Mazdutide

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What Is Mazdutide?

Mazdutide is a long-acting synthetic dual GLP-1 and glucagon receptor co-agonist developed under the developmental codes IBI362 (Innovent Biologics, in-licensed from Eli Lilly LY3305677). It is one of the most advanced compounds in the renewed wave of oxyntomodulin-derived dual-agonist pharmacology — an approach distinct from both the GLP-1-only programme (semaglutide) and the GLP-1/GIP dual-agonist programme (tirzepatide). The structural inspiration is oxyntomodulin itself, a 37-amino-acid product of preproglucagon processing in intestinal L-cells that natively activates both the GLP-1 and glucagon receptors. Endogenous oxyntomodulin has very short pharmacokinetics; mazdutide engineers around this with a fatty-acid acyl tether at a lysine residue that drives reversible serum-albumin binding and extends the plasma half-life sufficiently for once-weekly subcutaneous administration in clinical research.

Mazdutide has a mature molecular weight of approximately 4,865 Da including the acyl modification. The structural scaffold preserves the dual-receptor pharmacology of oxyntomodulin while engineered substitutions confer resistance to DPP-4-mediated proteolytic cleavage that would otherwise produce rapid clearance. Mazdutide is the lead Chinese metabolic peptide programme, with Phase 3 trials (GLORY-1 in obesity, DREAMS-1 and DREAMS-2 in type 2 diabetes) reporting body-weight reductions of approximately 15–17% at the highest dose tier over 48 weeks. Outside China, mazdutide is not approved by the FDA, EMA, MHRA, or any other major Western regulator. In China, mazdutide has been approved by the NMPA under its initial commercial brand — making it one of the first dual-agonist incretin peptides to receive regulatory clearance for human use anywhere. The research-grade mazdutide sold here is supplied uitsluitend voor laboratoriumonderzoek and is not intended for human or veterinary administration. For the triple-agonist comparator that adds GIP on top of the same GLP-1/glucagon combination, see our Retatrutide product page.

Mechanism of Action — Dual GLP-1 / Glucagon Receptor Co-Agonism

What makes mazdutide mechanistically distinctive among current dual-agonist metabolic peptides is that it pairs the canonical GLP-1 satiety / glycaemic axis with the glucagon receptor energy-expenditure axis — not the GIP receptor axis used by tirzepatide. The dual-receptor profile produces complementary effects across three principal compartments documented in published research:

• GLP-1 receptor activation — satiety, β-cell insulin secretion, gastric emptying — Mazdutide activates the GLP-1 receptor on pancreatic beta-cells (glucose-dependent insulin secretion), hypothalamic arcuate-nucleus POMC neurons (central satiety signalling), and gastric vagal afferents (delayed gastric emptying). This arm overlaps with the mechanism of semaglutide and the GLP-1 component of tirzepatide and retatrutide.
• Glucagon receptor activation — energy expenditure, hepatic lipid mobilisation, brown adipose activation — The defining feature of mazdutide is the simultaneous activation of the glucagon receptor. Glucagon-receptor agonism increases resting energy expenditure modestly, drives hepatic fatty-acid oxidation and lipid mobilisation from steatotic liver, and contributes to brown adipose tissue activation in published rodent research. The energy-expenditure component is what distinguishes glucagon-containing multi-agonists (mazdutide, retatrutide, survodutide) from the body-weight effect of GLP-1-only and GLP-1/GIP-dual peptides — the latter produce weight loss almost entirely through reduced energy intake, while glucagon-containing agonists add a metabolic-rate component.
• Receptor-activity balance and the “glucagon paradox” — The pharmacological challenge in glucagon-receptor co-agonism is achieving a beneficial net effect: glucagon alone raises glucose by stimulating hepatic glucose output, which would worsen rather than improve glycaemic control. Mazdutide’s GLP-1 component overrides the glucagon-driven glucose effect through the dominant glucose-lowering action on insulin and glucagon-suppression at beta- and alpha-cells, while the glucagon arm preserves the lipid-mobilisation and energy-expenditure benefits. The relative GLP-1-to-glucagon receptor potency is engineered to favour glucose-lowering net effect — an important difference from triple agonists like retatrutide where GIP also contributes.

