This product has a broad-spectrum antibacterial effect and strong antibacterial activity, and has strong antibacterial activity against most Enterobacteriaceae. It also has antibacterial effects on Gram-positive bacteria such as Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes, Mycoplasma pneumoniae, and Chlamydia pneumoniae, but has poor effects on anaerobic bacteria and enterococci. Its mechanism of action is to inhibit the activity of bacterial DNA gyrase, prevent the synthesis and replication of bacterial DNA, and cause bacterial death.

The second generation cephalosporin antibiotics have similar or slightly worse antibacterial activity against Gram-positive cocci than the first generation cephalosporins, but are quite stable against beta-lactamase produced by Staphylococci and Gram-negative bacilli. Methicillin-resistant Staphylococci, Enterococci and Listeria are resistant, and other positive cocci (including anaerobic cocci) are sensitive to this product. The antibacterial activity against Staphylococcus aureus is worse than that of cefazolin, and 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. may be sensitive to this product; indole-positive Proteus, Citrobacter and Acinetobacter are poorly sensitive to this product, Serratia is mostly resistant, Pseudomonas aeruginosa, Campylobacter and Bacteroides fragilis are resistant to this product. 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.

Extract from the above information

This product is a proton pump inhibitor of gastric parietal cells. It can specifically inhibit the secretory microtubules and tubular vesicles in the cytoplasm of the parietal cell apical membrane, thereby effectively inhibiting the secretion of gastric acid. Since H, K-ATPase is the last process of acid secretion of parietal cells, this product has a strong acid inhibition ability. It can not only non-competitively inhibit gastric acid secretion caused by gastrin, histamine, choline, food, and stimulation of the vagus nerve, but also inhibit part of the basic gastric acid secretion that is not affected by choline or H2 receptor blockers. It also has a strong and lasting inhibitory effect on gastric acid secretion caused by dibutyl cyclic adenosine monophosphate (DCAMP) stimulation that cannot be inhibited by H2 receptor antagonists. In addition, this product also has an inhibitory effect on pepsin secretion, has no obvious change in gastric mucosal blood flow, and does not affect body temperature, gastric cavity temperature, arterial blood pressure, venous hemoglobin, arterial oxygen partial pressure, carbon dioxide partial pressure and arterial blood pH.