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c/cagrilintide·submitted 5 months ago by u/emeka_chowdhury

why does nobody talk about CagriSema

Trial Databranch of 8 comments

why does nobody talk about CagriSema. I am not trying to be the "source?" guy. I would just like a source. Why this compound is not simply another agonist, which is how it gets described everywhere else. Amylin is co-secreted with insulin and signals satiety through its own receptor complexes. It is a different axis…

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8 comments, started 5 months ago
u/zeynep_duarte12 points·5 months ago

nausea profile in the combination trials is the thing to read carefully

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u/hana_pereira10 points·5 months ago

Not convinced. Amylin signalling is not a GLP-1 pathway and the mechanism you are proposing conflates them.

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[removed]4 points·5 months ago

[removed by moderator]

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u/amylin_amyamylin4 points·5 months ago

the interesting data is the combination, not the monotherapy

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u/sequence_checkerresearch peptides2 points·5 months ago

amylin analogue, different receptor family, different story

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u/hugo_pires1 point·5 months ago

Complementary mechanisms are the rationale for pairing: satiety signalling alongside incretin signalling, rather than more agonism at the same receptor.

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u/pavel_halvorsen6 points·5 months ago

That is preclinical work and the thread is treating it as a human finding.

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u/helga_vermeulen5 points·5 months ago

Right, and the tolerability data in the combination arms is the part worth reading properly rather than summarising.

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Amylin analog pharmacology and the CagriSema combination: why amylin and GLP-1 co-agonism produces a different satiety profile, the REDEFINE readouts, and the very limited pool of people handling cagrilintide as research material.

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