Or, Gfp, further on speculative groping in the dark(my specialty): is there something compensatory about high-impacts themselves . . . via BDNF production with a neuroprotective effect, inhibiting the formation of the "signal" which I strongly agree is most likely within the brain, and, within the brain, I would further guess within the Hippocampus. It may be by some paradoxical quirk the high impacts(although associated with seizures ect . . .)may turn out to be more promising and safe in the end. Who knows? Is it too early to call this a class effect. Yes. But if the signal occurs in the brain and within the hippocampus: my question would be why not a class effect? Then the question turns to how hard was ORG24448 pushed, how high was 516 pushed? Like the FDA decision, things are not always 'binary' in the end. Compound specific, class effect, how about a subclass effect as consequence of some metabolite in the CX717 related structures? Finally, what if the signal is due to calpain/spectrin? Whatever the mechanism of action of the signal, ampakines are different with potencies and brain regions and sub-brain regions, are more or less neurotrophic than one another and presumably, even if a class-effect(or subclass effect)signal is seen, it may well turn out that CX717 shows the signal at say I gram/kg per day and attentional boosting effects at 10mg/kg day whereas another more potent ampakine will have a 200 or even a 1000 fold distinction between attentional boosting effects and the origination of the 'signal.' For all of these reasons(and so many more I can't begin to consider), I would strongly hope and urge Cortex to ensure that this signal is not seen in CX701 and other backups or clearly differentiate the levels where the signal occurs from CX717. Of course, the final irony is we don't even know what it means in the first place! Where the monkey's sick, the rats? For the signal at this juncture is like the monolith in that old science fiction movie!
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