GLP3-RT
Investigational GLP-1/GIP/glucagon triple agonist (Retatrutide-class)
GLP3-RT is the catalog name for a Retatrutide-class triple agonist — a single synthetic peptide that activates three metabolic receptors at once: the GLP-1, GIP, and glucagon receptors. The molecule it refers to is retatrutide (research code LY3437943), an investigational drug in late-stage clinical development. The GLP-1 and GIP arms suppress appetite and improve blood-sugar control; adding glucagon-receptor activity is intended to raise energy expenditure on top of that, which is the rationale behind the unusually large weight reductions seen in its trials. In a Phase 2 obesity study, the highest dose reduced body weight by about 24% over 48 weeks. Crucially, retatrutide is NOT an FDA-approved medicine — it is investigational, still in Phase 3 trials, and is not the same as the approved GLP-1 drugs semaglutide or tirzepatide. Everything known about it comes from controlled clinical trials conducted under medical supervision; this page reports that research and is not medical or dosing advice.
The short version
GLP3-RT is the catalog label for a triple agonist — the molecule is called retatrutide (lab code LY3437943). "Triple agonist" means one peptide that switches on three different receptors that control appetite, blood sugar, and energy use.
Two of those receptors (GLP-1 and GIP) are the same ones targeted by well-known weight-loss drugs; they reduce hunger and improve blood-sugar handling. The third (the glucagon receptor) is the twist: activating it is meant to make the body burn more energy, which is why retatrutide produced larger weight loss than older drugs in its trials — about 24% at the top dose over roughly a year.
The single most important thing to understand: retatrutide is NOT an approved medicine. It is still being tested in late-stage clinical trials and has not been approved by the FDA for any use. It is also not the same drug as Ozempic/Wegovy (semaglutide) or Mounjaro/Zepbound (tirzepatide), which are approved — retatrutide is a separate, investigational molecule.
Everything on this page comes from controlled clinical trials run under medical supervision. It is presented as research information, not as a recommendation, a protocol, or medical advice.
Molecular identity
Specs
- Molecular weight
- ~4,731 Da
- Molecular formula
- C221H342N46O68
- Monoisotopic mass
- 4728.47 Da
- Structure / class
- Synthetic lipidated peptide; GLP-1/GIP/glucagon triple receptor agonist (retatrutide / LY3437943)PubChem CID 171390338; Guide to Pharmacology 13769
- CAS / UNII
- 2381089-83-2 · NOP2Y096GVPubChem CID 171390338; FDA UNII
- Molecular target
- GLP-1 receptor + GIP receptor + glucagon receptor (GCGR) triple agonistGuide to Pharmacology 13769
- Half-life
- ~6 days (supports once-weekly SC dosing)PMID 38858523 (retatrutide phase 2a)Half-life curve →
- Regulatory status
- Investigational; not FDA-approved (Phase 3, TRIUMPH program)ClinicalTrials.gov
Plain English
Mechanism
Retatrutide is a single synthetic peptide that acts as an agonist (a molecule that switches a receptor on) at three receptors simultaneously: the glucagon-like peptide-1 receptor (GLP-1R), the glucose-dependent insulinotropic polypeptide receptor (GIPR), and the glucagon receptor (GCGR). In the discovery pharmacology, it was characterized as having balanced glucagon-receptor and GLP-1-receptor activity with relatively greater GIP-receptor activity.
The therapeutic logic of combining all three is additive. GLP-1 and GIP receptor agonism drive appetite suppression and improved glycemic control — the established mechanism of the GLP-1 drug class. Adding glucagon-receptor agonism is intended to increase energy expenditure, so that the molecule both reduces energy intake and raises energy output; this is the proposed basis for the larger weight loss observed versus single- or dual-receptor agonists.
Structurally it is a large synthetic lipidated peptide of roughly 4.7 kDa. It carries a fatty-diacid chain attached through a linker, which lets the peptide bind to circulating albumin and so resist rapid clearance — the basis for its long, once-weekly dosing interval. It also incorporates non-natural amino acids (including α-aminoisobutyric acid and α-methyl-leucine) that increase resistance to enzymatic breakdown. (The precise residue count, parent-backbone attribution, and exact lipid chain length vary between secondary sources and are not stated here; the receptor profile, the albumin-binding acylation strategy, and the molecular formula above are what the primary record supports.)
