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Drug Repurposing Hypothesis Generation Using the "RE:fine Drugs" System

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Desarrollo de Fármacos

Samar Padder¹, Jesus J Campagna¹, Sujyoti Chandra¹

¹University of California, Los Angeles (UCLA), Los Angeles, CA, USA.

Alzheimer's & dementia : the journal of the Alzheimer's Association

|December 25, 2025

Resumen

Este resumen es generado por máquina.

Un nuevo fármaco, DDL-218, mejora los niveles neuroprotectores de Sirtuina 1 (SirT1) al contrarrestar los efectos de la apolipoproteína E4 (ApoE4). Este candidato a terapia para la enfermedad de Alzheimer (EA) mejoró la memoria en modelos preclínicos.

Palabras clave:

Neurociencia Farmacología Genética Enfermedad de Alzheimer Sirtuina 1 Apolipoproteína E4 DDL-218

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Área de la Ciencia:

Neuroscience; Pharmacology; Genetics

Sus antecedentes:

Alzheimer's disease (AD) involves amyloid plaques and tau tangles.; Apolipoprotein E4 (ApoE4) is a major genetic risk factor for sporadic AD.; ApoE4 represses Sirtuin 1 (SirT1), a crucial neuroprotective protein, exacerbating AD progression.

Objetivo del estudio:

Discover and preclinically evaluate DDL-218, a small-molecule SirT1 enhancer.; Target ApoE4 to reverse its repressive effects on SirT1 expression.; Assess DDL-218's therapeutic potential for Alzheimer's disease.

Principales métodos:

High-throughput screening identified SirT1 enhancer candidates.; Medicinal chemistry and in silico modeling optimized lead compounds.; In vitro and in vivo studies in ApoE4-expressing neuronal cells and AD mouse models were performed.; Mechanisms were investigated using proteomics, chromatin immunoprecipitation, and qRT-PCR.

Principales resultados:

DDL-218 increased SirT1 protein and mRNA by upregulating NFYB and PRMT5.; Drug treatment displaced ApoE4 from the SirT1 promoter, boosting SirT1 expression.; DDL-218 improved memory in AD mouse models and enhanced brain SirT1, NFYB, and PRMT5 mRNA.; Proteomics indicated upregulation of neuronal function proteins like PTprn2; DDL-218 demonstrated brain penetration and safety.

Conclusiones:

DDL-218 effectively enhances SirT1 by counteracting ApoE4, showing therapeutic promise for AD.; The compound improved cognition and neural pathways in preclinical AD models.; Further research is warranted to establish DDL-218's targets, mechanism, and efficacy in diverse ApoE4-related AD models.