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MariTide (Maridebart Cafraglutide) Results: Phase 2 Data, Monthly GLP-1/GIP Mechanism and MARITIME Status

Short answer: MariTide (maridebart cafraglutide, code AMG 133) is Amgen’s investigational obesity drug — a peptide–antibody conjugate that agonises the GLP-1 receptor and antagonises the GIP receptor, with a ~21-day half-life (as reported by Amgen) supporting once-monthly subcutaneous dosing. Phase 2 (NEJM, 2025) reported mean body-weight change at 52 weeks of −12.3% to −16.2% across the dose arms in obesity without type-2 diabetes, against −2.5% on placebo (treatment-policy estimand). It is in the Phase 3 MARITIME programme, which has not published results in the peer-reviewed literature as of November 2026, and the sources reviewed report no marketing authorisation . MariTide is a proprietary conjugate, not a reference peptide — New-U does not sell it. Part of our next obesity-research wave overview.

Plain-English summary. MariTide is an unapproved investigational drug. The FDA, MHRA and EMA have not authorised it. It is also structurally a biologic (an antibody conjugate), not a simple peptide that research-compound suppliers stock. This page is general information, not legal or medical advice; do not use unapproved compounds on people.

What MariTide actually is

Most obesity drugs are peptides. MariTide is not — it is a peptide–antibody conjugate : a monoclonal-antibody scaffold with GLP-1 analogue peptides chemically attached. That architecture is the whole point. Antibodies circulate for weeks, so bolting the active peptides onto an antibody backbone stretches the half-life to roughly 21 days (as reported by Amgen) — about three times semaglutide’s ~7 days — which is what makes once-monthly (and potentially less-frequent) dosing realistic.

Its developmental code was AMG 133 ; the generic name is maridebart cafraglutide . Amgen’s 2026 discovery paper (Wu et al., J Med Chem 2026, PMID 41941715) describes conjugating synthetic GLP-1 peptides to an IgG-based anti-GIPR antibody, which markedly prolonged systemic exposure of the intact peptide. A 2026 review in Antibody Therapeutics (Yie et al., PMID 42592044) uses maridebart cafraglutide as its central case study for antibody–peptide conjugate design. The molecular and pharmacology detail is indexed under PubMed: maridebart cafraglutide.

The GIP paradox: agonise GLP-1, block GIP

Here is the genuinely counter-intuitive part. Tirzepatide, the most successful incretin drug to date, activates the GIP receptor. MariTide does the opposite — it blocks it — while still agonising GLP-1. And yet both produce major weight loss. How can activating and blocking the same receptor both work?

GLP-1 receptor agonism — the shared engine: slows gastric emptying, suppresses appetite centrally, improves glucose-dependent insulin secretion.

GIP receptor antagonism — the differentiator. The leading hypotheses are that chronic GIP agonism ends up desensitising the receptor (so an agonist and an antagonist converge on a similar downstream state), and that central versus peripheral GIP signalling pull in different directions. The honest answer is that the field has not settled this; it is an active research question.

For the contrasting GIP- agonist design, see our tirzepatide research guide.

The Phase 2 evidence

Before Phase 2, a Phase 1 study (Véniant et al., Nat Metab 2024, PMID 38316982) reported an acceptable safety and tolerability profile with dose-dependent weight loss, maintained for up to 150 days after the last dose in the multiple-ascending-dose cohorts.

The Phase 2 trial (Jastreboff et al., N Engl J Med 2025;393:843–857, PMID 40549887) was published online in June 2025 and presented at the American Diabetes Association’s 85th Scientific Sessions. It was a double-blind, placebo-controlled, dose-ranging trial of 592 participants in two cohorts, with doses given every 4 or 8 weeks, with or without dose escalation. The primary end point was percent change in body weight from baseline to week 52. Figures below are the published treatment-policy (intention-to-treat) estimates; ranges span the active dose arms:

Population Mean weight change at 52 weeks Notable Obesity, without type-2 diabetes (n=465) −12.3% to −16.2% (placebo −2.5%) Primary end point, treatment-policy estimand Obesity, with type-2 diabetes (n=127) −8.4% to −12.3% (placebo −1.7%) HbA1c −1.2 to −1.6 percentage points (placebo +0.1)

On safety, the published abstract reports that gastrointestinal adverse events were common with maridebart cafraglutide, though less frequent with dose escalation and a lower starting dose, and that no unexpected safety signals emerged. NEJM published correspondence on the trial, with the authors’ reply, in December 2025. These are results for Amgen’s investigational product in a clinical trial, not for any research material.

