Mazdutide | Buy Research-Grade Mazdutide in Europe | ≥99% Purity

Mazdutide is a synthetic dual GLP-1 receptor and glucagon receptor agonist peptide, available to buy in Europe for laboratory research into incretin pharmacology, energy homeostasis, hepatic lipid metabolism, glucose regulation biology, and the emerging field of dual incretin-glucagon receptor co-agonism as a metabolic research strategy.

Laboratories and research institutions across the EU can order verified, research-grade Mazdutide with fast international dispatch to Europe, full batch documentation, and ≥99% purity confirmed by HPLC and Mass Spectrometry.

✅ ≥99% Purity — HPLC & Mass Spectrometry Verified

✅ Batch-Specific Certificate of Analysis (CoA)

✅ Sterile Lyophilised Powder | GMP Manufactured

✅ Fast Dispatch to EU & Europe | Tracked Shipping

What is Mazdutide?

Mazdutide (IBI362) is a synthetic fatty acid-conjugated peptide dual agonist of the GLP-1 receptor (GLP-1R) and glucagon receptor (GcgR) — two G-protein coupled receptors with complementary but distinct roles in metabolic regulation — developed by Innovent Biologics as a once-weekly research and clinical candidate compound for studying the pharmacological consequences of simultaneous incretin and glucagon pathway co-activation in metabolic biology.

The GLP-1 receptor and glucagon receptor are structurally related class B GPCRs that share the glucagon peptide superfamily as their endogenous ligands — GLP-1 acting through GLP-1R to drive insulin secretion, suppress glucagon, slow gastric emptying, and activate CNS satiety circuits, and glucagon acting through GcgR to drive hepatic glucose production, stimulate lipolysis, increase energy expenditure, and promote fatty acid oxidation. While these two receptors have historically been considered to have opposing metabolic effects — GLP-1R activation lowering blood glucose and GcgR activation raising it — research has established that their co-activation produces a metabolically favourable combination of effects that neither receptor pathway achieves alone.

The key insight driving dual GLP-1R/GcgR agonism research is that glucagon’s metabolic actions extend well beyond its classical glycogenolytic role — with GcgR activation in adipose tissue and liver driving lipolysis, fatty acid oxidation, and energy expenditure through mechanisms that complement rather than oppose GLP-1R-mediated glucose regulation when both pathways are engaged simultaneously. Mazdutide’s balanced GLP-1R/GcgR co-agonism exploits this complementarity — with GLP-1R activation maintaining glycaemic control that prevents the hyperglycaemic consequences of GcgR activation, while GcgR activation drives the lipolytic, hepatic, and thermogenic effects that amplify weight reduction and metabolic reprogramming beyond what GLP-1R activation alone produces.

Mazdutide’s fatty acid conjugation — similar in principle to the albumin-binding strategies used in Semaglutide and Cagrilintide — extends its half-life to enable once-weekly dosing in pre-clinical research protocols, making it a practically useful research tool for studying sustained dual GLP-1R/GcgR co-activation and its metabolic consequences in European laboratory settings.

What Does Mazdutide Do in Research?

In laboratory settings, Mazdutide is studied as a dual GLP-1R/GcgR agonist with broad metabolic regulatory activity, with research applications centred on energy homeostasis, hepatic biology, adipose tissue metabolism, and incretin-glucagon combination pharmacology. EU and European researchers working with Mazdutide typically focus on:

