Aztreonam (SQ-26,776), a monocyclic beta-lactam antibiotic originally isolated from Chromobacterium violaceum, possesses bactericidal activity.

Aztreonam causes significant suppression of human colony forming unit-erythroid (cfu-e), burst forming unit-erythroid (bfu-e) and colony forming unit-granulocyte macrophage (cfu-gm) at both peak and trough serum concentrations in human bone marrow cells. [1] Aztreonam is hydrolyzed at measurable rates by class A beta-lactamases, a TEM-2 type penicillinase and the Proteus vulgaris cephalosporinase with a broad substraterange. Aztreonam is extremely stable as to the typical class C cephalosporinase of Citrobacter freundii, and acts as a competitive and progressive inhibitor for the beta-lactamase. [2] Aztreonam (AZT) combined with clindamycin (CLDM) has synergistic effects on Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pneumoniae, and Haemophilus influenzae, which are sensitive or quasi-sensitive to CLDM, in the presence of CLDM at MIC or sub-MIC. [3] Aztreonam reduces the cfu of some strains by 1 log unit without preserving the integrity of cystic fibrosis airway cell monolayers, while decreasing the biofilms of other clinical isolates by 4 log units and protecting the monolayers from being compromised. [4]

Aztreonam (300 mg/kg) results in a significant decrease in the content of hepatic microsomal P450, while no significant change is observed in hepatic cytochrome b5 content and NADPH-cytochrome c (P450) reductase activity. [5]