$89.99
Buy Mazdutide Online from SourceTides. IBI362 | LY3305677 | CAS 2259884-03-0 | GLP-1R + GCGR dual agonist | Oxyntomodulin analog | MW 4,563.1 g/mol | C₂₁₀H₃₂₂N₄₆O₆₇ | ≥99% HPLC (C20 fatty acid confirmed by MS) | Endotoxin <1 EU/mg (LAL) | Full CoA | Lyophilised | Dry-ice cold chain.
GLP-1R Ki = 28.6 nM | GCGR Ki = 17.7 nM | Insulin secretion EC50 = 5.2 nM. Active in both Gcgr-/- and Glp1r-/- mice (dual independent receptor validation). Phase 1b/2 clinical trials published (eClinicalMedicine, Nat Commun, Diabetes Care). Dedicated MAFLD/NAFLD clinical programme. Phase 3 T2D (China) underway. Not WADA-prohibited. For in-vitro laboratory research use only. Not for human consumption.
Buy Mazdutide Online | IBI362 | GLP-1R/GCGR Dual Agonist | Oxyntomodulin Analog | ≥99% Purity | CoA | SourceTides
Buy Mazdutide Online from SourceTides.
Mazdutide (IBI362; LY3305677; CAS 2259884-03-0) is a long-acting synthetic oxyntomodulin analog engineered as a balanced dual agonist of the GLP-1 receptor (GLP-1R) and the glucagon receptor (GCGR).
It was developed by Innovent Biologics (code: IBI362) and licensed to Eli Lilly for Western markets (code: LY3305677).
Its 33-amino acid backbone is derived from oxyntomodulin — the endogenous gut hormone that naturally activates both GLP-1R and GCGR — with multiple stability-enhancing modifications including an Aib (α-aminoisobutyric acid) residue at position 2 and a C20 fatty diacid moiety attached at Lys²⁰ via a hydrophilic PEG-linker for albumin binding and once-weekly half-life.
Mazdutide binds human GLP-1R (Ki = 28.6 nM) and GCGR (Ki = 17.7 nM) with balanced dual agonism — stimulating GLP-1R-mediated satiety, insulin secretion, and glucose control while simultaneously activating GCGR-driven hepatic fat oxidation, energy expenditure, and adipose tissue lipolysis.
This dual mechanism distinguishes it from GLP-1R-only agonists and positions it as one of the most clinically advanced GLP-1R/GCGR dual agonists with published Phase 1b and Phase 2 human data.
Mazdutide has a remarkable pharmacological validation finding: it reduces body weight in both GCGR-knockout and GLP-1R-knockout mice — confirming that each receptor independently contributes to its weight-reducing effects, and that neither receptor alone is strictly necessary.
Multiple published Phase 1b/2 trials in Chinese adults and adolescents, plus an ongoing Phase 3 programme, make it one of the most deeply documented dual GLP-1R/GCGR agonists available for research.
Every SourceTides vial is lyophilised, tested at ≥99% HPLC purity, and ships with a full lot-specific Certificate of Analysis.
For in-vitro laboratory research use only. Not for human consumption.
Mazdutide — Technical Specifications
| Parameter | Specification |
|---|---|
| INN / Common Name | Mazdutide |
| Development Codes | IBI362 (Innovent Biologics); LY3305677 (Eli Lilly); OXM-3 |
| CAS Number | 2259884-03-0 |
| PubChem CID | 167312357 |
| Molecular Formula | C₂₁₀H₃₂₂N₄₆O₆₇ |
| Molecular Weight | 4,563.1 g/mol |
| Peptide Backbone | 33 amino acids; synthetic oxyntomodulin analog; C-terminal glycinamide; Aib (α-aminoisobutyric acid) at position 2 for metabolic stability |
| Half-Life Extension | C20 fatty diacid moiety attached to Lys²⁰ via hydrophilic PEG-like linker (2× OEG units + γ-glutamic acid spacer); albumin binding extends plasma half-life to ~7 days; enables once-weekly SC dosing |
| Origin | Derived from oxyntomodulin (OXM) — endogenous gut hormone produced in intestinal L-cells from proglucuagon; naturally activates both GLP-1R and GCGR; Mazdutide is a stabilised, long-acting analog of this endogenous dual agonist |
| Receptor Targets | GLP-1R (Glucagon-Like Peptide-1 Receptor; Gs-coupled Class B GPCR) + GCGR (Glucagon Receptor; Gs-coupled Class B GPCR) |
| GLP-1R Binding Affinity | Ki = 28.6 nM (human); Ki = 25.1 nM (mouse) |
| GCGR Binding Affinity | Ki = 17.7 nM (human); Ki = 15.9 nM (mouse) |
| Insulin Secretion EC50 | 5.2 nM (mouse islets) |
| KO Mouse Validation | Reduces body weight in both Gcgr-/- and Glp1r-/- knockout mice — confirms independent contribution of each receptor to weight-reducing effects |
| Developer | Innovent Biologics (Suzhou, China); licensed to Eli Lilly for Western markets; multiple Phase 1b/2 trials published; Phase 3 in T2D underway |
| Physical Form | White lyophilised powder; hygroscopic |
| Purity | ≥99% (RP-HPLC); identity confirmed by ESI-MS (MW 4563.1 Da confirmed; charge-state deconvolution); C20 fatty acid modification confirmed |
| Endotoxin | <1 EU/mg (LAL chromogenic assay) |
| Solubility | Soluble in sterile water and PBS pH 7.4; 1 mg/mL stock; may require gentle warming to 37°C for full dissolution due to fatty acid modification; do not vortex |
| Storage — Lyophilised | −20°C long-term (stable 18–24 months); 2–8°C short-term; protect from moisture and light |
| Storage — Reconstituted | 2–8°C for up to 7 days; −20°C for longer; avoid freeze-thaw; aliquot before freezing |
| Certificate of Analysis | Lot-specific CoA with every order; HPLC + ESI-MS (MW 4563.1; C20 modification confirmed) + endotoxin |
| Regulatory Status | Not FDA, EMA, TGA, or Health Canada approved; Phase 3 in China (T2D); research compound for laboratory use only |
| WADA Status | Not listed on 2024–2025 WADA Prohibited List; not prohibited |
What Is Mazdutide?
