Molecule guides
What Is Mazdutide? Oxyntomodulin-Based Dual Agonist: Structure, Mechanism and Research
Mazdutide (IBI362 / LY3305677) is a lipidated GLP-1 and glucagon receptor co-agonist derived from oxyntomodulin. Here is how it is built, how it signals and how laboratories work with it.
Mazdutide — referred to in publications as IBI362 and LY3305677 — is a lipidated co-agonist of the GLP-1 and glucagon receptors designed on an oxyntomodulin scaffold. Its origin is what sets it apart from other glucagon-containing duals: oxyntomodulin is a natural proglucagon-derived peptide that already activates both receptors, so mazdutide is an optimised form of a dual agonist that exists in nature, not a single-receptor agonist that had a second activity bolted on. Our research-grade mazdutide is supplied as lyophilized powder in sealed vials, strictly for laboratory use.
As of 2026 mazdutide is still investigational and has no marketing authorisation. Research-grade material is a reference chemical, and nothing on this page describes a protocol for human use.
Mazdutide defined
Proglucagon is cleaved into different products depending on the tissue. Pancreatic alpha cells turn it into glucagon, while intestinal L-cells produce GLP-1, GLP-2 and oxyntomodulin. Oxyntomodulin is glucagon plus an extra eight residues at the C-terminus, and this extension alters its receptor profile so that it stimulates both the GLP-1 and glucagon receptors — only weakly, and for just minutes before it is degraded, but at both receptors nonetheless. Dual receptor agonism is therefore already part of human physiology, and mazdutide is an effort to make it long-lasting and potent enough to be studied.
Its design uses the familiar tools of this drug class: substitutions that make it resistant to dipeptidyl peptidase-4, and a lipid side chain that binds reversibly to albumin. Its catalogue identifier is CAS 2259884-42-1, and it is also listed as IBI362 and LY3305677. Our specification sheet does not give a molecular weight, so laboratories needing an exact mass for molarity calculations should use the value on the lot certificate.
Design and structure
- Scaffold. Derived from oxyntomodulin: a glucagon core with the C-terminal extension that provides affinity for the GLP-1 receptor.
- Resistance to proteolysis. Changes close to the N-terminus prevent DPP-4 cleavage, the weakness that restricts every native proglucagon peptide to a few minutes of activity.
- Lipidation. A fatty-acid chain attached via a spacer encourages albumin binding, which published pharmacokinetic studies show extends circulation time to several days.
- Receptor balance. Published characterisation describes mazdutide as favouring the GLP-1 receptor, with a smaller yet pharmacologically relevant glucagon receptor component.
Mechanism of action
Both targets are class B GPCRs that signal through Gs to raise cAMP, yet they are found in different tissues and drive different physiology. In islet preparations, GLP-1 receptor activation enhances insulin release in a glucose-dependent way, and receptor populations in the hindbrain, hypothalamus and vagus nerve are thought to underlie the lower food intake and slower gastric transit observed in rodents. Glucagon receptor activation acts chiefly on the liver, where studies report greater fatty-acid oxidation and changes in hepatic lipid handling, together with higher whole-body energy expenditure in preclinical models.
The reasoning behind the class is that the two arms offset each other where they would clash and reinforce each other where they agree: glucose-dependent insulin secretion from the incretin arm counteracts the extra hepatic glucose output that glucagon receptor activation would otherwise cause, while the energy-expenditure effect of the glucagon arm is preserved. Because oxyntomodulin-based molecules carry a receptor balance shaped by evolution rather than set by design, the literature often uses them as a physiological benchmark for comparing purpose-built dual agonists.
Research applications
- Receptor and cell-based work. cAMP potency and binding assays on human GCGR and GLP-1R in recombinant cell systems to define the activity ratio, together with signalling-bias studies such as beta-arrestin recruitment.
- Rodent work. Food intake and body composition in diet-induced obesity models, indirect calorimetry to isolate the energy-expenditure contribution of the glucagon arm, and liver fat measurement in steatosis models.
- Clinical trials in humans. Phase 2 and phase 3 results have been published, and much of the programme ran in Chinese populations — relevant when comparing across the class, since trial population and baseline metabolic phenotype are not interchangeable. These trials concern an investigational medicine given under clinical supervision and tell us nothing about research-grade powder.
To see how mazdutide fits into the wider field, read our overview of next-generation GLP-1 molecules and the incretin signalling hub.
A design caveat applies to all glucagon-containing duals. Glucagon receptor pharmacology varies more between species than GLP-1 receptor pharmacology does, so a potency ratio measured on rodent receptors cannot be assumed to hold at human receptors. Claims that an effect comes from the glucagon arm are much more convincing when the study includes a glucagon receptor antagonist arm or a GLP-1 mono-agonist comparator such as semaglutide; without one, the result cannot be told apart from a stronger incretin effect at higher receptor occupancy.
