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A specimen of the Metabolic drawer Drawer A · Metabolic

MariTide

Investigational

A bispecific peptide-antibody conjugate combining GLP-1 receptor agonism with GIP receptor antagonism. Unique mechanism opposite to tirzepatide. The published Phase 2 trial (NCT05669599) showed up to ~16% weight loss at 52 weeks with once-monthly dosing. MARITIME Phase 3 program ongoing.

AMG 133 · maridebart cafraglutide

Research evidence
Moderate

12 human studies

Preclinical
14%
Clinical
86%

Based on 14 cited sources

Evidence Score68/100
Emerging / moderate
Research Depth73/100
Mechanism85/100
Plausibility80/100
Global Coverage55/100
Community Experience30/100
Effectiveness75/100

clinically demonstrated · moderate confidence

Demonstrated effect magnitude — not a recommendation or safety claim.

Research Depth 73: one published adequately-powered double-blind placebo-controlled Phase 2 RCT (Jastreboff NEJM 40549887, n=592, NCT05669599) at low RoB on weight (1A 28, 1B 16); total human N ~600-700 incl. Phase 1 (1C 9); direct obesity population/SC route/body-weight outcome (1D 13); substantial DIO-mouse + obese-monkey preclinical program (AMG 133 discovery 41941715, 1E 7). No second RCT, SR or meta-analysis yet (Phase 3 MARITIME ongoing), capping 1A. Mechanism 85: GLP-1R/GIPR targets with binding + functional + genetic/antagonist confirmation (GIPR variant work 38871982; gut GIPR signaling 39723966) (2A 38); incretin pathway largely mapped though the dual GIP-agonism/antagonism paradox is unresolved (2B 20); dose-response across Phase 2 doses + in-vivo models (2C 17); confirmed in mammalian in vivo incl. humans (2D 10). Plausibility 80: mechanism -> surrogate (weight, HbA1c) established, surrogate -> hard CV outcome still inferred (3A 28); coherent with incretin biology with the GIP paradox as residual tension (3B 21); multiple same-class agents (semaglutide, tirzepatide) reliably produce the effect (3C 18); tightly scoped obesity/T2D claim (3D 13). Global Coverage 55: pivotal RCT single-sponsor (Amgen) so clinical replication pending, but mechanism reproduced by independent academic groups across US/Denmark/UK/Canada/Korea (4A 18, 4B 16); ~50 PubMed records, mostly reviews + mechanistic (4C 16); Phase 3 trial registration, no approval yet (4D 5). Community Experience 30: investigational, not marketed - niche enthusiast discussion only (5A 8), <3-year track record (5B 8), limited/mixed reports (5C 7), no broad real-world tolerability signal beyond trial GI events (5D 7). Effectiveness basis clinical (moderate confidence): Phase 2 weight loss up to -16.2% vs -2.5% placebo (~14 pp placebo-adjusted), large effect far exceeding the ~5% obesity MCID, on weight/HbA1c surrogates; superior to placebo with no head-to-head vs tirzepatide/semaglutide and only one RCT, hence moderate.

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 30 AA · ~240 kDa
Also Known As
AMG 133 • maridebart cafraglutide
Class
Bispecific peptide-antibody conjugate
Length
30 amino acids
Mol. weight
~240 kDa
Sequence
GLP-1 analog + anti-GIPR antibody
Molecular Structure
GLP1
Ab
Hydrophobic
Polar
Positive
Negative

MariTide represents a unique approach in the incretin-based therapy space, combining GLP-1 agonism with GIP antagonism—the opposite of tirzepatide’s dual agonist mechanism.

How It Works (Simplified)

MariTide’s bispecific design targets metabolic pathways through two distinct actions:

GLP-1 Agonism

The GLP-1 peptide portion activates GLP-1 receptors, reducing appetite, improving glucose control, and slowing gastric emptying—standard incretin effects.

GIP Antagonism

The antibody portion blocks GIP receptors, potentially reducing fat storage signals and preventing GIP-driven metabolic effects—opposite to tirzepatide.

