Pre-Treatment with blarcamesine entirely prevented Abeta-induced cognitive decline
Confirmed significant biomarker-response in hippocampus
NEW YORK – August 20, 2025
Anavex Life Sciences Corp. (“Anavex” or the “Company”) (Nasdaq: AVXL), a clinical-stage biopharmaceutical company focused on developing innovative treatments for Alzheimer’s disease, Parkinson’s disease, schizophrenia, neurodevelopmental, neurodegenerative, and rare diseases, including Rett syndrome, and other central nervous system (CNS) disorders, today reported a peer-reviewed publication in the journal Neuroscience Letters, titled “Prevention of memory impairment and hippocampal injury with blarcamesine in an Alzheimer’s disease model.”[1]
This study shows that pre-treatment with blarcamesine prevented Amyloid beta-induced memory impairment and brain oxidative injury, suggesting that blarcamesine is an attractive candidate for Alzheimer’s disease pharmacological prevention.
“This preclinical study is exciting since it clearly demonstrates a preventative effect of blarcamesine in Alzheimer’s pathology and potentially might be able to prevent onset of Alzheimer’s disease in healthy individuals,” said Tangui Maurice, PhD, Research Director at University of Montpellier, France, and author of the publication. “These findings support the future direction of clinical trials with the objective of addressing blarcamesine’s potential as a safe and effective pharmacologic agent — applied as a convenient once-daily oral pill — for the prevention of Alzheimer’s disease.”
While placebo-controlled mice developed significant amyloid toxicity in the brain after the toxic Aβ25-35 peptide injection, animals pre-treated with blarcamesine showed significant protection, with less vulnerability to Aβ25-35-induced oxidative stress and reduced learning and memory deficits.
The mechanistic confirmation that blarcamesine restores impaired autophagy through SIGMAR1 activation—acting upstream of amyloid and tau pathologies—was previously established both in vitro and in vivo. Studies demonstrated enhanced autophagic flux in human cells and C. elegans, increased proteostasis capacity, and the ability to promote autophagosome biogenesis, autophagic cargo reception, and lysosome fusion.[2]
SIGMAR1 has emerged as a key therapeutic target in neurodegenerative disorders. Its activation enhances autophagy, facilitating degradation of amyloid-beta precursor protein (APP) and helping normalize Aβ production.[3] Beyond amyloid regulation, SIGMAR1 activation supports neurogenesis, reduces oxidative stress, suppresses neuroinflammation, and alleviates Aβ-induced toxicity. It further maintains endoplasmic reticulum (ER) integrity and modulates intracellular calcium signaling.[4] Collectively, these effects contribute to restoring cellular homeostasis and promoting neuroplasticity.[5]
“The findings in this publication further support the potential beneficial effect of blarcamesine in Alzheimer’s disease prevention. With once-daily oral blarcamesine administration retaining autophagy strength through upstream SIGMAR1 activation, downstream pathological manifestations of Amyloid beta might be prevented,” said Christopher U. Missling, PhD, President and Chief Executive Officer of Anavex.
The paper can be accessed online at: https://pubmed.ncbi.nlm.nih.gov/40784611/
This release discusses investigational uses of an agent in development and does not convey conclusions about efficacy or safety. There is no guarantee any investigational uses will complete development or gain regulatory approval. About Alzheimer’s Disease.
Alzheimer’s disease is a progressive degenerative brain disorder that gradually destroys memory and cognitive abilities. An estimated 7.2 million Americans currently have Alzheimer’s dementia. It is the most common cause of dementia among older adults and ranks as the third leading cause of death in the U.S. after heart disease and cancer. In 2020, Alzheimer’s and other dementias cost the nation approximately $781 billion, projected to rise to as high as $1.1 trillion by 2050.[6] More than 50 million people globally live with dementia, a number expected to rise to nearly 152 million by 2050.[7] Nearly 10 million new cases are diagnosed each year—one every three seconds—placing significant caregiving burdens on families and society.[8]
About Anavex Life Sciences Corp.
Anavex Life Sciences Corp. (Nasdaq: AVXL) is a publicly traded biopharmaceutical company developing novel therapeutics for neurodegenerative, neurodevelopmental, and neuropsychiatric disorders. Its lead candidate, ANAVEX®2-73 (blarcamesine), has completed multiple clinical trials for Alzheimer’s disease, Parkinson’s disease dementia, and Rett syndrome. ANAVEX®2-73 is an orally available drug candidate designed to restore cellular homeostasis by targeting SIGMAR1 and muscarinic receptors. Preclinical studies demonstrate its potential to halt or reverse Alzheimer’s disease progression. The company’s pipeline includes ANAVEX®3-71, a SIGMAR1 and M1 muscarinic receptor agonist showing disease-modifying activity in Alzheimer’s disease models. More information: www.anavex.com. Connect with Anavex on Twitter, Facebook, Instagram, and LinkedIn.
Forward-Looking Statements
Statements in this press release that are not historical facts are forward-looking statements involving risks and uncertainties. Actual results may differ materially due to factors described in the Company’s most recent Annual Report on Form 10-K. Readers should not place undue reliance on forward-looking statements, which speak only as of this date. Anavex undertakes no obligation to update any forward-looking statement.
For Further Information:
Anavex Life Sciences Corp.
Research & Business Development
Toll-free: 1-844-689-3939
Email: info@anavex.com
Investors:
Andrew J. Barwicki
Investor Relations
Tel: 516-662-9461
Email: andrew@barwicki.com
References
[1] Maurice, Tangui. “Prevention of memory impairment and hippocampal injury with blarcamesine in an Alzheimer’s disease model.” Neuroscience Letters, Aug. 2025.
[2] Christ, M. G. et al. “Sigma-1 Receptor Activation Induces Autophagy and Increases Proteostasis Capacity In Vitro and In Vivo.” Cells, 2019.
[3] Jaeger P. A., Pickford F., Sun C.-H., et al. PLoS One, 2010.
[4] Nguyen L. et al., Journal of Pharmacological Sciences, 2015; Moriguchi S. et al., PLoS One, 2013; Rosen D. A. et al., Science Translational Medicine, 2019; Maurice T. et al., Pharmacological Research, 2019.
[5] Advances in Experimental Medicine and Biology, 2017.
[6] NIH: nia.nih.gov/health/alzheimers; Alzheimer’s Association: alz.org/alzheimers-dementia/facts-figures
[7] Alzheimer’s Disease International. World Alzheimer Report 2019.
[8] AARP. 2020 Report: Caregiving in the United States.