Antibiotics, Journal Year: 2024, Volume and Issue: 13(12), P. 1169 - 1169
Published: Dec. 3, 2024
Mycobacteria tuberculosis (Mtb) infection causes (TB). TB is one of the most intractable infectious diseases, causing over 1.13 million deaths annually. Under harsh growing conditions, innate response mycobacteria to shut down its respiratory metabolism a basal level, transit into dormant, non-replicating phase preserve viability, and establish latent infection. Mtb utilizes non-canonical regulatory mechanisms, such as alternative oxidase pathways, survive in low oxygen/nutrient conditions. The bacterium’s survival native microenvironmental niches aided by ability evolve mutations drug binding sites, enhance overexpression various enzymes that activate β-lactam antibiotics hydrolysis, or stimulate efflux pathways ward off effect antibiotics. Bedaquiline 3,5-dialkoxypyridine analogs, sudapyridine squaramide S31f, have been shown be potent F1FO-ATP synthase inhibitors replicating brought oxidative phosphorylation focus an anti-TB target. In this review, we attempt highlight structural pathogen-specific epitopes F1-domain, ligand development on classes targeting Fo-domain, metabolic responses employs bedaquiline ensure
Language: Английский