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.
For anyone tracking the class: GLP-1 alone gets you appetite, GLP-1 plus GIP adds tolerability and lipid handling, and adding glucagon adds expenditure and liver-fat reduction. Each addition also adds a receptor system that can generate side effects.
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.
I would rather have one careful answer than five confident ones.
This one has a reasonably settled answer, so here it is. The distinction that resolves most of these threads is between what is true on average and what is true for one person. Both are real; they answer different questions and get quoted as if they were the same one.
PharmacoVig_BOS said:The distinction that resolves most of these threads is between what is true on average and what is true for one person.
That is correct as far as it goes, and here is where it stops going. 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.
Ask again with the specifics and you will get a better answer than this one.
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Browse GL Biochemdenise_HTX 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.
Same pattern here, and in the same order. Posting only so the count is not one.
Adding the clinical framing, because it changes how the question reads. The version of this that has an answer is narrower than the version being asked. Narrow it and it becomes tractable; leave it broad and the thread will produce nine confident and incompatible replies.