[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.
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.
Corrections welcome, especially the pedantic ones. Pedantry is how this board earns its reputation.
best — the order this archive was captured in
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.
Do you have the publication or a summary of it?
REDEFINE is the combination programme
Read the combination paper twice before saying anything here. The monotherapy and combination arms tell genuinely different stories.
amylin analogue, different receptor family, different story
this is a less-travelled board and the evidence base shows it
nothing here is approved as a standalone product and research material is not for human use
Are you comparing against a GLP-1 monotherapy result? They are not comparable.
independent purity data on this compound is thin
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.
Carried an assumption over from the tirzepatide board and was corrected within an hour. Deserved.
Is there any independent purity data on this compound that you have seen?
the interesting data is the combination, not the monotherapy
the monotherapy numbers are modest and that is not the point
Bought small deliberately because the evidence base is thin. That felt like the only defensible approach.
the co-agonism argument is about complementary mechanisms
- 1Dosing intuitions from the GLP-1 boards do not transfer. Different receptor…8 comments in this branch · started by u/iman_castellanos
- 2Reading the trial literature on this without misleading yourself. Separate…6 comments in this branch · started by u/egfr_watcher