URB447
Based on 1 Customer Validation
URB447 is a peripherally restricted CB1 cannabinoid antagonist (IC50: 313 nM and 41 nM for rat CB1 and human CB2 receptor respectively ). URB447 lowers food intake and body-weight gain in mice without entering the brain or antagonizing central CB1-dependent responses. URB447 can be used for research of obesity.
For research use only. We do not sell to patients.
- Purity : 99.5%
- CAS No.: 1132922-57-6
- Formula: C25H21ClN2O
- Molecular Weight:400.90
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Storage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
Biological Activity
Description
IC50 & Target
[1]|
CB1 313 nM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| CHO-K1 | IC50 |
41 nM
Compound: 8b, URB-447
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Displacement of [3H]WIN-55212-2 from human CB2 receptor expressed in CHO-K1 cells by liquid scintillation counting
Displacement of [3H]WIN-55212-2 from human CB2 receptor expressed in CHO-K1 cells by liquid scintillation counting
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[PMID: 19128970] |
In Vitro
URB447 (100 nM-30 μM) inhibits GTPγS binding induced by the CB agonist WIN55,212-2 (1 μM), with an EC50 of 4.9 μM in rat cerebellar membrane preparations[1].
URB447 (1 μM) inhibits β-adrenergic agonist Isoproterenol (10 μM) induced cAMP accumulation in Hek-293 cells stably expressing mouse CB2 receptors[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
URB447 (20 mg/kg, i.p.) blocks the analgesic effects of Methanandamide in Swiss mice, indicating URB447 inhibits peripheral CB1-mediated analgesia[1].
URB447 (20 mg/kg, i.p., once daily for 2 weeks) reduces food consumption and body-weight gain in obese ob/ob mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 1132922-57-6
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Appearance Solid
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Molecular Weight 400.90
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Formula C25H21ClN2O
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Color Light yellow to yellow
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SMILES
O=C(C1=C(C)N(CC2=CC=C(C=C2)Cl)C(C3=CC=CC=C3)=C1N)C4=CC=CC=C4
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
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
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Data Sheet (276 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)