Carpachromene
Based on 1 Customer Validation
Carpachromene is a potent α-glucosidase enzyme inhibitor. Carpachromene ameliorates insulin resistance in HepG2 cells via modulating IR/IRS1/PI3k/Akt/GSK3/FoxO1 pathway.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Reinheit : 98.84%
- CAS. Nr.: 57498-96-1
- Formel: C20H16O5
- Molecular Weight:336.34
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Speicherung:
-20°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
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Biologische Aktivität
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Chemical Information
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- Reinheit & Dokumentation
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Help & FAQs
Biologische Aktivität
Beschreibung
In Vitro
Carpachromene (0-100 μg/mL, 48 h) exhibits cytotoxicity against HepG2, HepG2/IRM, PLC/PRF/5 and Raji cancer cell lines[1].
Carpachromene (20 μg/mL) significantly increases the protein expression ratios of IR, IRS1, PI3K, Akt, GSK3, and FoxO1 in HepG2/IRM cells[1].
Carpachromene (20 μg/mL) improves cellular glycogen synthesis in HepG2/IRM cells[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. Nr. 57498-96-1
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Appearance Solid
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Molecular Weight 336.34
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Formel C20H16O5
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Color Light yellow to yellow
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SMILES
OC1=C2C(OC(C3=CC=C(O)C=C3)=CC2=O)=CC4=C1C=CC(C)(C)O4
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Structure Classification
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Initial Source
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
-20°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Protokoll
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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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
Reinheit & Dokumentation
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Data Sheet (267 KB)
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SDS (536 KB)
- English - EN (536 KB)
- Français - FR (536 KB)
- Deutsch - DE (536 KB)
- Norwegian - NO (536 KB)
- Español - ES (536 KB)
- Swedish - SV (536 KB)
- Italian - IT (536 KB)
- Korean - KR (536 KB)
- Portuguese - PT (536 KB)
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Handling Instructions (2659 KB)
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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