Mazdutide occupies a unique position in the GLP-1 family: it is the most clinically documented long-acting dual GLP-1R/GCGR agonist with an explicitly oxyntomodulin-derived backbone.
Understanding its biology requires understanding oxyntomodulin first — the natural hormone it was engineered to improve.
Oxyntomodulin (OXM) is a 37-amino acid proglucagon-derived peptide produced and released by intestinal L-cells in response to food intake.
It is co-secreted with GLP-1, PYY, and GLP-2 from the same L-cell.
Unlike GLP-1 — which is a specific, potent GLP-1R agonist — oxyntomodulin activates both GLP-1R and GCGR, though with lower affinity than either native ligand.
In humans, OXM administration reduces appetite, increases energy expenditure, and reduces food intake more than equimolar GLP-1 — the GCGR component’s energy expenditure effects add to GLP-1’s appetite suppression.
The problem with native oxyntomodulin is its plasma half-life of approximately 12 minutes — making it unsuitable for clinical use.
Mazdutide solves this through three structural modifications: (1) Aib substitution at position 2 prevents DPP-4-mediated cleavage at the His-Aib cleavage site; (2) C-terminal glycinamide blocks carboxypeptidase attack; and (3) the C20 fatty diacid at Lys²⁰ enables non-covalent albumin binding, extending the plasma half-life to approximately 7 days for once-weekly dosing.
The result is an OXM pharmacology that lasts a week rather than 12 minutes.
The key pharmacological design choice in Mazdutide vs other dual GLP-1R/GCGR agonists is the potency balance.
Mazdutide was deliberately designed with roughly balanced GLP-1R and GCGR activity (Ki values: GCGR 17.7 nM vs GLP-1R 28.6 nM — approximately 1.6:1 GCGR:GLP-1R ratio).
This is more GCGR-active than most competing dual agonists, reflecting a design philosophy that maximises the GCGR-driven energy expenditure and hepatic fat effects rather than diluting them to minimise any potential hyperglycaemic risk.
When you buy Mazdutide from SourceTides, you access research-grade IBI362/LY3305677 with MW 4563.1 Da confirmed and full lot-specific CoA.
The Oxyntomodulin Lineage: Why Mazdutide’s Origin Matters
The peptide GLP-1 family tree has two branches in metabolic research.
One branch — Semaglutide, liraglutide, exenatide — descends from GLP-1 itself, engineered for longer action but retaining GLP-1R selectivity.
The other branch descends from the broader proglucagon peptide family, where oxyntomodulin’s natural dual GLP-1R/GCGR activity provides the template.
Mazdutide belongs firmly to the oxyntomodulin branch.
This matters because the oxyntomodulin lineage carries intrinsic GCGR activity not as an add-on but as a native feature of the backbone — the peptide was designed around a molecule that evolved to activate both receptors simultaneously.
Retatrutide, by contrast, descends from a GIP backbone with GLP-1 and glucagon pharmacophores engineered in.
Both approaches produce GLP-1R/GCGR agonism, but through different structural lineages that may have different receptor binding geometries and downstream signalling biases.
This structural lineage distinction is scientifically meaningful because Mazdutide and Retatrutide, despite sharing two receptor targets, are different molecules with different affinities, different structural modifications, and potentially different receptor-coupling dynamics.
Studying both in the same model provides information about how the structural route to dual agonism affects biological outcomes — an important SAR question in the metabolic peptide field.
