ArticleScientific reports2026
Computational investigation of biochanin a targeting DEPTOR in Alzheimer's disease with in vitro cellular validation of neuroprotective activity.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Targeting protein-protein interactions in the BCL-2 family: opportunities for precision oncology.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
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Abstract
Trifolium pratense (TP) L. contains active phytoconstituents such as biochanin A are known to prevent oxidative stress–induced neuronal death in Alzheimer’s disease (AD). This study explored the molecular mechanism of TP phytoconstituents in AD therapy by network pharmacology and computational modelling. Common targets were analyzed via protein–protein interaction (PPI) in STRING and Cytoscape, followed by Gene Ontology (GO). Based on topological parameters DEPTOR (DEP domain–containing mTOR-interacting protein) was selected as a key target. Subsequently, molecular docking, molecular dynamics (MD) simulations, MM-PBSA free energy calculations, and DFT analyses were performed. It revealed that Biochanin A exhibited the highest MM/PBSA energy (− 150.04 kJ/mol) compared to the standard drug (− 24.01 kJ/mol) and formed stable interactions with key residues (Lys131 and Arg138). Moreover, the currently available therapy targeting the cholinesterase enzyme-related pathways is inadequate, as it displays only symptomatic treatment and fails to address the underlying neurodegenerative molecular mechanisms related to AD. In addition to computational analyses, in vitro validation was performed to confirm the neuroprotective effect of biochanin A. Using the MTT assay, increasing concentrations of Aβ₁–₄₂ (0.625–20 µM) were shown to reduce SH-SY5Y cell viability in a dose-dependent manner, with 10 µM Aβ₁–₄₂ causing ~ 48% reduction. Pretreatment with biochanin A (6.25–100 µM) significantly improved cell survival, with 100 µM restoring viability to ~ 82% of control levels (P < 0.01), indicating a dose-dependent neuroprotective effect without marked cytotoxicity below 100 µM. Overall, this integrative study reveals that biochanin A may target DEPTOR and stabilize mTOR regulatory interactions, suggesting a promising computationally supported and experimentally validated neuroprotective mechanism for Alzheimer’s disease therapy.
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