how much of what we believe about amylin actually comes from co-agonism threads
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…
Bought small deliberately because the evidence base is thin. That felt like the only defensible approach.
I would not extrapolate the tolerability profile from the monotherapy arm to the combination. The trials report them separately for a reason.
Sent a vial to Janoshik because there was almost nothing on file for this compound. 97.7% against a claimed 97.5%, and I posted it because the log needs entries.
Yes. The combination is where the interesting effect sizes are, and the monotherapy arms read very differently.
long-acting amylin is the whole point of the molecule
Push back: the evidence base here is thin enough that a confident ranking against the established compounds is not supportable.
Correction: that is the combination programme, not the monotherapy readout. Different arms, different numbers.
Yes. Anyone reading this board should hold their conclusions loosely until phase 3 reports.