Why people reach for it
Potential benefits
GLP3-RT (retatrutide) is the most potent agent in this family in the trial data — here's what draws interest to it, with the all-important caveat that it is investigational, not approved.
- The deepest weight loss seen in the class — Its headline draw: in a Phase 2 obesity trial the 12 mg dose reduced body weight by about 24% over 48 weeks — the steepest figure among the GLP-1-family agents, the reason it draws so much attention.
- A third lever the others don't have — On top of the GLP-1 and GIP arms that cut appetite, its glucagon-receptor arm is intended to raise energy expenditure — so the molecule is studied to both reduce intake and increase burn, the proposed basis for those larger reductions.
- Striking liver-fat reduction in trials — In a Phase 2a fatty-liver study, liver fat dropped by roughly 80% at the higher doses — an effect tied to the glucagon arm's direct action on hepatic fat that people increasingly pursue it for.
- Strong blood-sugar improvement — In its Phase 2 type 2 diabetes trial, HbA1c fell by up to about 2 percentage points alongside substantial weight loss — the incretin arms doing the glycemic work.
- A convenient once-weekly schedule — Its ~6-day half-life (from designed-in albumin binding) supports one injection a week, with no meal timing to manage.
- A clear add-on lever via amylin — Because it already saturates the incretin/glucagon receptors, the one non-overlapping appetite axis left is amylin — Cagrilintide is the reasoned complement people layer for extra satiety.
Sources:PMID 37366315PMID 37385280PMID 38858523PMID 35985340
What draws interest to GLP3-RT, based on what its supervised Phase 2/3 trials report and how it's used — not approved outcomes or medical claims. Retatrutide is investigational, not FDA-approved, and these figures come from monitored trials, not a promise of results.
Implied timing
Best time to dose
Implied best time
Anytime (consistent, weekly)
GLP3-RT is taken on one fixed day each week — the day you hold it matters, the hour does not.
- Its half-life is about 6 days, so blood levels stay broadly steady across the week — there is no daily peak to align with a clock. Picking one weekday and holding it is what keeps exposure even; a few hours' drift makes no meaningful difference.
- Effects build over weeks: appetite suppression deepens through the slow escalation and weight loss accrues over months, so the timing of any single dose does not change the outcome — week-to-week consistency does.
- It can be injected with or without food; meal timing has no effect on the subcutaneous dose, though a light meal or ginger tea on escalation days can blunt early nausea.
- The main day-to-day variable is nausea, sharpest during the steep titration — many people choose a morning dose so any early queasiness lands in waking hours rather than overnight.
No study establishes an ideal time of day for GLP3-RT — this is reasoned from its ~6-day half-life and how it's used in trials. The usual peptide-dosing default is the midday-to-evening window, but for a once-weekly agent the real lever is the same weekday each week, not the hour.
Sources:PMID 38858523
How to run it
Dosing & protocol
GLP3-RT (retatrutide) is a weekly subcutaneous injection — the same route used in every Phase 2 trial. Because it is the most potent agent in the GLP-1/GIP/glucagon class and produces the steepest weight loss, titration discipline matters most here: the Phase 2 trials started at 1 mg/week and escalated over weeks to the target dose, explicitly to manage the GI side effects that scale with dose. The figures below are anchored to that published trial titration (Jastreboff et al., NEJM 2023); retatrutide is investigational and not FDA-approved, so there is no approved dose to report.
Trial-anchored convention, not a personal regimen: every dose figure comes from the Phase 2 supervised clinical trials. Retatrutide is investigational; it is not FDA-approved for any use and has no regulatory dosing label. Nothing here is medical advice. WADA: monitored, not banned (verify before sign-off).
Trial-anchored dose / titration
The Phase 2 obesity trial (n=338, 48 weeks) used four dose arms reached by slow escalation from a 1 mg/week start.
- Starting dose:
- 1 mg once weekly SC — the Phase 2 trial start point. Beginning this low is non-negotiable at this potency: nausea and GI side effects are dose-dependent and most intense during escalation.
- Escalation targets:
- 4 mg/week (−17.1% body weight at 48 wks) · 8 mg/week (−22.8%) · 12 mg/week (−24.2%) — these are trial arms, not sequential rungs; the escalation pace was set by trial protocol under medical supervision.
- Pace principle:
- Hold each dose step until GI tolerance is established before moving up. The trials showed the largest benefit at the higher doses, but also the highest GI side-effect burden — slower escalation is the primary lever against nausea and vomiting.