How Mazdutide Works — Dual Receptor Mechanism
GLP-1R Activation: Appetite, Insulin, and Glucose Control
Mazdutide’s GLP-1R component drives the same mechanisms as all GLP-1R agonists.
Binding GLP-1R on pancreatic beta cells activates the Gs→cAMP→PKA cascade, driving glucose-dependent insulin secretion — amplifying beta cell insulin output only when blood glucose is elevated, avoiding hypoglycaemia at normal glucose levels.
GLP-1R on hypothalamic and brainstem neurons reduces appetite and food intake by decreasing neuropeptide Y (NPY) and agouti-related peptide (AgRP) expression while increasing POMC.
GLP-1R on stomach smooth muscle slows gastric emptying, extending meal-related satiety signals.
GLP-1R on alpha cells suppresses glucagon secretion, reducing hepatic glucose output.
These established GLP-1R mechanisms make Mazdutide directly comparable to Semaglutide for its GLP-1R component.
The clinical Mazdutide vs Semaglutide comparison is therefore an empirical test of what adding GCGR agonism contributes to GLP-1R pharmacology in humans.
GCGR Activation: Hepatic Fat, Energy Expenditure, and the Counterintuitive Metabolic Partner
Glucagon receptor activation is Mazdutide’s defining feature — the component that GLP-1R agonists lack entirely.
GCGR is expressed most densely in the liver, but also in adipose tissue, brain, kidney, and brown adipose tissue.
In the liver, GCGR activation stimulates hepatic fat oxidation (beta-oxidation), reduces de novo lipogenesis, and drives glycogenolysis.
This hepatic fat-burning effect is why GCGR agonism is particularly promising for MAFLD/NAFLD — conditions defined by hepatic fat accumulation.
Mazdutide has dedicated MAFLD clinical trials underway in China, targeting this specific hepatic mechanism.
In brown adipose tissue, GCGR activation increases UCP-1 (uncoupling protein 1) expression and thermogenesis, increasing resting energy expenditure.
This metabolic rate increase is the mechanism behind the incremental weight loss beyond GLP-1R alone — energy is burned even in the absence of reduced caloric intake.
The counterintuitive aspect: glucagon normally raises blood glucose by driving hepatic glycogenolysis.
In Mazdutide’s dual agonist context, the concurrent GLP-1R activation counteracts this glucose-raising effect: GLP-1R simultaneously suppresses glucagon secretion and stimulates insulin secretion.
The net effect is that GCGR’s fat-burning and energy-expenditure contributions are retained while the hyperglycaemic liability is suppressed by the GLP-1R partner — the same pharmacological insight behind Retatrutide and Trinity-X.
The Knockout Mouse Validation: Both Receptors Independently Contribute
One of the most pharmacologically significant findings in the Mazdutide preclinical literature is its activity in receptor-specific knockout mice.
Mazdutide reduces body weight in Gcgr-/- mice (no glucagon receptor) — confirming GLP-1R alone is sufficient to produce weight loss.
It also reduces body weight in Glp1r-/- mice (no GLP-1 receptor) — confirming GCGR alone can produce weight loss.
This means the two receptor-mediated weight loss mechanisms are genuinely independent — not obligately synergistic.
The full weight loss potential of Mazdutide comes from activating both simultaneously, but neither receptor is merely a passenger.
This finding has important implications for research design: using Mazdutide in a single-receptor-knockout background allows clean isolation of each receptor’s contribution to specific metabolic endpoints.
Mazdutide Clinical Evidence
| Trial | Design | Key Finding | Source |
|---|---|---|---|
| Phase 1b — Obesity (high dose; Chinese adults) | Randomised, placebo-controlled; 9 mg and 10 mg cohorts; 12–16 weeks; published in eClinicalMedicine (The Lancet) | 9 mg and 10 mg well tolerated; favourable safety profile; high-dose cohorts showed promising body weight loss; previously 6 mg achieved 6.4% weight loss at 12 weeks in earlier cohort; potential confirmed for moderate-to-severe obesity | eClinicalMedicine 2022 — PMID: 36267519 |
