Cerebral deposition of amyloid-β peptide (Aβ) plays a critical role in Alzheimer’s disease (AD) pathogenesis. Owing to its role in the generation of Aβ, the BACE1 enzyme has been a prime target for designing drugs to prevent or treat AD. However, recent failures of anti-amyloid therapies to slow the progression of AD have caused the field to consider studies in asymptomatic patients with amyloid pathology or combination approaches. Ideally, BACE inhibitors in these studies will maximize target engagement and have excellent safety profiles. This presentation will describe the discovery and early clinical development of LY3202626, a low-dose, CNS-penetrant BACE inhibitor capable of reducing CSF Aβ by &gt; 90%. This presentation will also include the disclosure of the chemical structure of LY3202626.

Discovery, structure disclosure, and early clinical development of LY3202626, a low-dose, CNS-penetrant BACE inhibitor

256th National Meeting (2018)

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