MariTide

Dosing from the Literature

Published for fat loss: 140 to 420 mg under the skin every 4 weeks, or 420 mg every 8 weeks, for 52 weeks, from the Phase 2 trial. Not published: an approved dose, or the three Phase 3 target doses.

Every dose below was given in an Amgen trial or stated by Amgen for one. They are trial doses, not recommendations, and no dose of MariTide is approved. Amgen’s Phase 3 weight-management trials start lower than Phase 2 did: at 21 mg, stepping up over eight weeks (Amgen, June 23, 2025).

What It Is

MariTide is Amgen’s name for maridebart cafraglutide, formerly AMG 133, an investigational obesity drug “subcutaneously administered monthly or less frequently” (Amgen, November 26, 2024). It is not a peptide. It is an antibody-peptide conjugate: “a fully human monoclonal anti-human GIPR antagonist antibody” conjugated “to two GLP-1 analogue agonist peptides using amino acid linkers” (Véniant et al., 2024). The antibody blocks the receptor for GIP; the peptides activate the receptor for GLP-1. GIP and GLP-1 are gut hormones that augment glucose-stimulated insulin secretion and help regulate weight (Véniant et al., 2024). Semaglutide and liraglutide, approved for weight management, act on the GLP-1 receptor, and tirzepatide activates both receptors (Wu et al., 2026).

Amgen’s case for blocking GIP started from genetics. Variants that lower GIPR expression or function are associated with lower BMI in Japanese, European and North American populations, and mice without the receptor are protected from diet-induced obesity (Véniant et al., 2024). Amgen’s antibodies against the receptor protected obese mice from weight gain, reduced weight in obese monkeys, and added to the weight loss of GLP-1 drugs given alongside (Killion et al., 2018). The company then attached GLP-1 peptides to the antibody so that one molecule does both (Lu et al., 2021). The antibody also sets the timing: conjugation stretched the apparent half-life of the GLP-1 part in monkeys “from minutes to over 9 days” (Wu et al., 2026), and in people the intact molecule’s half-life was about 14 to 16 days (Véniant et al., 2024). Amgen now says the design “supports starting with monthly dosing, and staying on MariTide with as few as 4 or 6 doses per year” (Amgen, August 4, 2026).

Two human trials are published: a Phase 1 in Nature Metabolism in 2024 and a 52-week Phase 2 in the New England Journal of Medicine in 2025 (Véniant et al., 2024; Jastreboff et al., 2025). ClinicalTrials.gov lists 28 studies of the drug, all sponsored by Amgen, 10 of them Phase 3; the earliest estimated Phase 3 primary completions are MARITIME-1 and MARITIME-2, in January 2027 (searched September 29, 2026). No MariTide product is approved: FDA’s drug databases return no record for it (searched September 29, 2026).

Mechanism of Action

The mechanism data come from cell assays, animal studies and the Phase 1 pharmacokinetics, published by Amgen scientists and their collaborators. How blocking GIP adds to GLP-1’s weight loss in people is not known.

• GIP receptor (GIPR) blockade — the antibody — In cells, AMG 133 fully antagonized native GIP at the human GIP receptor, with a half-maximal inhibitory concentration of 42.4 nM (26.5 nM at the monkey receptor, 822 nM at the rat’s). It did not fully block the mouse receptor at up to 3 µM, so Amgen’s mouse studies used a surrogate built on an anti-mouse GIPR antibody (Véniant et al., 2024).
• GLP-1 receptor (GLP-1R) activation — the two peptides — Each antibody carries two copies of a GLP-1(7–37) analogue with four substitutions (Aib8, Y16, E22, G36) on a (G4S)3K linker, attached at an engineered cysteine (E384C) on the antibody’s Fc region near the hinge (Wu et al., 2026). The published peptide sequence including the linker is H[Aib]EGTFTSDYSSYLEEQAAKEFIAWLVKGGG(GGGGS)₃K(BrAc), and the average molecular weight of the whole molecule is 153,514 Da. AMG 133 fully activated the human GLP-1 receptor with a half-maximal effective concentration of 24.4 pM, against 4.1 pM for native GLP-1 (Véniant et al., 2024).
• Antibody-length half-life — FcRn recycling — Conjugation to an antibody increases a peptide’s size, which reduces filtration by the kidney, and lets the neonatal Fc receptor (FcRn) recycle it. In the design work, a version conjugated at E384C had a half-life of 5.3 days in mice, against 1.2 days for dulaglutide, a GLP-1 Fc fusion drug, and that site was chosen (Wu et al., 2026). In Phase 1, blood levels peaked about 4 to 7 days after a dose; the half-life was about 14 to 16 days for the intact molecule (antibody with at least one peptide attached) and 21 to 24 days for the antibody with or without its peptides (Véniant et al., 2024).
• Both receptors at once — internalization and endosomal cAMP — In cells expressing both receptors, Amgen’s earlier GIPR-antibody/GLP-1 molecules bound both simultaneously and were rapidly internalized, which amplified cAMP production inside endosomes (Lu et al., 2021). The Phase 1 paper describes those molecules as having functional activities comparable to AMG 133’s (Véniant et al., 2024).
• Brain GIPR and GLP-1R (mouse data) — In obese, primarily male mice, a GIPR-antibody/GLP-1 conjugate needed both brain GIPR and brain GLP-1R for its full weight loss; it was detected in circumventricular organs of the brain and activated c-FOS in downstream regions involved in appetite (Liu et al., 2025). Antibodies reach the brain poorly, at about 0.1–0.4% of their plasma concentration, but both receptors are expressed outside the blood–brain barrier, including in the area postrema (Véniant et al., 2024).
• The GIPR paradox — Tirzepatide activates the GIP receptor and MariTide blocks it, yet clinical data suggest both add to GLP-1-driven weight loss (Douros et al., 2025). “The precise mechanism by which both GIPR antagonism and GIPR agonism result in weight loss in humans, when combined with GLP-1R agonism, is not known” (Véniant et al., 2024); the same paper points to data that repeated GIP exposure desensitizes the receptor. Amgen scientists set out the case for both approaches in a 2020 review (Killion et al., 2020), and a 2025 review traces how preclinical findings translated into clinical results for both drugs (Douros et al., 2025). A 2026 review notes “the lack of evidence for the anorectic effects of GIPR agonism or antagonism alone in humans” (Davies et al., 2026).

What the Research Shows

The animal work below was published by Amgen scientists. Some of it tested MariTide (AMG 133) itself and some tested its forerunners; each item says which.

• GIPR antibodies alone and with GLP-1 drugs (forerunners) — A mouse anti-GIPR antibody protected diet-induced obese mice from weight gain, with lower food intake; an anti-human GIPR antibody reduced weight in obese monkeys, more than in mice; and weight loss was greater in both species when the antibodies were given with GLP-1 receptor agonists (Killion et al., 2018). Amgen later reported the antibody plus liraglutide at 23.5% weight reduction in obese mice, and plus dulaglutide at 14.5% in obese monkeys (Wu et al., 2026).
• One molecule instead of two (forerunners) — GIPR-antibody/GLP-1 conjugates reduced body weight in mice and monkeys; weight loss was greater than with the antibody alone or a control antibody conjugate, and the respiratory exchange ratio fell in obese mice (Lu et al., 2021).
• AMG 133 in mice (a surrogate) — A mouse surrogate reduced weight dose-dependently in diet-induced obese mice given 0.5 or 2.5 mg/kg every 6 days for three doses, with lower food intake, blood glucose, insulin and lipids. Two high-dose mice lost more than 45% of their body weight and were excluded from the analysis (Véniant et al., 2024).
• AMG 133 in obese monkeys — Weekly injections of 0.25 or 0.75 mg/kg for 6 weeks lowered body weight 11% and 13% from baseline, with lower energy intake, fasting triglycerides, fasting insulin, total cholesterol and LDL cholesterol. Three treated monkeys were excluded because anti-drug antibodies cleared the drug (Véniant et al., 2024).
• What reviewers say — A 2024 commentary on the Phase 1 described “astounding body-weight loss, and an appreciable safety profile” (Novikoff & Müller, 2024). A 2026 review of the molecule’s design says early clinical trials “suggest that AMG133 may produce more pronounced GI adverse effects compared with semaglutide or tirzepatide” (Yie et al., 2026). No trial has compared them directly. A 2026 review of next-generation obesity drugs says maridebart cafraglutide, “combining GLP-1 agonism with glucose-dependent insulinotropic polypeptide (GIP) antagonism, enables once-monthly dosing”; the same review covers the amylin drugs, amycretin among them, and bimagrumab for “lean mass preservation during potent anorectic therapy” (Lempesis & Dalamaga, 2026).

Human Data

Two human trials of MariTide are published, both sponsored or funded by Amgen. Everything after them is registered but unpublished, or described only by Amgen.

• Phase 1 (Véniant et al., 2024; NCT04478708) — Randomized, double-blind and placebo-controlled, at three US sites from August 2020 to November 2022, in men and in women of nonreproductive potential aged 18 to 65, with a BMI of 30 to 40 and no history of diabetes. The paper reports 75 of the 110 people enrolled: 49 in single-dose cohorts (37 given 21 to 840 mg, 12 placebo) and 26 in three repeat-dose cohorts given 140, 280 or 420 mg or placebo every 4 weeks for three doses. Safety was the primary end point; weight was exploratory. Mean weight change was −7.4% at 140 mg after three doses (day 78) and −14.5% at 420 mg by day 85, against +1.5% on placebo; in the 420 mg group, weight was still 11.2% below baseline 150 days after the last dose. Four of the eight people in that group received only the first dose. Amgen sponsored the study and was involved in preparing the paper.
• Phase 2 (Jastreboff et al., 2025; NCT05669599) — Double-blind, placebo-controlled and dose-ranging: 592 adults, 465 with obesity (63% women, mean age 47.9, mean BMI 37.9) and 127 with obesity and type 2 diabetes (42% women, mean age 55.1, mean BMI 36.5), treated for 52 weeks. Mean weight change at week 52 by the treatment-policy estimand, an intention-to-treat approach: −12.3% to −16.2% across the MariTide groups, against −2.5% on placebo, in the obesity cohort; −8.4% to −12.3%, against −1.7%, in the diabetes cohort, where HbA1c changed by −1.2 to −1.6 percentage points against +0.1 on placebo. The trial was funded by Amgen.
• The “up to ~20%” figure — Amgen’s announcements use the efficacy estimand, which estimates results “as if treated participants had adhered to MariTide for the entire 52-week study period”: −16.3% to −19.9% against −2.6% in the obesity cohort, and −12.1% to −17.0% against −1.4% in the diabetes cohort (Amgen, June 23, 2025). Amgen says weight loss “had not plateaued by 52 weeks” (Amgen, June 23, 2025).
• The second year (unpublished) — People who had lost at least 15% by week 52 and were still taking the drug could continue, re-randomized to placebo, 70, 140 or 420 mg monthly, or 420 mg every 12 weeks (Amgen, June 23, 2025). More than 90% of eligible participants chose to continue (Amgen, November 26, 2024). Amgen’s summary of the results, with no numbers: “The large majority of participants maintained the weight loss achieved in Part 1 for an additional 52 weeks on a lower monthly dose or quarterly dose of MariTide” (Amgen, February 3, 2026).
• Type 2 diabetes, Phase 2 (unpublished; NCT06660173) — 409 adults with type 2 diabetes, randomized to several dose levels or placebo for up to 24 weeks, with the change in HbA1c at week 24 as the primary end point. Amgen reported a “robust and clinically meaningful reduction in both hemoglobin A1c (HbA1c) and weight with monthly MariTide at 24 weeks,” without figures (Amgen, February 3, 2026).
• Low starting doses, Phase 1 (NCT06976372; no paper on this study in PubMed) — Participants started on 21, 35 or 70 mg, then took 70 mg on day 15 and 350 mg on day 29. Vomiting occurred in 24.4% of those who started at 21 mg and 22.5% of those who started at 35 mg, and no one stopped for GI effects (Amgen, June 23, 2025). Amgen’s Phase 3 weight-management trials use a 21 mg start.
• Phase 3: MARITIME (ongoing) — MARITIME-1, adults with obesity or overweight without diabetes, 3,853 enrolled, 72 weeks (NCT06858839); MARITIME-2, adults with type 2 diabetes and obesity or overweight, 1,105 enrolled, 72 weeks (NCT06858878); both estimate primary completion in January 2027. Also registered: MARITIME-3-J in Japan (279 enrolled; NCT06987695), a cardiovascular outcomes trial (MARITIME-CV, 12,800 planned; NCT07037433), a heart-failure trial (MARITIME-HF, 5,056 planned; NCT07037459), two sleep-apnea trials (MARITIME-OSA-1 and -2, 250 planned each; NCT07225686, NCT07226765), a switch trial (MARITIME-SWITCH; NCT07575399) and two long-term extensions (NCT07684235, NCT07684144), plus a Phase 2b trial on liver fat and weight (180 planned; NCT07441252). Amgen says three more Phase 3 studies in type 2 diabetes “will be initiated in 2026” (Amgen, August 4, 2026).