Phase 3: the MARITIME programme

MariTide has advanced into the MARITIME Phase 3 programme, evaluating efficacy, safety and tolerability in people with obesity or overweight, with and without type-2 diabetes; Amgen’s 2026 J Med Chem paper describes AMG 133 as currently in Phase 3 trials. As of November 2026, no MARITIME results have been published in the peer-reviewed literature (PubMed search), so the Phase 2 figures above remain the only published efficacy data. Topline timing and any regulatory submission schedule are subject to change; refer to Amgen investor disclosures for the current position. Registered studies are listed on ClinicalTrials.gov.

How MariTide compares

Compound Receptor profile Format Cadence Status MariTide GLP-1 agonist + GIP antagonist Peptide–antibody conjugate ~Monthly Phase 3, no approval Tirzepatide GLP-1 + GIP agonist Peptide Weekly Approved Retatrutide GLP-1 + GIP + glucagon agonist Peptide Weekly Phase 3, no approval Semaglutide GLP-1 agonist Peptide Weekly Approved

MariTide’s distinctive selling points are the monthly cadence and the GIP-antagonist mechanism — both unusual in a field otherwise converging on weekly GIP agonists.

MariTide and research compounds

Because MariTide is an antibody conjugate rather than a short synthetic peptide, it sits outside what research-compound suppliers can characterise and verify by HPLC and mass spec. New-U does not sell MariTide , and any listing claiming to is selling something it cannot authenticate. The lawful, verifiable research references in the same therapeutic area are the established GLP-1-class peptides:

Semaglutide — the GLP-1 single-agonist reference.

Tirzepatide — the GLP-1 / GIP dual-agonist reference.

Retatrutide — the triple-agonist reference.

Each ships as a sealed, lyophilised reference peptide, with the per-batch Certificate of Analysis published online, verified to >99% HPLC purity, research use only .

Red flags on MariTide listings

Because there is no licensed MariTide product anywhere, treat any “buy MariTide” listing with maximum caution. Walk away if it:

Calls itself a “pharmacy” or “clinic” supplier of MariTide — no such supplier exists; it is not a medicine.

Quotes dosing schedules or weight-loss promises — that re-characterises it as an unlicensed medicine.

Claims to sell the antibody conjugate as a reference reagent — that is not a product a CoA can verify the way a short peptide can.

Has no batch-specific CoA, sells “ready-to-inject” pens, or operates Telegram-only with no legal entity.

Frequently Asked Questions

What is MariTide? Amgen’s investigational obesity drug maridebart cafraglutide (AMG 133) — a peptide–antibody conjugate that agonises GLP-1 and antagonises GIP, dosed about once a month.

Is MariTide approved? No. As of November 2026 the sources reviewed report no marketing authorisation; it is in the Phase 3 MARITIME programme, and no MARITIME results have been published in the peer-reviewed literature.

How much weight loss did it show? In the Phase 2 trial (NEJM 2025), mean body-weight change at 52 weeks was −12.3% to −16.2% across the dose arms in obesity without type 2 diabetes (placebo −2.5%) and −8.4% to −12.3% in obesity with type 2 diabetes (placebo −1.7%), on the treatment-policy (intention-to-treat) estimand.

Why block GIP when tirzepatide activates it? An open question — likely receptor desensitisation and central-vs-peripheral GIP signalling. Both designs produce weight loss; the mechanism is unsettled.

Can I buy MariTide as a research compound? No — it is a proprietary antibody conjugate, not a verifiable reference peptide. New-U catalogues the established GLP-1-class references instead.

Primary sources & further reading

New England Journal of Medicine — Once-Monthly Maridebart Cafraglutide for the Treatment of Obesity — A Phase 2 Trial (Jastreboff et al., 2025; PMID 40549887)

New England Journal of Medicine — Correspondence and authors’ reply on the Phase 2 trial (December 2025; PMIDs 41337722, 41337723, 41337724)

Nature Metabolism — A GIPR antagonist conjugated to GLP-1 analogues promotes weight loss with improved metabolic parameters in preclinical and phase 1 settings (Véniant et al., 2024; PMID 38316982)

Journal of Medicinal Chemistry — Discovery of AMG 133, a GIPR antagonist and GLP-1 receptor agonist antibody–drug conjugate for the treatment of obesity (Wu et al., 2026; PMID 41941715)

Antibody Therapeutics — Design and therapeutic rationale of antibody–peptide conjugates: insights from maridebart cafraglutide (AMG133) (Yie et al., 2026; PMID 42592044)

Amgen — Phase 2 obesity results, ADA 2025

U.S. National Library of Medicine — PubMed: maridebart cafraglutide

ClinicalTrials.gov — MARITIME programme

U.S. FDA — FDA (no MariTide approval as of publication)

External links are provided for research reference only; New-U is not affiliated with the cited organisations and links carry no endorsement either way.

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