• Dual GLP-1R/GcgR pharmacology research — Mazdutide is one of the most advanced and well-characterised dual GLP-1R/GcgR agonist research tools available — enabling studies of how simultaneous co-activation of GLP-1 and glucagon receptor pathways influences metabolic outcomes and how the pharmacodynamic interactions between these two pathways produce effects distinct from either pathway alone.
• Energy expenditure and thermogenesis research — GcgR activation drives increased energy expenditure through hepatic and adipose tissue mechanisms — including upregulation of fatty acid oxidation, thermogenic gene expression in brown adipose tissue, and sympathetic nervous system activation. Mazdutide is used to study how GcgR-mediated energy expenditure enhancement combines with GLP-1R-driven appetite suppression to produce greater energy deficit than single receptor pathway activation.
• Hepatic lipid metabolism and NASH research — glucagon receptor activation in the liver drives fatty acid oxidation and reduces hepatic lipid accumulation through multiple mechanisms including PPARα activation and FGF21 upregulation. Mazdutide is studied in models of non-alcoholic steatohepatitis (NASH) and hepatic steatosis — characterising how dual GLP-1R/GcgR co-activation influences liver lipid content, hepatic inflammation, and fibrosis parameters.
• Obesity and adiposity biology — pre-clinical and clinical studies have examined Mazdutide in obesity models — documenting effects on body weight, adipose depot mass, body composition parameters, and the metabolic consequences of combined incretin and glucagon pathway activation on fat metabolism. These findings have positioned Mazdutide as a high-interest research tool for studying dual-mechanism metabolic peptide pharmacology.
• Glucose homeostasis research — despite GcgR’s classical role in raising blood glucose, Mazdutide’s GLP-1R co-activation maintains glycaemic control by driving insulin secretion and suppressing the hyperglycaemic consequences of glucagon receptor activation. Studies examine the net glycaemic effects of dual agonism and how the balance of GLP-1R versus GcgR activity influences glucose regulation parameters.
• FGF21 biology research — glucagon receptor activation is a potent driver of FGF21 — the hepatokine with broad metabolic regulatory effects including adipose tissue browning, fatty acid oxidation, and insulin sensitisation. Mazdutide-driven GcgR activation provides a pharmacological tool for studying GcgR-mediated FGF21 induction and its downstream metabolic consequences in pre-clinical metabolic research.
• Brown adipose tissue and adipose browning research — GcgR activation promotes thermogenic programming in adipose tissue — including UCP1 upregulation and features of brown/beige adipocyte differentiation. Studies use Mazdutide to examine how GcgR-driven adipose browning contributes to the increased energy expenditure and metabolic rate associated with dual GLP-1R/GcgR agonism.
• Appetite regulation and CNS satiety research — both GLP-1R and GcgR are expressed in hypothalamic and brainstem appetite-regulating circuits — with GLP-1R activation suppressing appetite through well-characterised arcuate nucleus and nucleus tractus solitarius mechanisms, and GcgR activation contributing additional satiety-promoting signals. Mazdutide is used to examine how dual receptor activation influences CNS appetite circuits and the neuronal mechanisms underlying combined incretin-glucagon satiety signalling.
• Insulin secretion and beta cell biology — GLP-1R activation on pancreatic beta cells drives glucose-dependent insulin secretion — a well-characterised incretin effect that Mazdutide shares with GLP-1R-selective agonists like Semaglutide. Studies examining Mazdutide in beta cell biology characterise how GcgR co-activation modifies the insulinotropic effects of GLP-1R activation and the net consequences for pancreatic endocrine function.
• Lipid metabolism and dyslipidaemia research — studies have examined Mazdutide effects on circulating lipid profiles — including triglycerides, LDL, HDL, and free fatty acids — characterising how dual GLP-1R/GcgR activation influences systemic lipid homeostasis parameters in metabolic disease models.
• Comparative dual and triple agonist pharmacology — Mazdutide is studied alongside other dual and triple metabolic receptor agonists — including Tirzepatide (GLP-1R/GIPR), Retatrutide (GLP-1R/GIPR/GcgR), and CagriSema (GLP-1R/amylin) — as part of the broader research landscape examining how different metabolic receptor combination strategies influence energy homeostasis outcomes and metabolic parameter profiles.
• Cardiovascular metabolic research — GLP-1R agonism has well-documented cardiovascular biology and GcgR activation influences cardiac function and vascular tone through direct and indirect mechanisms. Studies examine Mazdutide’s cardiovascular metabolic profile — including effects on cardiac function parameters, vascular biology, and the interaction between dual agonism and cardiovascular metabolic regulation.

