“These data continue to highlight the potential of fosgonimeton as a novel therapeutic approach for Alzheimer's disease targeting multiple facets of its complex pathophysiology,” said
Key findings reported in the study publication regarding fosgonimeton in preclinical models of Alzheimer’s disease include:
- In primary rat cortical neurons challenged with Aβ, fosgonimeton treatment improved neuronal survival, protected neurite networks, and reduced tau hyperphosphorylation following Aβ injury.
- Fosgonimeton attenuated Aβ-induced mitochondrial stress and apoptotic signaling.
- Fosgonimeton enhanced activation of pro-survival effectors extracellular signal-regulated kinase (ERK) and protein kinase B (AKT). It also reduced activity of glycogen synthase kinase 3 beta (GSK3β), one of the main kinases involved in tau hyperphosphorylation.
- Fosgonimeton mitigated Aβ-induced deficits in Unc-like kinase 1 (ULK1) and Beclin-1 expression, suggesting a potential effect on autophagy.
- Fosgonimeton improved cognitive performance in an Aβ rat model of Alzheimer’s disease.
“There is an urgent need for new treatments that tackle the multifactorial pathologies of Alzheimer’s disease (AD), especially for people with mild-to-moderate AD, an advanced stage of the disease,” said
The article is available on the Neurotherapeutics website and from the
About Fosgonimeton
Fosgonimeton is a potentially first-in-class, once daily, subcutaneously administered small molecule drug candidate. Targeting the protection and repair of neuronal networks, fosgonimeton has disease-modifying potential to address a broad range of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and dementia with Lewy bodies.
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