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The next generation of metabolic research is no longer focused solely on GLP-1.
Researchers are increasingly investigating whether combining GLP-1 signalling with other hormonal pathways can produce different metabolic effects.
One of the most closely watched examples is zenagamtide, the investigational compound previously known as amycretin.
Developed by Novo Nordisk, zenagamtide is particularly unusual because a single molecule targets both GLP-1 and amylin receptor systems.
And during 2026, the programme has moved considerably further forward.
Phase 3 studies are now underway in obesity, while Novo Nordisk has also been advancing Phase 3 development in type 2 diabetes.
So what is zenagamtide, is it the same thing as amycretin, and how does it differ from drugs such as semaglutide, tirzepatide and emerging amylin compounds?
Is zenagamtide the same as amycretin?
Yes.
Zenagamtide is the newer name for the compound previously widely known as amycretin.
This is worth establishing immediately because both names continue to appear online and in earlier scientific literature.
Researchers following amycretin haven’t missed a different compound — the development programme has simply moved forward under the zenagamtide name.
Its development code is NNC0487-0111.
For search purposes, therefore:
Zenagamtide = amycretin.
What is zenagamtide?
Zenagamtide is an investigational unimolecular peptide agonist of GLP-1 and amylin receptors.
“Unimolecular” is important.
Rather than combining two separate medicines, researchers have engineered activity affecting both hormonal systems into a single molecule.
That differentiates zenagamtide from combination approaches such as CagriSema or the EloraTZP programme we recently covered.
Those combine separate compounds.
Zenagamtide attempts to incorporate complementary receptor activity within one molecule.
What does GLP-1 do?
GLP-1 — glucagon-like peptide-1 — is an incretin hormone involved in glucose regulation, insulin secretion, gastrointestinal signalling and appetite.
The success of GLP-1 receptor agonists transformed metabolic drug development.
But researchers increasingly recognise that GLP-1 is only one component of a much larger hormonal network.
That is where amylin becomes particularly interesting.
What is amylin?
Amylin is a peptide hormone released alongside insulin by pancreatic beta cells.
It contributes to signals involved in satiety, food intake and gastrointestinal function.
Rather than asking whether amylin could replace GLP-1, current research increasingly asks whether the two systems could complement one another.
Zenagamtide is one attempt to answer that question.
How does zenagamtide work?
Zenagamtide activates both GLP-1 and amylin receptor systems.
That makes its mechanism fundamentally different from several well-known metabolic compounds.
Semaglutide primarily targets the GLP-1 receptor.
Tirzepatide targets GIP and GLP-1 receptors.
Retatrutide targets GIP, GLP-1 and glucagon receptors.
Zenagamtide instead brings together:
GLP-1 + amylin.
That means researchers are investigating a different combination of biological signals rather than simply adding another incretin receptor.
Is zenagamtide a peptide?
Yes.
This is another useful distinction from the orforglipron article we recently covered.
Orforglipron is a non-peptide small molecule.
Zenagamtide is peptide-based.
Yet researchers are investigating both oral and injectable versions of zenagamtide.
That makes the oral programme particularly interesting from a peptide-science perspective, because achieving useful oral delivery of peptide-based compounds has historically been challenging.
Is zenagamtide a tablet or an injection?
Potentially both.
Novo Nordisk has been developing:
once-weekly subcutaneous zenagamtide, and
once-daily oral zenagamtide.
Both approaches have progressed through clinical research, and the company’s Phase 3 programme includes development of oral as well as injectable formulations.
This makes zenagamtide unusual.
The question isn’t simply whether one administration route will replace another. Researchers can investigate whether different formulations could ultimately suit different clinical situations.
What have the zenagamtide trials found?
Several results have attracted attention.
In earlier research involving adults with overweight or obesity, once-weekly subcutaneous amycretin — now zenagamtide — produced substantial mean body-weight changes across the investigated dose groups.
For example, one group receiving the investigated 60 mg regimen had an estimated mean change of −24.3% at 36 weeks, compared with −1.1% with placebo.
Importantly, this was an earlier-stage study involving only 125 randomised participants, and the researchers noted a large number of withdrawals, so the results shouldn’t be treated as equivalent to evidence from a completed large Phase 3 programme.
That’s precisely why the ongoing Phase 3 research matters.
What did the type 2 diabetes research find?
More recently, Novo Nordisk presented Phase 2 results in adults with type 2 diabetes at the American Diabetes Association’s 2026 Scientific Sessions.
