why does nobody talk about amylin
The title is the whole question — why does nobody talk about amylin — but here is why I am asking. Amylin is co-secreted with insulin and acts on satiety and gastric emptying through its own receptor complexes. An amylin analogue is therefore not a variant of an incretin agonist — it is a different signalling axis.…
Combination and monotherapy arms must be read separately. Efficacy and tolerability both differ substantially between them and summaries routinely blur the two.
Complementary mechanisms are the rationale for pairing: satiety signalling alongside incretin signalling, rather than more agonism at the same receptor.
Not convinced. Amylin signalling is not a GLP-1 pathway and the mechanism you are proposing conflates them.
Push back: the evidence base here is thin enough that a confident ranking against the established compounds is not supportable.
Small fix — amylin analogue, not a GLP-1 analogue. The whole mechanism argument changes on that word.
Careful — that is a dosing intuition carried over from another board and there is no basis for it here.
Correction: that is the combination programme, not the monotherapy readout. Different arms, different numbers.
phase 3 data will change most of what gets said here