Answers are grounded in this paper and cite their sources.
High-throughput screening identified potent FabX inhibitors in H. pylori, suggesting new antibacterial strategies.
Unsaturated fatty acids (UFAs) are essential for the membrane function in most bacteria. In Helicobacter pylori (H. pylori), a gastric pathogen, UFA biosynthesis depends on the bifunctional dehydrogenase/isomerase FabX, a promising target against H. pylori. Herein, we report the first FabX inhibitor, P61G11 (compound 1, IC50 = 3.7 ± 0.2 μM), identified via high-throughput screening and featuring a 1,3,4-thiadiazole sulfonamide scaffold. The costructure of FabX-1 reveals occupancy of the L-shaped substrate-binding tunnel via hydrophobic interactions and hydrogen bonds. Structure-based optimization led to more potent derivatives, among which compound 47 showed potent inhibition (IC50 = 0.128 ± 0.002 μM), representing a 29-fold improvement. Compound 47 also demonstrated strong in vitro antibacterial activity (MIC = 0.5-1 μg/mL), when combined with membrane permeabilizers, efflux pump inhibitors, and clarithromycin, and exhibited narrow-spectrum efficacy against H. pylori, providing a novel strategy for anti-H. pylori therapy.
No takes yet. Share an insight, caveat, or question.
Ruan et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: