Enicepatide, formerly known by its development code CT-388, is Roche’s investigational dual GLP-1/GIP receptor agonist for obesity and type 2 diabetes, given as a once-weekly subcutaneous injection. An early 24-week phase 1 extension cohort produced 18.8% placebo-adjusted weight loss; in the larger phase 2 trials, the highest dose (24 mg weekly) produced 22.5% placebo-adjusted weight loss in obesity and a 2.65-percentage-point HbA1c reduction alongside 15.5% weight loss in type 2 diabetes. It is not approved anywhere, and Roche has named it its lead obesity asset.
Research snapshot
| Peptide category | Metabolic / incretin — dual GIP/GLP-1 receptor agonist, described in its peer-reviewed Phase 1 publication as biased toward cAMP signaling |
| Primary research interest | Obesity and overweight; type 2 diabetes |
| Highest available evidence | Published human clinical trial data (Phase 1 single- and multiple-ascending-dose, peer-reviewed); the Phase 1 24-week extension and both Phase 2 trials are company-reported, not yet peer-reviewed |
| Human research available | Yes — Phase 1 published (short-term) and company-reported (24-week extension); Phase 2 complete for both obesity and type 2 diabetes populations; Phase 3 recruiting across multiple trials |
| Development status | Phase 3 — Roche’s designated lead obesity asset from the Carmot Therapeutics acquisition |
| Regulatory status | Not approved anywhere; Roche has said it may seek regulatory submission for obesity as early as 2028 |
| Last reviewed | September 27, 2026 |
Technical identity
| Primary name | Enicepatide (INN) |
| Alternative names | CT-388 (original Carmot Therapeutics development code); RO7795068 and RG6640 (Roche/Genentech internal codes) |
| Peptide sequence | Not independently verified from a primary source. A commercial vendor lists a full modified sequence, but this has not been confirmed against a primary registry or publication and is not reproduced here. |
| Amino-acid length | Not reliably established from a primary source |
| Molecular formula | C226H345FN48O67, per a peer-reviewed Phase 1 publication (PMC12771327) |
| Molecular weight | Approximately 4,825 Da, per the same peer-reviewed publication; a commercial vendor separately lists 4,825.44 Da, consistent within rounding |
| CAS Registry Number | Not reliably established — two secondary sources conflict (2919675-94-6 vs. 2869147-44-2), with no primary registry confirmation of either |
| PubChem CID | Not established |
| UNII | Not established |
| DrugBank ID | Not established |
| Chemical modifications | Lipidated peptide; described in the peer-reviewed Phase 1 paper as a unimolecular dual agonist engineered for biased signaling |
| Peptide class | Dual GIP/GLP-1 receptor agonist, cAMP-signaling-biased |
| Primary biological target | GLP-1 receptor and GIP receptor |
| Developer or originator | Discovered by Carmot Therapeutics; Carmot acquired by Roche (via Genentech), completed December 2023 |
| Development status | Phase 3 |
What is enicepatide (CT-388)?
Enicepatide is Roche’s entry in the dual GLP-1/GIP agonist race for obesity and type 2 diabetes, the same drug class that includes tirzepatide, VK2735, and retatrutide. It started life as CT-388, one of three clinical-stage obesity and diabetes assets Roche acquired when it bought Carmot Therapeutics, a smaller biotech, for $2.7 billion in a deal completed December 2023. Somewhere between its 2021 phase 1 registration and its August 2024 phase 2 registration, the compound picked up the formal international nonproprietary name enicepatide, though the exact announcement establishing that name could not be pinned to a specific date or document during this review; both names are still used interchangeably in company communications and trial registrations.
Roche has since made its priorities among the three ex-Carmot assets explicit. On July 24, 2026, Roche discontinued a sibling compound, acmopatide (CT-868), even though the company’s own CEO said the drug “met all the requirements”; the stated reasoning was strategic focus rather than a failed trial, with Roche saying it would rather advance one molecule across several indications than run two obesity and diabetes candidates in parallel. Enicepatide is the asset that stayed, described by Roche around the same time as showing “best-in-class” weight-loss potential, with a broad phase 3 program now covering obesity, type 2 diabetes, and cardiovascular outcomes, and a company statement that regulatory submission for obesity could come as early as 2028.
What makes enicepatide scientifically distinct from other dual agonists in this class is a design choice Carmot describes as biased agonism. Most GPCR drugs, when they activate a receptor, also trigger a secondary internal process called beta-arrestin recruitment, which tends to shut the receptor down and pull it inside the cell, an effect called receptor internalization, that can blunt a drug’s effect over repeated dosing. Enicepatide was specifically engineered to strongly activate the signaling pathway that matters for its effect, cAMP production, while minimizing that beta-arrestin and internalization process at both the GLP-1 and GIP receptors. Whether this design choice produces a real-world clinical advantage over other dual agonists has not been established by any head-to-head trial; it is a mechanistic hypothesis with laboratory support, not a proven clinical benefit.
Roche’s first real public evidence that the drug worked came early: a 24-week phase 1 extension cohort reported in May 2024 showed 18.8% placebo-adjusted weight loss, with the effect still climbing at the end of that period and no plateau reported. That was months before the larger, formal phase 2 obesity trial confirmed a similar top-line result of 22.5% at the highest dose. As of this review, enicepatide is in phase 3 development for both obesity and type 2 diabetes, with additional trials recruiting in China and one combination trial paired with petrelintide, an amylin analog also in Roche’s pipeline. It is not approved anywhere.
How does it work?
Plain-English explanation
Like other dual agonists, enicepatide activates two gut-hormone receptors at once, GLP-1 and GIP, which together reduce appetite, slow stomach emptying, and improve insulin release. What is different about enicepatide’s design is an attempt to make the “on” signal last longer and stay cleaner, by minimizing a cellular process that would otherwise dial the receptor back down after each dose.
Technical explanation
A peer-reviewed phase 1 publication reports enicepatide’s receptor pharmacology in detail: at the GLP-1 receptor, EC50 of 0.087 nM with 99% maximal cAMP signaling efficacy, but only 4% beta-arrestin-2 recruitment efficacy and 6% receptor internalization efficacy. At the GIP receptor, EC50 of 2.47 nM with 92% maximal cAMP efficacy, 28% beta-arrestin-2 recruitment efficacy, and internalization below detectable levels. Relative to the native hormones, the same source reports enicepatide is roughly 4-fold less potent than native GLP-1 at the GLP-1 receptor but roughly 42-fold less potent than native GIP at the GIP receptor, described in the paper as a GLP-1-receptor-skewed profile, explicitly contrasted with tirzepatide’s GIP-preferring profile. The molecule was discovered through Carmot’s “Chemotype Evolution” platform, described by the company as a high-throughput, nanoliter-scale iterative chemistry and screening method; no independent side-by-side comparison of this discovery platform to competitors’ methods was located.
Potential benefits and research applications
Weight reduction in obesity and overweight
What is being investigated: body-weight reduction, first over 24 weeks in a phase 1 extension cohort, then over 48 weeks in the formal phase 2 obesity trial, in adults with obesity or overweight plus a weight-related comorbidity. Evidence: 24-week phase 1 extension results (Roche press release, 2024-05-16), and a phase 2 trial (NCT06525935, completed, 469 participants), results reported via Roche and Genentech press releases (2026-01-27), corroborated by trade press. Strength: the phase 1 SAD/MAD data is peer-reviewed; the extension and full phase 2 trial are large, registered, randomized, placebo-controlled, and company-reported, one of the strongest tiers this site recognizes, though pending fuller publication. Limitation: only the highest, 24 mg, dose’s phase 2 results have been disclosed publicly, and the 24-week extension cohort’s exact dose was not disclosed.
