Repurposing FDA-approved drugs as multi-target neuroprotective agents for Alzheimer’s disease via computational screening and experimental validation

β-site APP-cleaving enzyme 1 (BACE1, a β-secretase) is a key aspartyl protease that initiates the proteolytic processing of the amyloid precursor protein (APP) to form the amyloid-β (Aβ) peptide. Given that Aβ aggregation and plaque formation are a central pathological feature of Alzheimer’s disease (AD), BACE1 remains a critical therapeutic target. Furthermore, the complexity of AD pathology necessitates the identification of novel multi-target agents. This study employed a structure-based virtual screening, targeting the BACE1 approach to identify the potential BACE1 inhibitors from FDA-approved drug scaffolds derived from the ZINC database. Top-ranked candidates were subsequently validated through extensive 500 ns molecular dynamics (MD) simulations and in vitro assays of BACE1 inhibition activity. Furthermore, multi-AD-related target profiling of candidates was conducted using molecular docking and a series of in vitro assays. Among them, ZINC000019796155 emerged as a promising multi-target compound. Biochemical analysis revealed that ZINC000019796155 exhibited moderate inhibitory effects against BACE1. Subsequent assays confirmed its capacity to inhibit butyrylcholinesterase (BuChE) action and Aβ aggregation, function as a free radical scavenger, and provide neuroprotection against H₂O₂-induced oxidative stress in cellular models. Furthermore, western blot analysis elucidated the mechanism of neuroprotection, indicating that ZINC000019796155 inhibits the apoptotic pathway while simultaneously suppressing the formation of Aβ plaques and neurofibrillary tangles (NFTs). These findings highlight ZINC000019796155 as a validated scaffold with a known safety profile for AD. While further structural optimization and preclinical in vivo studies are necessary, this study underscores the potential of ZINC000019796155 as a multi-target neuroprotective agent for AD treatment.

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Publication Details

Journal
Scientific Reports
Published
2026-04-07
DOI
https://doi.org/10.1038/s41598-026-46708-2
Primary Topic
Cholinesterase and Neurodegenerative Diseases
Type
article
Field-Weighted Citation Impact
0.00

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article

Repurposing FDA-approved drugs as multi-target neuroprotective agents for Alzheimer’s disease via computational screening and experimental validation

Pattaporn Poonsawas, Chantana Boonyarat, Khemjira Phemphunananchai, Jutarop Phetcharaburanin et al.
Scientific Reports
Cholinesterase and Neurodegenerative Diseases
article

Repurposing FDA-approved drugs as multi-target neuroprotective agents for Alzheimer’s disease via computational screening and experimental validation

Pattaporn Poonsawas, Chantana Boonyarat, Khemjira Phemphunananchai, Jutarop Phetcharaburanin, Pornthip Waiwut
article en

Abstract

β-site APP-cleaving enzyme 1 (BACE1, a β-secretase) is a key aspartyl protease that initiates the proteolytic processing of the amyloid precursor protein (APP) to form the amyloid-β (Aβ) peptide. Given that Aβ aggregation and plaque formation are a central pathological feature of Alzheimer’s disease (AD), BACE1 remains a critical therapeutic target. Furthermore, the complexity of AD pathology necessitates the identification of novel multi-target agents. This study employed a structure-based virtual screening, targeting the BACE1 approach to identify the potential BACE1 inhibitors from FDA-approved drug scaffolds derived from the ZINC database. Top-ranked candidates were subsequently validated through extensive 500 ns molecular dynamics (MD) simulations and in vitro assays of BACE1 inhibition activity. Furthermore, multi-AD-related target profiling of candidates was conducted using molecular docking and a series of in vitro assays. Among them, ZINC000019796155 emerged as a promising multi-target compound. Biochemical analysis revealed that ZINC000019796155 exhibited moderate inhibitory effects against BACE1. Subsequent assays confirmed its capacity to inhibit butyrylcholinesterase (BuChE) action and Aβ aggregation, function as a free radical scavenger, and provide neuroprotection against H₂O₂-induced oxidative stress in cellular models. Furthermore, western blot analysis elucidated the mechanism of neuroprotection, indicating that ZINC000019796155 inhibits the apoptotic pathway while simultaneously suppressing the formation of Aβ plaques and neurofibrillary tangles (NFTs). These findings highlight ZINC000019796155 as a validated scaffold with a known safety profile for AD. While further structural optimization and preclinical in vivo studies are necessary, this study underscores the potential of ZINC000019796155 as a multi-target neuroprotective agent for AD treatment.

Scientific ReportsVol. 16(1)
Khon Kaen University (TH), Ubon Ratchathani University (TH)
Khon Kaen University, National Science and Technology Development Agency
Good health and well-being
Openalex Percentile: Top 29%
Cholinesterase and Neurodegenerative Diseases
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