| Phase 2 — Type 2 Diabetes (Chinese adults) | Published in Diabetes Care (top-tier diabetes journal); multiple doses; primary endpoint HbA1c reduction + weight loss | Robust HbA1c reduction; significant body weight loss; multiple cardiometabolic benefits; favourable safety profile with manageable GI side effects; Phase 3 in T2D Chinese patients launched on basis of these results | Diabetes Care — Innovent Phase 2 full results |
| Phase 1b — Type 2 Diabetes (Chinese adults) | Randomised controlled trial; published in Nature Communications 2022 (PMID: 35768413) | Mazdutide improved glycaemic control (HbA1c, fasting glucose) and reduced body weight in T2D Chinese patients; confirmed GLP-1R/GCGR dual mechanism in a diabetic population; Nature Communications publication validates research-grade significance | Nat Commun 2022 — PMID: 35768413 |
| Phase 1b — Adolescent Obesity (China) | Phase 1b; met primary endpoint; December 2025 announcement by Innovent | Significant weight loss and metabolic benefits confirmed in Chinese adolescents with obesity; primary endpoint met; first GLP-1R/GCGR dual agonist trial data in the adolescent population | Innovent Press Release Dec 2025 |
| Preclinical — Cognitive Function (diabetic mice) | Multi-omics; STZ-induced diabetic mouse model; three doses (50, 100, 200 µg/kg); published PMC 2025 | Mazdutide mitigated diabetes-associated cognitive dysfunction; reduced neuroinflammation; improved hippocampal biology; metabolomics and transcriptomics analysis identified neuroprotective pathways; extends Mazdutide’s research applications beyond metabolic endpoints to CNS-metabolic intersection | PMC12205698 — Cognitive dysfunction 2025 |
| Preclinical — Knockout Mouse Receptor Validation | In vivo; Gcgr-/- and Glp1r-/- mice; body weight and food intake endpoints | Weight reduction in both knockout strains confirms both receptors independently contribute to Mazdutide’s weight loss; each receptor is neither obligatory nor merely accessory — both are active and independent; definitive receptor attribution data | Published preclinical KO data — Cayman/Biomol reference |
Mazdutide in the GLP-1/Dual Agonist Landscape
| Compound | Receptors | Structural Origin | Peak Published Weight Loss | Key Distinction | SourceTides |
|---|---|---|---|---|---|
| GLP-1 (native) | GLP-1R | Endogenous; proglucagon-derived | Minimal (t½ ~2 min) | Pharmacology reference; GLP-1R positive control | Buy GLP-1 |
| Glucagon (native) | GCGR | Endogenous; proglucagon-derived | Not an obesity drug standalone | GCGR pharmacology reference for Mazdutide’s glucagon component | Buy Glucagon |
| Semaglutide | GLP-1R | GLP-1 analog | ~15% (STEP-1; 68 weeks) | FDA-approved GLP-1R mono-agonist; Mazdutide’s GLP-1R arm comparator; gold standard for GLP-1R-only effects | Buy Semaglutide |
| Tirzepatide | GLP-1R + GIPR | GIP analog | ~22.5% (SURMOUNT-1; 72 weeks) | FDA-approved; adds GIPR not GCGR — the other major dual agonism strategy; compare vs Mazdutide for GIP vs Glucagon contribution | Buy Tirzepatide |
| Mazdutide (this product) | GLP-1R + GCGR | Oxyntomodulin analog | 6.4% (12 weeks, 6 mg dose; Phase 1b) — longer-term data from Phase 2/3 pending | Most clinically documented GLP-1R/GCGR dual agonist; oxyntomodulin origin; MAFLD clinical programme; balanced dual agonism; KO mouse receptor validation | Buy Mazdutide |
| Retatrutide | GLP-1R + GIPR + GCGR | GIP backbone | 24.2% (Phase 2 NEJM; 48 weeks) | Adds GIPR to GLP-1R/GCGR vs Mazdutide; triple agonist vs dual; GIP-backbone vs OXM-backbone structural comparison | Buy Retatrutide |
| Trinity-X | GLP-1R + GIPR + GCGR | Proprietary tri-agonist | No published standalone data | Trade-name tri-agonist; compare Mazdutide (dual) vs Trinity-X (triple) to measure GIPR addition contribution | Buy Trinity-X |
What Is Mazdutide Used for in Research?
