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Re: nidan7500 post# 292752

Wednesday, 01/13/2021 5:54:24 PM

Wednesday, January 13, 2021 5:54:24 PM

Post# of 463611
Well, it's a -mab, monoclonal antibody.

...comment on difference of A2-73 MOA vs this new "treatment".


I haven't (and won't) follow this new Alzheimer's drug, "donanemab." I know nothing more than I can discern from the webpage article that was posted.

Offhand, the therapeutic data look good. Any slowing of the progression of Alzheimer's symptoms is always regarded as a positive, inasmuch as so few drugs can do this. Alzheimer's is pretty recalcitrant; ultimately resistant to every therapy used to date. There are no cures; only a few approved drugs that merely slow, for but a time, the progression of the disease (such as aricept). Ultimately, those drugs fail; the patient dies of Alzheimer's.

Here are the positive statements about the new drug:

The two-year study, which has now concluded its second phase before entering a third and final phase, found patients’ decline was slowed by as much as 32 per cent over 18 months – a reduction researchers described as “statistically significant”.

And,

Six to 12 months following the treatment, the amaloid [sic] plaques were gone and did not return, said Dr. Daniel Skovronsky.

Well and good; beats aricept I believe.

But, how does all of this compare against blarcamesine? Very different. I won't be selling any of my AVXL shares so as to purchase some shares of Eli Lilly, the apparent owner of the drug. Very different approaches, those of Anavex and Eli Lilly. The Anavex drug, blarcamesine, fixes things at their start in the neuron; preventing the things that, downstream, cause the production and aggregation of amyloid plaques. The Eli Lilly drug directly targets those waste proteins, after they've been produced and deposited. Blarcamesine keeps them from ever forming in the first place.

The pathologies (cellular anomalies) that produce or allow the amyloids to form and accumulate are not apparently addressed by the new drug. They are simply removed after they form. Now, if that can continue perennially, keeping neurons free from accumulated amyloids, the drug will be an effective Alzheimer's treatment (requiring uninterrupted dosings for the rest of the patients' lives).

But let's wait and see. The factors that cause Alzheimer's are not binary, on or off. Instead, with age, they continue to become ever more dominant and powerful. At some point, it's very likely that the drug will not be able to keep up with the increasing production of the waste amyloid proteins. End of treatment, lethally.

Two very different, contrasting mechanisms of action (MOAs). Anavex fixes things at the sigma-1 receptor protein, with propitious (there's the word) downstream outcomes, while the new Eli Lilly drug tries to clear the amyloid wastes after they form. It apparently does not fix or stop the process that allowed their formation.
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