Anavex Life Sciences Corp (AVXL)

[falconer66a]

Blarcamesine works differently; with safety and success.

...as the AD trial results may not be as good or will not show efficacy (like so many AD trials)

That perspective or anticipation presumes, of course, that the Anavex mechanism of action (MOA) is similar to all the other, failed Alzheimer’s trials; virtually all of which target beta-amyloid and tau waste proteins. None of those approaches (new drugs) have yielded either safety or efficacy. They’ve always failed; always will. Trying to reduce or prevent Alzheimer’s waste proteins by re-shaping or re-directing immunological processes fails, every time.

I’m a biologist knowledgeable in cellular physiology. Better than most I can understand the diverse, effective mechanisms and downstream normalizations of blarcamesine’s sigma-1 receptor activation. Totally and utterly different from any other Alzheimer’s drug.

Be assured, if Anavex were directly targeting the waste proteins of Alzheimer’s, I would have saved my dollars; wouldn’t own a share of AVXL. Among others, two controlling facts validate my AVXL position: a) blarcamesine has a now-proven MOA that restores and promotes normal cellular processes in neurons, and b) as described in yesterday’s Needham presentation, blarcamesine has shown strong safety and efficacy in Phase 1 and Phase 2 human trials.

There is no reason whatsoever to believe the on-going Phase 3 Alzheimer’s trial will fail. Just the opposite. Blarcamesine is safe and works in both preclinical murine (lab rodent) models of CNS disease and likewise in every human trial. For the FDA, the Phase 3 trial will seal the deal. There is no conceivable mechanism by which it can fail. (Ok, let’s hear them. I’ll record them, and re-post them later this year when the Phase 3 data are released. Let’s see who got it right.)