I'd be willing to bet the answer would be--they don't know. Right now they are still operating on the level of empirical observation, what is seen under what circumstances. Explaining it, why that occurs, is a whole other step that may not currently be answerable. Which is why I previously made the discrimination--explaining why something happens in healthy tissue would be a question Cortex would have to answer--but if it doesnt happen there, and only happens in dead tissue, that should not be a question that has to be answered in order for Cortex to run studies on living patients. Now, if they were to propose sacrificing those patients and choosing between fixative and frozen slice preparation, that would be a different story.
To play devil's advocate with myself: One could ask, are there any other implications of what appears to be a dose-related level of molecular...presence? Do only massive doses far above clinically relevant doses get enough drug into the cellular-area-of-interest that there is anything for the fixative to interact with? (As appears to be the case). As Gfp wondered recently, could there be a metabolite? Without any living tissue histo changes or behavioral effects, that should not be a reason to halt relatively short-duration Phase II studies (especially in ADHD). But longterm tox/safety trials are required for product approval, and this would be an issue that could surface again in that context. In other words, the FDA can and should give permission for Phase IIb trials to resume, while maintaining an interest in whether anything else might pop up in longterm administration.
NeuroInvestment
Market Data 
Markets 
AI