- Duration at target:
- The Phase 2 obesity trial ran 48 weeks at the target dose. The type 2 diabetes trial ran 36 weeks (up to 12 mg/week, −16.94% body weight, HbA1c −2.02%). These are study durations, not prescriptions.
Subcutaneous administration
One injection per week, subcutaneously — the molecule's ~6-day half-life (albumin-binding, designed-in) makes less frequent dosing possible.
- Injection site:
- Abdomen (two inches clear of the navel), lateral thigh, or upper arm fat. Rotate sites week-to-week to prevent local irritation and lipohypertrophy.
- Day / timing:
- Pick one consistent day of the week and hold it. Time of day is flexible — retatrutide's long half-life means a few hours' drift has no meaningful effect on exposure. Most users choose morning to pair any early nausea with waking hours rather than sleep.
- Food window:
- No required food window for SC injection. That said, starting dose-escalation days with a light meal or ginger tea before eating can blunt the GI hit. Smaller, lower-fat meals throughout the titration phase reduce delayed gastric emptying symptoms.
- Measuring the dose:
- Drawn on a U-100 insulin syringe from the reconstituted vial. The reconstitution card below converts each milligram dose to syringe units — verify with the on-page calculator.
Cycle / duration
There are no washout data for retatrutide — it is investigational and single-agent trials only. Duration guidance is therefore extrapolated from the trial lengths and the biology.
- Active phase:
- Phase 2 trials ran 24–48 weeks at target dose. Weight loss plateaus around 36–48 weeks at max dose in the trial data — once stable, reassess goals before continuing.
- Discontinuation:
- Expect partial weight regain on stopping — consistent with the GLP-1 class. The trials did not study maintenance dosing or step-down protocols; this is an open gap.
- No washout requirement documented:
- Unlike pulse peptides (BPC-157, TB-500), there is no published reason to cycle off. The Phase 2 trials ran continuously. Cycling off for washout is not supported by trial data — it is just an absence of long-term continuation data beyond 48 weeks.
Reconstitution at a glance
The on-page calculator does this live; the quick reference for a 10 mg vial at the default 2 mL BAC water mix:
- Mixing:
- 10 mg vial + 2 mL bacteriostatic water = 5,000 mcg per mL. On a U-100 (100-unit, 1 mL) insulin syringe: 1 mg = 20 IU · 2 mg = 40 IU · 4 mg = 80 IU · 8 mg = 160 IU (two syringes) · 12 mg = 240 IU (three syringes).
- Higher-dilution option:
- Adding 5 mL BAC water instead gives 2,000 mcg/mL — easier measurement for the 1–4 mg starting doses (1 mg = 50 IU). Switch back to the 2 mL standard once at the 8–12 mg target.
Substrate the signal needs
Nutritional cofactor precision
GLP3-RT is the most potent agent in the GLP-1 family — triple agonism (GLP-1 + GIP + glucagon) produces the deepest weight loss and the deepest nutritional obligations. Three cofactor jobs dominate: (1) preserve lean mass across a 20–24% weight loss, (2) blunt GI side effects during the steep titration, and (3) support the glucagon arm's liver-fat clearance so it does not deplete key co-factors.
Reasoned from GLP-1/GIP/glucagon triple-agonist physiology and weight-loss nutrition — not a retatrutide supplement trial. Every supplement dose is community convention matched to the mechanism, not a retatrutide-specific finding.
Preserve lean mass (highest priority — deepest weight-loss risk in the class)
At 20–24% body-weight loss, GLP3-RT carries the highest lean-mass risk of any agent on this site. The glucagon arm also increases hepatic amino-acid turnover, compounding the demand.
- Protein:
- 1.6–2.0 g per kg of body weight per day — the minimum to support muscle-protein synthesis in a steep deficit. With appetite this suppressed, protein must be deliberate: prioritize it at every meal before fat or carbohydrate. Push toward 2.0 g/kg if resistance training is concurrent.
- Resistance training:
- Non-negotiable. GLP-1-class weight loss splits approximately 75% fat / 25% lean mass without resistance training; with it, lean-mass loss is substantially reduced. Minimum 2–3 sessions per week of compound movements.
- Creatine:
- 3–5 g/day monohydrate — supports muscle phosphocreatine during resistance training and has an independent lean-mass retention signal in caloric-restriction models. Taken daily (no loading needed); dissolve in water with a meal to prevent GI irritation during titration.
