This product is a second-generation sulfonylurea antidiabetic drug, which is effective for most patients with type 2 diabetes. It can reduce fasting and postprandial blood sugar and reduce glycosylated hemoglobin (HbAlc) by 1% to 2%. The main function of this type of drug is to stimulate pancreatic b cells to secrete insulin, but the prerequisite is that pancreatic b cells still have a certain function of synthesizing and secreting insulin. Its mechanism is to specifically bind to the sulfonylurea receptor on the b cell membrane, thereby closing the K channel, causing changes in membrane potential, opening the Ca2 channel, and increasing intracellular Ca2, which promotes insulin secretion. In addition, there are extra-pancreatic effects, including improving the insulin resistance of peripheral tissues (such as liver, muscle, and fat).

Lowers cholesterol (TC), triglycerides (TG), increases high-density lipoprotein (HDL), suitable for patients with various hyperlipidemia

Proton pump inhibitor. This product is a fat-soluble weakly alkaline drug that is easily concentrated in an acidic environment. Therefore, after oral administration, it can be specifically distributed in the secretory tubules of the gastric mucosal parietal cells and converted into the active form of sulfenamide in this high-acid environment. It then irreversibly combines with the sulfhydryl group of the H,K-ATPase (also known as the proton pump) in the secretory membrane of the parietal cells through a disulfide bond to form a complex of sulfenamide and the proton pump, thereby inhibiting the activity of the enzyme and blocking the final step of gastric acid secretion. Therefore, this product has a strong and lasting inhibitory effect on gastric acid secretion caused by various reasons.

Proton pump inhibitor. This product is a fat-soluble weakly alkaline drug that is easily concentrated in an acidic environment. Therefore, after oral administration, it can be specifically distributed in the secretory tubules of the gastric mucosal parietal cells and converted into the active form of sulfenamide in this high-acid environment. It then irreversibly combines with the sulfhydryl group of the H,K-ATPase (also known as the proton pump) in the secretory membrane of the parietal cells through a disulfide bond to form a complex of sulfenamide and the proton pump, thereby inhibiting the activity of the enzyme and blocking the final step of gastric acid secretion. Therefore, this product has a strong and lasting inhibitory effect on gastric acid secretion caused by various reasons.

This product is a second-generation cephalosporin antibiotic. After oral administration, it is hydrolyzed into cefuroxime to exert its antibacterial effect. Its activity against Gram-positive cocci is similar to or slightly worse than that of the first-generation cephalosporins, but it is quite stable against β-lactamase produced by Staphylococci and Gram-negative bacilli. Except for methicillin-resistant Staphylococci, Enterococci and Listeria, other positive cocci (including anaerobic cocci) are sensitive to this product. Its antibacterial activity against Staphylococcus aureus is worse than that of cefazolin. 1-2 mg/L can inhibit all Staphylococcus aureus that are sensitive and resistant to penicillin, respectively. It has strong antibacterial activity against Haemophilus influenzae, and Escherichia coli, Proteus mirabilis, etc. are sensitive to this product; indole-positive Proteus, Citrobacter and Acinetobacter are poorly sensitive to this product, most Serratia are resistant, Pseudomonas aeruginosa, Campylobacter and Bacteroides fragilis are resistant to this product. The mechanism of action is to inhibit the synthesis of bacterial cell walls.