It is also very misleading to say that Donepezil is a superior S1R receptor. 2-73 has given benefit for years, months is the most anyone can expect from Donepezil. There is a conflating of efficacy and chemical binding which is very deceptive.
There is limited data to compare DZP effects to 2-73. Within that limited preclinical data DZP does outperform 2-73 in at least one model but there are no models I've seen where the reverse is true - please provide an example. This is not at all the same as conflating efficacy and chemical binding...please point to an instance where I conflated the two.
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.
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