Nandinine
Nandinine is an orally active derivative of Berberine (HY-N0716). Nandinine enhances AMPK activity, inhibits the activation of IKKβ/NF-κB, and regulates the phosphorylation of IRS-1. Nandinine reverses the abnormal production of adipokines, promotes insulin-mediated glucose uptake, and alleviates insulin resistance. Nandinine improves glucose tolerance and increases the insulin sensitivity index in mice. Nandinine can be used in studies related to insulin resistance.
For research use only. We do not sell to patients.
- CAS No.: 572-76-9
- Formula: C19H19NO4
- Molecular Weight:325.36
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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All AMPK Isoforms
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Biological Activity
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IKKβ |
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| THP-1 | IC50 |
36.41 nM
Compound: 9, S-(-)-5
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Inhibition of tissue factor procoagulant activity in LPS-stimulated human THP1 cells preincubated for 1 hr before LPS addition measured after 5 hrs
Inhibition of tissue factor procoagulant activity in LPS-stimulated human THP1 cells preincubated for 1 hr before LPS addition measured after 5 hrs
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[PMID: 23199480] |
Nandinine (10 µM; 1 h) significantly reverses the dysregulated adipokine secretion in differentiated 3T3-L1 adipocytes induced by Mac-CM by reducing the levels of pro-inflammatory TNF-α and IL-6 and restoring the level of anti-inflammatory adiponectin[1].
Nandinine (10 µM; 1 h) significantly inhibits the activation of the IKKβ/NF-κB pathway in post-differentiation 3T3-L1 adipocytes induced by Mac-CM[1].
Nandinine (10 µM; pretreated for 1 hour and co-incubated with Mac-CM for 30 minutes) significantly restores insulin-mediated signal transduction and glucose uptake in Mac-CM-treated differentiated 3T3-L1 adipocytes by regulating IRS-1 phosphorylation and the activity of the downstream PI3K/Akt/GLUT-4 pathway[1].
Nandinine (10 µM; 1 h) significantly activates AMPK in differentiated 3T3-L1 adipocytes under normal conditions and those treated with Mac-CM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:differentiated 3T3-L1 adipocytes
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Concentration:10 µM
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Incubation Time:1 h pretreatment; 30 min stimulation with Mac-CM
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Result:Reversed Mac-CM-induced increases in IKKβ phosphorylation.
Reversed Mac-CM-induced increases in IκBα phosphorylation.
Reversed Mac-CM-induced increases in p65 phosphorylation.
Reversed Mac-CM-induced increases in nuclear p65 expression.
Reduced the Mac-CM-enhanced interaction between IκBα and IKKβ.
All changes were statistically significant at P < 0.01 compared to Mac-CM-only treatment.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ICR mice (male, 6-8 weeks of age)[1]
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Dosage:100 mg/kg; 200 mg/kg
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Administration:p.o.; single dose
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Result:Restored glucose disposal compared to Mac-CM-only treated mice.
Reduced the area under the curve for glucose (AUC-G) compared to Mac-CM-only treated mice.
Decreased the homeostasis model assessment of insulin resistance (HOMA-IR) index compared to Mac-CM-only treated mice.
Chemical Information
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CAS No. 572-76-9
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Molecular Weight 325.36
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Formula C19H19NO4
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SMILES
OC1=C2CN3[C@](CC2=CC=C1OC)([H])C4=CC(OCO5)=C5C=C4CC3
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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