Blunt GI side effects (nausea / constipation — dose-escalation phase)
GI adverse events occurred in ~35% of participants in the Phase 2 type 2 diabetes trial. Nausea peaks during escalation; constipation accumulates with slowed gastric motility.
- Ginger (nausea):
- 1–2 g standardized ginger extract per day, divided with meals. Ginger acts on 5-HT3 and NK1 receptors — the same anti-nausea pathways GLP-1-class drugs stress. Take on escalation-dose days before the first meal.
- Vitamin B6 (nausea):
- 25–50 mg pyridoxine daily, particularly during the first 4–8 weeks of dose escalation. Synergistic with ginger on GI motility; standard first-line nausea cofactor.
- Magnesium + fiber + hydration (constipation):
- Magnesium glycinate 300–400 mg at bedtime — gentle osmotic laxative effect; also replaces the magnesium depleted by reduced food volume. Pair with 25–35 g/day dietary fiber (psyllium husk 5–10 g is the fastest lever) and ≥2.5 L water daily. Slowed gastric emptying means stool sits longer — constipation is mechanical, not optional to address.
Electrolytes and micronutrient insurance
Eating substantially less means absorbing substantially less. At 20–24% weight loss, micronutrient gaps are the highest-probability under-managed risk after lean mass.
- Electrolytes (Na / K / Mg):
- Sodium 1,000–2,000 mg/day added (deficit eating + any GI losses deplete it fast), potassium 2,000–3,000 mg/day via food or supplement, magnesium 300–400 mg/day. Fatigue and muscle cramps at caloric restriction are electrolyte deficiency until proven otherwise.
- Multivitamin:
- A complete multivitamin daily — minimum safety net for B12, iron, calcium, zinc, and folate when food volume is severely reduced. B12 and iron are the most common deficiencies reported in GLP-1-class use; choose a formulation with methylcobalamin B12 for absorption.
Glucagon-arm liver and energy support
The glucagon receptor drives hepatic fat oxidation (trials: ~80% liver-fat reduction) and increases amino-acid catabolism in the liver. Supporting hepatic function keeps this mechanism running cleanly.
- Choline:
- 500–1,000 mg choline bitartrate or CDP-choline daily. Choline is the rate-limiting substrate for hepatic fat export (VLDL assembly); as the glucagon arm mobilizes liver fat, choline keeps the export pathway from bottlenecking. Food sources: eggs (147 mg each), liver, beef — prioritize these at protein meals.
- Omega-3 (EPA/DHA):
- 2–3 g combined EPA/DHA daily from fish oil. Omega-3s independently activate hepatic fat oxidation pathways (PPARα), directionally aligned with the glucagon arm, and reduce liver-derived inflammation (NF-κB). Take with meals to reduce fish-burp reflux; enteric-coated formulations avoid this entirely.
- Glycemic awareness:
- The glucagon arm raises fasting glucose slightly in some participants (GCGR activation releases hepatic glycogen). Monitor fasting glucose during escalation — relevant especially if pre-diabetic or diabetic. The GLP-1 arm's insulin-secreting effect usually offsets this, but the balance shifts with dose. This is a monitoring signal, not a supplement.
Combinations + timing
Stacking notes + timing windows
GLP3-RT already activates GLP-1, GIP, and glucagon — the full incretin/glucagon receptor set. Adding any other incretin or glucagon agonist (semaglutide, tirzepatide, survodutide) is redundant: they overlap every receptor retatrutide already drives. The only non-overlapping appetite axis is amylin. Beyond appetite, the two leverage points are lean-mass preservation (the most important) and GI tolerance during the steep titration.
Mechanistic reasoning — no combination with retatrutide has been tested in a trial. Retatrutide itself is investigational (not FDA-approved), so every stack carries the additional caveat that its own safety profile is still being established. WADA: retatrutide is monitored, not banned — verify before competition use.
GLP3-RT + Cagrilintide (amylin axis — the only non-overlapping satiety lever)
Cagrilintide is an amylin analog — it acts through the amylin receptor (calcitonin receptor family), a satiety pathway entirely separate from GLP-1/GIP/glucagon. This is the CagriSema logic applied to a triple agonist.
- Why it works:
- Amylin and GLP-1/GIP/glucagon converge on satiety from different brainstem nuclei. Cagrilintide does not duplicate any of GLP3-RT's three receptor arms — it adds a fourth, mechanistically distinct satiety signal. Reasoned, not trial-tested with retatrutide; the CagriSema Phase 3 data (semaglutide + cagrilintide) supports the logic.
