Anavex Life Sciences Announces Publication of Foundational Data for ANAVEX®2-73 (blarcamesine) in Multiple Sclerosis (MS)
Published in Journal of Neuroimmunology, Results Highlight ANAVEX®2-73 (blarcamesine) Shown to Protect and Repair Myelin Forming Cells
ANAVEX®2-73 (blarcamesine) Provides optimal Protection of Oligodendroglia against Glutamate Toxicity
NEW YORK – February 24, 2020
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 announced the publication in the peer-reviewed Journal of Neuroimmunology, titled “Sigma-1 Receptor Agonists as Potential Protective Therapies in Multiple Sclerosis“ featuring preclinical data of ANAVEX®2-73 (blarcamesine) relevant to multiple sclerosis.
“A unique feature of ANAVEX®2-73 (blarcamesine), compared to another sigma-1 receptor agonist we studied, is that while these molecules increase proliferation of oligodendrocyte precursor cells (OPCs), ANAVEX®2-73 (blarcamesine) does not inhibit the maturation of these OPCs to oligodendrocytes (OLs), also called oligodendroglia”, said Professor Robert P. Lisak, MD the Parker Webber Chair in Neurology, Professor of Neurology and Professor of Biochemistry, Microbiology and Immunology at Wayne State University School of Medicine and lead author of the paper. “This is an important feature since OPCs can replace lost OLs by maturing into new potential myelin-producing cells. In other words, ANAVEX®2-73 (blarcamesine) might promote remyelination by both providing more OPCs and not delaying their maturation into mature OLs. Further data also demonstrates that ANAVEX®2-73 (blarcamesine) provides protection for OLs, OPCs, as well as central nervous system neurons in addition to helping repair by increasing the pool of OPCs that can go on to matter to OLs.“
Multiple sclerosis (MS) is a chronic disease of the central nervous system (CNS) characterized by inflammation, demyelination, loss of oligodendrocytes (OLs) and axonal damage in the white matter accompanied by reactivity of astrocytes and microglia. There are effective disease-modifying therapies (DMTs) approved for treatment of patients with relapsing remitting MS, however, none of these DMTs are cures and many have significant side effects.
The study also described that ANAVEX®2-73 (blarcamesine) provides optimal protection of oligodendroglia against glutamate toxicity in vitro.
“MS is a lifelong disease that has a significant impact on the people affected and their caregivers. We are encouraged by these findings providing additional evidence for the neuroprotective and neurorestorative effects of ANAVEX®2-73 (blarcamesine), as well as further expanding its potential application,” said Christopher U. Missling, PhD, President and Chief Executive Officer of Anavex.
The full paper can be accessed online at: (https://www.sciencedirect.com/science/article/abs/pii/S0165572819305831).
About Multiple Sclerosis (MS)
Multiple sclerosis (MS) is a chronic autoimmune disease that causes damage to nerve fibers in the central nervous system (CNS), including the brain, spinal cord and optic nerve. This can disrupt communication between the CNS and other parts of the body, resulting in a wide range of physical and cognitive symptoms such as muscle weakness, visual loss, poor balance, chronic pain, tremors, short-term memory loss and other difficulties associated with dementia.
About Anavex Life Sciences Corp.
Anavex Life Sciences Corp. (Nasdaq: AVXL) is a publicly traded biopharmaceutical company dedicated to the development of 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, pain and various types of cancer. Anavex’s lead drug candidate, ANAVEX®2-73 (blarcamesine), recently completed a successful Phase 2a clinical trial for Alzheimer’s disease. ANAVEX®2-73 (blarcamesine) is an orally available drug candidate that restores cellular homeostasis by targeting sigma-1 and muscarinic receptors. Preclinical studies demonstrated its potential to halt and/or reverse the course of Alzheimer’s disease. ANAVEX®2-73 (blarcamesine) also exhibited anticonvulsant, anti-amnesic, neuroprotective and anti-depressant properties in animal models, indicating its potential to treat additional CNS disorders, including epilepsy. The Michael J. Fox Foundation for Parkinson’s Research previously awarded Anavex a research grant, which fully funded a preclinical study to develop ANAVEX®2-73 (blarcamesine) for the treatment of Parkinson’s disease. ANAVEX®3-71, which targets sigma-1 and muscarinic receptors, is a promising preclinical drug candidate demonstrating disease-modifying activity against the major hallmarks of Alzheimer’s disease in transgenic (3xTg-AD) mice, including cognitive deficits, amyloid and tau pathologies. In preclinical trials, ANAVEX®3-71 has shown beneficial effects on mitochondrial dysfunction and neuroinflammation. Further information is available at www.anavex.com. You can also connect with the company on Twitter, Facebook and LinkedIn.
Statements in this press release that are not strictly historical in nature are forward-looking statements. These statements are only predictions based on current information and expectations and involve a number of risks and uncertainties. Actual events or results may differ materially from those projected in any of such statements due to various factors, including the risks set forth in the Company’s most recent Annual Report on Form 10-K filed with the SEC. Readers are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. All forward-looking statements are qualified in their entirety by this cautionary statement and Anavex Life Sciences Corp. undertakes no obligation to revise or update this press release to reflect events or circumstances after the date hereof.
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