You have 0 items in your cart
The metabolic research landscape is becoming much larger than a handful of familiar GLP-1 compounds.
One emerging name is enicepatide, previously known primarily by its development code CT-388.
Enicepatide is an investigational once-weekly dual GLP-1 and GIP receptor agonist being developed by Roche following its acquisition of Carmot Therapeutics.
The mechanism immediately invites comparison with tirzepatide.
Both compounds target the GLP-1 and GIP receptor systems.
But they are separate molecules, and enicepatide is now progressing through its own clinical development programme.
So what is enicepatide, what have researchers found so far, and how does it actually differ from tirzepatide and other next-generation metabolic compounds?
What is enicepatide?
Enicepatide is an investigational peptide designed to activate:
GLP-1 receptors
and
GIP receptors.
It was previously called CT-388, and that development code still appears frequently in older articles, clinical-trial information and online searches.
So:
Enicepatide = CT-388.
The compound originated at Carmot Therapeutics, which Roche acquired in 2024 as part of its expansion into metabolic research.
Is enicepatide a GLP-1?
It’s more accurately described as a dual GLP-1/GIP receptor agonist.
This distinction matters.
A traditional GLP-1 receptor agonist primarily targets the GLP-1 receptor.
Enicepatide is designed to activate two incretin-related pathways simultaneously.
The basic comparison looks like this:
Semaglutide: GLP-1
Tirzepatide: GIP + GLP-1
Enicepatide: GIP + GLP-1
Retatrutide: GIP + GLP-1 + glucagon
Enicepatide therefore sits within the increasingly competitive dual-incretin category.
Is enicepatide the same as tirzepatide?
No.
This will probably become one of the most common questions surrounding the compound.
Tirzepatide and enicepatide both activate GIP and GLP-1 receptors, but they are completely separate molecules.
Tirzepatide was developed by Eli Lilly and is already an authorised medicine.
Enicepatide remains an investigational compound undergoing clinical trials.
Two compounds targeting the same receptors also shouldn’t automatically be expected to behave identically.
Differences in molecular design can affect receptor activity, pharmacokinetics, tolerability and other biological characteristics.
How does enicepatide work?
Enicepatide is designed to activate the body’s GIP and GLP-1 receptor systems.
Both GIP and GLP-1 are incretin hormones involved in metabolic signalling following food intake.
GLP-1 signalling has effects involving glucose-dependent insulin secretion, glucagon regulation, gastrointestinal function and appetite.
GIP also participates in nutrient and insulin-related signalling.
Dual agonists attempt to influence both pathways simultaneously.
Tirzepatide demonstrated that this strategy can produce substantial metabolic effects, which has encouraged further research into different dual-incretin molecules.
Enicepatide is one of the most advanced examples.
Is enicepatide a peptide?
Yes.
This makes it quite different from the oral compounds we’ve recently covered at Klarity Research.
Orforglipron and aleniglipron are non-peptide small molecules.
Enicepatide is peptide-based.
It is being investigated as a once-weekly subcutaneous compound, rather than as a daily tablet.
That gives us an important distinction within the wider series.
Researchers aren’t universally trying to replace injectable peptides.
Both peptide and small-molecule technologies are being developed simultaneously.
What have the enicepatide trials found?
Clinical development has produced encouraging early and mid-stage findings.
Earlier Phase 1 research reported substantial reductions in body weight among participants receiving CT-388.
The programme subsequently progressed into larger Phase 2 research.
By September 2026, enicepatide was among the increasingly crowded group of obesity candidates moving towards late-stage development, with Roche planning Phase 3 development.
As with all experimental compounds, these results need to be interpreted within the context of the individual study.
Headline percentages from different trials aren’t reliable head-to-head comparisons.
Enicepatide vs tirzepatide: which is better?
At this stage, there isn’t sufficient evidence to say that one is better than the other.
This is an important distinction because searches increasingly compare every new compound with tirzepatide.
Both target:
GIP + GLP-1.
But tirzepatide has a much larger body of completed clinical evidence and real-world use behind it.
Enicepatide remains under investigation.
Comparing a percentage from an enicepatide trial with a percentage from an unrelated tirzepatide study doesn’t provide a scientifically reliable answer.
Study populations, doses, durations and statistical approaches can all differ.
A proper head-to-head trial would be considerably more informative.
