Always appreciate these explanations. Your theory seems sound to this layman, and is also what the company is operating on. As for the mouse models, they are a vital tool, and can be predictive. Being models only though, I cringe if someone takes them as proof of efficacy (which you sometimes see here). Many successful animal studies don't translate to humans, for many reasons that have to do not directly with the compound but with the imperfection of the animal model itself. Would love to hear your view on the animal models used for 2-73. Eg, the lesion scarring in MJFF's PD study.
Furthermore given the complexity of the CNS, 2-73 might be a therapeutic key to a multi-lock door. That is, it might "fail" until used in combination with another therapy(s). Or it might demonstrate only incremental benefit until then - which is a better outcome because the FDA might still approve it for commercialization. I suspect most cancer therapies fall into this category.
I think it's important to stress that our success depends on several hypotheses being true, including: the S1 receptor's roles, its validity as a therapeutic target, and 2-73's agonistic effect. We are dealing with many hypotheses here, not yet truths. It is also worth mentioning that 2-73 might work even when all the relevant hypotheses are incorrect. This could make some folks' heads spin, but biological science is that complex. There are effective drugs that don't have a clear MOA. A lot of them have their origins in folk medicine.
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