All research applications are for in vitro and pre-clinical use only.

What Do Studies Say About Mazdutide?

Mazdutide has generated a rapidly growing and high-profile research literature — with pre-clinical studies establishing the pharmacological rationale for GLP-1R/GcgR dual agonism and clinical research programmes documenting significant metabolic effects in human subjects at a scale that has attracted substantial European and global research attention.

Dual receptor pharmacology characterisation: Foundational pharmacology studies characterised Mazdutide’s balanced GLP-1R and GcgR agonism — documenting its receptor binding affinities, cAMP activation potency at each receptor, and in vitro selectivity profile relative to other class B GPCRs. These studies established Mazdutide’s dual agonist pharmacological identity and provided the receptor-level characterisation underpinning interpretation of its in vivo metabolic effects.

Pre-clinical metabolic findings: Pre-clinical studies in dietary obesity and metabolic disease models documented Mazdutide producing greater reductions in body weight, adipose mass, and hepatic lipid content than GLP-1R-selective agonists alone — consistent with the additive metabolic contributions of GcgR-driven energy expenditure, lipolysis, and fatty acid oxidation on top of GLP-1R-mediated appetite suppression and gastric emptying delay. These pre-clinical findings provided the mechanistic and pharmacodynamic rationale for clinical investigation.

NASH and hepatic research: Studies examining Mazdutide in hepatic steatosis and NASH models have documented meaningful reductions in liver fat content, hepatic triglyceride accumulation, and inflammatory and fibrotic liver parameters — findings attributed to GcgR-driven hepatic fatty acid oxidation and FGF21 upregulation alongside GLP-1R-mediated improvements in insulin sensitivity. These hepatic findings have positioned Mazdutide as a research tool of particular interest for NASH biology research.

FGF21 induction: Studies have characterised Mazdutide’s robust induction of FGF21 through GcgR activation in liver tissue — documenting dose-dependent increases in circulating FGF21 levels and the downstream metabolic consequences of GcgR-driven FGF21 elevation including adipose tissue browning markers and fatty acid oxidation gene expression. These FGF21 findings have contributed to understanding of the hepatic mechanisms through which GcgR activation produces metabolic benefits beyond glycogenolysis.

Clinical research findings: Mazdutide has been examined in Phase II clinical trials — with published findings documenting substantial reductions in body weight, improvements in glycaemic parameters, and reductions in hepatic fat content in participants with obesity and type 2 diabetes. These clinical findings — among the most striking reported for a metabolic peptide in recent years — have driven significant European research interest in the GLP-1R/GcgR dual agonism approach and established Mazdutide as one of the most actively investigated compounds in metabolic pharmacology research.

Energy expenditure characterisation: Studies have characterised Mazdutide-associated increases in energy expenditure parameters — including resting metabolic rate and thermogenic gene expression in adipose tissue — that are not observed with GLP-1R-selective agonists alone. These energy expenditure findings have provided mechanistic context for the greater weight reduction produced by dual GLP-1R/GcgR agonism compared to GLP-1R monotherapy and have established the GcgR-driven metabolic rate component as a key distinguishing feature of the dual agonist research profile.

Comparative agonist research: Studies comparing Mazdutide to GLP-1R-selective agonists and other dual agonists have characterised the specific contributions of GcgR co-activation to the overall metabolic profile — documenting the incremental effects on body weight, liver fat, energy expenditure, and FGF21 attributable to GcgR engagement on top of GLP-1R activation. These comparative findings have contributed to mechanistic understanding of how different receptor combination strategies influence metabolic outcomes in the broader multi-agonist pharmacology research landscape.

