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 question I want answered is why adding glucagon agonism to an anti-obesity drug is not self-defeating, given that glucagon raises blood glucose.
Tell me what I have not thought of.
Short answer first, then the reasoning. The useful move here is to separate what is established from what is widely repeated. Those two sets overlap less than the confident tone of most write-ups suggests, and the second set is where nearly all the disagreement on this board comes from.
Dr.GastroMayo said:The useful move here is to separate what is established from what is widely repeated.
Agreeing with Dr.GastroMayo, and the qualification matters more than the agreement. 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 BiochemDr.BariatricHTX 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.
Second this.
Adding the clinical framing, because it changes how the question reads. Whatever the answer turns out to be, the method for getting there is the same: state the assumption, do the arithmetic in public, and invite the correction. That is slower than asserting, and it is the only version that survives being wrong.