| Research Field | Application | Why Mazdutide |
|---|---|---|
| Obesity and body composition | DIO rodent models; body weight reduction; fat vs lean mass; adiposity; energy intake and expenditure; food intake | Multiple published clinical trials establish human-relevant dose response; KO mouse data provides clean receptor-attribution design framework; use Mazdutide + selective antagonists (Exendin(9-39) for GLP-1R; L-168,049 for GCGR) to isolate each receptor’s contribution in identical DIO protocols |
| NAFLD / MAFLD / NASH | Hepatic steatosis; liver fat reduction; NASH fibrosis; hepatic insulin resistance; NAS scoring; ALT/AST; liver triglyceride content | The most clinically advanced GLP-1R/GCGR agonist with a dedicated MAFLD clinical trial programme; GCGR-driven hepatic beta-oxidation is the primary hepatic fat-reduction mechanism; studied alongside LIPO-C for hepatic lipid biology and Glucagon for GCGR-specific liver fat comparisons |
| Type 2 diabetes | Glucose-stimulated insulin secretion (GSIS); OGTT; HbA1c-proxy models; beta-cell function; glucagon suppression; fasting glucose | Phase 2 T2D trial published in Diabetes Care; Phase 1b T2D data in Nature Communications; most published clinical T2D data of any GLP-1R/GCGR dual agonist; insulin secretion EC50 = 5.2 nM confirmed from mouse islets |
| GCGR receptor attribution research | GLP-1R vs GCGR contribution dissection; Gcgr-/- and Glp1r-/- mouse models; receptor selectivity pharmacology; OXM vs GLP-1 differential biology | The validated Gcgr-/- and Glp1r-/- activity data makes Mazdutide the ideal compound for studying dual agonism receptor attribution — both knockouts are validated, documented, and publishable as experimental designs |
| Cognitive function / neurometabolic research | Diabetes-associated cognitive dysfunction; hippocampal biology; neuroinflammation; metabolomics-transcriptomics multi-omics; CNS-metabolic intersection | 2025 PMC study (PMC12205698) confirmed Mazdutide mitigates diabetes-associated cognitive dysfunction in mice via multi-omics-identified neuroprotective pathways; extends research applications beyond metabolic endpoints; studied alongside Pinealon, NAD⁺, and Selank Amidate in neurometabolic intersection panels |
| GLP-1R/GCGR vs GLP-1R/GIPR comparison | Dual agonism pharmacology comparison; GCGR vs GIPR as GLP-1R partner; hepatic fat vs adipose biology; energy expenditure mechanism dissection | Comparing Mazdutide (GLP-1R/GCGR) vs Tirzepatide (GLP-1R/GIPR) in identical metabolic models directly measures how GCGR vs GIPR contribute differently to weight loss, hepatic fat, and insulin secretion when paired with GLP-1R; the fundamental dual agonism SAR experiment |
| Energy expenditure and thermogenesis | Brown adipose thermogenesis; UCP-1 expression; resting metabolic rate; respiratory quotient; indirect calorimetry | GCGR activation drives BAT thermogenesis independently of GLP-1R; comparing Mazdutide vs Semaglutide in calorimetry protocols directly measures GCGR’s energy expenditure contribution above GLP-1R alone |
Mazdutide Pharmacokinetics and Handling
| Parameter | Value / Notes | Research Implication |
|---|---|---|
| Plasma half-life | ~7 days (once-weekly dosing enabled by C20 fatty diacid albumin binding); dramatically extended vs native oxyntomodulin (~12 min) | For rodent in-vivo studies: once-weekly SC injection is the validated dosing frequency; measure metabolic endpoints 3–7 days post-dose for peak-to-trough characterisation; steady-state reached by week 3–4 |
| In-vitro receptor assay | GLP-1R Ki = 28.6 nM; GCGR Ki = 17.7 nM; insulin secretion EC50 = 5.2 nM; use 1–1000 nM range for cell-based cAMP and calcium flux assays | Run 8-point dose-response from 0.1–1000 nM; include Glucagon and GLP-1 as reference agonists for each receptor; confirm receptor expression in your cell system |
| Rodent in-vivo dose | 15–30 nmol/kg SC (single dose) in published rodent studies; 30 nmol/kg SC once weekly for chronic DIO studies; acute dose confirmed: 15 nmol/kg significantly reduces food intake and body weight in diabetic mice | Start at 15 nmol/kg SC once weekly in DIO mouse; measure body weight, food intake, blood glucose weekly; collect tissue at 4–8 weeks for liver histology, adipose weight, and plasma endpoints |
| Reconstitution note | May require gentle warming to 37°C and slow gentle rotation (not vortex) for full dissolution due to C20 fatty acid modification; white particulate visible before full dissolution is normal for fatty acid-conjugated peptides | Dissolve in sterile PBS pH 7.4 at 37°C for 15–30 minutes with slow end-over-end rotation; check solution is clear before filtering through 0.22 µm and using; do not microwave or heat above 40°C |
| Key metabolic endpoints | Body weight; food intake; fasting glucose; OGTT; insulin; HOMA-IR; liver weight and triglycerides; ALT/AST; adipose tissue mass; energy expenditure (indirect calorimetry); UCP-1 (BAT thermogenesis) | Liver endpoints (weight, histology, TG, ALT/AST) are particularly important given Mazdutide’s dedicated MAFLD programme; UCP-1 provides the mechanistic evidence for GCGR-driven thermogenesis contribution |
Mazdutide Quality Control at SourceTides
Every batch of Mazdutide from SourceTides undergoes these tests before release.