Glycemic control and weight loss in type 2 diabetes
What is being investigated: HbA1c reduction and weight loss over 48 weeks in people who are overweight or obese with type 2 diabetes. Evidence: a phase 2 trial (NCT06628362, 447 participants), results reported via Roche press release (2026-09-22) and corroborated by trade press. Strength: large, randomized, placebo-controlled phase 2 evidence, again company-reported pending full publication. Limitation: only the 24 mg dose’s results have been disclosed, and the trial’s own listed completion date is essentially concurrent with this review, so some detail may still be emerging.
What dosage information circulates?
Figures in this section summarize amounts and schedules reported in published research or circulating online. Their inclusion documents what is reported and does not establish that a regimen is verified, safe, effective, or appropriate.
| Reported use or research objective | Route reported | Amount reported | Frequency reported | Reported duration | Evidence or source category |
|---|---|---|---|---|---|
| Phase 1 single-ascending-dose (SAD) | Subcutaneous | 0.5, 2.0, 5.0, 6.0, and 7.5 mg (single dose per cohort) | Single dose | Observed through day 8 | Published human clinical trial (PMC12771327) |
| Phase 1 multiple-ascending-dose (MAD) | Subcutaneous | Titrated regimens up to 12 mg | Weekly | Observed through day 29 | Published human clinical trial (PMC12771327) |
| Phase 1 open-label extension | Subcutaneous | Dose not publicly disclosed | Once weekly | 24 weeks (18.8% placebo-adjusted weight loss reported) | Company-reported (Roche press release, May 16, 2024) |
| Phase 2, obesity/overweight | Subcutaneous | Up to 24 mg (only dose level publicly disclosed) | Once weekly | 48 weeks (22.5% placebo-adjusted weight loss reported) | Company-reported; not yet peer-reviewed |
| Phase 2, type 2 diabetes | Subcutaneous | Up to 24 mg (only dose level publicly disclosed) | Once weekly | 48 weeks (2.65-point HbA1c reduction and 15.5% weight loss reported) | Company-reported; not yet peer-reviewed |
| Phase 3 (multiple registered trials) | Subcutaneous | Dose not disclosed; Roche has stated it will explore doses above 24 mg | Not disclosed | Ongoing | Registered, unpublished |
| Practitioner or community protocols | — | Not consistently reported | — | — | No independent vendor or community dosing convention was identified, distinct from registered trial doses. Discussion in communities such as r/enicepatide and r/GLP1ResearchTalk consists of trial-participant discussion and reposted official data, not an independently circulating protocol. |
Amounts studied in human research
The peer-reviewed phase 1 program tested single ascending doses of 0.5, 2.0, 5.0, 6.0, and 7.5 mg subcutaneously, and multiple ascending weekly titrated regimens up to 12 mg, through day 29. A separate 24-week extension cohort from the same phase 1 program used an undisclosed dose. Both phase 2 trials, in obesity and in type 2 diabetes, tested doses up to 24 mg once weekly over 48 weeks, but Roche has only publicly disclosed results for the 24 mg arm in either trial; the lower-dose arms’ results have not been reported in any source checked. Doses for the ongoing phase 3 program have not been disclosed; Roche has stated only that it intends to explore doses above 24 mg in future work.
Amounts studied in animal research
Not identified in the sources reviewed for this page. Public disclosures on enicepatide have focused on the human trial program.
Practitioner and community-reported protocols
Not consistently reported. No independent vendor or community dosing convention for enicepatide or CT-388 was identified during this review, separate from the registered trial doses above. Active Reddit communities exist, including r/enicepatide, r/GLP1ResearchTalk, and discussion within r/mounjarouk, but they consist of trial-participant experiences and reposted official data rather than an independent dosing convention. Because enicepatide has no legitimate retail or research-use supply chain, anything purchased under either name from an online vendor should be treated with the same caution given to any unregulated research-chemical listing.
