Quinoline-4-carboxylic acid derivatives are privileged scaffolds in drug discovery, with potential as inhibitors of human dihydroorotate dehydrogenase (HsDHODH), a clinically validated target in cancer and autoimmune diseases. Here, we report computational and structural studies of a series of 6-fluoro-2-(aryl)quinoline-4-carboxylic acids, focusing on their mechanistic basis of inhibition. Molecular docking and molecular dynamics simulations predicted stable binding of compounds 2d and 2e within the HsDHODH binding site. These findings, corroborated by MM-PBSA free energy calculations, suggest a solvent-assisted anchoring mechanism that differs from the binding mode of brequinar. Enzymatic assays confirmed nanomolar potency for compound 2d (IC50 = 27 ± 1 nM), comparable to brequinar, while other derivatives displayed micromolar activity. Crucially, X-ray crystallography of the 2d–HsDHODH complex provided direct structural confirmation of the computationally predicted binding mode. In parallel, ADME modeling predicted a lower Log P for 2d compared with brequinar, pointing to more favorable physicochemical properties. Together, these results establish compound 2d as a potent and drug-like HsDHODH inhibitor and illustrate how integrated computational and structural approaches can elucidate binding determinants of known scaffolds and guide future inhibitor design.
Viana et al. (Mon,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: