N-(E)-Caffeoyldopamine
N-(E)-Caffeoyldopamine is an inhibitor of α-glucosidase that can be purified from Clerodendranthus Spicatus. N-(E)-Caffeoyldopamine shows a 53.73% inhibitory activity againstα-glucosidase. N-(E)-Caffeoyldopamine can be studied in diabetes research.
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- CAS No.: 103188-49-4
- Formule: C17H17NO5
- Masse moléculaire:315.32
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Stockage:
4°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Activité biologique
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HepG2 | CC50 |
229 μM
Compound: 8d
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Cytotoxicity against human HepG2 cells assessed as cell viability incubated for 12 days by WST-1 assay
Cytotoxicity against human HepG2 cells assessed as cell viability incubated for 12 days by WST-1 assay
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[PMID: 37216809] |
| PC-12 | CC50 |
>150 μM
Compound: 6i
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Cytotoxicity against rat PC12 cells measured for 24 hrs by WST-assay
Cytotoxicity against rat PC12 cells measured for 24 hrs by WST-assay
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[PMID: 38740144] |
Chemical Information
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CAS No. 103188-49-4
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Appearance Solid
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Masse moléculaire 315.32
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Formule C17H17NO5
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SMILES
OC=1C=CC(=CC1O)CCNC(/C=C/C2=CC(O)=C(O)C=C2)=O
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Structure Classification
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Initial Source
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
4°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Protocole
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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
Pureté et documentation
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Fiche technique (264 KB)
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SDS (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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Instruction de manipulation (2659 KB)
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)