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A specimen of the Metabolic drawer Drawer A · Metabolic

CT-388

Investigational

A dual GLP-1/GIP receptor agonist (INN enicepatide; also RO7795068) acquired by Roche through the $2.7 billion Carmot Therapeutics acquisition in 2024. The published Phase 1 trial (NCT04838405) showed 4.7-8.0% mean weight loss vs 0.5% placebo over 4 weeks; a more widely reported ~18.8% placebo-adjusted figure at 24 weeks comes from an unpublished Phase 1 extension reported via press release. Phase 2 obesity and T2D trials are completed or ongoing and Phase 3 began in 2026, positioning it as a competitive obesity therapeutic with a mechanism similar to tirzepatide.

RG-6912

Research evidence
Moderate

6 human studies

Preclinical
25%
Clinical
75%

Based on 8 cited sources

Evidence Score54/100
Early / limited
Research Depth55/100
Mechanism76/100
Plausibility85/100
Global Coverage24/100
Community Experience8/100
Effectiveness77/100

clinically demonstrated · low confidence

Demonstrated effect magnitude — not a recommendation or safety claim.

Research Depth 55: one published CT-388 Phase 1 double-blind placebo-controlled RCT (NCT04838405, PMID 41319798) at the small early-phase tier (1A 25, single RCT n<50; 1B 9 some-concerns sponsor-run early study; 1C 3 total N well under 50; 1D 12 direct population/route/outcome match — SC, overweight/obese, bodyweight; 1E 6 substantial multi-model preclinical program in mice and monkeys incl. MASH pathology). The widely-cited 18.8% placebo-adjusted weight loss at 24 weeks is from an unpublished Phase 1b (press-release/conference, no PubMed primary), so it does not raise the human-tier band. Mechanism 76: GLP-1R/GIPR are named validated targets with functional (cAMP-biased) agonism confirmed for CT-388 and class-level knockout confirmation (Samms 34003802; El 37277609) (2A 30 binding+functional, exact Ki undisclosed); incretin pathway largely mapped (2B 22); dose-response across human 0.5-12 mg plus in-vivo mouse/monkey models (2C 14); confirmed in mammalian in vivo (2D 10). Plausibility 85: mechanism->surrogate(weight/glucose)->clinical-weight-loss chain demonstrated in the RCT itself (3A 30); fully coherent with incretin pathophysiology validated by FDA-approved tirzepatide (3B 24); multiple same-class agents reliably produce weight loss (3C 18); tightly scoped single-mechanism claim (3D 13). Global Coverage 24: CT-388-specific evidence is single-developer (Carmot/Genentech/Roche), one primary paper, <5 CT-388 studies, US+Mexico trial sites only, investigational with regulator trial registration (4A 6 / 4B 7 / 4C 6 / 4D 5). Community Experience 8: dossier confirms no meaningful real-world user discussion (5A 3 / 5B 2 / 5C 0 / 5D 3); investigational, not yet available. Effectiveness basis clinical (low confidence): published 4-week RCT data -4.7% to -8.0% bodyweight vs -0.5% placebo already far exceeds the ~5% weight-loss MCID with a large effect on a patient-relevant outcome (E1 26 / E2 22 / E3 13 / E4 16), but rests on a single small short-duration sponsor-run early-phase trial with no head-to-head and longer-term efficacy unpublished.

Scored June 2026 How we rate →
~
Evidence Level
moderate
Not approved for human use by any regulatory agency
Limited human clinical trial data
Consult a healthcare provider before use
Not FDA Approved WADA Prohibited
Identity
SCALE · 1:1 N-TERMINUS C-TERMINUS 39 AA · ~4,500 Da (estimated)
Also Known As
RG-6912
Class
Modified peptide dual agonist
Length
39 amino acids
Mol. weight
~4,500 Da (estimated)
Sequence
Proprietary (not publicly disclosed)
Molecular Structure
Hydrophobic
Polar
Positive
Negative

CT-388 (INN enicepatide; also RO7795068) is a dual GLP-1/GIP receptor agonist that has completed Phase 1 and Phase 2 obesity trials, with Phase 3 trials beginning in 2026. Its mechanism is well-characterized based on the established biology of incretin hormones.

How It Works (Simplified)

CT-388 activates two hormone receptors simultaneously to reduce appetite and improve metabolism:

GLP-1 Receptor

Signals fullness to the brain, slows stomach emptying, and enhances glucose-dependent insulin release from the pancreas.

GIP Receptor

Synergizes with GLP-1 for enhanced insulin secretion and directly improves fat cell function and lipid metabolism.

Appetite Control

Dual receptor activation creates stronger satiety signals than single-receptor drugs, leading to reduced food intake.

Metabolic Effects

Improves insulin sensitivity, reduces blood glucose levels, and may improve lipid profiles through multiple pathways.

