CT-388 is an investigational once-weekly injection from Roche that activates the GLP-1 and GIP receptors — the same two targets as tirzepatide — but is engineered to do it differently. It is a "signalling-biased" agonist, built to switch the receptors on without switching them off. In its phase 1 trial it produced up to 8% weight loss in 29 days. It is now in phase 3 and is not approved anywhere.
Three names, one molecule
The naming causes real confusion, so it is worth settling first.
- CT-388 — the development code, and the name most coverage still uses.
- CT388 — the same thing without the hyphen.
- Enicepatide — the international nonproprietary name, now used in the trial registry.
The "CT" comes from Carmot Therapeutics, the company that developed it. Roche acquired Carmot, so the molecule that appears in older material as a small-biotech asset is now a large-pharma phase 3 programme. There is no brand name yet, because there is no approval.
Where it stands
| Status | Investigational — phase 3, recruiting |
| Developer | Hoffmann-La Roche (formerly Carmot Therapeutics) |
| Nonproprietary name | Enicepatide |
| Targets | GLP-1 and GIP receptors, signalling-biased |
| Administration | Once-weekly subcutaneous injection |
| Registered studies | 7 |
| Published result | −4.7% to −8.0% at day 29 (phase 1) |
Study count and phase read from ClinicalTrials.gov on 13 August 2026. Where it sits against the rest of the field is in the GLP-1 pipeline tracker.
What "signalling-biased" actually means
This is the part that makes CT-388 more than another tirzepatide, and it is almost always skipped.
When a drug activates a receptor, two things happen. The receptor sends its signal — for GLP-1 and GIP that signal runs through a molecule called cAMP. And the receptor is then pulled inside the cell, a process called internalisation, which takes it out of service for a while. Internalisation is how a cell protects itself from being shouted at continuously.
CT-388 is engineered to maximise the first and minimise the second. Its published characterisation shows it activating both receptors with minimal internalisation compared with the natural hormones. The theory is that a receptor left on the surface keeps responding, so the drug does more with less desensitisation.
That is a genuinely different bet from the one tirzepatide made. Tirzepatide's advance was which receptors to hit; CT-388's is how to hit them. Both could be right, and only one has been proven at scale. The dual-receptor rationale itself is covered in how tirzepatide works.
The published results, and how to read them
One clinical study has been published: a phase 1, double-blind, randomised, placebo-controlled trial in otherwise healthy participants with overweight or obesity, testing single doses of 0.5 to 7.5 mg or four weekly doses of 5 to 12 mg.
Mean weight change at day 29 was −4.7% to −8.0% across doses, against −0.5% on placebo. Tolerability was described as generally good, with most adverse events mild or moderate and a profile consistent with other incretin drugs. Glycaemic measures improved, and the pharmacokinetics supported weekly dosing.
Now the caveat, which matters more than the number. That is twenty-nine days. Tirzepatide's 20.9% and semaglutide's 14.9% are figures at 68 to 72 weeks. Putting 8% beside them as though they were comparable would be wrong by roughly a factor of eighteen in elapsed time.
What 8% in four weeks does suggest is a steep early trajectory, and phase 1 trials are not designed to show where a curve ends. It is a reason to pay attention, not a result to rank.
What is not known
- Weight loss over a full course. No phase 2 or 3 efficacy data has been published. Everything past day 29 is unknown.
- Whether the biased-agonism premise holds. The theory is elegant and the preclinical work supports it. Elegant theories fail in phase 3 routinely.
- Tolerability at length. Twenty-nine days in healthy volunteers cannot show what a year does.
- How it compares. No head-to-head against tirzepatide or semaglutide is registered.
Can you get it?
No. CT-388 is not approved by any regulator, cannot be prescribed and is not sold through any legitimate channel. It is also, so far, less visible in the grey market than retatrutide — which is a matter of luck rather than protection, and anything appearing under the name would carry the same problems set out in can you buy retatrutide: unverified identity, unverified strength, no accountability.
Being in phase 3 and recruiting means the trials are still enrolling, which is the only legitimate route to receiving it. That is a conversation for a clinician, not a website.
