Complestatin exerts antibacterial activity by the inhibition of fatty acid synthesis

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Complestatin exerts antibacterial activity by the inhibition of fatty acid synthesis
Yun Ju Kwon; Hyun Ju Kim; Won Gon Kim
Bibliographic Citation
Biological & Pharmaceutical Bulletin, vol. 38, no. 5, pp. 715-721
Publication Year
Bacterial enoyl-acyl carrier protein (ACP) reductase has been confirmed as a novel target for antibacterial drug development. In the screening of inhibitors of Staphylococcus aureus enoyl-ACP reductase (FabI), complestatin was isolated as a potent inhibitor of S. aureus FabI together with neuroprotectin A and chloropeptin I from Streptomyces chartreusis AN1542. Complestatin and related compounds inhibited S. aureus FabI with IC50 of 0.3-0.6 μM. They also prevented the growth of S. aureus as well as methicillin-resistance S. aureus (MRSA) and quinolone-resistant S. aureus (QRSA), with minimum inhibitory concentrations (MICs) of 2-4 μg/mL. Consistent with its FabI-inhibition, complestatin selectively inhibited the intracellular fatty acid synthesis in S. aureus, whereas it did not affect the macromolecular biosynthesis of other cellular components, such as DNA, RNA, proteins, and the cell wall. Additionally, supplementation with exogenous fatty acids reversed the antibacterial effect of complestatin, demonstrating that it targets fatty acid synthesis. In this study, we reported that complestatin and related compounds showed potent antibacterial activity via inhibiting fatty acid synthesis.
AntibacterialComplestatinEnoyl-acyl carrier protein reductaseFatty acid synthesisStaphylococcus aureus
Pharmaceutical Soc Japan
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Division of Research on National Challenges > Infectious Disease Research Center > 1. Journal Articles
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