Sokol,
I did not get into this in the earlier post in order to stay on point. My understanding is that donepezil, a Sigma-1 agonist, is not understood to present memory benefits from that activity, but from its other known effect. This is from Wikipedia's description of DZP's MOA:
"Donepezil binds and reversibly inactivates the cholinesterases, thus inhibiting hydrolysis of acetylcholine. This increases acetylcholine concentrations at cholinergic synapses.The precise mechanism of action of donepezil in patients with Alzheimer's disease is not fully understood. Certainly, Alzheimer's disease involves a substantial loss of the elements of the cholinergic system and it is generally accepted that the symptoms of Alzheimer's disease are related to this cholinergic deficit, particularly in the cerebral cortex and other areas of the brain." [Emphasis added and footnotes omitted.]
In fact, the temporary symptomatic memory improvement DZP provides to AD patients meshes with what is understood about the advantage of increased acetylcholine at those synapses. By contrast, 2-73's MOA is based on a broad agonism of the Sigma-1 receptor, and the preliminary clinical information suggests the same. (I have just read a 2017 post on this board citing Missling as referring to 2-73 as a natural agonist of the Sigma-1 receptor.) In other words, even though both drugs are Sigma-1 agonists, only 2-73 appears to have its MOA based on that receptor. I am, of course, unaware of any research behind DZP's effect on the Sigma-1 receptor.
Once again, I would like Doc's views on this.
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