the co-agonism thing finally clicked for me and I want to write it down
Thinking out loud about this: the co-agonism thing finally clicked for me and I want to write it down.
Nothing containing this compound is approved as a standalone product, and research-use-only material is not approved for human use.
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.
Sent a vial to Medutest because there was almost nothing on file for this compound. 98.1% against a claimed 97.5%, and I posted it because the log needs entries.
Would rather be corrected in public than confident in private.
best — the order this archive was captured in
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.
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phase 3 data will change most of what gets said here
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.
Not convinced. Amylin signalling is not a GLP-1 pathway and the mechanism you are proposing conflates them.
How many separate lots has anyone here tested?
Monotherapy arm or combination arm?
the monotherapy numbers are modest and that is not the point
That is preclinical work and the thread is treating it as a human finding.
That result is preclinical. Worth flagging, since the thread has been reading it as human data.
Is there any independent purity data on this compound that you have seen?
Is there any independent purity data on this compound that you have seen?
This is the distinction that keeps this board honest — different axis, not a stronger version of the same one.
Yes. The combination is where the interesting effect sizes are, and the monotherapy arms read very differently.
Which trial and which readout?
Independent purity data on this compound is sparse compared with the older molecules, simply because far fewer members have paid for testing. Sparse data means wide uncertainty, not a verdict.
Which receptor family are you attributing that effect to?
the interesting data is the combination, not the monotherapy
Independent result added to the log. Thank you for paying for it — there are very few on this compound.
Read the combination paper twice before saying anything here. The monotherapy and combination arms tell genuinely different stories.
nausea profile in the combination trials is the thing to read carefully
Disagree — you are quoting a combination arm as though it were monotherapy. Those are different results.
Do you have the publication or a summary of it?
Complementary mechanisms are the rationale for pairing: satiety signalling alongside incretin signalling, rather than more agonism at the same receptor.
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.
read the combination arms separately from the monotherapy arms
This. Complementary mechanisms rather than more of the same is the actual argument for the pairing.
amylin and GLP-1 are not redundant pathways
REDEFINE is the combination programme
Asked a question here that turned out to be based on a mechanism confusion. Three people untangled it patiently.
- 1Do you have the publication or a summary of it?9 comments in this branch · started by u/viktor_erdogan