[Trial Data] REDEFINE 1 — what cagri adds on top of sema
REDEFINE 1 — what cagri adds on top of sema. It is the sort of thing everyone half-believes and nobody writes down.
Asked a question here that turned out to be based on a mechanism confusion. Three people untangled it patiently.
Bought small deliberately because the evidence base is thin. That felt like the only defensible approach.
Why this compound is not simply another agonist, which is how it gets described everywhere else.
Amylin is co-secreted with insulin and signals satiety through its own receptor complexes. It is a different axis from the incretin system, not a parallel version of it. That is why the combination story is interesting: two mechanisms that address appetite differently, rather than more agonism at one receptor.
It is also why the dosing intuitions people bring from the semaglutide and tirzepatide boards do not transfer. Different receptors, different exposure-response, and no published schedule anybody here can reason from.
Tell me where this is wrong. That is the useful part of posting it.
best — the order this archive was captured in
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.
The tolerability tables were more informative than the headline numbers, which is usually the case and never how it gets summarised.
satiety signalling rather than incretin signalling
Careful — that is a dosing intuition carried over from another board and there is no basis for it here.
do not assume the dosing intuitions from the GLP-1 boards transfer
Carried an assumption over from the tirzepatide board and was corrected within an hour. Deserved.
Independent result added to the log. Thank you for paying for it — there are very few on this compound.
What does the tolerability table in that paper actually say?
Complementary mechanisms are the rationale for pairing: satiety signalling alongside incretin signalling, rather than more agonism at the same receptor.
Disagree — you are quoting a combination arm as though it were monotherapy. Those are different results.
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Which receptor family are you attributing that effect to?
Small fix — amylin analogue, not a GLP-1 analogue. The whole mechanism argument changes on that word.
Correction: that is the combination programme, not the monotherapy readout. Different arms, different numbers.
the interesting data is the combination, not the monotherapy
Disagree — you are quoting a combination arm as though it were monotherapy.
Agreed, and the combination arms are where the interesting numbers actually live.
Agreed, and the combination arms are where the interesting numbers actually live.
This is the distinction that keeps this board honest — different axis, not a stronger version of the same one.
Which trial and which readout?
nothing containing this is approved as a standalone product
- 1Disagree — you are quoting a combination arm as though it were monotherapy.…10 comments in this branch · started by u/viktor_nkemelu
- 2The engineering problem was duration: native amylin is short-acting and…8 comments in this branch · started by u/egfr_watcher