The C20 fatty acid modification confirmation is the critical QC checkpoint unique to this compound — confirming the albumin-binding, half-life-extending moiety is present.
| Test | Method | Specification | Why It Matters |
|---|---|---|---|
| Purity | RP-HPLC (C18; UV 220 nm) | ≥99% peak area purity | Separates full-length Mazdutide from deletion sequences and from the unconjugated 33-AA backbone (which would lack the C20 fatty acid and have substantially shorter half-life, compromising once-weekly dosing kinetics) |
| Identity and C20 Modification | ESI-MS (charge-state deconvolution; MW 4563.1 Da) | Confirmed MW 4563.1 g/mol; C20 fatty diacid modification confirmed by mass (loss of C20 diacid moiety would reduce MW by ~424 Da) | The C20 fatty diacid is the half-life-extending modification. Without it, Mazdutide behaves like a short-acting peptide. The ~424 Da mass contribution of the fatty acid modification is directly confirmed by MS — any preparation without this mass is not long-acting Mazdutide. |
| Endotoxin | LAL chromogenic assay | <1 EU/mg | LPS activates inflammatory insulin resistance in hepatocytes and adipocytes — directly confounding Mazdutide’s glycaemic control, hepatic fat, and adipose biology endpoints |
| Appearance | Visual inspection | White lyophilised powder; no discolouration or aggregation | Fatty acid-conjugated peptides can form aggregates if mishandled; white powder confirms correct lyophilisation; discolouration may indicate Trp or Tyr oxidation |
| Certificate of Analysis | Lot-specific PDF | HPLC + MS (4563.1 Da; C20 fatty acid confirmed) + endotoxin + dates | C20 fatty acid mass confirmation is the unique CoA element for Mazdutide — the identifier that distinguishes long-acting from unmodified versions; required documentation for any once-weekly dosing research protocol |
Mazdutide Regulatory Status
| Jurisdiction | Status | Notes |
|---|---|---|
| China (NMPA) | Not yet approved; Phase 3 in T2D underway; Phase 2 results in T2D published in Diabetes Care | Innovent Biologics conducting Phase 3 programme for T2D in China. Not commercially approved. Research-grade supply only. |
| USA (FDA) | Not approved; not DEA-controlled; licensed to Eli Lilly (LY3305677) for Western development; research compound only | Eli Lilly holds the Western rights. No FDA IND/NDA for commercial sale. Not a scheduled substance. SourceTides supplies research-grade for laboratory use only. |
| EU / UK / Australia / Canada | Not approved in any jurisdiction; not a controlled substance; research compound only | No regulatory approval in these jurisdictions. Not a controlled substance. Research laboratory access. See the SourceTides shipping policy. |
| WADA | Not listed on 2024–2025 WADA Prohibited List; not prohibited | No performance-enhancing classification. Verify annually at wada-ama.org. |
Peer-Reviewed References
| # | Citation | Link |
|---|---|---|
| 1 | Jiang H et al. (2022). Safety and efficacy of mazdutide (IBI362) 9 mg and 10 mg in Chinese adults with overweight or obesity. eClinicalMedicine. PMID: 36267519. | PubMed PMID: 36267519 |
| 2 | Xu W, Yang J et al. (2022). Phase 1b RCT of IBI362 (LY3305677) in Chinese patients with T2D. Nat Commun. 13:3613. PMID: 35768413. | PubMed PMID: 35768413 — Nature Communications |
| 3 | Chen T et al. (2022). The Design and Optimization of Monomeric Multitarget Peptides for the Treatment of Multifactorial Diseases — describes Mazdutide structure-activity design. J Med Chem. 65(5):3685–3705. | PubMed — J Med Chem 2022 |
| 4 | Mazdutide — diabetes-associated cognitive dysfunction. Multi-omics mechanistic study in diabetic mice. PMC. 2025. PMC12205698. | PMC12205698 — Cognitive dysfunction 2025 |
| 5 | Innovent Biologics. (December 2025). Mazdutide Phase 1b in Chinese Adolescents with Obesity meets primary endpoint. Press release. | Innovent Press Release Dec 2025 |
| 6 | Wikipedia: Mazdutide. CAS 2259884-03-0; formula; mechanism; clinical development; IBI362/LY3305677. | Wikipedia: Mazdutide |
Frequently Researched Alongside Mazdutide
These compounds are most commonly studied alongside Mazdutide in metabolic, obesity, NAFLD, and GLP-1/GCGR receptor research:
- Semaglutide — FDA-approved GLP-1R mono-agonist; the essential comparator for Mazdutide’s GLP-1R component; comparing Mazdutide vs Semaglutide directly measures what adding GCGR to GLP-1R achieves in weight loss, hepatic fat, and energy expenditure endpoints
- Tirzepatide — FDA-approved GLP-1R + GIPR dual agonist; the key structural comparator — both are dual agonists pairing GLP-1R with a second receptor, but Mazdutide’s partner is GCGR and Tirzepatide’s is GIPR; comparing both in identical metabolic models reveals whether GCGR or GIPR is the more effective GLP-1R partner for specific endpoints