None of the 28 registered studies compares MariTide head-to-head with semaglutide or tirzepatide; the efficacy trials compare it with placebo, except MARITIME-SWITCH, which compares two MariTide dosing schedules (ClinicalTrials.gov, searched September 29, 2026). The evidence meter on the MariTide card reads “Human trials” because a placebo-controlled weight-loss trial of the drug itself is published.

Reconstitution & Storage

No document read for this page describes a powder form of MariTide, so there is nothing to reconstitute. Every documented form is a ready-made liquid:

• Phase 1 vials — “Participants received AMG 133 in vials containing 70 mg ml−1 of AMG 133,” injected under the skin of the abdomen in the morning, fasting (Véniant et al., 2024).
• Later trial products — A completed Phase 1 study compared “a liquid drug product in vial” with “a frozen liquid drug product in vial” (NCT07717814); the Phase 2 diabetes trial lists a “Solution for subcutaneous injection” (NCT06660173); two completed Phase 1 studies compared two subcutaneous presentations (NCT07226778, NCT07313761), and a study comparing two drug products is not yet recruiting (NCT07832799).
• The planned device — Amgen: MariTide “is expected to be delivered as a single dose in a convenient, handheld, patient-friendly, autoinjector device” (Amgen, November 26, 2024).
• Storage — No storage conditions for any clinical MariTide product are published. The only storage statement found is a laboratory reagent supplier’s: TargetMol supplies maridebart cafraglutide “as a sterile solution in a buffered formulation system” and lists “-20°C for 1 year,” for research use only (TargetMol data sheet T9901A-169).

Arithmetic only, not a recommendation: at the Phase 1 vial strength of 70 mg/mL, 140 mg is 2 mL, 280 mg is 4 mL and 420 mg is 6 mL (U-100 insulin syringe: 100 units = 1 mL). The later trial products’ concentrations are not published.

