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Iclaprim
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Andrew Stewardson, M. Lindsay Grayson
Iclaprim is active against Gram-positive bacteria including Staphylococcus aureus (including methicillin-resistant, vancomycin-intermediate, and vancomycin-resistant strains), streptococci, and enterococci. It also has limited in vitro activity against Gram-negative pathogens including Entero-bacteriaceae and respiratory pathogens such as Haemophilus influenzae, Moraxella catarrhalis, Legionella pneumophila, and Chlamydophila pneumoniae.
Novel developments in the treatment of acute bacterial skin and skin structure infections
Published in Expert Opinion on Pharmacotherapy, 2019
Rupal K. Jaffa, Kelly E. Pillinger, Danya Roshdy, Jacqueline A. Isip, Timothy R. Pasquale
Iclaprim is a diaminopyrimidine with an underutilized mechanism of action, selective bacterial dihydrofolate reductase inhibitor (DHFR). While trimethoprim is the only other currently available DHFR, iclaprim has demonstrated an advantage of increased potency (8- to 32-fold) compared to trimethoprim for all Gram-positive isolates [54]. Iclaprim is an ideal agent for the use in skin infections as it displays a large volume of distribution with high concentrations in skin compartment and demonstrates rapid in vitro bactericidal activity against common pathogens encountered including resistant organisms. In an in vitro study evaluating susceptibility against MRSA isolates which were nonsusceptible to daptomycin, linezolid, or vancomycin, iclaprim maintained activity (MIC < 1 ug/ml) to majority of the isolates [52].
Iclaprim: a differentiated option for the treatment of skin and skin structure infections
Published in Expert Review of Anti-infective Therapy, 2018
Stephanie Noviello, David B. Huang, G. Ralph Corey
Iclaprim is differentiated from other antibiotics used to treat ABSSSI. Unlike other antibiotics, of which there are many that act on the cell wall, cell membrane or protein synthesis, iclaprim’s mechanism of action is selective bacterial DHFR inhibition, of which only trimethoprim is currently available. Iclaprim was designed using X-ray crystallography to be more potent than trimethoprim and to overcome select TMP-R due to its additional hydrophobic interactions in the conserved substrate-binding pocket of bacterial DHFR. Iclaprim retains activity against select trimethoprim-resistant DHFRs, including the F98Y mutant enzyme most commonly associated with TMP-R in S. aureus and the I100L mutation associated with TMP-R in S. pneumoniae. Iclaprim’s increased potency allows use as monotherapy without the need for co-administration of sulfonamides thereby avoiding the sulfonamide-associated safety issues such as rashes, hypersensitivity reactions (e.g. Stevens Johnson Syndrome), blood dyscrasias, nephrotoxicity, drug–drug interactions leading to hypoglycemia or gastrointestinal hemorrhage, and life-threatening hyperkalemia [31]. Therefore, iclaprim’s activity is similar to that of trimethoprim-sulfamethoxazole, but without its safety drawbacks.