Abstract

The therapeutic effect of the plant-derived component vincetene against neurological diseases was evaluated applying a combined in silico method. Positive drug-likeness was anticipated by pharmacokinetic outlining using SwissADME, which also ascertained no P-glycoprotein substrate interaction, elevated gastrointestinal absorption, and blood-brain barrier permeability. Vincetene attained a bioavailability score of 0.55, exposed no cytochrome P450 inhibition, and coincided with the Lipinski, Veber, Ghose, Egan, and Muegge criteria. While non-carcinogenicity, non-mutagenicity, and non-cytotoxicity were categorically witnessed, toxicological approximations engendered by ProTox-II suggested likely hepatotoxicity, neurotoxicity, immunotoxicity, and respiratory toxicity. A study of network pharmacology uncovered 49 genes that intersected involving targets linked to vincetene and those linked to ataxia, meningitis, and encephalitis. Principal hub genes classified via protein–protein interaction (PPI) network include PI3KCA, AKT2, AKT3, MTOR, and HSP90AA1. Vincetene's role in pathways such as PI3K-Akt, HIF-1, and ErbB signaling, which are essential for neuronal survival, synapse repair, and stress response processes, was elucidated by gene ontology and pathway enrichment analysis. With strong hydrogen bond interfaces comprising fundamental amino acid residues, molecular docking assessments showed that vincetene showed stable binding to three disease-relevant proteins: 2Z83 (-7.6 kcal/mol), 5KTR (-6.1 kcal/mol), and 1Q5K (-8.8 kcal/mol). These findings suggest that vincetene exerts multi-targeted neuroprotective effects and holds promise as a neurotherapeutic lead compound. Overall, this study provisions the tactical repositioning of vincetene for the supervision of complex neurological disorders, paving the way for future experimental research.