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c/cagrilintide·submitted 1 year ago by u/pancreatitis_scare

how much of what we believe about amylin actually comes from co-agonism threads

Trial Databranch of 6 comments

Question in the title, detail here: how much of what we believe about amylin actually comes from co-agonism threads. Dosing intuitions from the GLP-1 boards do not transfer. Different receptor family, different exposure-response, and no published schedule for members to reason from. Carried an assumption over from…

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6 comments, started 1 year ago
u/lukas_vermeulen0 points·1 year ago

The engineering problem was duration: native amylin is short-acting and aggregation-prone. A long-acting analogue suitable for weekly administration is what makes the combination clinically interesting.

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u/pancreatitis_scareOP1 point·1 year ago

amylin and GLP-1 are not redundant pathways

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[deleted]1 point·1 year ago

[deleted]

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u/milos_vestergaard1 point·1 year ago

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

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u/helga_vermeulen1 point·1 year ago

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

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u/yannick_petrov1 point·1 year ago

Agreed that the monotherapy numbers look modest out of context and that the context is the whole story.

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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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