The fatty-acid acyl tether attached at a lysine residue binds reversibly to circulating serum albumin, producing a plasma depot that extends the effective half-life to support once-weekly subcutaneous dosing in clinical research. Subcutaneous administration is the standard research route. The mechanism for sustained-release distribution is analogous to semaglutide’s C18 and tirzepatide’s C20 fatty-acid systems but with different chain length and linker chemistry tuned to mazdutide’s dual-receptor pharmacology.

Published Research Applications

Mazdutide is used in laboratory research contexts that investigate:

• Obesity and body-composition research — preclinical DIO rodent models, body-composition (DEXA/MRI), food-intake assays, respiratory exchange ratio and resting energy expenditure; canonical dual GLP-1/glucagon research peptide
• Type 2 diabetes preclinical research — glycaemic control, HbA1c surrogates, glucagon-suppression dynamics, insulin sensitivity in high-fat-diet and db/db rodent models; head-to-head with single-agonist GLP-1 and dual GLP-1/GIP comparators
• MASLD/MASH (metabolic-dysfunction-associated liver disease) — hepatic triglyceride content, ALT/AST, fibrosis staging; particular interest because of the glucagon arm’s lipid-mobilising activity in steatotic liver
• Energy-expenditure research — resting energy expenditure measurement, brown adipose tissue activation, thermogenic gene expression; mechanistic dissection of the glucagon-driven metabolic-rate component
• Comparative dual-agonist research — head-to-head with the alternative dual-agonist Tirzepatide (GLP-1/GIP) and the triple-agonist Retatrutide (GLP-1/GIP/glucagon); receptor-stacking strategy research
• Cardiovascular and renal research — effects on blood pressure, lipid profiles, atherosclerosis progression in ApoE^-/- models; emerging dataset given mazdutide’s Phase 3 maturation
• Glucagon-axis pharmacology — isolated glucagon-receptor pharmacology characterisation, hepatic glucose output dynamics, glucagon-suppression vs glucagon-agonism balance in dual-agonist molecules
• Comparative incretin research — benchmarking against single-agonist GLP-1 (Semaglutide), dual-agonist GLP-1/GIP (Tirzepatide), and triple-agonist GLP-1/GIP/glucagon (Retatrutide).

For broader context on where mazdutide fits within the multi-agonist metabolic-peptide landscape, see Retatrutide as the triple-agonist comparator that adds GIP, Tirzepatide as the alternative dual-agonist using GIP instead of glucagon, Semaglutide as the single-agonist baseline, and Cagrilintide as the amylin-axis combination-pharmacology alternative. Browse the full onderzoekspeptiden catalogus voor gerelateerde verbindingen.

Beschikbare sterktes en concentraties

MedsBase stocks Mazdutide in two lyophilized vial sizes calibrated to typical research protocol lengths. Each strength is available in 10-vial or 20-vial pack formats with full reconstitution guidance:

Both strengths are the same chemical form (lyophilized powder, 99%+ HPLC purity). Phase 3 clinical doses are 4–9 mg weekly, so research-grade vials at 5 mg or 10 mg represent single-to-multi-week supplies of clinical-equivalent dosing for in-vivo work. Mazdutide is a comparatively scarce research peptide because of structural complexity and active clinical development, which is reflected in the per-mg price relative to mature small synthetic peptides.

How It Compares — Mazdutide vs Retatrutide

Mazdutide and Retatrutide are the two canonical glucagon-receptor-containing multi-agonist metabolic peptides in current research. They share the GLP-1 + glucagon backbone and differ in whether they also activate the GIP receptor — Retatrutide does (triple agonist), Mazdutide does not (dual agonist). The comparison is one of the cleanest in current metabolic-peptide pharmacology because the GLP-1 and glucagon arms are shared, isolating the contribution of the GIP component.

The principal pharmacological question separating the two is the value of GIP receptor activation on top of GLP-1 + glucagon. Retatrutide’s Phase 2 body-weight effect is larger, suggesting GIP adds substantial benefit, but the more selective dual-agonist profile of mazdutide produces a potentially cleaner side-effect signal that may matter for long-term tolerability research. For glucagon-axis-specific pharmacology, mazdutide is the cleaner research tool because it isolates the GLP-1 + glucagon combination without the confound of GIP. For maximum-magnitude body-weight research, the triple-agonist retatrutide remains the canonical reference.

Opslag en Reconstituering

Voor reconstituering: store lyophilized vials refrigerated at 2–8 °C in original packaging for short-term working stock. For unopened long-term storage, freeze at −20 °C. Lyophilized mazdutide is stable under refrigeration for up to 24 months and at −20 °C for up to 36 months. Avoid freeze-thaw cycles on the lyophilized powder.

