Posting this because the summary going around does not say what the paper says, and the difference matters for how people here are using it.
Amylin analogues act on a different satiety circuit — area postrema and dorsal raphe — rather than the arcuate pathway GLP-1 agonists use. Because the mechanisms are complementary rather than additive on the same receptor, the combination gets more effect without the tolerability cost of simply pushing GLP-1 higher. REDEFINE-2 put cagrisema near 22.7% against about 15.8% for semaglutide alone.
Where I think it is weakest: the population was selected and supported in ways a real cohort is not, so I would read the effect size as a ceiling rather than an expectation.
What I am after is whether the amylin component adds anything beyond what a higher GLP-1 dose would achieve. If the honest answer is that nobody knows, that is a useful answer and I would rather have it.
Note on sourcing:
Figures above are from the primary publication rather than the press summary. If a number here disagrees with one you have, post yours and we will work out which of us is reading a secondary source.