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.
The bit I cannot resolve on my own is why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose.
If the honest answer is that nobody knows, that is a useful answer and I would rather have it.
Answering the narrow version, because the broad one does not have a single answer. The mechanism and the magnitude are separate questions. Agreeing that something happens says nothing about whether it happens enough to act on.
Dr.ObesityLA said:The mechanism and the magnitude are separate questions.
No disagreement with Dr.ObesityLA. 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 Biochemraj_cambridge 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.
This matches mine closely enough to be worth saying so out loud.
From the other side of the consultation, briefly. It helps to say which part of this you are uncertain about. A precise question gets a precise answer; a general one gets everybody’s favourite anecdote.