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Anavex Reports ANAVEX 2-73 Results in Preclinical Model of Alzheimer’s Disease

Published: Monday, November 04, 2013
Last Updated: Monday, November 04, 2013
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ANAVEX 2-73 dose-dependently blocks Tau and amyloid-beta (“amyloid”) proteins and memory deficit in a mouse model of Alzheimer’s disease (AD).

A reduction in these two main hallmarks of Alzheimer’s has the potential to stop, slow or reverse the disease.  The report also suggests that, because it is targeting the mixed muscarinic and Sigma-1 receptors, ANAVEX 2-73 is able to achieve its effect further “upstream” in the Alzheimer’s disease cascade.  This compares to most other current AD clinical development compounds that are mainly downstream and single-targeted approaches, which might be limited by adverse effects.  More interestingly, the mixed muscarinic and Sigma-1 agonist ANAVEX 2-73 exhibited powerful effects despite its moderate affinity for these receptors, emphasizing its great advantage for potential therapy in Alzheimer’s disease.

Tangui Maurice, PhD, CNRS Research Director, Head of Team 2 ‘Endogenous Neuroprotection in Neurodegenerative Diseases’, at the University of Montpellier and INSERM, and one of the study authors, said, “ANAVEX 2-73 also dose-dependently reduced C99 levels in the hippocampus, an effect which researchers are currently trying to achieve with BACE inhibitors.  In the mouse model we also confirmed the central role of the kinase GSK-3 beta in Alzheimer’s disease toxicity through drugs acting either directly as GSK-3 beta inhibitors, or indirectly, as mixed muscarinic and Sigma-1 ligands. Both can efficiently alleviate these two major alterations observed in the Alzheimer’s animal model, as well as in Alzheimer’s patient brains. However, by targeting GSK-3 beta indirectly as ANAVEX 2-73 does through muscarinic and Sigma-1 ligands, we could avoid the toxicity seen by directly targeting GSK-3 beta.”

Christopher U. Missling, PhD, President and Chief Executive Officer of Anavex, said, “Using further upstream targets that efficiently block tau phosphorylation and amyloid overproduction might be a more comprehensive approach in successfully treating this complex disease. Together with previously confirmed findings demonstrating the ability of ANAVEX 2-73 to reduce mitochondrial oxidative stress, this publication strengthens the case for a potential pharmacological treatment for Alzheimer’s disease.”

The report, entitled “Blockade of Tau Hyperphosphorylation and Amyloid-beta1–42 Generation by the Aminotetrahydrofuran Derivative ANAVEX2-73, a Mixed Muscarinic and Sigma-1 Receptor Agonist, in a Nontransgenic Mouse Model of Alzheimer’s Disease,” is based on a scientific study conducted in France at the University of Montpellier and INSERM.


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