In the once-weekly injectable programme, reductions in HbA1c were observed alongside body-weight reductions reaching approximately 14.6% at 36 weeks at the highest investigated dose.
The oral version was also investigated.
Novo Nordisk subsequently confirmed that zenagamtide would advance into Phase 3 development for type 2 diabetes.
Zenagamtide vs semaglutide: what’s the difference?
The most obvious difference is receptor activity.
Semaglutide: GLP-1
Zenagamtide: GLP-1 + amylin
But there is another reason this comparison is becoming particularly interesting.
Novo Nordisk’s Phase 3 programme includes studies designed to compare zenagamtide directly with semaglutide.
That should eventually provide much more useful evidence than attempting to compare headline percentages from unrelated trials.
Until those studies report, cross-trial comparisons should be treated cautiously.
Zenagamtide vs tirzepatide: which is different?
Again, the key difference is the biology.
Tirzepatide combines:
GIP + GLP-1 receptor agonism.
Zenagamtide combines:
GLP-1 + amylin receptor agonism.
Both therefore extend beyond GLP-1 alone, but through completely different secondary pathways.
There currently isn’t enough direct comparative evidence to conclude which approach is superior.
For researchers, the more interesting question is what these different combinations teach us about the relative roles of GIP, amylin and other metabolic signals.
Zenagamtide vs CagriSema
This comparison is especially interesting because both involve GLP-1 and amylin biology.
CagriSema combines two separate components: semaglutide and cagrilintide.
Zenagamtide is instead designed as a single molecule with GLP-1 and amylin receptor activity.
So while their broad biological rationale overlaps, their molecular design is quite different.
This reflects a wider trend in metabolic research: researchers are investigating not only which receptors to target, but also the best molecular architecture for targeting them.
What is the AMAZE Phase 3 programme?
Zenagamtide has now moved into a substantial Phase 3 obesity programme known as AMAZE.
Novo Nordisk reported that the obesity programme began during the first quarter of 2026, with studies investigating doses reaching as high as 40 mg.
The programme includes studies of injectable and oral zenagamtide, as well as direct comparator research.
This represents a significant change from where amycretin stood only a relatively short time ago.
It’s no longer simply an interesting early-stage compound.
It’s now one of the major late-stage programmes to watch.
Is zenagamtide approved in the UK?
No.
As of October 2026, zenagamtide remains investigational.
Phase 3 development does not mean a medicine has been approved.
Large clinical trials still need to establish its efficacy and safety, after which regulatory review would be required before any potential authorisation.
That distinction is particularly important when experimental compounds begin receiving significant attention online.
When could zenagamtide become available?
There isn’t a confirmed UK launch date.
The Phase 3 programme is ongoing, and some of the major studies aren’t expected to complete for several years.
Any claims that zenagamtide is already an approved or routinely available medicine should therefore be treated cautiously.
Why has the name changed from amycretin?
Drug-development names frequently evolve as compounds progress through clinical development.
Amycretin became widely recognised during the earlier research programme, so it will probably remain a common search term for some time.
However, zenagamtide is increasingly the name researchers and Novo Nordisk are using as development advances.
For anyone following the science, knowing both names is useful.
Why does zenagamtide matter?
Zenagamtide illustrates something much bigger happening in metabolic research.
The first major wave focused heavily on GLP-1.
The next expanded towards GIP + GLP-1.
Researchers then moved into triple agonism, amylin analogues, glucagon-containing molecules and numerous other pathways.
Zenagamtide represents another branch:
GLP-1 + amylin within a single peptide molecule.
Alongside EloraTZP, petrelintide, eloralintide and other programmes we’ve covered at Klarity Research, it shows just how important amylin biology is becoming within next-generation metabolic science.
The bigger picture
There may ultimately be no single pathway that defines the next generation of metabolic research.
Instead, researchers are exploring multiple strategies simultaneously:
GLP-1 plus GIP.
GLP-1 plus glucagon.
GLP-1 plus amylin.
GIP, GLP-1 and glucagon together.
Selective amylin receptor activation.
Small-molecule oral GLP-1 agonism.
And combinations involving multiple separate compounds.
Zenagamtide is particularly interesting because it combines two established areas of metabolic biology in one peptide molecule, while also being investigated through both injectable and oral delivery.
With Phase 3 development now underway, it is a compound we’ll be hearing considerably more about.
At Klarity Research, we’ll continue following emerging peptide and metabolic research as the evidence develops.
For educational and research information only. This article is not medical advice.