- Retatrutide — GLP-1R + GIPR + GCGR triple agonist; shares GLP-1R and GCGR with Mazdutide but adds GIPR and uses a GIP backbone rather than OXM; comparing Mazdutide (OXM-backbone dual) vs Retatrutide (GIP-backbone triple) dissects both the GIPR contribution and the structural backbone effect simultaneously
- Trinity-X — Trade-name GLP-1R/GIPR/GCGR triple agonist; used alongside Mazdutide in protocols comparing dual GLP-1R/GCGR (Mazdutide) vs triple GLP-1R/GIPR/GCGR (Trinity-X) to measure GIPR’s marginal contribution to the Mazdutide dual mechanism
- Glucagon — Endogenous GCGR agonist; the selective GCGR reference for isolating Mazdutide’s glucagon receptor arm; using Glucagon alone alongside Mazdutide in hepatic fat and energy expenditure studies confirms which effects are GCGR-mediated
- GLP-1 — Endogenous GLP-1R agonist; the selective GLP-1R reference for isolating Mazdutide’s GLP-1R arm; essential positive control for all GLP-1R cell-based assays and in-vivo receptor attribution experiments
- LIPO-C Injectable — Multi-nutrient lipotropic with hepatic fat clearance and beta-oxidation support; studied with Mazdutide in NAFLD/MAFLD research combining hormonal GCGR-driven hepatic fat reduction (Mazdutide) and nutritional lipotropic hepatic fat clearance (LIPO-C)
- AOD-9604 Peptide — hGH C-terminal fragment; direct β₃-AR adipocyte lipolysis (non-receptor-mediated, non-hormonal mechanism); studied with Mazdutide in comprehensive fat-loss protocols combining receptor-mediated appetite suppression and energy expenditure (Mazdutide) with direct adipocyte triglyceride hydrolysis (AOD-9604)
- Ipamorelin 10 mg — Selective GH secretagogue; studied with Mazdutide in body composition research where lean mass preservation during weight loss is the endpoint — GH/IGF-1 axis (Ipamorelin) preserves muscle mass while Mazdutide drives fat reduction
- Sermorelin 10 mg — GHRH agonist for GH axis lean mass support; studied with Mazdutide in obesity + sarcopenia research protocols combining GLP-1R/GCGR fat reduction (Mazdutide) and GH axis anabolic support (Sermorelin)
- NAD⁺ Injectable — Sirtuin substrate; mitochondrial metabolism; SIRT3 regulates hepatic fatty acid oxidation — the same GCGR-driven pathway Mazdutide activates; studied with Mazdutide in NAFLD and mitochondrial ageing panels for combined hormonal (Mazdutide) and metabolic cofactor (NAD⁺) approaches to hepatic fat
- Pinealon 10 mg — CNS neuroprotective bioregulator; studied with Mazdutide in neurometabolic panels building on Mazdutide’s 2025 cognitive dysfunction PMC data — combining direct neuroprotection (Pinealon) and metabolic improvement of the CNS-diabetes interface (Mazdutide)
- Selank Amidate 10 mg — IL-6 suppression and GABAergic anxiolytic; studied with Mazdutide in neuroinflammation and metabolic-anxiety intersection research connecting the cognitive dysfunction (Mazdutide 2025 data) and neuroinflammatory (Selank) biology
- BPC-157 — Tissue repair; hepatic cytoprotection via VEGFR2/NO; studied with Mazdutide in NAFLD protocols combining hormonal hepatic fat reduction (Mazdutide GCGR component) and hepatic tissue cytoprotection and repair (BPC-157)
- Kisspeptin-10 10 mg — GnRH pulse generator; reproductive neuroendocrinology; studied with GLP-1 family in research on metabolic-reproductive axis interactions, where energy availability (GLP-1R/GCGR signalling) and reproductive hormone (Kisspeptin/GnRH) biology converge
Frequently Asked Questions
You can buy Mazdutide (IBI362; LY3305677; CAS 2259884-03-0) directly from SourceTides.
Every order includes a lot-specific Certificate of Analysis with the RP-HPLC chromatogram (≥99% purity), ESI-MS identity confirmation (MW 4563.1 Da; C20 fatty acid modification confirmed by mass), and LAL endotoxin result (<1 EU/mg).
All vials are lyophilised white powder and dispatched on dry-ice cold chain. See the SourceTides shipping policy for dispatch details.
Semaglutide is a GLP-1R mono-agonist — it activates one receptor. Mazdutide is a dual agonist — it activates two receptors simultaneously: GLP-1R and GCGR.
The practical consequence for research is that Mazdutide produces all the effects of GLP-1R activation (appetite suppression, insulin secretion, glucagon suppression, gastric emptying delay) plus the GCGR-specific effects that Semaglutide cannot produce: hepatic fat oxidation (particularly relevant for NAFLD/MAFLD), brown adipose thermogenesis and increased energy expenditure, and broader proglucagon-derived metabolic biology. This is why the direct head-to-head comparison between Mazdutide and Semaglutide in identical metabolic models is the definitive experiment for quantifying what GCGR adds to GLP-1R therapy.
Structurally: Semaglutide is derived from GLP-1; Mazdutide is derived from oxyntomodulin — the endogenous dual agonist gut hormone. SourceTides supplies both for research comparison protocols.
Both Mazdutide and Tirzepatide are dual agonists that pair GLP-1R with a second metabolic receptor — but the second receptor is completely different.
