Amylin analogue mechanism: satiety signalling separate from GLP-1 — does this still hold?

Gastric emptying: both amylin and GLP-1 slow it, through partly overlapping but distinct mechanisms. Whether the slowing at a higher magnitude produces disproportionate nausea or is tolerable is a question phase 3 exists to answer.

This is the sort of thing that ought to be settled and apparently is not.

Taking post #4 at face value and following it one step further.

What is genuinely unknown about long-term amylin agonism: real-world response rates, whether effect is durable with continued use, whether satiety adaptation occurs over months or years, safety profile in populations not enrolled in the trials.

That is the practical version. The rigorous version is longer and says the same thing.

Checked the Amylin analogue mechanism claim against the primary source this morning. It survives, with a narrower scope than the version quoted here. Posting the narrower scope.

Cagrilintide is a long-acting amylin analogue, which puts it in a different mechanistic family from the incretin agonists it is usually discussed alongside. Amylin signalling contributes to satiety through a distinct pathway.

I read post #17 twice before replying, because I had assumed the opposite.

Having read the whole Amylin analogue mechanism thread before replying: the question in the first post has not actually been answered yet, and three of us have answered a nearby one instead.