Anavex Life Sciences Corp (AVXL)

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Two Potential Blarcamesine Mechanisms

... more support for Anavex's MOA.

Yes, indeed, this new report from neurologists at Massachusetts General Hospital (associated with Harvard) provide further evidence that blarcamesine (Anavex 2-73) is able to either stop the progression of Alzheimer’s disease, or even reverse or prevent it.

For those who missed it, read the report closely, here:
https://www.massgeneral.org/news/press-release/researchers-link-high-calcium-levels-in-mitochondria-to-neuronal-death-in-alzheimers

When I first encountered Anavex science, several years ago, I examined all of the published research articles on (then) “Anavex 2-73,” (now, “blarcamesine”). Therapeutic results for a number of central nervous system (CNS) disorders — all in murines, lab rodents — were quite remarkable; yielding results that conventional drugs or therapies could not. Too good to be true; at least if ever tried in real humans. At the time, it was difficult to explain how this rather simple molecule could have so many good, “downstream” health-restorative effects.

I am a biologist (retired advanced placement biology teacher; presently a researcher leading a university team using ecological processes to solve a major environmental problem; working with a major federal grant just awarded to us). I understand cellular physiology and biochemical processes. It was clear to me (and others) that the Anavex sigma-1 receptor antagonist, Anavex 2-73, after binding to and activating the sigma-1 receptor protein, allowed that protein then to function normally.

One function (too complicated to describe in less than a dozen paragraphs, with illustrative graphics) is to support the function of the endoplasmic reticula, tiny organelles that properly fold proteins into functioning enzymes. Those properly-folded enzymes mediate virtually all of the hundreds of chemical reactions in cells. But if any of those enzyme proteins are mis-folded, essential reactions are compromised. Pathology results.

So, restoration or support of proper protein folding by Anavex 2-73 in endoplasmic reticula was a plausible mechanism of action (MOA) explaining the positive therapeutic results. Simply, Anavex 2-73 caused proteins to be properly folded into fully-functioning enzymes. Some of those enzymes properly reduce and destroy cellular wastes, such as the amyloids that pathogenically accumulate to cause Alzheimer’s. That’s what I’ll call the Anavex MOA No. 1.

But now, with this new research, there might be an Anavex MOA No. 2; the drug’s facilitation of proper calcium ion transport. This needs to be affirmed in transgenic lab rodents with the human genes for Alzheimer’s. Simply replicate the new study, but this time add some blarcamesine to the rodents’ drinking water; then see what happens, grossly (observed behaviors), and biochemically. I’d bet a dozen or so of my AVXL shares that normalized calcium modulation will result. The new study shows that with this, severity or occurrence of Alzheimer’s could be reduced or prevented.

Altogether, more solid evidence that the Anavex molecule is not too good to be true. It’s multiple, positive therapeutic outcomes are ever more firmly based and affirmed by its unique biochemistry.

And Anavex Life Sciences Corp has another proprietary analog, Anavex 3-71, for which murine studies indicate even stronger and wider therapeutic efficacies.

The means by which these occur are no longer so mysterious.