Tirzepatide’s second receptor is GIPR (GIP receptor) — the receptor for glucose-dependent insulinotropic polypeptide, an incretin hormone that augments insulin secretion and modulates adipose tissue. GIPR is primarily a metabolic synergist for GLP-1R’s pancreatic and adipose effects.
Mazdutide’s second receptor is GCGR (glucagon receptor) — the receptor for glucagon, which drives hepatic fat oxidation, brown adipose thermogenesis, and energy expenditure. GCGR adds a fundamentally different metabolic dimension: it increases caloric burning rather than (primarily) reducing caloric intake.
The research implication: Mazdutide vs Tirzepatide in identical protocols answers the fundamental question — for metabolic disease, which is the more powerful GLP-1R partner: GCGR (energy expenditure + liver fat) or GIPR (incretin augmentation + adipose)? This is one of the most important open questions in multi-agonist metabolic peptide pharmacology. SourceTides supplies both for this comparison.
The finding that Mazdutide reduces body weight in both Gcgr-/- mice (no glucagon receptor) and Glp1r-/- mice (no GLP-1 receptor) is one of the most pharmacologically informative pieces of preclinical data for any dual agonist.
It tells you two things definitively. First: GLP-1R activation alone is sufficient to produce weight loss — the GCGR component is not required for Mazdutide to work. Second: GCGR activation alone is also sufficient to produce weight loss — the GLP-1R component is not required either.
This means the two receptor mechanisms are genuinely independent, not obligately synergistic. The combined effect of Mazdutide in wild-type animals (activating both simultaneously) is additive from two independent mechanisms — not a single mechanism requiring both receptors together.
For research design: this validation provides a clean experimental framework. Using Mazdutide in Gcgr-/- mice isolates the pure GLP-1R contribution to each endpoint. Using it in Glp1r-/- mice isolates the pure GCGR contribution. Any endpoint that differs between the two knockouts is differentially regulated by the two receptor systems. This design cannot be done with Semaglutide (GLP-1R only) or with compounds that have no validated knockout data.
Mazdutide is a research-grade peptide and is not a controlled substance in any of these jurisdictions. It is not DEA-scheduled in the USA, not controlled under the Misuse of Drugs Act 1971 in the UK, and not a CDSA controlled substance in Canada. In Australia, it is not scheduled — verify current TGA status for institutional compliance.
Mazdutide (IBI362/LY3305677) is in Phase 3 clinical development for T2D in China (Innovent Biologics) and is licensed to Eli Lilly for Western development, but it has not been approved by any regulatory authority as of May 2026. It is not WADA-prohibited.
SourceTides supplies for in-vitro laboratory research use only. See the SourceTides shipping policy for jurisdiction-specific details.
Mazdutide requires slightly different reconstitution than most peptides because of its C20 fatty acid modification. Dissolve lyophilised Mazdutide in sterile PBS (pH 7.4) at 1 mg/mL. The fatty acid may require gentle warming — heat solution to 37°C and slowly rotate end-over-end for 15–30 minutes until fully dissolved. Do not vortex, sonicate, or heat above 40°C. Filter through 0.22 µm syringe filter before use.
For in-vitro receptor assays (GLP-1R/GCGR cAMP accumulation, β-arrestin): working concentration 1–1000 nM; include Glucagon and GLP-1 as reference agonists for each receptor.
For in-vivo rodent DIO studies: 15–30 nmol/kg SC once weekly; collect metabolic endpoints weekly (body weight, food intake, fasting glucose); collect tissue at 4–8 weeks for liver histology, adipose mass, and plasma biomarkers. Store reconstituted stock at 2–8°C for up to 7 days or −20°C in aliquots for longer. Full guidance in the CoA with every SourceTides Mazdutide order.
SourceTides accepts Visa, Mastercard, American Express, cryptocurrency, and bank transfers for institutional orders. All payments go through secure, encrypted gateways.
For institutional purchase orders, bulk research procurement, or custom quantities, contact the team via the SourceTides contact page. Orders are reviewed for research compliance before dispatch.
All SourceTides products, including Mazdutide (IBI362; LY3305677; CAS 2259884-03-0), are for in-vitro laboratory research use only.
Mazdutide is in Phase 3 clinical development (China) but is not approved by the FDA, EMA, TGA, or Health Canada.
These products are not for human consumption.
By purchasing, the buyer confirms authorised researcher status and accepts responsibility for compliance with all applicable regulations.
| Weight | 0.01 lbs |
|---|---|
| Dimensions | 5 × 5 × 5 in |
| Purity | ≥99% HPLC, C20 Fatty Acid Confirmed (ESI-MS), MW 4563.1 Da |
| Receptor Targets | |
| Form | Lyophilised Powder (once-weekly half-life; C20 albumin-binding) |
| CAS Number | 2259884-03-0 |
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