- The protocol:
- GLP3-RT titrated to target dose (see above) + cagrilintide on its own independent titration schedule (typical research range: 0.3–2.4 mg once weekly SC, also slow-escalated). Do not start both simultaneously — establish GLP3-RT tolerance first, then layer cagrilintide.
- Outcome:
- The combination users reason toward for maximum satiety depth and the steepest possible deficit, accepting that it is the most complex GI-management scenario in the class. Lean-mass preservation cofactors (protein + creatine + resistance training) become even more critical here.
GLP3-RT + GH secretagogue (ipamorelin / CJC-1295 — lean-mass preservation)
Ipamorelin + CJC-1295 drive GH-mediated protein synthesis and lipolysis — a separate anabolic signal that works against the lean-mass loss that makes GLP3-RT's depth a double-edged sword.
- Why it works:
- GLP3-RT creates a steep caloric deficit; GH secretagogues promote lean-mass retention and fat mobilization through the GHRH/ghrelin → GH → IGF-1 axis. These do not touch GLP-1/GIP/glucagon receptors — fully complementary levers. The glucagon arm's amino-acid catabolism in the liver makes the anabolic counterweight more, not less, important.
- The protocol:
- Ipamorelin 200–300 mcg + CJC-1295 (no-DAC) 100–200 mcg subcutaneously, 1–2× daily on a 5-on/2-off cycle — timed pre-bed or pre-training on an empty stomach (food and insulin blunt the GH pulse). GLP3-RT continues weekly on its own schedule. Creatine 3–5 g/day and 1.6–2.0 g/kg protein are non-negotiable alongside.
- Outcome:
- The stack most users reason toward when the goal is maximum fat loss with minimum muscle loss. The GH axis does not reduce GLP3-RT's GI side-effect burden — maintain nausea cofactors independently.
GLP3-RT + BPC-157 (GI comfort during steep titration)
BPC-157 is studied for gut-lining healing and GI motility normalization — directly relevant when GLP3-RT's slowed gastric emptying and nausea are the primary tolerability obstacles.
- Why it works:
- BPC-157 promotes angiogenesis (new blood-vessel growth) into the gut lining and has been studied in rodent GI-injury models for restoring motility and reducing mucosal damage. GLP3-RT's GI side effects are dose-dependent and mechanical — a gut-supportive agent is a different lever, not a redundant one.
- The protocol:
- BPC-157 250–500 mcg once daily SC (abdomen site, rotated with GLP3-RT weekly injection site). Run throughout the titration phase — typically the first 8–16 weeks. If GI tolerance is established, BPC-157 can be tapered off; lean-mass and liver cofactors take over as the primary support.
- Outcome:
- The combination users reach for when GI side effects are limiting dose escalation or when gut symptoms persist beyond the early titration weeks. Does not reduce the weight-loss efficacy of GLP3-RT and carries no receptor overlap.
Reconstitution math
Reconstitution calculator
Reconstitution calculator
Calculated for a 1 mL U-100 insulin syringe (100 units/mL).
Units per dose
80
Draw to this mark on a U-100 syringe
- Volume per dose
- 0.8 mL
- Doses per vial
- 2
- Concentration
- 5 mg/mL
One vial lasts
- Daily
- 2 days
- Every other day
- 5 days
- 5×/week
- 3 days
- Large draw (80 units). Double-check the vial size and dose — a mcg/mg mix-up produces values like this.
Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.
From the studies
Side effects from research
Across its Phase 2 trials, retatrutide's most common adverse events were gastrointestinal — nausea, diarrhea, vomiting, and constipation — which were dose-related and mostly mild to moderate, and which the trials managed with gradual dose escalation. In the type 2 diabetes trial, gastrointestinal adverse events occurred in about 35% of retatrutide participants versus roughly 13% on placebo.
The obesity trial also reported a dose-dependent increase in heart rate that peaked around 24 weeks and then declined — a genuine trial-observed signal worth noting. All of these findings come from controlled clinical trials conducted under medical supervision; they describe what was observed in a monitored study population and are not a safety characterization of unsupervised use. Because retatrutide is investigational and not approved, there is no regulatory safety labeling for it.
