Thanks for re-posting these data — phenomenal, indeed! A3-71
I was not aware of the first poster. Albeit from murine-derived data (from a rat species, not humans), the data are, from my perspective, even more prognostic for favorable treatments in humans than the CTAD data were. Those data showed profound stabilization or improvement of Alzheimer’s symptoms, along with a remarkable safety profile. Those two factors, alone, should move Anavex 2-73 closely toward FDA approval.
But none of the people in the trial had their brains assessed for A2-73's removal of amyloid beta deposits (if it even occurred). Here, after dosing with Anavex 3-71, Alzheimer's rats’ brains were sectioned and stained, showing conclusive proof of A-beta clearance with Anavex 3-71.
So, in both this murine study and the human CTAD report there’s solid evidence of enduring symptomatic stabilization or improvement. But the rat study, with A-3-71, also shows A-beta clearance.
Ain’t that something? The Big Pharmas have been trying to do that for years, with consecutive failures. But little Anavex gets it done, without side effects.
Clearly, now, Anavex 3-71 profoundly treats Alzheimer’s by two mechanisms. The first, is the drug’s re-connection of endoplasmic reticula with associated mitochondria, allowing restored, normalized enzyme production and function.
The second is by beta amyloid clearance, the target mechanism no other drug company has yet (or is likely to) attain. Their drugs simply have too many side effects, or don’t work sufficiently.
The question arises, how, perhaps, might A3-71 be able to clear the waste proteins, when other drugs have such difficulty? I think it’s rather clear. A3-71, itself, does not clear the waste proteins. But when enzyme homeostasis is restored by it within the neuron, normal waste-clearing enzymes can function once again.
Out, damned amyloid!