→ Peptide Calculator — vial-to-syringe math

Side Effects & Risks

• Nausea and vomiting (Phase 1) — In the repeat-dose cohorts, nausea affected 5 of 6 people at 140 mg, 4 of 6 at 280 mg and 8 of 8 at 420 mg, against 1 of 6 on placebo; vomiting affected 4 of 6, 5 of 6 and 6 of 8, against none. The events were mostly mild and came mainly after the first dose, starting 8 to 12 hours after it and lasting about 72 hours; of participants given at least two doses, 68% had GI events after the first dose and 9% after later doses. Four of the eight people in the 420 mg group withdrew before their second dose after mild GI events. No severe or serious adverse events were reported (Véniant et al., 2024).
• Nausea and vomiting (Phase 2) — “Gastrointestinal adverse events were common with maridebart cafraglutide, although less frequent with dose escalation and a lower starting dose. No unexpected safety signals emerged” (Jastreboff et al., 2025). Amgen puts discontinuations for GI events in the dose-escalation arms at up to 7.8% (Amgen, June 23, 2025) and for any adverse event at about 11% (Amgen, November 26, 2024).
• Pancreas — In Phase 1, one participant given a single 140 mg dose and one given repeat 140 mg doses had amylase and lipase elevations that resolved without clinical sequelae (Véniant et al., 2024). The Phase 2 trial excluded people with a history of pancreatitis (NCT05669599), and MARITIME-1 and -2 exclude chronic pancreatitis or acute pancreatitis within 180 days (NCT06858839; NCT06858878).
• Heart rate — In Phase 1, heart rate rose within the normal range after dosing, without a dose relationship: at day 5, by 13.6 ± 8.2 beats per minute at 21 mg and 4.2 ± 8.7 at 840 mg. Neither tachycardia nor palpitations were reported as adverse events (Véniant et al., 2024). Amgen’s QT study (NCT07229157) was completed in August 2026; no results are posted.
• Bone — GIPR is expressed in osteoblasts and osteoclasts, and GIPR knockout mice show reduced cortical bone mass (Yie et al., 2026). Amgen, in a statement on its Phase 1 data: “Amgen does not see an association between the administration of MariTide (maridebart cafraglutide, formerly AMG 133) and bone mineral density changes. The Phase 1 study results do not suggest any bone safety concern” (Amgen, company statement). Of Phase 2: “There was no association between the administration of MariTide and bone mineral density changes” (Amgen, November 26, 2024). A 2026 review says the trials “included close BMD monitoring” and “detected no meaningful declines in BMD” (Yie et al., 2026). The Phase 1 paper’s main text and the Phase 2 abstract give no bone data.
• Immune response — In the Phase 1 results posted on ClinicalTrials.gov, binding anti-drug antibodies appeared in 0% to 50% of participants per dose cohort, and antibodies neutralizing native GLP-1 in 1 of 6 participants in each of two single-dose cohorts (NCT04478708). In obese monkeys, three animals lost drug exposure to anti-drug antibodies (Véniant et al., 2024).
• Blood sugar — Phase 1 participants had no diabetes; fasting glucose fell, and no hypoglycemia-related adverse events were reported (Véniant et al., 2024). The Phase 2 abstract gives no hypoglycemia figures.
• Who the trials leave out — The Phase 2 trial and MARITIME-1 and -2 exclude people with a personal or family history of medullary thyroid carcinoma or multiple endocrine neoplasia type 2, and MARITIME-1 and -2 also exclude unstable major depression or another severe psychiatric disorder within 2 years, and any lifetime suicide attempt (NCT05669599; NCT06858839; NCT06858878). MARITIME-2 excludes proliferative diabetic retinopathy, diabetic macular edema, or retinopathy needing acute treatment (NCT06858878). These are exclusion rules, not reported harms.
• Pregnancy and contraception — The Phase 1 enrolled only men and women of nonreproductive potential (Véniant et al., 2024). An Amgen study of MariTide’s effect on a combined oral contraceptive in postmenopausal women is active, with no results (NCT07523711).
• A dose lasts weeks — With a half-life of about 14 to 24 days, weight in the Phase 1 420 mg group was still 11.2% below baseline 150 days after the last dose (Véniant et al., 2024).
• Identity and purity — No MariTide product for human use outside Amgen’s trials is documented. TargetMol lists “Maridebart cafraglutide” as a laboratory reagent for ELISA, FACS and functional assays, “for Research Use Only· Not for Human or Veterinary or Therapeutic Use”; its data sheet gives two different human GIPR values, 46.4 nM and 42.4 nM (TargetMol data sheet T9901A-169).
• WADA — The 2026 Prohibited List does not name MariTide. S0 prohibits at all times “Any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use (e.g. drugs under pre-clinical or clinical development or discontinued, designer drugs, substances approved only for veterinary use).” The List names no GLP-1 or GIP drug in any section, and MariTide has no approval.
• Drug interactions — Unpublished. Amgen has completed a gastric-emptying study (NCT07429032) and an ondansetron interaction study (NCT07310563) with no results posted; the oral contraceptive study is active (NCT07523711).

Bloodwork & Monitoring

No monitoring guidance for MariTide has been published, and there is no label. The trials measured these:

• Weight, BMI and waist circumference — Exploratory end points in Phase 1; body weight at week 52 was the Phase 2 primary end point and body weight at week 72 is the primary end point of MARITIME-1 and -2 (Véniant et al., 2024; NCT05669599; NCT06858839; NCT06858878).
• Glucose control — Fasting glucose, insulin, C-peptide, glucagon and HbA1c in Phase 1; HbA1c, fasting insulin, fasting glucose and HOMA2 indices in Phase 2 (Véniant et al., 2024; NCT05669599).
• Pancreatic enzymes — Amylase and lipase were tracked as GI safety laboratory tests in Phase 1 (Véniant et al., 2024).
• Heart — Vital signs and 12-lead electrocardiograms were Phase 1 safety end points (Véniant et al., 2024); a dedicated QT study is complete without posted results (NCT07229157).
• Lipids and inflammation — Fasting lipids, free fatty acids and high-sensitivity C-reactive protein in Phase 1; C-reactive protein fell with dose in the repeat-dose cohorts (Véniant et al., 2024).
• Bone mineral density — A 2026 review says the trials “included close BMD monitoring” (Yie et al., 2026); no bone density figures appear in the documents read for this page.
• Anti-drug antibodies — Measured in Phase 1 (NCT04478708).
• Which tests fit a given person — A question for a licensed healthcare provider. This page can’t answer it.

