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Saturday, August 19, 2017 1:29:10 PM
astounding to me that this point is passed over so casually.
Quote:This is one we have covered before on quite a few occasions. It’s also one that, across the period, has taken a bit of a beating in mainstream financial news media. The mechanism of action of its lead candidate has the potential to render what amounts to billions of dollars of Alzheimer’s research wasted and wider market forces seem not to want the asset to successfully reach commercialization.
If the new MOA constitutes BTD not only for AD but multiple CNS indications?
This issue has been discussed before and no knowledgeable poster has any any answer to this other than "maybe muscarinic modulation will make a difference" or "maybe it activates the S1R a different way". Those maybes are dubious for a number of reasons but whatever the case they remain maybes and talking about a MOA as if you expect there's something novel is premature. Morever, its very unlikely.
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