...do you see any indication(s) that any of Anavex molecules could be useful in successfully treating BiPolar Disorder?
No, unfamiliar with any definitive information on the ability of blarcamesine (or other Anavex sigma-1 receptor agonists) to moderate or control bipolar disorder.
But until the drugs are tried, either in murines with bipolar genotypes, or in actual humans with the disorder, the possibility shouldn’t be ruled out. The number and kinds of central nervous system diseases and conditions that the Anavex molecules can treat continues to grow.
How could a single, rather simple molecule provide a diverse multitude of therapeutic outcomes? Given the unique mechanism(s) of action (MOA) the sigma-1 receptor agonists possess, it might work.
Of course, the most beneficial outcome of Anavex sigma-1 receptor agonist therapy is its promotion and modulation of proper, healthful protein folding. Mis-folded proteins (in the form of enzymes) are involved in a large number of CNS diseases. Bent-out-of-shape enzymes (which are mis-folded proteins) are simply unable to catalyze essential chemical reactions. So, might bipolar disorder result from poorly functioning (mis-folded) brain enzymes? Very possible.
As I’ve mentioned previously, I’m certain that the brains at Anavex Life Sciences Corp have conducted any number of undisclosed murine trials to discover the breadth of diseases their molecules can address. Simply, blarcamesine is given to rats or mice who have the same genetic pathologies as humans. This paper tells of the development of animal models with BP: https://dmm.biologists.org/content/2/5-6/238
I have a mild, uncomplicated case of hereditary spastic paraplegia (HSP); with tight, spastic legs and a compromised gait. An extremely obscure paper (the copy of which I lost when my hard drive failed) showed that rats with my CNS condition, when given blarcamesine (Anavex 2-73) in their drinking water rapidly, (in a few weeks or less) re-gained normalized motor control of their legs.
In that case, the MOA is understandable. As shown in the Rett trial (in humans), blarcamesine increases the production of gama-aminobutyric acid (GABA) and suppresses the over-production of glutamate. With these more optimized levels, spasticity is obviated. The GABA turns down the hyperexcitability the excess glutamate induces.
But in either case, bipolar disorder or HSP, there will be no release of early, preliminary murine trials. Anavex almost surely has had a good number of these trials performed on a diversity of CNS diseases. The time to tell about those early animal trials will be only after blarcamesine gains regulatory approval somewhere (Australia?) to sell blarcamesine. Then, the public will want to know what else the drug can treat. In the public mind, that approval will thorougly validate Anavex. But to make any claims now about new diseases being targeted by Anavex drugs would only prompt naysaying. We have ample amounts of that already.
Can’t wait for that New York Times article to appear, entitled, “New Drug Treats CNS Disease.” Everything different after that.