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Ramoplanin, a potent cyclic lipoglycodepsipeptide antibiotic, has been reported to be active against aerobic and anaerobic gram-positive bacteria. Mechanistic studies show that Ramoplanin prevents cell wall peptidoglygan formation and further enzymatic processing via binding to lipid II, a key intermediate moeity. Ramoplanin has also displayed a low affinity for Lipid I, a substrate for the MurG step of cell wall formation. >> Read More
Ramoplanin is an actinomycetes-derived antibiotic with broad-spectrum activity against Gram-positive bacteria that has been evaluated in clinical trials for the treatment of gastrointestinal vancomycin-resistant enterococci (VRE) and Clostridium difficile infections. Recent studies have proposed that ramoplanin binds to bacterial membranes as a C2 symmetrical dimer that can sequester Lipid II, which causes inhibition of cell wall peptidoglycan biosynthesis and cell death. In this study, ramoplanin was shown to bind to anionic and zwitterionic membrane mimetics with a higher affinity for anionic membranes and to induce membrane depolarization of methicillin-susceptible Staphylococcus aureus (MSSA) ATCC 25923 at concentrations at or above the minimal bactericidal concentration (MBC). The ultrastructural effects of ramoplanin on S. aureus were also examined by transmission electron microscopy (TEM), and this showed dramatic changes to bacterial cell morphology. The correlation observed between membrane depolarization and bacterial cell viability suggests that this mechanism may contribute to the bactericidal activity of ramoplanin.
Cheng, M., Huang, J. X., Ramu, S., Butler, M. S., & Cooper, M. A. (2014). Ramoplanin at bactericidal concentrations induces bacterial membrane depolarization in Staphylococcus aureus. Antimicrobial agents and chemotherapy, 58(11), 6819-6827.
Ramoplanin, a novel antibiotic with activity against aerobic and anaerobic gram-positive bacteria, acts to prevent cell wall peptidoglycan formation by binding to a key intermediate moiety, lipid II. It has been fast-tracked by the US FDA for the prevention of enterococcal infections and the treatment of Clostridium difficile. The minimum inhibitory concentration(90s) have been < or = 1.0 microg/ml against gram-positive organisms examined. In carriers of vancomycin-resistant enterococci, a double-blind, placebo-controlled Phase II trial of two doses of ramoplanin versus placebo showed proof of concept. A second Phase II trial also demonstrated the equivalence of ramoplanin compared with vancomycin for the treatment of C. difficile colitis. The clinical value and place in therapy of ramoplanin is dependent upon the results of Phase III trials addressing its utility in suppressing carriage of target organisms in the gastrointestinal tract or in the nares.
Fulco, P., & Wenzel, R. P. (2006). Ramoplanin: a topical lipoglycodepsipeptide antibacterial agent. Expert review of anti-infective therapy, 4(6), 939-945.