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

Cagrilintide alone is discussed less than in combination because the published data is almost entirely from combination trials. The phase 2 combination data was consistent with more effect than either component alone, but phase 2 cannot establish whether that is synergy or simply additivity.

This follows post #4 rather than contradicting it.

For anyone arriving from a search: the marked solution above is the direct answer, and the replies underneath it add the caveats that make it safe to use.

Reading the phase 2 paper: it establishes tolerability and efficacy in a selected population on a defined dose escalation. It does not establish the lowest effective dose or the durability over years.

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.

Coming back to post #17, because the follow-up matters more than the original answer.

Is synergy the right word for the combination data? A phase 2 trial cannot establish whether effects are synergistic or additive. Synergy is a mechanistic claim that requires a designed experiment to support it. The combination works, but the mechanism is unsettled.