[Discussion] can we stop arguing about satiety until somebody posts a number
Question in the title, detail here: can we stop arguing about satiety until somebody posts a number. 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.…
Reading the trial literature on this without misleading yourself.
Separate the monotherapy arms from the combination arms before you do anything else. They report different effect sizes and different tolerability, and almost every summary that circulates blends them.
Then read the tolerability tables rather than the headline. In combination work the interesting question is whether adding a second mechanism adds effect without adding proportionate side effects, and that question is answered in a table nobody quotes.
Finally, note the durations. Comparing a shorter readout here with a longer one from an established compound is not a comparison at all.
amylin and GLP-1 are not redundant pathways
That result is preclinical. Worth flagging, since the thread has been reading it as human data.
Not convinced. Amylin signalling is not a GLP-1 pathway and the mechanism you are proposing conflates them.
Correction: that is the combination programme, not the monotherapy readout. Different arms, different numbers.
Correction: that is the combination programme, not the monotherapy readout.
Adding the standing caveat — nothing here is approved standalone and research material is not for human use.