Mazdutide vs Related Metabolic Receptor Agonist Research Compounds

Compound	Targets	Mechanism	Key Research Distinction
Mazdutide	GLP-1R + GcgR	Dual incretin-glucagon co-agonism	Hepatic lipid reduction, FGF21 induction, energy expenditure via GcgR
Semaglutide	GLP-1R	GLP-1 receptor agonism	Reference GLP-1R agonist — single pathway
Tirzepatide	GLP-1R + GIPR	Dual incretin co-agonism	GLP-1/GIP dual agonism — no glucagon component
Retatrutide	GLP-1R + GIPR + GcgR	Triple agonism	All three receptors — most comprehensive metabolic agonism
CagriSema	GLP-1R + Amylin receptor	Incretin + amylin co-activation	Amylin pathway — distinct from glucagon mechanism
Cotadutide	GLP-1R + GcgR	Dual incretin-glucagon co-agonism	Comparable mechanism — comparative dual GLP-1R/GcgR research

Buying Mazdutide in Europe — What’s Included

Every order of Mazdutide dispatched to EU and European research institutions includes:

• Batch-Specific Certificate of Analysis (CoA)
• HPLC Chromatogram
• Mass Spectrometry Confirmation
• Sterility and Endotoxin Testing Reports
• Reconstitution Protocol
• Technical Research Support

Frequently Asked Questions — Mazdutide EU

Can I Buy Mazdutide in the EU and Europe?

Yes. We supply research-grade Mazdutide with fast tracked international dispatch to all EU member states and wider European destinations including Germany, France, Netherlands, Spain, Italy, Poland, and beyond. Packaging is designed to maintain peptide integrity throughout transit and all orders include full batch documentation. Mazdutide is supplied strictly for laboratory research use only.

What is the Glucagon Receptor and How Does its Co-Activation Benefit Metabolic Research?

The glucagon receptor (GcgR) is a class B GPCR expressed primarily in the liver — where it mediates glucagon’s classical glycogenolytic and gluconeogenic effects — and also in adipose tissue, heart, kidney, and brain. Beyond its hepatic glucose-raising role, GcgR activation drives fatty acid oxidation, reduces hepatic lipid accumulation through PPARα activation, induces FGF21 secretion with downstream metabolic effects, promotes thermogenic programming in adipose tissue, and increases energy expenditure through sympathetic nervous system activation. When combined with GLP-1R co-activation — which prevents the hyperglycaemic consequences of GcgR engagement — these metabolic effects of glucagon receptor activation become accessible as research tools for studying lipolysis, energy expenditure, and hepatic fat metabolism without glycaemic confounding.

What is the Difference Between Mazdutide and Tirzepatide in Metabolic Research?

Mazdutide and Tirzepatide are both dual metabolic receptor agonists but target different receptor combinations. Tirzepatide combines GLP-1R and GIPR (glucose-dependent insulinotropic polypeptide receptor) activation — with both receptors being incretin pathways influencing insulin secretion and appetite regulation. Mazdutide combines GLP-1R and GcgR activation — pairing an incretin receptor with the glucagon receptor to add energy expenditure promotion, hepatic lipid reduction, and FGF21 induction to the GLP-1R biology. The two compounds represent mechanistically distinct dual agonism strategies — Tirzepatide for studying dual incretin co-activation, Mazdutide for studying incretin-glucagon co-activation — with different receptor biology profiles and metabolic effect distributions relevant to different research questions.

What is the Difference Between Mazdutide and Retatrutide in Research?

Retatrutide is a triple GLP-1R/GIPR/GcgR agonist — combining all three metabolic receptor pathways simultaneously. Mazdutide is a dual GLP-1R/GcgR agonist — providing GLP-1R and GcgR co-activation without the GIPR component. Mazdutide is more useful as a research tool for specifically studying the GLP-1R/GcgR combination pharmacology without GIPR confounding, while Retatrutide is the reference compound for studying the pharmacological consequences of all three receptor pathways engaged simultaneously. The two compounds are complementary research tools for dissecting the relative contributions of different receptor combinations in the multi-agonist metabolic pharmacology landscape.

