This material is suppliedΒ exclusively as a laboratory research chemicalΒ forΒ in vitro scientific study. All descriptions and documentation are providedΒ for informational and educational purposes only.
This compound isΒ not approvedΒ for human or animal consumption, injection, ingestion, inhalation, topical use, or any other biological application. It must be handled only by qualified, trained personnel in a properly equipped laboratory.
This product isΒ notΒ a drug, supplement, food, cosmetic, or therapeutic agent, and it may not be rebranded, repackaged, or marketed as any such item.Β Misuse, mislabeling, or unauthorized application is strictly prohibited.
Nothing on this website constitutes medical advice, professional guidance, or a recommendation of use.
(Dual GLP-1R / GCGR Agonist β Research Use Only)
Mazdutide (also known as IBI362) is a synthetic peptide-based dual-agonist targeting both the glucagon-like peptide-1 receptor (GLP-1R) and the glucagon receptor (GCGR).
In vitro studies show that Mazdutide activates Gs-coupled GPCR signaling, driving adenylate cyclase, cAMP accumulation, and downstream phosphorylation of PKA, CREB, and AMPK-linked metabolic regulators. Dual receptor activation produces coordinated effects on glucose metabolism, fatty-acid utilization, and hepatocellular gene expression.
Mazdutide binds and activates:
| Receptor | Research Role |
|---|---|
| GLP-1R | cAMP-PKA signaling, insulinotropic transcription, neuroendocrine effects |
| GCGR | Hepatic fatty-acid oxidation, AMPK activation, gluconeogenic gene modulation |
Both receptors belong to class B GPCR family and signal primarily via Gs-protein activation β adenylate cyclase β cAMP.
Mazdutide stimulation results in:
β intracellular cAMP
PKA phosphorylation
CREB transcription factor activation
Representative CREB-regulated genes:
PCK1 (PEPCK)
G6PC
PPARGC1A (PGC-1Ξ±)
INS gene transcription in Ξ²-cell models
GCGR activation stimulates:
β cAMP-PKAβdependent AMPK signaling
β Ξ²-oxidation and mitochondrial oxidative metabolism
Typical gene targets monitored in vitro:
CPT1A, CPT2 (fatty-acid transport)
ACOX1, ACADL (fatty-acid oxidation)
NRF1, TFAM (mitochondrial biogenesis)
GLP-1R agonism can induce PI3K/Akt phosphorylation, especially in pancreatic and neuronal cell lines.
Downstream targets include:
mTOR, GSK3Ξ²
BCL2 family (cell-survival pathways)
FOXO1 transcriptional control
Dual GLP-1R/GCGR activation alters liver transcriptional programs:
| Functional Category | Gene Examples |
|---|---|
| Gluconeogenesis | PCK1, G6PC |
| Mitochondrial Oxidation | CPT1A, ACADL, ACOX1 |
| Cholesterol & Lipid Transport | ABCG5, ABCG8, SREBF1 |
| Mitochondrial Biogenesis | NRF1, TFAM |
Research frequently notes a shift toward fatty-acid oxidation over lipid storage.
In neuronal culture systems:
cAMP/PKA β CREB β POMC transcription
Reduced NPY / AgRP gene activity
Potential modulation of hypothalamic metabolic circuits
| Component | Role in Mazdutide Mechanism |
|---|---|
| cAMP | Primary intracellular second messenger |
| PKA | Phosphorylation of CREB, ACC, GSK3Ξ² |
| CREB | Transcription factor for metabolic gene networks |
| ACC (acetyl-CoA carboxylase) | PKA-mediated inhibition β β fatty-acid oxidation |
| AMPK | Energy-sensing kinase activated indirectly via GCGR |
β p-CREB, p-AMPK, p-Akt
β mitochondrial gene transcription (NRF1, TFAM)
β fatty-acid oxidation gene expression (CPT1A, ACOX1)
Changes in neuropeptide gene signaling (β POMC, β AgRP/NPY)
Synthetic dual GLP-1R/GCGR agonist
Strong cAMP-PKA-CREB activation
Crosstalk with AMPK and PI3K/Akt pathways
Modulation of metabolic gene clusters governing:
gluconeogenesis,
fatty-acid oxidation,
mitochondrial biogenesis,
neuroendocrine signaling
Mazdutide is offered exclusively for controlled in-vitro laboratory research.
Not for human or animal use, ingestion, injection, or therapeutic application.
| Weight | N/A |
|---|---|
| Size | 100 Mg |
