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.
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- CAS No.: 572-76-9
- 화학식: C19H19NO4
- 분자량:325.36
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보관:
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
- 순도&문서
- 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
|
[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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분자량 325.36
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화학식 C19H19NO4
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SMILES
OC1=C2CN3[C@](CC2=CC=C1OC)([H])C4=CC(OCO5)=C5C=C4CC3
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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