Why cagrilintide alone is discussed so much less than in combination — does this still hold?

Why cagrilintide alone is discussed so much less than in combination — does this still hold? — that is the question, and I have not found it answered plainly anywhere I have looked.

Session topic: SURMOUNT-4 (JAMA, 2024). Please read it before posting; the discussion is much better when everyone has.

The question I would like us to start with is what the trial set out to estimate, rather than what it found. Once that is on the table we can talk about whether the design could have answered it, and only then about the numbers.

Specific things I would like covered: the population and how far it generalises, how discontinuation was handled, whether the comparator was a fair one, and what the absolute rather than relative effect looks like.

I will summarise at the end and the summary will feed the relevant digest page.

Worth separating two things that post #2 runs together.

Practical note that does not fit anywhere else. Whatever you conclude from this topic, write down what you did and when. The single most useful thing in your own records is not any individual result; it is that they are dated and consecutive.

For anyone arriving from searches on "amylin agonist": this subcategory discusses published clinical evidence and what it does and does not establish. It does not endorse or recommend the compounds discussed.

Coming back to post #20, because the follow-up matters more than the original answer.

Amylin signalling is distinct from GLP-1 signalling. Amylin slows gastric emptying and promotes satiety through a different receptor and different neural pathways. The hypothesis behind combination is two complementary satiety mechanisms with one injection.