For anyone choosing among the glucagon-containing duals, the experimental variable that matters is the receptor ratio, not the compound's name. Two molecules hitting both receptors can behave quite differently if one leans ten times further toward the incretin arm — and that ratio depends on the assay: cAMP potency measured in a recombinant over-expressing cell line may not carry over to primary hepatocytes with native receptor levels. If a study hinges on the balance between arms, the rigorous course is to measure the ratio in your own system instead of borrowing a published value from a different one. Where the aim is simply a physiologically derived dual agonist reference, mazdutide is the sensible default, because its balance originates from oxyntomodulin rather than from an optimisation target.
Available formats and vial sizes
Current vial sizes and prices appear on the mazdutide product page within the GLP-1 and incretin peptides collection.
Reconstitution and storage at the bench
This is a calculation, not an instruction for use: 4 mL of bacteriostatic water added to a 20 mg vial gives 5 mg/mL (5,000 mcg/mL), so 0.2 mL of the solution contains 1,000 mcg of peptide. If an assay needs a defined buffer, dilute alkaline or phosphate systems are typical for this class — check compatibility with your detection chemistry beforehand.
Introduce the diluent slowly down the inside of the vial, swirl instead of shaking and make sure the solution is fully clear before use. Sealed lyophilized material is stored at minus 20 degrees Celsius, away from light and moisture; reconstituted solution is kept at 2 to 8 degrees Celsius, protected from light, and used within the study period. Divide into aliquots at reconstitution so that repeated freeze-thaw cycles do not degrade the stock. Our reconstitution guide has further detail.
Purity and reading the certificate of analysis
A mazdutide certificate should include an HPLC chromatogram showing main-peak area percentage, a mass-spectrometric identity result, net peptide content, lot number and date of analysis. Confirming identity is especially important for this molecule for two reasons: glucagon-containing duals look structurally alike, and mazdutide appears in the literature under three names, making it harder than it should be to match a supplier's claim to a published characterisation. Where our specification sheet gives no molecular weight, rely on the lot certificate for molar calculations. See how to read a COA.
For purchasing, the key point is that molecules in this class are not interchangeable. Two glucagon-containing duals bought at the same nominal purity may give different results in the same assay because their receptor ratios differ, and neither result is wrong. Documenting which compound, lot and certificate a data set rests on is therefore part of the experimental record rather than paperwork — and it is the only way another laboratory working from the same published description can reproduce the result.
Regulatory position
As of 2026 mazdutide has no marketing approval in the United States and is still investigational. For molecules whose trials are concentrated in particular regions, regulatory status varies by jurisdiction, and a filing or approval in another market does not alter the status of research-grade material. Our mazdutide is supplied as a laboratory reference chemical, for research use only and not for human consumption.
Related compounds and comparisons
Its closest structural comparator is survodutide, the other glucagon-containing dual in our range, covered in survodutide vs mazdutide. For a triple agonist that adds GIP to the same receptor pair, see retatrutide; for the GIP-containing dual, see tirzepatide.
Questions
What is oxyntomodulin, and why is it relevant to mazdutide?
Oxyntomodulin is a naturally occurring proglucagon product — glucagon with an additional eight-residue C-terminal tail — that activates both the GLP-1 and glucagon receptors, weakly and only briefly. Mazdutide is built on that template, making it a stabilised form of an existing endogenous dual agonist rather than a single-receptor agonist given a second activity after the fact.
Which receptors are activated by mazdutide?
It acts on the GLP-1 receptor and the glucagon receptor, both class B G-protein-coupled receptors that signal through Gs. Published data show a bias toward GLP-1 receptor activity, with a smaller but pharmacologically relevant contribution at the glucagon receptor.
What do the codes IBI362 and LY3305677 refer to?
They are both development codes for mazdutide and appear across the preclinical and clinical literature. Searching by code frequently turns up mechanistic papers that a search on the generic name misses — useful when checking a supplier's claim against published receptor data.
How does mazdutide compare with survodutide?
Both act on the same two receptors but are built on different backbones: mazdutide on oxyntomodulin, survodutide on the wider proglucagon pharmacophore. Because this is a genuine structural difference, published potency figures for the two cannot automatically be compared, even though the receptor pair is identical.
Has mazdutide been approved anywhere?
It has no US marketing approval as of 2026 and remains an investigational compound. Status differs between jurisdictions for molecules with regionally focused trial programmes, but an approval elsewhere does not change the status of research-grade material, which is sold only as a laboratory reference chemical.
Why does the trial population matter when interpreting mazdutide data?
Much of the published programme was run in Chinese populations. Baseline metabolic phenotype, comparator standards and endpoint definitions vary between regions, so comparisons with trials in other populations should take this into account rather than treating the figures as directly interchangeable.
How should mazdutide be stored and prepared in the laboratory?
Keep sealed lyophilized powder at minus 20 degrees Celsius, away from light and moisture. Bacteriostatic water is the usual diluent for reconstitution, with dilute alkaline or phosphate buffers used when an assay calls for them. Store reconstituted solution at 2 to 8 degrees Celsius and aliquot it to prevent repeated freezing and thawing.