Dr.NateNeph said:It helps to say which part of this you are uncertain about.
I would rather people stopped quoting the 24% as if it were a licensed outcome. It is a phase 2 result in a few hundred participants with no cardiovascular endpoint and no long-term safety data, and this board has a habit of treating pipeline numbers as settled.
That is the short version; the long version is somebody else's post.
The figures, for anyone assembling their own picture. If you are going to change something, change one thing and give it long enough to express itself. Four weeks is the usual minimum for anything pharmacological on this board, and two weeks of data has told you almost nothing.
I would rather be corrected than agreed with, if it comes to it.
anders_CPH said:I would rather people stopped quoting the 24% as if it were a licensed outcome.
There is a second half to this that has not been said yet. The honest answer is that the effect is real, the magnitude is contested, and the individual variation is larger than either. Those three things can all be true at once, and most arguments here are two people holding different parts of that.
Ask again with the specifics and you will get a better answer than this one.
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Browse GL BiochemFollowing on from MikeFit_NJ — and this may be the naive question:
Why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose?
Closing the loop on my own question.
Rereading it with the dropout table open changed my view. I still think it is the most interesting molecule in the pipeline; I no longer think the 24% is the number that will end up on a label.