Extended Half-Life

The antibody component greatly prolongs systemic exposure, enabling a once-monthly dosing interval—among the longest in the obesity drug class.

Sustained Efficacy

Phase 2 data showed no weight loss plateau at 52 weeks, with curves still declining, suggesting potential for continued benefit beyond initial treatment periods.

Key Research: The peer-reviewed Phase 2 dose-ranging trial (Jastreboff et al., NEJM 2025; PMID 40549887; NCT05669599) reported up to -16.2% body weight at 52 weeks vs -2.5% with placebo in the obesity cohort, with once-monthly dosing. Topline results were first presented at ADA 2025. Amgen Press Release

Important Limitations

  • GIP antagonism vs agonism debate unresolved—both approaches show efficacy
  • No head-to-head trials against tirzepatide or semaglutide
  • Phase 3 MARITIME program ongoing; final efficacy/safety data pending (~2027)
  • Long-term cardiovascular and safety outcomes not yet established
  • Currently investigational—not approved for clinical use
i. GLP-1 Receptor Activation · Appetite & Glucose
MariTide GLP-1 portionGLP-1R activationHypothalamic satiety signalingReduced appetite + Improved glycemic control
ii. GIP Receptor Blockade · Fat Metabolism
MariTide anti-GIPR antibodyGIPR blockadeAltered adipose tissue signalingModified nutrient partitioning
Mechanism GLP-1 receptor agonism reducing appetite and improving glycemic control
Established 12 direct studies
Benefit shown to achieve significant weight loss
Evidence Level
High
12 Human
2 Animal
Mechanism GIP receptor antagonism altering nutrient partitioning and fat storage
Supported 8 direct studies
Benefit appears to enhance metabolic outcomes through novel GIP blockade
Evidence Level
Moderate
8 Human
2 Animal
Mechanism Extended half-life antibody portion enabling monthly dosing
Established 10 direct studies
Benefit shown to provide convenient once-monthly administration
Evidence Level
High
10 Human
2 Animal
Mechanism Confidence
Established
Supported
Emerging
Evidence Level
High
Moderate
Low
Very Low
Phase 01 1
Week 1-4

Once-monthly subcutaneous dosing begins, often with a lower starting dose and gradual escalation. Gastrointestinal side effects (nausea, vomiting, diarrhea) are most common during initial dosing. Early appetite suppression is typically observed.

Phase 02 2
Week 4-8

Continued dose escalation and weight-loss trajectory. GI symptoms typically diminish as the body adjusts to the medication.

Phase 03 3
Week 8-24

Maintenance dosing. Phase 2 data (NCT05669599) showed substantial and progressive weight loss through this period with no plateau.

Phase 04 4
Week 24-52

Continued weight loss with curves still declining at 52 weeks. In the published Phase 2 trial, mean body-weight reduction reached up to -16.2% in the obesity (non-diabetic) cohort.

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 (4 indicators)
Supplied through legitimate clinical trial or healthcare provider
Proper cold chain storage maintained
Clear documentation of product authenticity
Administered under medical supervision
Warning Signs (3 indicators)
Product obtained outside of clinical trials or legitimate medical channels
Unclear storage or handling history
Missing documentation or certificates
Bad Signs (4 indicators)
Product sold by unverified online vendors
No cold chain verification
Significantly below expected pricing
Claims of availability before regulatory approval
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

Both target GLP-1 receptors but with opposing GIP mechanisms (MariTide antagonizes, tirzepatide agonizes). Should not be combined due to overlapping primary mechanisms.

Both are GLP-1 receptor agonists. Combining would result in additive GLP-1 activation and potentially severe GI adverse events. Not recommended.

Overlapping GLP-1 agonism and opposing GIP mechanisms. Not suitable for combination due to pharmacological conflicts.

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.

14 Sources 12 Human 2 Preclinical

Key Studies Cited

Full reference list available on request. All citations link to PubMed for verification.

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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