Counting rather than debating, for once. The debate can happen underneath.
Sceptical rather than excited about the triple agonist, and I would like somebody to talk me out of the scepticism with data rather than enthusiasm.
What I am after is why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose.
Roughly, people seem to land in one of these:
Say which and say why — the why is the useful half.
Taking the question as asked, rather than the general version of it. Start from the measurement rather than the conclusion. Almost every disagreement here turns out to be two people measuring different things and comparing the numbers anyway.
Ask again with the specifics and you will get a better answer than this one.
KevinCompounds said:Start from the measurement rather than the conclusion.
No disagreement with KevinCompounds. One condition attached. The phase 2 numbers were about 24% mean weight loss at 48 weeks on the top dose, with the curve still descending at the end of the study. A curve that has not flattened is a real finding, but it also means the true plateau is unknown, and phase 2 populations are small and selected.
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Browse GL BiochemSteveThurs said:Sceptical rather than excited about the triple agonist, and I would like somebody to talk me out of the scepticism with data rather than enthusiasm.
Adding a me-too, because a thread of one person's experience is not much use. Nothing to add that would improve it.
Adding the clinical framing, because it changes how the question reads. There is a difference between no evidence and evidence of no effect, and this subject is one where the two get swapped freely in both directions.