Commonly Stacked With

No published or registered study tests MariTide with another peptide, and no document read for this page shows people combining it with one. The combinations below are the ones Amgen’s registered studies include, recorded as registered.

→ Peptide Calculator — vial-to-syringe math

Legal Status

Related Compounds

People researching MariTide often also look at these:

Next Steps

References

1. Véniant MM, Lu SC, Atangan L, Komorowski R, Stanislaus S, Cheng Y, Wu B, Falsey JR, Hager T, Thomas VA, et al. A GIPR antagonist conjugated to GLP-1 analogues promotes weight loss with improved metabolic parameters in preclinical and phase 1 settings. Nat Metab. 2024;6(2):290-303. PMID: 38316982. (Open access; full text read. The Phase 1 trial, NCT04478708.)
2. Jastreboff AM, Ryan DH, Bays HE, Ebeling PR, Mackowski MG, Philipose N, Ross L, Liu Y, Burns CE, Abbasi SA, Pannacciulli N; MariTide Phase 2 Obesity Trial Investigators. Once-Monthly Maridebart Cafraglutide for the Treatment of Obesity — A Phase 2 Trial. N Engl J Med. 2025;393(9):843-857. PMID: 40549887. (Abstract read; the full text was not accessible.)
3. Killion EA, Wang J, Yie J, Shi SD, Bates D, Min X, et al. Anti-obesity effects of GIPR antagonists alone and in combination with GLP-1R agonists in preclinical models. Sci Transl Med. 2018;10(472):eaat3392. PMID: 30567927.
4. Lu SC, Chen M, Atangan L, Killion EA, Komorowski R, Cheng Y, et al. GIPR antagonist antibodies conjugated to GLP-1 peptide are bispecific molecules that decrease weight in obese mice and monkeys. Cell Rep Med. 2021;2(5):100263. PMID: 34095876.
5. Liu CM, Killion EA, Hammoud R, Lu SC, Komorowski R, Liu T, et al. GIPR-Ab/GLP-1 peptide-antibody conjugate requires brain GIPR and GLP-1R for additive weight loss in obese mice. Nat Metab. 2025;7(6):1266-1281. PMID: 40301582.
6. Wu B, Falsey JR, Netirojjanakul C, Herberich B, Holder JR, Sham K, et al. Discovery of AMG 133, a Glucose-Dependent Insulinotropic Polypeptide Receptor Antagonist and Glucagon-Like Peptide 1 Receptor Agonist Antibody-Drug Conjugate for the Treatment of Obesity. J Med Chem. 2026;69(8):9348-9362. PMID: 41941715. (Open access; full text read.)
7. Killion EA, Lu SC, Fort M, Yamada Y, Véniant MM, Lloyd DJ. Glucose-Dependent Insulinotropic Polypeptide Receptor Therapies for the Treatment of Obesity, Do Agonists = Antagonists? Endocr Rev. 2020;41(1):bnz002. PMID: 31511854.
8. Douros JD, Mowery SA, Knerr PJ. The Premise of the Paradox: Examining the Evidence That Motivated GIPR Agonist and Antagonist Drug Development Programs. J Clin Med. 2025;14(11):3812. PMID: 40507574.
9. Davies I, Holst JJ, Rosenkilde MM, Tan TMM. The Paradox and Future of GLP-1/GIP Combination Therapies: Efficacy and Mechanisms. Annu Rev Nutr. 2026;46(1):387-414. PMID: 42166683.
10. Yie J, Mou Z, Liu X. Design and therapeutic rationale of antibody-peptide conjugates: insights from maridebart cafraglutide (AMG133) and emerging applications. Antib Ther. 2026;9(3):367-380. PMID: 42592044. (Open access; full text read.)
11. Novikoff A, Müller TD. Antagonizing GIPR adds fire to the GLP-1R flame. Trends Endocrinol Metab. 2024;35(7):566-568. PMID: 38763780.
12. Lempesis IG, Dalamaga M. Obesity pharmacotherapy reimagined: The era of multi-receptor agonists and next-generation metabolic modulators, perspectives and controversies. Metabol Open. 2026;30:100463. PMID: 41948476. (Abstract read.)
13. Amgen. Amgen Announces Robust Weight Loss With MariTide in People Living With Obesity or Overweight at 52 Weeks in a Phase 2 Study. Press release, November 26, 2024. amgen.com/newsroom/press-releases/2024/11/. Read September 29, 2026.
