genuine question about amylin that I am slightly embarrassed to ask
Something I noticed reading old threads that I have not seen said out loud.
The advice on REDEFINE in this community changed substantially around the start of last year, and nobody went back and updated the older posts. So depending on which thread the search engine hands you, you get two contradictory answers with the same confidence.
I have listed what I think the current consensus is below. Correct me — that is the point of posting it.
best — the order this archive was captured in
REDEFINE readouts are phase 21 data
REDEFINE phase 2 readouts are interesting but 2 person CagriSema is different from 2 trial CagriSema.
Three years on this site and the questions have not changed at all. Which is depressing or reassuring depending on the day.
Strongly agree. REDEFINE is phase 15, not final.
Sceptical. If this were true we would see it reflected in the data and we do not.
This is correct. The co-agonism is real.
This is the "correlation is mechanism" thing again. You changed three variables at once.
tendon and CagriSema literature in rodents is interesting
the co-agonism question is real and interesting
the amylin agonist pool is small, community is satiety
This is correct. The co-agonism is real.
CagriSema is a fixed combo in trials, not user-mixed
Yeah, amylin is doing different work than GLP-1.
Are we talking amylin or GLP-1 here?
the co-agonism question is real and interesting
Yeah, amylin is doing different work than GLP-1.
Adding to this: co-agonism is doing more work than the comment implies.
not approved anywhere, keep posts descriptive, not instructional
amylin receptor distribution is different from GLP-1
the amylin agonist pool is small, community is satiety
the mechanism is different, the side effect profile reflects it
- 1Strongly agree. REDEFINE is phase 15, not final.8 comments in this branch · started by u/elin_lundgren
- 2Yeah, amylin is doing different work than GLP-1.8 comments in this branch · started by u/niels_norgaard