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Re: georgejjl post# 328922

Friday, 09/03/2021 6:34:31 PM

Friday, September 03, 2021 6:34:31 PM

Post# of 463623
Info errors. But data very promising.

This was a claim in today’s fragile X announcement:

Blarcamesine is an experimental agonist (inhibitor) of the protein sigma-1 receptor (S1R).

It was also claimed:

By blocking S1R, blarcamesine may improve synapse health, which could be therapeutic in fragile X and other neurological diseases characterized by synapse dysfunction.


Two mistakes. Blarcamesine does not inhibit the sigma-1 receptor, it activates it. Instead of “inhibitor” the word should have been “activator.”

And, no, “blocking S1R,” the sigma-1 receptor protein, is not “therapeutic.” Just the opposite. Blarcamesine (Anavex 2-73) binds to that protein, thereby propitiously activating its several downstream cellular processes, which allow the neuron to function properly.

The rest of the information presented in the media release is all positive. Let the human trials begin. They will yield the same good therapeutic results seen in the mice with fragile X. The genes and molecules are the same in mice and men (well, children with fragile X syndrome).

Another central nervous system (CNS) disease or condition that blarcamesine will treat (or even prevent): 1. Rett syndrome, 2. Parkinson’s disease dementia, 3. Alzheimer’s disease, and now, 4. Fragile X syndrome. Defining clinical trials for the first three are ongoing. As per the announcement, fragile X will be the next Anavex clinical trial in real humans.

I would add, fragile X syndrome is a form of autism. Blarcamesine may well successfully treat other forms of this debilitating disease family.
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