Why it is worth tracking
Two reasons, neither of them the day-29 figure.
It is a Roche programme in phase 3. Large manufacturers do not run phase 3 obesity trials on hunches; the cost of one runs to hundreds of millions. That is a company acting on internal data the rest of us have not seen.
And it tests a different idea. Most of the pipeline is adding receptors — two, then three, then combinations with amylin. CT-388 keeps tirzepatide's two targets and changes the quality of the signal instead. If that works, it opens a direction the receptor-counting approach does not.
What else is in development, with phase and sponsor for each, is in the GLP-1 pipeline tracker. The approved options available now are ranked in the best GLP-1 for weight loss.
Everything on CT-388
- What is CT-388? — the short version, and the three-names problem.
- CT-388 weight loss — the day-29 figure, and why it cannot be compared with 72-week results.
- CT-388 side effects — one published sentence, and what it does and does not commit to.
- CT-388 vs Zepbound — same targets, and a specific criticism of how they are hit.
- CT-388 vs Wegovy — one extra receptor and one untested idea.
- CT-388 vs Ozempic — no overlapping evidence at all.
Scientific References
2 sources- 1
Chakravarthy MV, Rodriguez R, Hergarden A, et al.
Effects of CT-388, a once-weekly signaling-biased dual GLP-1/GIP receptor agonist, on weight loss and glycemic control in preclinical models and participants with obesity
Molecular Metabolism ยท 103 ยท 2026PMID: 41319798
NIH - 2
U.S. National Library of Medicine
ClinicalTrials.gov โ enicepatide (CT-388) registered studies: 7 total, maximum phase 3, recruiting, lead sponsor Hoffmann-La Roche; read 13 August 2026
ClinicalTrials.gov ยท 2026
References open in a new tab. Content is reviewed against peer-reviewed literature as part of our editorial policy.
About the author
Editor, Modern Weight Science
Claudiu Gheorghe is the editor of Modern Weight Science. He is not a physician. His role is to synthesize peer-reviewed studies, clinical-trial data, and FDA prescribing information into clear, plain-language explanations, and to make sure every factual claim on the site traces back to a cited source. Any decision about starting, changing, or stopping a medication belongs with a licensed clinician who knows your history.
Every claim is checked against peer-reviewed research through our review process and fact-checking policy.
Frequently Asked Questions
What is CT-388?
An investigational once-weekly injection from Roche that activates the GLP-1 and GIP receptors โ the same two targets as tirzepatide โ but is engineered as a signalling-biased agonist, meaning it drives the receptors' signal while causing minimal receptor internalisation. It is in phase 3 and is not approved anywhere.
Is CT-388 the same as enicepatide?
Yes. Enicepatide is the international nonproprietary name and CT-388 is the development code, from Carmot Therapeutics, the company that created it. Roche acquired Carmot, so the same molecule appears in older material as a small-biotech asset and in the trial registry under its nonproprietary name. There is no brand name because there is no approval.
How much weight loss does CT-388 cause?
The one published clinical study, a phase 1 trial, reported mean weight change of โ4.7% to โ8.0% at day 29 across doses, against โ0.5% on placebo. That is a four-week figure and cannot be set beside the 20.9% and 14.9% quoted for tirzepatide and semaglutide, which are measured at 68 to 72 weeks. No longer-term efficacy data has been published.
How is CT-388 different from Zepbound?
It aims at the same two receptors โ GLP-1 and GIP โ but changes how it activates them. Ordinary agonists cause the receptor to be pulled inside the cell after signalling, taking it temporarily out of service. CT-388 is engineered to signal strongly with minimal internalisation, on the theory that a receptor left on the surface keeps responding. Whether that translates into better results in a long trial is unproven.
When will CT-388 be available?
There is no approval date. It is in phase 3 and recruiting, with seven registered studies. A manufacturer files after its pivotal trials report and a regulator then takes its own time, so any date in circulation is a projection. Enrolling in a trial is currently the only legitimate way to receive it.
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Not medical advice. This guide is for general education only. GLP-1 medications, dosing, and treatment suitability are decisions for you and a licensed clinician who knows your full medical history.