What circulates E5
| Reported use | Route | Amount reported | Frequency | Reported length |
|---|---|---|---|---|
| Phase 1 single-ascending-dose safety | Subcutaneous injection | 0.5 mg, 2.0 mg, 5.0 mg, 6.0 mg, or 7.5 mg | Single dose | Measured through day 8 |
| Phase 1 multiple-ascending-dose safety | Subcutaneous injection | Titrated regimens up to 12 mg (e.g. 5/8/12/12 mg across weeks) | Once weekly, titrated | Measured through day 29 |
| Phase 1 extension cohort, 24-week readout | Subcutaneous injection | Not disclosed; same overall dose range as the phase 1 program (0.5-12 mg) | Once weekly | 24 weeks |
| Weight management, phase 2 (obesity) | Subcutaneous injection | Up to 24 mg (highest disclosed dose; lower arms undisclosed) | Once weekly | 48 weeks |
| Glycemic control, phase 2 (type 2 diabetes) | Subcutaneous injection | Up to 24 mg (highest disclosed dose; lower arms undisclosed) | Once weekly | 48 weeks |
| Community, forum, or vendor protocol | Not applicable | No independent dosing convention identified | Not applicable | Not applicable |
No established or reliably sourced consumer dosing information was identified. Every dosage figure documented on this page comes from Roche's, Genentech's, or Carmot's own registered clinical trials or press releases; there is no approved product.
Active Reddit communities (r/enicepatide, r/GLP1ResearchTalk, discussion within r/mounjarouk) consist of reposted official data and trial-participant discussion, not an independent vendor or gray-market dosing convention. No such convention was identified during this review.
Recorded as an observation about what is published elsewhere. No figure here is a dose, a protocol, or a recommendation, and nothing in this section is evidence that any amount is safe or effective.
Side effects, risks, and limitations
Gastrointestinal side effects were the dominant adverse-event category across every enicepatide trial reviewed. In phase 1, GI events (nausea, vomiting, decreased appetite) occurred in 40% to 100% of participants depending on cohort, described as mostly mild to moderate and transient, alongside one serious adverse event, intractable vomiting at the single 7.5 mg dose, and one unrelated retinal detachment; no multiple-ascending-dose cohort participants discontinued for adverse events. The 24-week extension cohort reported “no new or unexpected safety signals,” with mild-to-moderate GI effects again the most common, though specific rates were not disclosed. In the phase 2 obesity trial, 5.9% of enicepatide-treated participants discontinued for adverse events versus 1.3% on placebo. In the phase 2 diabetes trial, 2.0% discontinued versus 0.0% on placebo, with GI effects again described as predominantly mild to moderate.
This overall pattern, GI-dominant side effects with low but nonzero discontinuation, is consistent with the broader incretin dual-agonist class and is not, on the evidence reviewed, a distinct safety signal specific to enicepatide. No long-term safety data exists yet; the longest completed human trials run 48 weeks. Trial eligibility criteria exclude participants with a personal or family history of medullary thyroid carcinoma and a history of pancreatitis, reflecting standard precaution for this drug class rather than an observed safety finding specific to enicepatide.
Regulatory and developmental status
Enicepatide (CT-388) is not approved for any use anywhere. It is in phase 3 development across multiple registered trials: an obesity-indication trial without type 2 diabetes (NCT07351045, recruiting, enrollment target 2,000, started March 2026), an obesity-indication trial with type 2 diabetes (NCT07351058, recruiting, enrollment target 1,600, started March 2026), a trial in Chinese patients (NCT07670416, recruiting, started July 2026), and a Chinese phase 1 pharmacokinetics and safety study (NCT07626515, recruiting). Roche has publicly stated it intends to begin a glycemic-control program and cardiovascular outcomes trials in the first half of 2027, and has said a regulatory submission for the obesity indication could come as early as 2028, stated as a company projection rather than a commitment. Two phase 3 trials referred to in a Roche press release as ENITH-1 and ENITH-2 appear to correspond to the obesity-indication trials above, though this name-to-registration mapping was not independently confirmed and should not be stated as settled.
