DGAT-1 inhibitor 3
DGAT-1 inhibitor 3 (compound 10) is a potent DGAT-1 inhibitor with an IC50 value of 0.038 µM. DGAT-1 inhibitor 3 has the potential for the research of obesity and diabetes.
For research use only. We do not sell to patients.
- CAS No.: 1231243-91-6
- Formula: C21H20F3N3O3
- Molecular Weight:419.40
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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
IC50: 0.038 µM (0.038 µM)[1]
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| CHO-K1 | EC50 |
1.803 μM
Compound: 10
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Inhibition of human DGAT1 expressed in CHO-K1 cells after 1 hr using palmitoyl-1-14C-coenzyme A by phospholipid flashplate assay
Inhibition of human DGAT1 expressed in CHO-K1 cells after 1 hr using palmitoyl-1-14C-coenzyme A by phospholipid flashplate assay
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[PMID: 21413799] |
Chemical Information
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CAS No. 1231243-91-6
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Appearance Solid
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Molecular Weight 419.40
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Formula C21H20F3N3O3
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Color White to off-white
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SMILES
O=C(C1=C(C(F)(F)F)OC(C2=CC=CC=C2)=N1)NC3=CC=C(N(CCOC)C)C=C3
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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 (266 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)