Anavex Life Sciences Announces New Publication in Medical Journal: Blarcamesine Prevented Cognitive Impairment in Animal Model of Alzheimer’s Disease
Anavex Life Sciences (NASDAQ:AVXL) announced a new peer-reviewed publication in Neuroscience Letters demonstrating that blarcamesine prevented cognitive decline in an Alzheimer's disease animal model. The study showed that pre-treatment with blarcamesine successfully prevented Amyloid beta-induced memory impairment and brain oxidative injury.
The research confirmed that blarcamesine works through SIGMAR1 activation, which enhances autophagy and helps normalize Aβ production. The drug, administered as a once-daily oral pill, demonstrated significant protection in pre-treated animals, showing less vulnerability to Aβ25-35-induced oxidative stress and reduced learning and memory deficits compared to placebo-controlled mice.
Anavex Life Sciences (NASDAQ:AVXL) ha pubblicato un nuovo articolo peer-reviewed su Neuroscience Letters che dimostra come blarcamesine abbia prevenuto il declino cognitivo in un modello animale di Alzheimer. Lo studio ha evidenziato che il trattamento preventivo con blarcamesine ha evitato l'insorgenza di deficit di memoria e i danni ossidativi cerebrali indotti dalla Amyloid beta.
La ricerca ha confermato che blarcamesine agisce tramite attivazione di SIGMAR1, migliorando l'autofagia e contribuendo a normalizzare la produzione di Aβ. Somministrato come compressa orale una volta al giorno, il farmaco ha mostrato una protezione significativa negli animali pretrattati, che sono risultati meno sensibili allo stress ossidativo indotto da Aβ25-35 e hanno evidenziato minori deficit di apprendimento e memoria rispetto ai controlli con placebo.
Anavex Life Sciences (NASDAQ:AVXL) anunció una nueva publicación revisada por pares en Neuroscience Letters que demuestra que blarcamesina previno el deterioro cognitivo en un modelo animal de la enfermedad de Alzheimer. El estudio mostró que el tratamiento preventivo con blarcamesina evitó el deterioro de la memoria y el daño oxidativo cerebral inducidos por la Amyloid beta.
La investigación confirmó que blarcamesina actúa mediante la activación de SIGMAR1, lo que aumenta la autofagia y ayuda a normalizar la producción de Aβ. Administrado como una pastilla oral una vez al día, el fármaco proporcionó una protección significativa en animales pretratados, que mostraron menor vulnerabilidad al estrés oxidativo inducido por Aβ25-35 y menos déficits de aprendizaje y memoria en comparación con los ratones control con placebo.
Anavex Life Sciences (NASDAQ:AVXL)는 Neuroscience Letters에 동료심사(peer-reviewed) 논문을 새로 발표했으며, 해당 논문은 blarcamesine이 알츠하이머 동물모델에서 인지저하를 예방했다고 보고했습니다. 연구에서는 blarcamesine을 사전 투여한 결과 Amyloid beta로 유발된 기억장애와 뇌의 산화적 손상을 효과적으로 막았음을 보여주었습니다.
연구진은 blarcamesine이 SIGMAR1 활성화를 통해 작용하며, 이로써 자가포식(autophagy)을 촉진하고 Aβ 생성의 정상화를 돕는다고 확인했습니다. 하루 한 번 복용하는 경구용 정제로 투여된 이 약물은 사전 투여된 동물에서 유의한 보호 효과를 보였고, Aβ25-35로 인한 산화적 스트레스에 대한 민감성이 낮고 학습 및 기억 장애가 위약 대조군보다 적었습니다.
Anavex Life Sciences (NASDAQ:AVXL) a annoncé une nouvelle publication évaluée par des pairs dans Neuroscience Letters montrant que la blarcamesine a empêché le déclin cognitif dans un modèle animal de la maladie d'Alzheimer. L'étude a montré qu'un prétraitement par blarcamesine a prévenu les troubles de la mémoire et les lésions oxydatives cérébrales induits par l'Amyloid beta.
La recherche a confirmé que la blarcamesine agit via l'activation de SIGMAR1, ce qui renforce l'autophagie et contribue à normaliser la production d'Aβ. Administré sous forme de comprimé oral une fois par jour, le médicament a démontré une protection significative chez les animaux prétraités, qui ont présenté une moindre vulnérabilité au stress oxydatif induit par Aβ25-35 et moins de déficits d'apprentissage et de mémoire comparés aux souris sous placebo.