14. Amgen. Results From Amgen’s Phase 2 Obesity Study of Monthly MariTide Presented at the American Diabetes Association 85th Scientific Sessions. Press release, June 23, 2025. amgen.com/newsroom/press-releases/2025/06/. Read September 29, 2026. (Efficacy estimand; the PK-LDI study; the Phase 3 dose escalation.)
15. Amgen. Amgen Reports Fourth Quarter and Full Year 2025 Financial Results. Press release, February 3, 2026. amgen.com/newsroom/press-releases/2026/02/. Read September 29, 2026. (Phase 2 second-year and type 2 diabetes results, described without numbers.)
16. Amgen. Amgen Reports Second Quarter 2026 Financial Results. Press release, August 4, 2026. amgen.com/newsroom/press-releases/2026/08/. Read September 29, 2026. (MARITIME program status.)
17. Amgen. Amgen Provides Statement on MariTide Phase 1 Data. Company statement, undated on the page (it anticipates Phase 2 topline data “later this year”). amgen.com/newsroom/company-statements/. Read September 29, 2026.
18. ClinicalTrials.gov. NCT04478708: Single and Multiple Ascending Dose Study of AMG 133 in Participants With Obesity. Results posted (anti-drug antibodies). Read September 29, 2026.
19. ClinicalTrials.gov. NCT05669599: Dose-ranging Study to Evaluate the Efficacy, Safety, and Tolerability of AMG 133 in Adult Subjects With Overweight or Obesity, With or Without Type 2 Diabetes Mellitus. Read September 29, 2026.
20. ClinicalTrials.gov. NCT06858839 (MARITIME-1) and NCT06858878 (MARITIME-2): Phase 3, 72 weeks, placebo-controlled. Read September 29, 2026.
21. ClinicalTrials.gov. Other Phase 2 and 3 studies: NCT06660173 (type 2 diabetes), NCT07441252 (liver fat), NCT06987695 (MARITIME-3-J), NCT07037433 (MARITIME-CV), NCT07037459 (MARITIME-HF), NCT07225686 and NCT07226765 (MARITIME-OSA-1 and -2), NCT07575399 (MARITIME-SWITCH), NCT07684235 and NCT07684144 (extensions). Read September 29, 2026.
22. ClinicalTrials.gov. Phase 1 studies: NCT06976372 (low starting doses), NCT07717814 (liquid and frozen liquid products), NCT07226778 and NCT07313761 (two subcutaneous presentations), NCT07832799 (two drug products), NCT07310563 (ondansetron), NCT07523711 (oral contraceptive), NCT07229157 (QT), NCT07429032 (gastric emptying), NCT07160257 (insulin sensitivity). Read September 29, 2026.
23. ClinicalTrials.gov. Search for the intervention “AMG 133,” September 29, 2026: 28 studies, all sponsored by Amgen; 15 recruiting, active or not yet recruiting.
24. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S0, Non-approved substances. wada-ama.org.
25. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the Federal Food, Drug, and Cosmetic Act (categories 1–3). Updated May 14, 2026. fda.gov/media/94155/download.
26. Code of Federal Regulations. 21 CFR 216.23, Bulk drug substances that can be used to compound drug products in accordance with section 503A. ecfr.gov. Read September 29, 2026.
27. FDA and National Library of Medicine databases: Drugs@FDA, drug label and NDC endpoints (api.fda.gov) and DailyMed, searched for “maridebart,” “cafraglutide” and “MariTide,” September 29, 2026: no records.
28. TargetMol. Maridebart cafraglutide data sheet (Cat. No. T9901A-169) and Maridebart data sheet (Cat. No. T81862). targetmol.com. Read September 29, 2026.

Related Research

• CagriSemaCagrilintide + Semaglutide (Novo Nordisk)
• RetatrutideGIP / GLP-1 / Glucagon Triple Agonist (Eli Lilly)
• TirzepatideDual GIP / GLP-1 Receptor Agonist — activates the receptor MariTide blocks
• GlumitideSelective GIP Receptor Agonist (Eli Lilly)
• SemaglutideWeekly GLP-1 Receptor Agonist
• DulaglutideGLP-1-Fc Fusion Receptor Agonist
• AmycretinUnimolecular GLP-1 and Amylin Receptor Agonist
• BimagrumabAntibody studied for lean mass preservation in obesity