Anavex Life Sciences Reports New Publication in Scientific Journal Demonstrating the Potential of ANAVEX3-71 to Prevent Cognitive Decline in Alzheimer’s Disease

ANAVEX3-71 treatment prevents cognitive impairment, reduces amyloid, and neuroinflammation even after a long drug washout

ANAVEX3-71 halts neurodegeneration and prevents cognitive decline in a transgenic Alzheimer’s disease model

Confirmation of Anavex’s upstream SIGMAR1 oral small molecule drug platform in Alzheimer’s disease

NEW YORK, Oct. 25, 2023 (GLOBE NEWSWIRE) -- Anavex Life Sciences Corp. (“Anavex” or the “Company”) (Nasdaq: AVXL), a clinical-stage biopharmaceutical company developing differentiated therapeutics for the treatment of neurodegenerative and neurodevelopmental disorders, including Alzheimer's disease, Parkinson's disease, Rett syndrome, and other central nervous system (CNS) diseases, today reported a new peer-reviewed publication in the journal Neurobiology of Aging, titled “Early treatment with an M1 and sigma-1 receptor agonist prevents cognitive decline in a transgenic rat model displaying Alzheimer-like amyloid pathology”, featuring the orally available small molecule ANAVEX3-71 (AF710B).¹

This study ascertains potential disease-modifying properties of ANAVEX3-71 (AF710B) on Alzheimer’s disease (AD) pathology and could be a drug candidate for a once daily oral preventive strategy.

ANAVEX3-71 activates the sigma-1 receptor (SIGMAR1) and the M1 muscarinic receptor (M1R). Data suggests that activation of SIGMAR1 results in the restoration of homeostatic function within the body and is pivotal to restoring neural cell balance and promoting neuroplasticity.² Previous studies of ANAVEX3-71 have demonstrated its potential to treat Alzheimer’s disease (AD)-like pathology at advanced stages of disease in animal models.^3,4

ANAVEX3-71, an orally available small molecule, has already successfully completed a Phase 1 human clinical trial demonstrating good safety and tolerability signals at all doses studied.⁵

In this publication, transgenic rats that develop AD-like symptoms as they age were treated with ANAVEX3-71 for 7-months before they developed amyloid plaques, followed by a 4-week washout period. Preventative treatment with ANAVEX3-71 reduced levels of insoluble and soluble amyloid-beta as well as plaque deposition in the aging cortex and hippocampus, areas heavily impacted by AD. Notably, the reduction in amyloid pathology was accompanied by a reduction in inflammatory glial activity which is connected to the disease cascade in AD and other dementias. ANAVEX3-71 treatment downregulated the proinflammatory IL-1β and IL-6 cytokines, which are known to be associated with AD. Additionally, ANAVEX3-71 treatment boosted brain derived neurotrophic factor (BDNF) which reinforces the evidence that ANAVEX3-71 protects neurons.