Reconstitueringsprocedure: inject bacteriostatic water down the side wall of the vial (not directly onto the lyophilized cake). For a 5 mg vial, 2.0 mL of bacteriostatic water yields a 2.5 mg/mL working concentration — 0.04 mL delivers 100 mcg; 0.2 mL delivers 500 mcg; ~1.6 mL delivers a 4 mg clinical-equivalent research dose. Swirl gently — do niet shake — and allow 5–10 minutes for full dissolution (acylated peptides dissolve more slowly than smaller unmodified peptides). A correctly reconstituted solution should be clear and colourless with no visible particles.

Na reconstitutie: store refrigerated at 2–8 °C and use within 30 days for optimal stability. Do not freeze the reconstituted solution — freeze-thaw cycles degrade peptide integrity. Discard any vial showing cloudiness, precipitate, or discolouration.

Veelgestelde vragen

What is Mazdutide used for in research?

Mazdutide is used in laboratory research investigating the dual GLP-1 / glucagon receptor co-agonist axis, obesity and body-composition regulation, type 2 diabetes preclinical models, MASLD/MASH liver disease, energy-expenditure and thermogenesis, and comparative multi-agonist incretin pharmacology against single-agonist GLP-1, dual GLP-1/GIP (tirzepatide), and triple GLP-1/GIP/glucagon (retatrutide) compounds. It is the most-cited Chinese-origin metabolic peptide in current literature. The research-grade mazdutide sold here is niet FDA-approved and is supplied strictly for laboratory research use only.

How is Mazdutide different from Semaglutide?

Semaglutide is a single GLP-1 receptor agonist. Mazdutide adds glucagon receptor agonism on top of GLP-1. The added glucagon component contributes an energy-expenditure mechanism — increased resting metabolic rate, hepatic lipid mobilisation, and brown adipose activation — that GLP-1-only agonists don’t produce. In comparable Phase 3 trials, mazdutide produces a somewhat larger body-weight effect than semaglutide alone (15–17% vs ~15%) but the principal practical difference is the mechanistic rationale for the weight loss: semaglutide largely through reduced food intake, mazdutide through both reduced intake and increased energy expenditure.

How is Mazdutide different from Tirzepatide?

Both are dual incretin agonists, but they activate different second receptors. Tirzepatide is GLP-1 + GIP. Mazdutide is GLP-1 + glucagon. The two receptor combinations produce qualitatively different metabolic profiles: GIP (tirzepatide) adds adipocyte lipolysis under fasting conditions and modest effects on energy expenditure; glucagon (mazdutide) adds substantial energy expenditure and hepatic lipid mobilisation. Tirzepatide has the larger Phase 3 dataset and larger body-weight effect; mazdutide has the unique mechanism for MASLD/MASH research given the glucagon-driven hepatic lipid component.

How is Mazdutide different from Retatrutide?

Retatrutide is a triple agonist (GLP-1 + GIP + glucagon). Mazdutide is a dual agonist that shares the GLP-1 + glucagon arms but lacks the GIP component. Retatrutide’s Phase 2 body-weight effect is larger than mazdutide’s Phase 3 result, suggesting GIP receptor activation adds substantial benefit on top of GLP-1 + glucagon. For research isolating the GLP-1 + glucagon combination specifically, mazdutide is the cleaner tool because it avoids the GIP confound; for maximum body-weight effect, retatrutide remains the canonical reference.

What is the typical Mazdutide research dose?

Published preclinical and clinical research protocols use weekly subcutaneous dosing with a titration schedule starting at 1.5–3 mg and increasing to maintenance doses of 4–9 mg weekly — the dose range used in GLORY-1 and DREAMS-1 Phase 3 trials. A 5 mg vial reconstituted with 2.0 mL bacteriostatic water yields 2.5 mg/mL — ~1.6 mL equals a 4 mg clinical-equivalent research dose.

Is Mazdutide FDA approved?

No. Mazdutide is not FDA-approved in the United States, nor is it EMA- or MHRA-approved. It has been approved by China’s NMPA for human use (one of the first dual GLP-1/glucagon agonists to receive any regulatory approval worldwide), but Western regulatory submission is still pending or ongoing as of current literature. All mazdutide sold by research-use-only suppliers outside China is for laboratory investigation and should not be administered to humans.

