GLP-1R agonist 1
GLP-1R agonist 1 is a fused imidazole GLP-1 receptor agonist with EC50 = 0.12 nM. GLP-1R agonist 1 exhibits weak inhibitory effect on hERG, with hERG potassium channel blockade IC50 = 22 μM. GLP-1R agonist 1 can be used for research on GLP-1-related diseases, such as diabetes.
For research use only. We do not sell to patients.
- CAS No.: 2711019-49-5
- Formula: C32H29ClFN3O5
- Molecular Weight:590.04
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
GLP-1 0.12 nM (EC50) |
In Vitro
GLP-1R agonist 1 (compound 4) (incubation for 6 h) activates the GLP-1 receptor, elevates intracellular cAMP levels, and induces CRE-dependent luciferase expression; GLP-1 agonistic activity EC50=0.12 nM, Emax=104%[1].
GLP-1R agonist 1 blocks hERG potassium current with IC50=22 μM; it has a weak inhibitory effect on hERG channels, reducing the risk of hERG-related cardiac side effects[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 2711019-49-5
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Molecular Weight 590.04
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Formula C32H29ClFN3O5
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SMILES
C[C@@]1(C2=C(C=C(C=C2)Cl)F)OC3=C(C4=CCN(CC(N(C5=C6)C[C@@H]7CCO7)=NC5=CC=C6C(O)=O)CC4)C=CC=C3O1
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)