STAT3/NF-κB-IN-3
STAT3/NF-κB-IN-3 is an orally active STAT3/NF-κB inhibitor with anti-inflammatory and antioxidant activities, which specifically blocks the phosphorylation of NF-κB and STAT3 proteins. STAT3/NF-κB-IN-3 downregulates the expression of iNOS and NOX-2 in macrophages, reduces intracellular levels of ROS and MDA, and upregulates the expression of antioxidant genes at the same time. In a mouse model of acute liver failure induced by LPS/D-GalN, STAT3/NF-κB-IN-3 alleviates liver necrosis and inflammatory cell infiltration, and reduces the release of pro-inflammatory cytokines such as IL-6 and IL-12 via the TLR4 pathway. STAT3/NF-κB-IN-3 can be used in studies related to acute liver failure.
For research use only. We do not sell to patients.
- Formula: C17H22O5
- Molecular Weight:306.35
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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
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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STAT3 |
NF-κB |
IL-6 |
IL-12 |
iNOS |
NOX2 |
STAT3/NF-κB-IN-3 (compound 27) (incubated for 6-24 h) potently inhibits LPS-induced TNF-α secretion in RAW 264.7 cells, with an IC50 of 2.84 μM and a selectivity index > 35.2[1].
STAT3/NF-κB-IN-3 (5-10 μM; 6-24 h) inhibits LPS-induced production of proinflammatory cytokines and suppresses the phosphorylation of NF-κB and STAT3 in RAW 264.7 cells and primary mouse bone marrow-derived macrophages (BMDMs)[1].
STAT3/NF-κB-IN-3 (5-10 μM; 6-24 h) alleviates LPS-induced oxidative stress and enhances the expression of antioxidant defense genes in RAW 264.7 cells and primary mouse bone marrow-derived macrophages (BMDMs)[1].
STAT3/NF-κB-IN-3 selectively inhibits TLR4-mediated inflammatory responses in RAW 264.7 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
STAT3/NF-κB-IN-3 (40 mg/kg; p.o.; daily; 3 days) protects against LPS/D-GalN-induced acute liver failure in a TLR4-dependent manner, as its hepatoprotective, anti-inflammatory, and signaling-inhibitory effects are abolished in Tlr4−/− mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (male, 8-10 weeks old, 25 g, LPS/D-GalN-induced acute liver failure)[1]
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Dosage:10 mg/kg; 20 mg/kg; 40 mg/kg
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Administration:p.o.; daily; 3 days
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Result:Significantly reduced serum ALT and AST levels compared to vehicle-treated mice, with the 40 mg/kg dose showing the strongest effect.
Significantly reduced the liver index (liver-to-body weight ratio) at 40 mg/kg and 20 mg/kg doses compared to vehicle-treated mice.
Significantly suppressed serum levels of pro-inflammatory cytokines IL-6 and IL-12 compared to vehicle-treated mice.
Significantly downregulated hepatic mRNA expression of TNF-α, CCL20, IL6, IL1β, NOX-2, and iNOS compared to vehicle-treated mice.
Significantly suppressed hepatic phosphorylation of NF-κB p65 and STAT3 at 40 mg/kg dose compared to vehicle-treated mice.
Attenuated hepatic necrosis, inflammatory cell infiltration, and intrahepatic hemorrhage compared to vehicle-treated mice, with the 40 mg/kg dose showing the most pronounced improvement.
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Animal Model:C57BL/6 (male, 8-10 weeks old, 25 g, LPS/D-GalN-induced acute liver failure)
Tlr4−/− (male, 8-10 weeks old, 25 g, LPS/D-GalN-induced acute liver failure, C57BL/6 genetic background)[1] -
Dosage:40 mg/kg
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Administration:p.o.; daily; 3 days
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Result:Significantly reduced liver index, serum ALT and AST levels, serum IL-6 and IL-12 levels, hepatic mRNA expression of TLR4, CCL20, IL6, IL1β, NOX-2, and iNOS, and hepatic phosphorylation of NF-κB p65 and STAT3 in wild-type mice compared to vehicle-treated wild-type mice.
Failed to significantly reduce liver index, serum ALT and AST levels, serum IL-6 and IL-12 levels, hepatic mRNA expression of CCL20, IL6, IL1β, NOX-2, and iNOS, or hepatic phosphorylation of NF-κB p65 and STAT3 in Tlr4−/− mice compared to vehicle-treated Tlr4−/− mice.
Attenuated hepatic damage in wild-type mice but did not further improve hepatic architecture in Tlr4−/− mice compared to their vehicle-treated group.
Chemical Information
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Molecular Weight 306.35
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Formula C17H22O5
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SMILES
CCCCCCC(C1=CC(OC(C)=O)=CC=C1OC(C)=O)=O
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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)
STAT3/NF-κB-IN-3 Related Classifications
HY-184736 Related Classifications
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