Sennidin A
Sennidin A is an anthraquinone derivative and a HCV NS3 helicase inhibitor with an IC50 of 0.8 μM against HCV NS3 helicase. Sennidin A induces Akt phosphorylation at Ser-473 and Thr-308 and promotes GLUT4 translocation to the plasma membrane. Sennidin A inhibits HCV replication. Sennidin A stimulates glucose incorporation and 2-Deoxyglucose uptake in cells. Sennidin A does not induce tyrosine phosphorylation of the insulin receptor or insulin receptor substrate-1. Sennidin A can be used for research on type 2 diabetes and hepatitis C.
For research use only. We do not sell to patients.
- CAS No.: 641-12-3
- Formula: C30H18O10
- Molecular Weight:538.46
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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Biological Activity
Description
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Helicase |
GLUT4 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| Huh-7 | EC50 |
>80 μM
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Antiviral activity against Huh-7 cells harboring HCV genotype 1b subgenomic replicon assessed as reduction in luciferase activity after 72 hrs.
Antiviral activity against Huh-7 cells harboring HCV genotype 1b subgenomic replicon assessed as reduction in luciferase activity after 72 hrs.
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26262613 |
| Huh-7 | CC50 |
>80 μM
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Cytotoxicity against human Huh-7 cells assessed by MTS assay after 72 hrs.
Cytotoxicity against human Huh-7 cells assessed by MTS assay after 72 hrs.
|
26262613 |
In Vitro
Sennidin A (0-300 μM; 30 min) stimulates glucose uptake in rat adipocytes in a dose-dependent manner, exerting insulin-mimetic and additive effects[1].
Sennidin A (300 μM; 30 min) does not induce tyrosine phosphorylation of IR or IRS-1 in rat adipocytes[1].
Sennidin A (300 μM; 30 min) stimulates the translocation of GLUT4 from low-density microsomes to the plasma membrane in rat adipocytes[1].
Sennidin A (100-300 μM; 30 min) induces Akt phosphorylation at Ser-473 and Thr-308 in rat adipocytes[1].
Sennidin A (30 min) potently inhibits HCV NS3 helicase in a cell-free FRET helicase assay with an IC50 of 0.8 µM[2].
Sennidin A (72 h) shows weak anti-HCV activity in Huh-7 cells harboring the HCV genotype 1b subgenomic replicon, with an EC50 greater than 80 µM[2].
Sennidin A (72 h) exhibits low cytotoxicity in Huh-7 cells, with a CC50 greater than 80 µM[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Huh-7
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Concentration:Various concentrations
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Incubation Time:72 h
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Result:Exhibited a CC50 value for cytotoxicity greater than 80 µM.
Chemical Information
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CAS No. 641-12-3
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Molecular Weight 538.46
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Formula C30H18O10
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SMILES
O=C1C2=C(O)C=C(C(O)=O)C=C2[C@@]([C@@]3([H])C4=CC(C(O)=O)=CC(O)=C4C(C5=C(O)C=CC=C35)=O)([H])C6=CC=CC(O)=C16
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Structure Classification
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Initial Source
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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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Kinase activity and phosphorylation assays
Kinase activity assays measure the ability of kinases to transfer phosphate groups from ATP to specific substrates, while phosphorylation assays detect the presence and levels of phosphorylated proteins. Common methods include radiolabeled ATP incorporation (e. g. ,), ADP release detection via bioluminescence (e. g. ,[3]), enzyme-linked immunosorbent assays (ELISA) for phospho-specific epitopes (e. g. ,[6]), and microtiter-based formats for high-throughput screening (e. g. ,[8]). The ADP-Glo assay quantifies kinase activity by measuring ADP produced during phosphorylation using a luciferase-based system. Radiometric assays involve autoradiography or scintillation counting after incorporation of 32P-labeled ATP into substrate proteins. ELISA-based approaches rely on phospho-specific antibodies to detect activated kinases in cell lysates or purified samples.
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Western Blot
Western blotting (WB) is a commonly used experimental method in molecular biology, biochemistry, and immunogenetics for identifying and quantifying target proteins. It combines gel electrophoresis with immunoassay, enabling researchers to analyze protein expression, post-translational modifications, and molecular weight.
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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 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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Protocol for Kinase activity and phosphorylation assays
Kinase activity assays measure transfer of phosphate from ATP to a protein or peptide substrate, generating phosphorylated substrate, ADP, or incorporated radiolabeled phosphate as the readout; phosphorylation assays measure site-specific phosphorylation in cells or tissues as a proxy for kinase-pathway activation, inhibition, or substrate regulation. Phosphorylation can be detected by phospho-specific Western blot, immunoprecipitation kinase assay, phospho-immunofluorescence, phospho-flow cytometry, luminescent ADP detection, radiolabeled ATP incorporation, or reporter-based pathway assays, and these readouts can be applied to cancer cells, primary neurons, mouse tumors, organoids, inflammatory macrophages, ferroptosis studies, and mitophagy studies when the kinase target is biologically relevant.
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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)
Sennidin A Related Classifications
HY-N6936 Related Classifications
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