Aztreonam (also known as SQ 26776) is a synthetic monocyclic beta-lactam antibiotic, used to treat Gram-negative aerobic bacteria infection. It has a very high affinity for penicillin-binding protein 3 (PBP-3). 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. 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.[1-3]
In Vitro
Aztreonam (SQ-26,776) is a synthetic monocyclic beta-lactam antibiotic (a monobactam), with the nucleus based on a simpler monobactam isolated from Chromobacterium violaceum. It was approved by the U.S. Food and Drug Administration in 1986. It is resistant to some beta-lactamases, but is inactivated by extended-spectrum beta-lactamases. Aztreonam has no useful activity against gram-positive or anaerobic microorganisms[1]. Aztreonam (SQ-26) is similar in action to penicillin. It inhibits mucopeptide synthesis in the bacterial cell wall, thereby blocking peptidogly can crosslinking. It has a very high affinity for penicillin-binding protein 3 (PBP-3) and mild affinity for PBP-1a. Aztreonam (SQ-26) binds the penicillin-binding proteins of gram-positive and anaerobic bacteria very poorly and is largely ineffective against them. Aztreonam (SQ-26) is bactericidal but less so than some of the cephalosporins[2].
In Vivo
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[3]
[1]. Kobayashi Y, et al. Synergy with aztreonam and arbekacin or tobramycin against Pseudomonas aeruginosa isolated from blood. J Antimicrob Chemother. 1992 Dec;30(6):871-2.
[2]. Guay DR, et al. Aztreonam, a new monobactam antimicrobial. Clin Pharm. 1985 Sep-Oct;4(5):516-26. [3]. Ohmori S, et al. Pharmacology,?994, 48(3), 137-142.