Enicepatide vs retatrutide
These compounds differ more substantially.
Enicepatide targets:
GIP + GLP-1
Retatrutide targets:
GIP + GLP-1 + glucagon
Retatrutide therefore adds a third receptor system.
That doesn’t automatically mean that a triple agonist is superior to a dual agonist.
Adding receptor activity can alter both desired and unwanted biological effects.
Researchers need clinical evidence rather than simply counting the number of receptors targeted.
Enicepatide vs VK2735
This is another comparison likely to become increasingly common.
Both are investigational GIP/GLP-1 dual agonists.
However, their development programmes differ.
VK2735 is being investigated in both injectable and oral formulations.
Enicepatide is currently primarily being developed as a once-weekly injectable peptide.
They therefore provide researchers with another opportunity to investigate how different molecular designs targeting the same receptor systems perform.
What is CT-996?
This is where Roche’s programme becomes more interesting.
Enicepatide isn’t Roche’s only metabolic compound.
Another compound originating from Carmot is CT-996, now known as tifeglipron.
Unlike enicepatide, tifeglipron is an oral small-molecule GLP-1 receptor agonist.
So Roche is effectively investigating several different technological approaches:
injectable dual incretin agonism through enicepatide
and
oral small-molecule GLP-1 agonism through tifeglipron.
That demonstrates just how diversified metabolic drug development has become.
And importantly, tifeglipron gives us another future article without having to write it immediately after the other oral GLP-1 pieces.
Is enicepatide in Phase 3?
The programme is moving towards late-stage development.
Roche has indicated plans to advance enicepatide into Phase 3, putting it among a growing group of next-generation obesity compounds competing beyond the currently established medicines.
Phase 3 will be particularly important because larger studies provide much stronger evidence regarding efficacy, tolerability and longer-term outcomes than early clinical research.
Is enicepatide approved?
No.
Enicepatide remains investigational.
It has not received marketing authorisation as an obesity or diabetes medicine.
This is important because online discussion sometimes blurs the distinction between promising clinical-trial results and regulatory approval.
They aren’t the same thing.
Is enicepatide available in the UK?
Not as an approved medicine.
There is currently no authorised enicepatide product available for routine prescribing in the UK.
Any eventual availability would depend upon successful completion of clinical development followed by regulatory review.
When will enicepatide be available?
There is no confirmed UK launch date.
Phase 3 research still needs to establish the compound’s performance in larger populations.
Drug-development timelines can also change substantially depending upon trial results and regulatory requirements.
For that reason, specific online claims about an enicepatide release date should be treated cautiously.
Why develop another GLP-1/GIP agonist if tirzepatide already exists?
This is perhaps the most interesting question.
Once researchers establish that a particular biological mechanism works, development doesn’t stop.
Different molecules targeting the same receptors may have different characteristics involving:
- receptor activity;
- duration of action;
- tolerability;
- manufacturing;
- dose requirements;
- combination potential;
- and pharmacokinetics.
The pharmaceutical industry contains many examples of several medicines targeting broadly the same biological mechanism while possessing meaningfully different properties.
Dual GIP/GLP-1 agonism is likely to follow the same pattern.
Are researchers moving beyond GLP-1?
Increasingly, yes — although GLP-1 remains central to much of the research.
The emerging landscape now includes compounds targeting:
GLP-1 alone
GIP + GLP-1
GIP + GLP-1 + glucagon
GLP-1 + amylin
selective amylin receptors
activin pathways
GDF15
FGF21
and several completely different mechanisms.
This is why the next generation of metabolic science is becoming much more interesting than simply searching for the “next Ozempic.”
There may ultimately be multiple distinct families of metabolic compounds.
The bigger picture
Enicepatide demonstrates something important about the evolution of metabolic research.
The discovery that a particular receptor combination can be effective doesn’t end the scientific question.
It begins another one:
How can that receptor combination be improved?
Researchers can alter molecular architecture, receptor bias, duration of activity, formulation and combination strategies while still working with the same underlying biological pathways.
Enicepatide therefore shouldn’t simply be viewed as another tirzepatide competitor.
It’s part of a much broader attempt to understand how dual incretin signalling can be optimised.
At Klarity Research, we’ll continue following enicepatide and the wider next-generation metabolic pipeline as new clinical evidence emerges.
For educational and research information only. This article is not medical advice.