The third generation of oral cephalosporins kill bacteria by inhibiting bacterial cell wall synthesis. They are stable to most β-lactamases and have good antibacterial effects on Gram-positive cocci such as pneumococci and Streptococcus pyogenes, and Gram-negative bacilli such as Haemophilus influenzae (including enzyme-producing strains), Moraxella catarrhalis (including enzyme-producing strains), Escherichia coli, Proteus mirabilis, and Neisseria gonorrhoeae (including enzyme-producing strains). In vitro, they also have antibacterial activity against Streptococcus pneumoniae, Parainfluenzae, Proteus vulgaris, Klebsiella pneumoniae, Pasteurella multocida, Providencia, Salmonella, Shigella, Serratia marcescens, Citrobacter heteromorphis, and Citrobacter malonate, but their clinical effectiveness has not yet been established. They have poor antibacterial effects on Staphylococcus, and have no antibacterial effects on Pseudomonas aeruginosa, Enterobacter, Bacteroides fragilis, and Clostridium.

The third generation of oral cephalosporins kill bacteria by inhibiting bacterial cell wall synthesis. They are stable to most beta-lactamases and have good antibacterial effects on Gram-positive cocci such as pneumococci and Streptococcus pyogenes, and Gram-negative bacilli such as Haemophilus influenzae (including enzyme-producing strains), Moraxella catarrhalis (including enzyme-producing strains), Escherichia coli, Proteus mirabilis, and Neisseria gonorrhoeae (including enzyme-producing strains). In vitro, they also have antibacterial activity against Streptococcus pneumoniae, Parainfluenzae, Proteus vulgaris, Klebsiella pneumoniae, Pasteurella multocida, Providencia, Salmonella, Shigella, Serratia marcescens, Citrobacter heteromorphis, and Citrobacter malonate, but their clinical effectiveness has not yet been established. They have poor antibacterial effects on Staphylococcus, and have no antibacterial effects on Pseudomonas aeruginosa, Enterobacter, Bacteroides fragilis, and Clostridium.

It achieves bactericidal effect by inhibiting biosynthesis of sensitive bacterial cell walls. When used in combination with sulbactam, it has obvious synergistic effect.

It has an irreversible inhibitory effect on most important β-lactamases produced by β-lactam antibiotic-resistant strains, and can protect β-lactam antibiotics from hydrolysis and destruction by β-lactamases of resistant bacteria. When used in combination with cefoperazone, it has a significant synergistic effect.

It is a third-generation cephalosporin that kills bacteria by inhibiting the biosynthesis of the cell wall of sensitive bacteria.

It has an irreversible inhibitory effect on most important β-lactamases produced by β-lactam antibiotic-resistant strains, and can protect β-lactam antibiotics from hydrolysis and destruction by β-lactamases of resistant bacteria; it can combine with certain penicillin-binding proteins to enhance the sensitivity of this compound preparation

A non-selective β-adrenergic receptor blocker, it blocks both β1 and β2 receptors, has no obvious local anesthetic effect and intrinsic sympathomimetic effect; it has an intraocular pressure-lowering effect on patients with both high and normal intraocular pressure, with a maximum intraocular pressure-lowering amplitude of 7 mmHg; the drug effect can be detected within one hour of instillation, reaches a peak in 2 to 6 hours, and can last for 24 hours after a single dose; the intraocular pressure-lowering mechanism is mainly to reduce the production of aqueous humor

It has antibacterial activity against some Gram-positive and Gram-negative bacteria and is a broad-spectrum antibiotic. In particular, it has a stronger antibacterial effect than other oral cephalosporin antibiotics against Streptococcus (except enterococci) and pneumococci among Gram-positive bacteria, and against gonococci, Branhamella, Escherichia coli, Clostridium, Saccharomyces, Proteus, and Haemophilus influenzae among Gram-negative bacteria. Its mechanism of action is bactericidal. It has extremely strong stability against β-lactamases produced by various bacteria and shows superior antibacterial activity against bacteria that produce β-lactamases. The mechanism of action is to prevent the synthesis of bacterial cell walls. Its point of action varies depending on the species, and it has a higher affinity with 1 (1a, 1b, 1c) and 3 in penicillin-binding protein (PBP).