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Thursday, July 27, 2017 2:37:09 PM
Falconer, what are your thoughts on 2-73 or 3-71 in a combination therapy with MANF or CDNF?
Far be it for me, a retired high school biology teacher, to render any sort of exhaustive assessment of these two molecules as enhancements of Anavex 2-73 or 3-71. Good question, nonetheless. Here’s what I see, in a quick skim of available info.
MANF (mesencephalic-astrocyte-derived neurotrophic factor) is a naturally-occurring protein produced by the body, reducing or preventing apoptosis (induced cell death) in disease or injury.
Injection of this molecule is proposed to assist the body’s own MANF in restoring cell health.
Herantis’ CDNF (Conserved Dopamine Neurotrophic Factor) protects and repairs dopamine neurons in a neurotoxin-induced experimental Parkinson’s disease model in rats. Whether this can happen in humans with real (not induced) Parkinson’s awaits clinical proof trials.
I don’t see any obvious ways Anavex molecules could be made more effective in disease treatments by either of these candidate drugs, for their respective diseases. All three drugs work in very different ways, with very different mechanisms of action.
Anavex 2-73 and 3-71 reconnect dislodged cellular organelles (mitochondria and endoplasmic reticula). With that, those organelles resume normal functions and the cell resumes normal function, normal health ensues in the involved nerves or other tissues.
MANF is, in fact, not a new, unique drug; merely a synthesis and administration of an existing body protein. The Anavex drugs are not likely to improve its function, nor vice-versa.
I think Anavex 2-73 and 3-71 will work just fine by themselves, with no need or assistance of some external molecules. The crucial thing is that the Anavex molecules have unique mechanisms of action, unlike (and better) than any drugs on the market or in other company’s labs. They are unique sigma-1 receptor agonists, improving and restoring the functions of intracellular sigma-1 receptors. MANF and CDNF aren’t involved in the restoration of cellular homeostasis. As with so many other drugs for neurodegenerative diseases, the Anavex drugs fix things within the cell at the start of the disease process. These other two drugs try to fix things at the end of the cascade of disease processes.
They may well work, which would be just fine. But the chances that they might improve efficacies of Anavex molecules, I think, are remote.
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