Zhejiang Yatai Pharmaceutical Co., Ltd.

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. Then, it 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 third-generation cephalosporin antibiotic. It has high antibacterial activity against Escherichia coli, Klebsiella pneumoniae and other Enterobacteriaceae, Haemophilus influenzae, Pseudomonas aeruginosa, etc. It also has good antibacterial effects on nitrate-negative bacilli, Alcaligenes, etc. Most beta-lactamases produced by bacteria are highly stable, so it can still have antibacterial activity against multi-drug resistant strains of most of the above-mentioned Gram-negative bacilli. Gram-positive cocci such as pneumococci and hemolytic streptococci are highly sensitive to this product, but this product has only moderate activity against staphylococci, while enterococci and methicillin-resistant Staphylococci are often resistant to this product. This product has certain antibacterial activity against anaerobic bacteria such as Peptococcus and Peptostreptococci, but has poor antibacterial effect against Bacteroides fragilis. Its mechanism of action is to bind to penicillin-binding proteins (PBPs) on the bacterial cell membrane, acylate the transpeptidase, inhibit the synthesis of the bacterial septum and cell wall, affect the cross-linking of the cell wall mucopeptide components, inhibit cell division and growth, elongate the bacterial morphology, and finally dissolve and die.

It is a selective β1-adrenergic receptor blocker with no membrane stabilizing effect and endogenous sympathomimetic activity. However, it does not inhibit the bronchodilator effect of isoproterenol. Its mechanism of lowering blood pressure and reducing myocardial oxygen consumption is the same as that of propranolol. Large-scale clinical trials have confirmed that atenolol can reduce the mortality rate of acute myocardial infarction within 0 to 7 days. The therapeutic dose has no significant inhibition on myocardial contractility.

It achieves bactericidal effect by inhibiting the synthesis of bacterial cell wall. It has bactericidal effect on a wide range of common clinical bacteria and can resist hydrolysis by a variety of beta-lactamases. Bacteria sensitive to this product include Gram-positive bacteria, Gram-negative bacteria, anaerobic bacteria, etc.

This product acts specifically on the gastric mucosal parietal cells, reducing the activity of H/KATPase in the parietal cells, thereby inhibiting the secretion of gastric acid. Compared with omeprazole and lansoprazole, this product has a weaker inhibitory effect on cytochrome P450-dependent enzymes. No adverse effects were found in either short-term or long-term administration of pantoprazole. This drug is non-carcinogenic, does not impair fertility, and does not induce teratogenesis. After continuous use of pantoprazole at a dose of 40 to 80 mg/d for 2.5 years, there was no change in various experimental parameters of liver enzymology and cholesterol metabolism.