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Re: longtermbeliever post# 464545

Sunday, 07/21/2024 8:50:19 AM

Sunday, July 21, 2024 8:50:19 AM

Post# of 464604
2-73 dislocates S1 from the MAM - hence "chaperone" protein. The hope is that it does this without effecting the S1's MOA, allowing it to fulfill its innate role. That's one of the key differences between mere S1 'agonist' (eg, donepezil) and 'potent agonist'. (There's also selectivity, etc.) Then there's the hope that potently agonizing S1 leads to therapeutic effects in the target indication - AD in this case. You need successful controlled clinical trials to show this. (Despite what knuckleheads claim to already know.)

The company is now making an argument that we have shown this, and has already gotten one major regulator to agree to evaluate our accumulated pre-clinical and clinical data. Folks like Sabbagh are on board, but he's 'on board' in both the figurative and literal sense; he is not an independent evaluator. The CHMP rapporteurs are. Having a peer-reviewed paper will be somewhat helpful, as that provides more validity and cover for what is a very big decision for the EMA. Luckily for the company, all regulators are hungry to approve a helpful, safe, convenient, and affordable AD therapy.

I suspect the company was hoping the paper would be published by now, in time for the summer conferences. It is certainly due now. Looking forward to the paper, and our completed MAA.

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