Key Research: Chakravarthy MV et al. (2025) reported the first published CT-388 clinical data, including the Phase 1 trial (NCT04838405). PMID:41319798 Willard FS et al. (2020) established the mechanistic basis for cAMP-biased GLP-1/GIP dual agonism (in the related agent tirzepatide). PMID:32730231

Important Limitations

  • CT-388 is investigational and not yet FDA approved
  • Only Phase 1 efficacy data are peer-reviewed (4-week timepoint); the ~18.8% at 24 weeks is from an unpublished press release, and Phase 2/3 results are pending
  • Specific receptor binding affinities not publicly disclosed
  • Head-to-head comparisons with tirzepatide not yet available
  • Long-term cardiovascular outcomes data not yet established
i. GLP-1 Receptor Pathway · Appetite & Glucose
CT-388GLP-1R activationHypothalamus POMC/CART ↑Reduced appetitePancreatic β-cellsGlucose-dependent insulin ↑GI tractDelayed gastric emptying
ii. GIP Receptor Pathway · Metabolic Enhancement
CT-388GIPR activationPancreatic β-cellsSynergistic insulin secretionAdipose tissueImproved lipid metabolismBrainEnhanced satiety signaling
Mechanism GLP-1 receptor activation reducing appetite and slowing gastric emptying
Established 6 direct studies
Benefit shown to reduce body weight in obesity
Evidence Level
Moderate
6 Human
2 Animal
2 In Vitro
Mechanism GIP receptor activation enhancing insulin secretion and adipocyte function
Established 4 direct studies
Benefit appears to improve glycemic control in type 2 diabetes
Evidence Level
Moderate
2 Human
2 Animal
3 In Vitro
Mechanism Dual incretin receptor synergy producing enhanced satiety signaling
Supported 3 direct studies
Benefit appears to achieve greater weight loss than GLP-1 agonists alone
Evidence Level
Moderate
1 Human
2 Animal
2 In Vitro
Mechanism Confidence
Established
Supported
Emerging
Evidence Level
High
Moderate
Low
Very Low
Phase 01 1
Week 1-4

Based on the published Phase 1 trial: initial GI adaptation period with potential nausea and decreased appetite. Mean weight loss of 4.7-8.0% vs 0.5% placebo was observed by day 29, with improved glycemic parameters.

Phase 02 2
Week 4-12

Continued weight loss expected as dose escalation proceeds and GI side effects typically diminish, based on incretin-class experience. CT-388 data beyond 4 weeks are not yet published.

Phase 03 3
Week 12-24

A reported ~18.8% placebo-adjusted weight loss by 24 weeks comes from an unpublished Phase 1 extension (press release only, not peer-reviewed) and should be treated as preliminary. Peer-reviewed 24-week and 48-week data from the Phase 2 trials are pending.

Phase 04 4
Week 24+

Based on tirzepatide data, continued weight loss expected through 52-72 weeks. Maintenance of weight loss requires ongoing treatment. Long-term CT-388 data pending Phase 2/3 results.

Research-based observations

This timeline reflects observations from published clinical and preclinical studies. Individual responses may vary significantly. This is not a guarantee of effects or a dosing schedule. Consult qualified healthcare providers for personalized guidance.

Good Signs (6 indicators)
Manufactured under pharmaceutical GMP conditions (Roche)
Clear documentation of dose and administration instructions
Provided through legitimate clinical trial or prescription pathway
Proper cold chain maintenance during shipping
Comes with complete prescribing information
Single-use prefilled device or properly sealed vials
Warning Signs (5 indicators)
CT-388 is not yet approved - any commercial sale is unauthorized
Products claiming to be CT-388 from research chemical suppliers
Significantly lower price than expected for novel biologic
No clear chain of custody or manufacturing documentation
Offered outside of clinical trial setting before approval
Bad Signs (6 indicators)
Any product sold as CT-388 outside clinical trials (currently investigational only)
Research chemical supplier claiming to sell CT-388
No COA or obviously fraudulent documentation
Unclear or suspicious origin
Products from unregulated compounding sources
Any CT-388 product without Roche/clinical trial involvement
Positive quality indicator
Requires evaluation
Potential quality issue

For Research Evaluation Only

These quality indicators are general guidelines based on typical peptide characteristics. Professional laboratory testing (HPLC, mass spectrometry) provides definitive quality verification. This checklist is for initial visual evaluation only.

Synergistic
Compatible
Caution
Avoid

Different mechanisms (incretin vs GHRH). No known contraindications. Both target metabolic improvements through distinct pathways.

Both affect GI function. CT-388 slows gastric emptying significantly while BPC-157 has gastroprotective effects. Unclear if effects interact; monitor GI symptoms if combined.

Both are dual GLP-1/GIP receptor agonists with overlapping mechanisms. Combining would duplicate effects and increase risk of severe GI adverse events. No clinical rationale for combination.

CT-388 already activates GLP-1 receptors. Adding a GLP-1-only agonist would provide no additional benefit while increasing adverse event risk.

Overlapping GLP-1 receptor activation. Combining dual/triple agonists has no clinical rationale and would compound GI side effects.

Research Note: Interaction data is based on published literature, mechanistic understanding, and theoretical considerations. Most peptide combinations lack direct clinical study. This information is for educational purposes only and does not constitute medical advice. Always consult qualified healthcare providers.

This dossier synthesizes available evidence from peer-reviewed literature, regulatory documents, and clinical trial registries. Evidence strength ratings follow a modified GRADE approach.

For complete methodology details, see our Methodology page.

Important Disclaimer

This dossier is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before making health decisions.

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