<unk>  is a β-lactam antibiotic (which refers to the structural components of the drug molecule itself). As a class, β-lactams inhibit bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins (PBPs). This inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell walls, thus inhibiting cell wall biosynthesis. Bacteria eventually lyse due to ongoing activity of cell wall autolytic enzymes (autolysins and murein hydrolases) in the absence of cell wall assembly. Due to the mechanism of their attack on bacterial cell wall synthesis, β-lactams are considered to be bactericidal. Unlike β-lactams such as penicillin and amoxicillin, which are highly susceptible to degradation by β-lactamase enzymes (produced, for example, nearly universally by S. aureus),<unk>  boasts the additional benefit of resistance to β-lactamase degradation due to the structural configuration of the<unk>  molecule. The syn-configuration of the methoxyimino moiety confers stability against β-lactamases. Consequently, the spectrum of activity is broadened to include several β-lactamase-producing organisms (which would otherwise be resistant to β-lactam antibiotics), as outlined below.<unk> , like other β-lactam antibiotics, does not only block the division of bacteria, including cyanobacteria, but also the division of cyanelles, the photosynthetic organelles of the glaucophytes, and the division of chloroplasts of bryophytes. In contrast, it has no effect on the plastids of the vascular plants. This supports the endosymbiotic theory and indicates an evolution of plastid division in land plants.
Cefotaxime
Meropenem
Cefepime
Cefazolin
Aztreonam
Vancomycin
Ceftazidime
Imipenem