ArticlePloS one2026
Identification of new fucosyltransferase-8 inhibitors: An integrated biochemical, biophysical, and computational approach.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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7 authors.
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Abstract
The α-1,6-fucosyltransferase (FUT8) mediated core fucosylation is responsible for several pathophysiological processes, including prostate cancer progression. FUT8 is a promising therapeutic target owing to its effects on cell migration and its capacity to convert androgen-dependent prostate cancer cells into androgen-independent cells. This study, therefore, investigates potential FUT8 inhibitors as therapeutic options for prostate cancer by targeting FUT8-mediated core fucosylation using in vitro, biophysical, and computational approaches. Eight of the 265 compounds showed significant cytotoxicity against the prostate cancer (PC3) cell line in in vitro screening. These compounds demonstrated dose-dependent reductions in cell viability, with IC50 values ranging from 2.94 ± 0.04 to 75.82 ± 2.10 µM. These compounds were non-cytotoxic against the normal human fibroblast (BJ) cell line. Biophysical and in silico analyses were conducted on active compounds to obtain atomic-level structural details of interactions between FUT8 and ligands. Among these, compounds 1, 3, 6, and 7 showed significant Saturation Transfer Difference Nuclear Magnetic Resonance (STD-NMR) effects and induced a decrease in the melting temperature (Tm) of FUT8 in the differential scanning fluorimetry (DSF) assay (0.25°C-9°C), indicating ligand-associated destabilization of the protein. Molecular docking and molecular dynamics simulation results showed that compounds 1, 2, 3, 4, 6, and 7 stably interacted with the FUT8 binding site. These compounds also exhibited anti-migratory activity in a scratch cell assay, as indicated by scratch closure of only 3.14% to 14.18%, compared with 45.45% to 100% in the control group. Our study identified compounds 1, 3, 6, and 7 as promising leads against the FUT8 enzyme. Further mechanistic and in vivo studies are required to evaluate their mechanisms of action for FUT8-driven prostate cancer progression.
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