Plazomicin

Plazomicin exerts a bactericidal action against susceptible bacteria by binding to bacterial 30S ribosomal subunit. Aminoglycosides typically bind to the ribosomal aminoacyl-tRNA site (A-site) and induce a conformational change to further facilitate the binding between the rRNA and the antibiotic. This leads to codon misreading and mistranslation of mRNA during bacterial protein synthesis.

Plazomicin demonstrates potency against Enterobacteriaceae, including species with multidrug-resistant phenotypes such as carbapenemase-producing bacteria and isolates with resistance to all other aminoglycosides. Its antibacterial activity is not inhibited by aminoglycoside modifying enzymes (AMEs) produced by bacteria, such as acetyltransferases (AACs), phosphotransferases (APHs), and nucleotidyltransferases (ANTs). Plazomicin was shown to be effective against Enterobacteriaceae in presence of some beta-lactamases. In clinical settings and in vivo, bacteria shown to be susceptible toward plazomicin include Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, and Enterobacter cloacae. Other aerobic bacteria that may be affected by plazomicin are Citrobacter freundii, Citrobacter koseri, Enterobacter aerogenes, Klebsiella oxytoca, Morganella morganii, Proteus vulgaris, Providencia stuartii, and Serratia marcescens.