A computational approach to mycolic acid biosynthesis disruption in mycobacterium tuberculosis via molluscan metabolites as KasA inhibitors

Abstract The ongoing global health challenge posed by Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), is exacerbated by the emergence of drug-resistant strains. This study explores the potential of inhibiting the KasA protein, a key component of the bacterium’s type II fatty ac...

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Bibliographic Details
Main Authors: Abdullah R. Alanzi, Fatimah Mohammed Alsulais, Bayan Abdullah Alhaidhal
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-13329-0
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Summary:Abstract The ongoing global health challenge posed by Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), is exacerbated by the emergence of drug-resistant strains. This study explores the potential of inhibiting the KasA protein, a key component of the bacterium’s type II fatty acid synthase system (FAS-II) involved in mycolic acid biosynthesis. Inhibition of KasA could disrupt the integrity of the mycobacterial cell wall, which is crucial for its survival and virulence. In this study, we screened a library of 730 Molluscan metabolites using molecular docking techniques via the Glide tool, identifying ten compounds with significant binding affinities ranging from − 7.535 to -6.517 kcal/mol. The ADMET profiles of these compounds were evaluated, revealing acceptable toxicity levels for four selected candidates: CMNPD7125, CMNPD22991, CMNPD4542, and CMNPD12265. Additionally, molecular dynamics simulations confirmed the stability of these compounds within the KasA binding pocket, reinforcing their potential as effective inhibitors. This integrated approach combining molecular docking, ADMET analysis, and dynamic simulations advances the search for innovative treatments against drug-resistant TB and supports rational drug design efforts for future anti-tubercular agents.
ISSN:2045-2322