Quantitative System Pharmacology Analysis of Oral Valiltramiprosate/ALZ‐801 Predicts Slowing of Alzheimer’s Disease Progression by Anti‐Amyloid Oligomer and APOE4 Structural Corrector Modes of Action

The results suggest that the primary molecular MOA driver of valiltramiprosate to reduce AD neurodegenerative pathology is mediated by its anti-aggregation action, which in turn prevents formation of soluble neurotoxic oligomers and protofibrils without directly reducing amyloid plaques load. The APOE4 corrector MOA of valiltramiprosate may partially contribute to its clinical efficacy in APOE4/4 and APOE4/3 AD patients by switching the phenotype to APOE3/3 phenotype.