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XenaLives

12/24/18 8:32 AM

#175948 RE: OFP #175940

Red herring:




There are 2 themes in this regard that no one has addressed:
1. The weak affinity means that if 2-73 is co-administered with a higher affinity S1R agonist using the same binding site then 2-73 will be blocked in some extent from access to the site by the more tightly bound compound. This is such an elementary problem that AVXL almost certainly has data but they've chosen not to present it - a very bad sign with their history. Yet even know they are launching into another trial with DZP co-administered in a significant proportion of patients.
2. No preclinical evidence exists that 2-73 (that I know of or that anyone has presented on this board) exerts a superior agonist effect relative to known S1R agonists. This is very different from saying DZP is a superior agonist. The onus here is on the company to have an expectation of a superior effect and they have shown none. There is nothing favorably unique in the way they've shown 2-73 works.



1) The company has stated that this is not the case. "With their history"... No company shows all of its cards this early..

Yet even know (sic) they are launching into another trial with DZP co-administered in a significant proportion of patients.

Australia and Canada both have established protocols for deprescribling Donepezil so you have no basis for this assumption.

2) Donepezil loses its effect after a few months. It literally burns out and crashes. 2-73 activates when needed. Therein lies the rub and it is totally unique and unprecedented.