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Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder in which declining acetylcholinesterase activity increases the relative importance of butyrylcholinesterase (BChE) in cholinergic regulation. Compound 4u, a donepezil–melatonin hybrid, was previously reported to inhibit human BChE with a half-maximal inhibitory concentration of 56 nM. We investigated its BChE-bound dynamics using three independently propagated 200 ns molecular dynamics replicas and a 100 ns simulation of crystallographically bound tacrine, totaling 700 ns. Compound 4u remained within the binding gorge in all three replicas, with persistent critical-residue contacts and replica-dependent hydrogen bonding. Clustering, supported by an alternative distance-based clustering method, revealed two persistent bound-state ensembles with replica-dependent populations: one ensemble accounted for 74.5%, 16.5%, and 100.0% of snapshots sampled at 1 ns intervals from replicas 1–3, respectively. Equilibrium state populations and kinetic metastability were not established. Despite distinct dominant conformations, the replicas produced complete-trajectory molecular mechanics/generalized Born surface area (MM/GBSA) estimates (−47.11, −45.66, and −48.66 kcal/mol for replicas 1–3, respectively) and shared a stabilizing core involving Trp82, Leu286, Phe329, and Tyr332. Tacrine retained its crystallographic anchoring environment. These results indicate that compound 4u combines persistent BChE engagement with conformational adaptability, providing testable structural hypotheses for future analogue design and experimental validation.
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Haskologlu et al. (2026) studied this question.
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