Anavex Life Sciences (NASDAQ:AVXL) gab eine neue peer‑reviewte Publikation in Neuroscience Letters bekannt, die zeigt, dass blarcamesine kognitiven Abbau verhinderte in einem Alzheimer-Tiermodell. Die Studie belegte, dass eine Vorbehandlung mit blarcamesine Gedächtnisbeeinträchtigungen und oxidativen Hirnschaden durch Amyloid beta erfolgreich verhinderte.
Die Forschung bestätigte, dass blarcamesine über SIGMAR1-Aktivierung wirkt, wodurch die Autophagie gesteigert und die Aβ‑Produktion normalisiert wird. Als einmal täglich eingenommene orale Tablette verabreicht, zeigte das Mittel bei vorbehandelten Tieren einen signifikanten Schutz: geringere Anfälligkeit für Aβ25‑35‑induzierten oxidativen Stress und weniger Lern‑ und Gedächtnisdefizite im Vergleich zu placebokontrollierten Mäusen.
- Pre-treatment with blarcamesine completely prevented Amyloid beta-induced memory impairment
- Drug demonstrated significant protection against oxidative stress and memory deficits
- Convenient once-daily oral pill administration format
- Confirmed mechanism of action through SIGMAR1 activation
- Results are from preclinical animal studies only, not human trials
- No guarantee of successful translation to human clinical trials
Insights
Anavex's preclinical study shows blarcamesine prevents cognitive decline in Alzheimer's model, supporting its development as a preventative treatment.
A new peer-reviewed publication in Neuroscience Letters provides compelling evidence for Anavex's lead compound blarcamesine as a potential preventative treatment for Alzheimer's disease. The preclinical study demonstrated that pre-treatment with blarcamesine completely prevented memory impairment and hippocampal injury in an animal model of Alzheimer's.
The research confirmed that blarcamesine works through a distinct mechanism - activating SIGMAR1 (sigma-1 receptor), which enhances autophagy (cellular waste removal) and acts upstream of amyloid and tau pathologies. This is particularly significant as it suggests blarcamesine could potentially address the disease before irreversible damage occurs.
Unlike many Alzheimer's treatments that target amyloid plaques after they've formed, blarcamesine's mechanism targets earlier disease processes. The study showed that while untreated mice developed significant amyloid toxicity after toxic Aβ25-35 peptide injection, the blarcamesine-treated animals showed reduced vulnerability to oxidative stress and fewer learning/memory deficits.
The research provides strong molecular rationale for blarcamesine's therapeutic potential. SIGMAR1 activation supports multiple neuroprotective functions: enhanced autophagy for Aβ clearance, reduced oxidative stress, decreased neuroinflammation, and maintained endoplasmic reticulum integrity. The oral once-daily administration would also offer significant convenience compared to more invasive treatment options.
For Anavex, this publication represents important scientific validation for their clinical development program, potentially expanding blarcamesine's application from treatment to prevention of Alzheimer's - a much larger market opportunity with fewer competitive treatment options currently available.
Pre-Treatment with blarcamesine entirely prevented Abeta-induced cognitive decline
Confirmed significant biomarker-response in hippocampus
NEW YORK, Aug. 20, 2025 (GLOBE NEWSWIRE) -- 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 a 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 convenient once-daily oral pill — for the prevention of Alzheimer's disease.”
While placebo-controlled mice developed significant amyloid toxicity in the brains after the toxic Aβ25-35 peptide injection, in animals pre-treated with blarcamesine, significant protection was observed with less vulnerability to Aβ25-35-induced oxidative stress and less vulnerability to develop learning and memory deficits.
The mechanistic confirmation that blarcamesine particularly restores impaired autophagy through SIGMAR1 activation by acting upstream of amyloid and tau pathologies at the molecular level was previously established both in vitro and in vivo. Specifically, blarcamesine’s studies demonstrated effect of enhanced autophagic flux in human cells and in C. elegans as well as increased proteostasis capacity and ability to promote autophagosome biogenesis, autophagic cargo reception, and lysosome fusion.2
SIGMAR1 has emerged as a key therapeutic target in the treatment of neurodegenerative disorders. Its activation enhances autophagy, facilitating the degradation of amyloid-beta precursor protein (APP) and helping to normalize Aβ production.3 Beyond its role in amyloid regulation, SIGMAR1 activation supports neurogenesis, mitigates oxidative stress by reducing reactive oxygen species (ROS), suppresses neuroinflammatory responses, and alleviates Aβ-induced toxicity. It also plays a critical role in maintaining endoplasmic reticulum (ER) integrity and modulating intracellular calcium signaling.4 Collectively, these effects contribute to the restoration of cellular homeostasis, rebalancing neural function, 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 and hence retaining autophagy strength through upstream SIGMAR1 activation, the downstream potentially 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 is not intended to convey conclusions about efficacy or safety. There is no guarantee that any investigational uses of such product will successfully complete clinical development or gain health authority approval.
