigella, but has no obvious antibacterial effect on Streptococcus pneumoniae, Neisseria gonorrhoeae, and Neisseria meningitidis, and has no effect on Pseudomonas aeruginosa. The mechanism of action of this product is to interfere with bacterial folic acid metabolism. It mainly selectively inhibits the activity of bacterial dihydrofolate reductase, so that dihydrofolate cannot be reduced to tetrahydrofolate, and synthetic folic acid is the main component of nucleic acid biosynthesis. Therefore, this product prevents the synthesis of bacterial nucleic acids and proteins, and the binding of this product to bacterial dihydrofolate reductase is 50,000 to 60,000 times tighter than that to mammalian enzymes. The combination of this product and sulfonamides can double block the bacterial folic acid synthesis metabolism, have a synergistic effect, enhance the antibacterial activity of sulfonamides, and convert the antibacterial effect into a bactericidal effect, reducing the production of drug-resistant strains.