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Floridoside (2-(α-D-galactosyl)glycerol) is a compatible solute synthesized in red algae, known for its antioxidant, immunostimulatory, anti-inflammatory, and antimicrobial properties. However, the lack of target validation has limited mechanistic insights into its bioactivity. Mitogen-activated protein kinase 13 (MAPK13), a member of the p38 mitogen-activated protein kinase (p38 MAPK) family with unique structural and functional characteristics, plays an important role in respiratory tissue remodeling, tumor progression, and immune responses, making it an attractive therapeutic target. This study identifies MAPK13 as a high-affinity target of floridoside. In vitro kinase assays validated that floridoside effectively inhibits MAPK13 with a nanomolar inhibitory concentration (IC50 = 13.59 nM), significantly outperforming the classical inhibitor BIRB-796. Unbiased molecular dynamics simulations and steered molecular dynamics simulations reveal that floridoside binds within the MAPK13 hinge region via an ATP-competitive mechanism. Binding free energy analysis combined with computational alanine scanning highlight Asp-113 as a primary interaction hotspot, stabilized by persistent hydrogen bonds with Pro-108 and Met-110. Despite stable complex formation, the flexibility of the glycosidic bond and glycerol tail may limit binding persistence. Comparative simulations with 2-α-glucosylglycerol (2αGG), a stereoisomer of floridoside, demonstrate the sensitivity of MAPK13 binding to subtle structural variations. These findings elucidate the atomistic basis for floridoside’s bioactivity and establish it as a candidate natural scaffold for the design of isoform-selective p38 inhibitors.
Zhong et al. (Wed,) studied this question.
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