About Alzheimer’s Disease
Alzheimer’s disease is a progressive degenerative brain disorder that gradually destroys a person's memory and ability to learn, reason, make judgments, communicate and carry out daily activities. An estimated 7.2 million Americans currently have Alzheimer's dementia. Alzheimer’s is the most common cause of dementia among older adults and is estimated to rank as the third leading cause of death for older people in the United States, just behind heart disease and cancer. In 2020, Alzheimer's and other dementias cost the nation approximately
About Anavex Life Sciences Corp.
Anavex Life Sciences Corp. (Nasdaq: AVXL) is a publicly traded biopharmaceutical company dedicated to the development of novel therapeutics for the treatment of neurodegenerative, neurodevelopmental, and neuropsychiatric disorders, including Alzheimer's disease, Parkinson's disease, schizophrenia, Rett syndrome, and other central nervous system (CNS) diseases, pain, and various types of cancer. Anavex's lead drug candidate, ANAVEX®2-73 (blarcamesine), has successfully completed a Phase 2a and a Phase 2b/3 clinical trial for Alzheimer's disease, a Phase 2 proof-of-concept study in Parkinson's disease dementia, and both a Phase 2 and a Phase 3 study in adult patients and one Phase 2/3 study in pediatric patients with Rett syndrome. ANAVEX®2-73 is an orally available drug candidate designed to restore cellular homeostasis by targeting SIGMAR1 and muscarinic receptors. Preclinical studies demonstrated its potential to halt and/or reverse the course of Alzheimer's disease. ANAVEX®2-73 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 for the treatment of Parkinson's disease. We believe that ANAVEX®3-71, which targets SIGMAR1 and M1 muscarinic receptors, is a promising clinical stage 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, Instagram, and LinkedIn.
Forward-Looking Statements
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.
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
________________________
1 Maurice, Tangui. “Prevention of memory impairment and hippocampal injury with blarcamesine in an Alzheimer's disease model.” Neuroscience letters, 138349. Aug. 2025.
2 Christ, M G et al. “Sigma-1 Receptor Activation Induces Autophagy and Increases Proteostasis Capacity In Vitro and In Vivo.” Cells vol. 8,3 211. 2 Mar. 2019.
3 Jaeger PA, Pickford F, Sun C-H, et al. Regulation of amyloid precursor protein processing by the Beclin 1 complex. PloS one. 2010;5(6):e11102.
4 Nguyen L, Lucke-Wold BP, Mookerjee SA, et al. Role of sigma-1 receptors in neurodegenerative diseases. Journal of pharmacological sciences. 2015;127(1):17-29; Moriguchi S, Shinoda Y, Yamamoto Y, et al. Stimulation of the sigma-1 receptor by DHEA enhances synaptic efficacy and neurogenesis in the hippocampal dentate gyrus of olfactory bulbectomized mice. PloS one. 2013;8(4):e60863-e60863; Rosen DA, Seki SM, Fernández-Castañeda A, et al. Modulation of the sigma-1 receptor–IRE1 pathway is beneficial in preclinical models of inflammation and sepsis. Science Translational Medicine. 2019;11(478):eaau5266; Maurice T, Volle J-N, Strehaiano M, et al. Neuroprotection in non-transgenic and transgenic mouse models of Alzheimer's disease by positive modulation of σ1 receptors. Pharmacological research. 2019;144:315-330.
5 Advances in Experimental Medicine and Biology Volume 964 (2017) Sigma Receptors: Their Role in Disease and as Therapeutic Targets.
6 https://www.nia.nih.gov/health/alzheimers; https://www.alz.org/alzheimers-dementia/facts-figures.
7 Alzheimer's Disease International. World Alzheimer Report 2019. https://www.alz.co.uk/research/WorldAlzheimerReport2019.pdf.
8 AARP. 2020 Report: Caregiving in the U.S. https://www.aarp.org/content/dam/aarp/ppi/2020/05/full-report-caregiving-in-the-united-states.doi.10.26419-2Fppi.00103.001.pdf.
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