Sources:PMID 37366315PMID 37385280
As reported in literature
Research dosing ranges
These are the doses actually tested in the published HUMAN trials — the evidence the practical framing above leans on, shown separately so trial results are never mistaken for a recommended regimen. Retatrutide is investigational; the doses below are the arms tested in supervised Phase 2 trials, paired with the outcomes those trials reported. They are not a recommended regimen, and nothing here is dosing or medical advice. In every trial the drug was given as a once-weekly subcutaneous injection (under the skin) reached by gradual dose escalation (titration) to limit gastrointestinal side effects, alongside diet and lifestyle measures, under medical monitoring.
| Dose | Route | Model | Outcome | Sources: |
|---|---|---|---|---|
| 1 mg | SC weekly | Human (Phase 2 obesity, n=338) | −8.7% body weight at 48 weeks | PMID 37366315 |
| 4 mg | SC weekly | Human (Phase 2 obesity, n=338) | −17.1% body weight at 48 weeks | PMID 37366315 |
| 8 mg | SC weekly | Human (Phase 2 obesity, n=338) | −22.8% body weight at 48 weeks | PMID 37366315 |
| 12 mg | SC weekly | Human (Phase 2 obesity, n=338) | −24.2% body weight at 48 weeks vs −2.1% placebo | PMID 37366315 |
| up to 12 mg | SC weekly | Human (Phase 2 type 2 diabetes, n=281) | HbA1c up to −2.02%; body weight up to −16.94% at 36 weeks | PMID 37385280 |
| up to 12 mg | SC weekly | Human (Phase 2a MASLD/fatty liver) | Liver-fat reduction −81.4% (8 mg) / −82.4% (12 mg) at 24 weeks | PMID 38858523 |
Quick answers
Frequently asked
What is GLP3-RT / retatrutide?
GLP3-RT is a catalog label for a Retatrutide-class triple agonist. The molecule, retatrutide (research code LY3437943), is a single synthetic peptide that activates the GLP-1, GIP, and glucagon receptors at the same time. It is an investigational drug studied for obesity and type 2 diabetes.
Is retatrutide FDA-approved?
No. Retatrutide is investigational and not approved by the FDA for any use. As of 2026 it remains in Phase 3 clinical trials (the TRIUMPH program), with no marketing application filed. This page reports trial research only and is not medical advice.
Is it the same as Ozempic, Wegovy, Mounjaro, or Zepbound?
No. Those are approved drugs — semaglutide (Ozempic/Wegovy) and tirzepatide (Mounjaro/Zepbound). Retatrutide is a different, unapproved molecule that adds glucagon-receptor activity to the GLP-1/GIP mechanism. Being in the same broad class does not make it equivalent or approved.
How much weight did it cause in trials?
In a Phase 2 obesity trial, the highest dose (12 mg weekly) reduced body weight by about 24% over 48 weeks, versus about 2% on placebo. That figure is specific to a supervised Phase 2 trial with dose escalation and lifestyle measures — it is a study result, not a promise or a protocol.
What are the main side effects?
In trials, the most common were gastrointestinal — nausea, diarrhea, vomiting, and constipation — dose-related and mostly mild to moderate. A dose-dependent increase in heart rate was also observed. These were findings in monitored trial participants, not a safety profile for unsupervised use.
Can a research vial be confirmed to be real retatrutide?
No. This page describes the molecule retatrutide as characterized in the scientific literature. It cannot vouch that any research-grade preparation actually matches that structure or is pure — research chemicals are not subject to the identity and quality verification that approved medicines undergo.
Primary sources
References
- PubChem CID 171390338PubChem CID 171390338 (Retatrutide / LY3437943, free acid)
- PMID 35985340Coskun et al., Cell Metab 2022 (discovery, triple-agonist pharmacology, PK)
- PMID 36354040Urva et al., Lancet 2022 (LY3437943 Phase 1b, type 2 diabetes)
- PMID 37366315Jastreboff et al., N Engl J Med 2023 (Phase 2 obesity trial)
- PMID 37385280Rosenstock et al., Lancet 2023 (Phase 2 type 2 diabetes trial)
- PMID 38858523Sanyal et al., Nat Med 2024 (Phase 2a MASLD trial; half-life ~6 days)
- PMC11255275Li et al., Cell Discovery 2024 (structural insights into triple agonism at GLP-1R/GIPR/GCGR by retatrutide)
- ClinicalTrials.gov NCT05929066ClinicalTrials.gov — TRIUMPH Phase 3 program (NCT05929066 active; NCT05931367 completed; NCT06662383 vs tirzepatide)
Research use only · Not medical advice · Updated 2026-06-01