small win: cagrilintide stopped being a problem at week 60
small win: cagrilintide stopped being a problem at week 60. Numbers below. Ask me the boring questions, they are the useful ones.
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 the tirzepatide board and was corrected within an hour. Deserved.
That is everything I have. The rest is opinion and I have tried to keep it out.
best — the order this archive was captured in
This. Complementary mechanisms rather than more of the same is the actual argument for the pairing.
satiety signalling rather than incretin signalling
Right, and the tolerability data in the combination arms is the part worth reading properly rather than summarising.
Nothing containing this compound is approved as a standalone product, and research-use-only material is not approved for human use.
Nothing containing this compound is approved as a standalone product, and research-use-only material is not approved for human use.
Agreed, and the combination arms are where the interesting numbers actually live.
Small fix — amylin analogue, not a GLP-1 analogue. The whole mechanism argument changes on that word.
Small fix — amylin analogue, not a GLP-1 analogue.
This is the distinction that keeps this board honest — different axis, not a stronger version of the same one.
Complementary mechanisms are the rationale for pairing: satiety signalling alongside incretin signalling, rather than more agonism at the same receptor.
Nothing containing this compound is approved as a standalone product, and research-use-only material is not approved for human use.
Adding the standing caveat — nothing here is approved standalone and research material is not for human use.
do not assume the dosing intuitions from the GLP-1 boards transfer
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.
Are you comparing against a GLP-1 monotherapy result? They are not comparable.
That result is preclinical. Worth flagging, since the thread has been reading it as human data.
Independent result added to the log. Thank you for paying for it — there are very few on this compound.
read the combination arms separately from the monotherapy arms
phase 3 data will change most of what gets said here
Push back: the evidence base here is thin enough that a confident ranking against the established compounds is not supportable.
this is a less-travelled board and the evidence base shows it
REDEFINE is the combination programme
Correcting myself upthread: I gave the 23-week figure and the paper reports 72 weeks.
nothing containing this is approved as a standalone product
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.
amylin and GLP-1 are not redundant pathways
Correction: that is the combination programme, not the monotherapy readout. Different arms, different numbers.
nausea profile in the combination trials is the thing to read carefully
Combination and monotherapy arms must be read separately. Efficacy and tolerability both differ substantially between them and summaries routinely blur the two.
Not convinced. Amylin signalling is not a GLP-1 pathway and the mechanism you are proposing conflates them.
- 1do not assume the dosing intuitions from the GLP-1 boards transfer14 comments in this branch · started by u/declared_value_dv
- 2Nothing containing this compound is approved as a standalone product, and…6 comments in this branch · started by u/tomas_kimani