Anavex Life Sciences Corp (AVXL)

[falconer66a]

Blarcamesine can replace Aricept, immediately.

You had once written that Aricept may take up space on the Sigma1 molecule. I'm wonder if you still think that, as well how long do you think patients would have to stop taking it in order for blarcasamine to be more effective?

As I recall, there may be some evidence that Aricept can also bind to, become a sigma-1 receptor protein ligand. If that is so, it is inconsequential, inasmuch as there is no evidence that Aricept can activate the sigma-1 protein to the effective degree that blarcamesine does.

Within the cell there are thousands of different proteins and other non-protein molecules; all in the realm of organic chemistry, wherein molecules are mutually “sticky,” they bump into each other and often “stick,” at least for an instant. When that happens, the new molecular complex of both of the stuck-together molecules takes on entirely new chemical traits and actions. Aricept may well bind to the sigma-1 receptor, but very clearly it is unable to facilitate that protein’s seminal modulation of homeostatic processes.

The prime mechanism of action (MOA) of Aricept is as an acetylcholinesterase inhibitor. Simply, it suppresses the acetylcholinesterase enzyme. In so doing, it inhibits acetylcholinesterase from breaking down the neurotransmitter acetylcholine; proper acetylcholine concentrations are maintained; neurons are then able to properly “fire,” transmit messages. Those, of course, are essential in thinking, memory, etc.

Then, what might be the time required for blarcamesine to work in patients already being treated with Aricept? I see no reason this would not be immediate. After Aricept is stopped, it will be cleared quickly; it does not bind strongly (if much at all) to the sigma-1 receptor protein. Blarcamesine strongly and quickly binds to it, even at very low concentrations.