What is FGF21 and Why is its Induction by GcgR Activation Research-Relevant?

FGF21 (Fibroblast Growth Factor 21) is a hepatokine — a liver-derived endocrine factor — with broad metabolic regulatory effects including promotion of fatty acid oxidation, induction of adipose tissue browning and thermogenesis, improvement of insulin sensitivity, and reduction of hepatic lipid accumulation. GcgR activation in the liver is one of the most potent pharmacological inducers of FGF21 secretion — making GcgR-mediated FGF21 elevation a key mechanism through which dual GLP-1R/GcgR agonists like Mazdutide produce metabolic effects beyond those achievable through GLP-1R activation alone. Research using Mazdutide to study FGF21 induction contributes to understanding of GcgR-FGF21 axis biology and the downstream metabolic consequences of pharmacologically elevated FGF21 in obesity and metabolic disease models.

Why Doesn’t Mazdutide’s GcgR Activation Cause Problematic Hyperglycaemia in Research Models?

Classical glucagon action raises blood glucose through hepatic glycogenolysis and gluconeogenesis — the GcgR-mediated mechanism responsible for glucagon’s role in hypoglycaemia rescue. In Mazdutide’s dual agonist profile, GLP-1R co-activation drives glucose-dependent insulin secretion and suppresses endogenous glucagon — maintaining glycaemic control that prevents the hyperglycaemic consequences of GcgR activation. Studies have documented that the GLP-1R component of dual agonist compounds effectively offsets the glycaemic effects of GcgR activation — allowing the lipolytic, thermogenic, hepatic, and energy expenditure-promoting effects of GcgR activation to be harnessed without net hyperglycaemia. This pharmacodynamic interaction between the two receptor pathways is central to the dual agonism research concept and is characterised in studies using Mazdutide alongside GLP-1R-selective and GcgR-selective comparator compounds.

How Do I Reconstitute Mazdutide for Laboratory Use?

Allow the vial to reach room temperature before opening. Add sterile water or an appropriate laboratory buffer slowly down the vial wall and swirl gently — do not shake. Mazdutide is a fatty acid-conjugated peptide — prepare stock solutions at your protocol’s required concentration, aliquot, and store at -80°C to minimise freeze-thaw degradation. Standard peptide handling protocols apply. As with other fatty acid-conjugated peptides, consider adding a small amount of BSA to working buffers at very low concentrations to minimise adsorption to vessel surfaces.

How Quickly is Mazdutide Delivered to Europe?

Orders are dispatched promptly via tracked international courier. Delivery to EU and European destinations typically takes 3–7 working days depending on location, with packaging designed to protect peptide stability throughout transit.

Product Specifications

Parameter	Detail
Type	Synthetic Dual GLP-1R / GcgR Peptide Agonist
Also Known As	IBI362
Modification	Fatty acid conjugation — extended half-life, albumin binding
Primary Targets	GLP-1 Receptor (GLP-1R) + Glucagon Receptor (GcgR)
Dosing Profile	Once-weekly in pre-clinical research protocols
Primary Research Interest	Dual incretin-glucagon pharmacology, obesity, NASH, energy expenditure, FGF21 biology
Purity	≥99%
Verification	HPLC & Mass Spectrometry
Form	Sterile Lyophilised Powder
Solubility	Sterile water or laboratory buffer
Storage	-20°C, protected from light and moisture
Intended Use	Research use only

Research Disclaimer

Mazdutide is supplied exclusively for legitimate scientific research conducted within licensed laboratory environments. This product is not approved for human consumption, self-administration, or any therapeutic, clinical, or veterinary application. It must be handled solely by qualified researchers in compliance with applicable EU regulations, national legislation, and institutional ethics guidelines. By purchasing, you confirm this compound will be used exclusively for approved in vitro or pre-clinical research purposes.