How should Mazdutide be stored?

Lyophilized vials: refrigerated at 2–8 °C for short-term working stock, or −20 °C for long-term storage of unopened vials. Reconstituted solution: refrigerated at 2–8 °C, use within 30 days. Do not freeze reconstituted solution — freeze-thaw cycles degrade the peptide. Protect from direct light at all times.

How do I reconstitute Mazdutide?

Follow the reconstitution procedure above. Add bacteriostatic water down the side wall of the vial (not onto the lyophilized cake), swirl gently, and allow 5–10 minutes for full dissolution (acylated peptides dissolve more slowly than smaller unmodified peptides). Do niet shake the vial. A correctly reconstituted solution is clear and colourless. For a 5 mg vial + 2.0 mL diluent, the working concentration is 2.5 mg/mL.

Welke sterktes heeft MedsBase op voorraad?

MedsBase carries Mazdutide in 5 mg and 10 mg lyophilized vials. Each strength is available in 10-vial or 20-vial pack sizes. All vials are supplied at 99%+ HPLC purity with a certificate of analysis available on request.

Why does Mazdutide also activate the glucagon receptor?

The structural inspiration for mazdutide is oxyntomodulin, an endogenous 37-amino-acid product of preproglucagon processing in intestinal L-cells that natively activates both the GLP-1 and glucagon receptors. The dual pharmacology is therefore not engineered — it inherits from the natural oxyntomodulin scaffold. What is engineered is the resistance to DPP-4 cleavage and the fatty-acid acylation that produces once-weekly half-life, alongside fine-tuning of the relative GLP-1-vs-glucagon receptor potency to favour net glucose-lowering effect.

Does the glucagon component cause hyperglycaemia?

This is the classic “glucagon paradox” in dual-agonist research. Glucagon alone raises glucose by stimulating hepatic glucose output, which would worsen rather than improve diabetes. In mazdutide, the GLP-1 component overrides this through dominant glucose-lowering action on insulin and glucagon-suppression at beta- and alpha-cells, while the glucagon arm preserves the lipid-mobilisation and energy-expenditure benefits. Published research confirms net glucose-lowering despite glucagon receptor activation, demonstrating that the engineered GLP-1-to-glucagon potency ratio achieves the desired balance.

Does Mazdutide cause side effects in research?

The most consistent finding is gastrointestinal, similar to other GLP-1-axis peptides — nausea, transient appetite suppression, and delayed gastric emptying are dose-dependent and tend to attenuate over 4–8 weeks of continuous dosing as receptor tachyphylaxis develops. Glucagon-component-related findings include modest elevations in resting heart rate and (rarely) transient blood-pressure effects. Long-term safety data continues to accumulate from China Phase 3 trials and post-approval surveillance.

What is the half-life of Mazdutide?

Mazdutide has a plasma half-life sufficient to support once-weekly subcutaneous dosing in clinical research, achieved through reversible binding to serum albumin via the fatty-acid acyl tether. The exact half-life is somewhat shorter than semaglutide (~165 hours) but in the same once-weekly dosing regime. The dosing schedule and clinical trial design treat it as a fully once-weekly compound.

How long does Mazdutide take to show effects in preclinical research?

Acute pharmacodynamic effects on glucose tolerance and gastric emptying are detectable within hours of the first dose. Body-weight effects in DIO rodent models typically become statistically significant after 1–2 weeks of weekly dosing and continue to accrue through 8–16 weeks. Maximum effect on body composition develops over 16–24 weeks of continuous dosing, mirroring the human Phase 3 trajectory in GLORY-1.

Can I order Mazdutide for international shipping?

Yes. MedsBase ships Mazdutide worldwide from our dedicated peptide shipping network. Peptide-only orders qualify for our standalone peptide shipping service. All orders ship in temperature-controlled packaging with full tracking and are covered by our Reshipment Assurance Policy.

Other Peptides for Metabolic, Body-Composition, and Multi-Agonist Research

• Retatrutide — Triple GLP-1/GIP/glucagon agonist — adds GIP to mazdutide’s receptor profile
• Tirzepatide — Dual GLP-1/GIP agonist — alternative dual-agonist using GIP instead of glucagon
• Semaglutide — Single GLP-1 agonist — canonical baseline comparator
• Cagrilintide — Amylin analog — alternative combination-pharmacology approach (CagriSema)
• Tesamorelin — GHRH analog — visceral adiposity research

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