Second-generation cephalosporin antibiotics are rapidly hydrolyzed into cefuroxime after entering the body. They have strong antibacterial effects on most Gram-positive cocci, good effects on diphtheria and Gram-positive anaerobic bacteria, strong activity on Escherichia coli, Proteus mirabilis, Klebsiella pneumoniae and Haemophilus influenzae, sensitive to some Enterobacter aerogenes, indole-positive Proteus and Providencia, and are also sensitive to Salmonella typhi, Shigella, Neisseria gonorrhoeae and Neisseria meningitidis. They have poor effects on Bacteroides fragilis, and are resistant to Serratia, Alcaligenes, Acinetobacter and Pseudomonas aeruginosa. The mechanism of action is to bind to penicillin-binding proteins (PBPs) on the bacterial cell membrane, inhibit the synthesis of bacterial septa and cell walls, and ultimately lead to bacterial lysis and death.

Second-generation cephalosporin antibiotics, which are rapidly hydrolyzed into cefmandole after entering the body, have strong antibacterial effects on most Gram-positive cocci, have good effects on diphtheria and Gram-positive anaerobic bacteria, have strong activity against Escherichia coli, Proteus mirabilis, Klebsiella pneumoniae and Haemophilus influenzae, are sensitive to some Enterobacter aerogenes, indole-positive Proteus and Providencia, are sensitive to Salmonella typhi, Shigella, Neisseria gonorrhoeae and Neisseria meningitidis, have poor antibacterial effects on Bacteroides fragilis, and are resistant to Serratia, Alcaligenes, Acinetobacter and Pseudomonas aeruginosa. The mechanism of action is to bind to penicillin-binding proteins (PBPs) on the bacterial cell membrane, inhibit the synthesis of bacterial septa and cell walls, affect the cross-linking of cell wall mucopeptide components, inhibit cell division and growth, and eventually cause bacterial lysis and death.

It achieves bactericidal effect by inhibiting biosynthesis of sensitive bacterial cell walls. When used in combination with sulbactam, it has irreversible inhibitory effect on most β-lactamases, thus enhancing the antibacterial effect.

It has an irreversible inhibitory effect on most important β-lactamases produced by β-lactam antibiotic-resistant strains, protects β-lactam antibiotics from hydrolysis and enhances synergistic antibacterial effects.