Enicepatide is now Roche’s clearly designated lead obesity and diabetes asset from the Carmot acquisition: on July 24, 2026, Roche discontinued a sibling compound, acmopatide (CT-868), explicitly to concentrate development resources on enicepatide, despite CEO Thomas Schinecker stating acmopatide itself “met all the requirements” in its own trials. This was a portfolio-prioritization decision, not a safety or efficacy failure for the discontinued drug. No FDA Fast Track, Breakthrough Therapy, or other expedited-review designation was identified in any source checked. Date verified: 2026-09-25.
Frequently asked questions
What is enicepatide?
An investigational dual GLP-1/GIP receptor agonist, originally developed by Carmot Therapeutics under the code CT-388 and now owned and advanced by Roche, given as a weekly injection for obesity and type 2 diabetes. It is not approved anywhere.
Is CT-388 the same thing as enicepatide?
Yes. CT-388 was the original development code; enicepatide is the compound’s formal international nonproprietary name, assigned sometime between 2021 and 2024. Both names refer to the same molecule.
How does it work?
It activates the GLP-1 and GIP receptors at once, like tirzepatide, but is specifically engineered to favor one internal signaling pathway, cAMP, over another, beta-arrestin recruitment, at both receptors, a design difference intended to change how the drug behaves with repeated dosing, though this has not been proven to matter clinically yet.
What dosage has been studied?
Phase 1 tested single doses from 0.5 to 7.5 mg and titrated weekly regimens up to 12 mg. Both phase 2 trials tested up to 24 mg weekly, though only the 24 mg results have been publicly disclosed.
How much weight loss and glucose improvement has been shown?
An early 24-week phase 1 extension cohort showed 18.8% placebo-adjusted weight loss. In the phase 2 obesity trial, 22.5% placebo-adjusted weight loss at 24 mg over 48 weeks. In the phase 2 diabetes trial, a 2.65-percentage-point HbA1c reduction and 15.5% weight loss at 24 mg over 48 weeks.
Has it been studied in humans?
Yes. Phase 1 single- and multiple-ascending-dose data is published and peer-reviewed, a longer 24-week phase 1 extension is company-reported, phase 2 is complete for both obesity and diabetes, and phase 3 is recruiting.
What side effects have been reported?
Mostly gastrointestinal, nausea, vomiting, and decreased appetite, consistent with other drugs in this class, with modest, dose-related discontinuation rates.
Is enicepatide approved?
No, in any country, for any use. Roche has said a regulatory submission for obesity could come as early as 2028, described as a company projection, not a commitment.
Why did Roche drop a similar drug, acmopatide?
Not because it failed; Roche’s CEO said it “met all the requirements”; but because the company decided to concentrate its obesity and diabetes development resources on enicepatide instead of running two similar candidates in parallel.
What remains unknown?
The low- and middle-dose phase 2 results, since only the top dose has been disclosed, the exact dose used in the 24-week phase 1 extension cohort, the actual phase 3 dosing regimen, the compound’s exact peptide sequence and CAS number, both unverified, and any long-term safety or durability data beyond 48 weeks.
Bottom line
Enicepatide (CT-388) has one of the more scientifically detailed public data packages in the dual-agonist field. A peer-reviewed phase 1 paper spells out its exact receptor pharmacology and a deliberate biased-agonism design intended to distinguish it from tirzepatide and other competitors, and an early 24-week extension cohort, 18.8% weight loss, was the first real signal that the effect kept building well past a month of treatment. Roche has now made it the clear priority of its ex-Carmot pipeline, discontinuing a sibling compound specifically to focus resources here. What is genuinely strong: the phase 1 publication itself, and large, company-reported phase 2 results at the top dose, 22.5% weight loss in obesity, a 2.65-point HbA1c drop in diabetes. What is still missing: peer-reviewed publication of the 24-week extension or either phase 2 trial, any data on the lower-dose arms in both phase 2 trials, the actual phase 3 dosing plan, and a chemical identity that is fully nailed down, since the CAS number conflicts between sources and the full sequence has never been confirmed against a primary source. It is not approved anywhere and has no legitimate retail supply chain.