3'-Methoxy-4'-nitroflavone
3'-Methoxy-4'-nitroflavone (MNF) is a specific aryl hydrocarbon receptor (AhR) antagonist. 3'-Methoxy-4'-nitroflavone activates AhR by inhibiting CYP1, the metabolic enzyme of the endogenous ligand FICZ (HY-12451), leading to the accumulation of FICZ. 3'-Methoxy-4'-nitroflavone reverses the anti-apoptotic effect of TCDD, attenuates the activation of Akt and Erk1/2 kinases and the expression of TGFα induced by TCDD. 3'-Methoxy-4'-nitroflavone can be used in research related to breast tumor promotion, rheumatoid arthritis, multiple sclerosis and inflammatory bowel disease.
For research use only. We do not sell to patients.
- CAS No.: 145370-39-4
- Formula: C16H11NO5
- Molecular Weight:297.26
-
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]
-
Biological Activity
-
Chemical Information
- Purity & Documentation
- References
-
Help & FAQs
Biological Activity
3'-Methoxy-4'-nitroflavone (0.1-1000 nM; 24 h) inhibits TCDD-dependent DRE-driven luciferase activity in MCF-10A cells at concentrations as low as 10 nM[1].
3'-Methoxy-4'-nitroflavone (0.1-1000 nM; 3 days) reverses the TCDD-dependent inhibition of apoptosis in MCF-10A cells, with significant effects observed at concentrations of 100 nM and 1000 nM[1].
3'-Methoxy-4'-nitroflavone (0.1-1000 nM; 6 h) reduces the phosphorylation level of Akt in MCF-10A cells, with significant inhibition observed at 1 nM and complete inhibition achieved at 100 nM[1].
3'-Methoxy-4'-nitroflavone (0.1-1000 nM; 6 h) reverses TCDD-mediated Erk1,2 phosphorylation in MCF-10A cells at concentrations of 10 nM and above, and when acting alone, its 1 nM concentration enhances basal Erk1,2 activation[1].
3'-Methoxy-4'-nitroflavone (0.1-100 nM; 6 h) completely abolishes TCDD-dependent TGFα mRNA expression in MCF-10A cells at concentrations as low as 1 nM[1].
3'-Methoxy-4'-nitroflavone (0.5-2.5 μM) potently inhibits the basal ethoxyresorufin O-deethylase activity of human recombinant CYP1A1[2].
3'-Methoxy-4'-nitroflavone (0.05-2.5 μM; 1.5-20 h) inhibits 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced ethoxyresorufin O-deethylase activity in HaCaT cells in a dose-dependent manner in vitro[2].
3'-Methoxy-4'-nitroflavone (0.05-2.5 μM; 1.5-48 h) first inhibits then enhances FICZ-dependent CYP1A1 mRNA expression and ethoxyresorufin O-deethylase activity in HaCaT cells, with a significant enhancing effect observable upon prolonged incubation[2].
3'-Methoxy-4'-nitroflavone (0.05-2.5 μM; 0-40 h) induces aryl hydrocarbon receptor-dependent ethoxyresorufin O-deethylase activity in HaCaT cells, and this effect depends on endogenous FICZ in the culture medium[2].
3'-Methoxy-4'-nitroflavone (0.05 μM; 0-30 h) induces aryl hydrocarbon receptor-dependent CYP1A1 mRNA expression in HaCaT cells, a process that requires FICZ present in commercial cell culture media[2].
3'-Methoxy-4'-nitroflavone (50 nM; 48 h) induces ethoxyresorufin O-deethylase activity in HaCaT cells only in the presence of 0.1 pM FICZ[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Cell Line:MCF-10A human mammary epithelial cells
-
Concentration:0.1 nM, 1 nM, 10 nM, 100 nM, 1000 nM (co-treated with 10 nM TCDD)
-
Incubation Time:3 days
-
Result:Resulted in four times the number of apoptotic cells compared to TCDD alone at 100 nM.
Doubled the number of apoptotic cells compared to TCDD alone at 1000 nM.
-
Cell Line:MCF-10A human mammary epithelial cells
-
Concentration:0.1 nM, 1 nM, 10 nM, 100 nM, 1000 nM (co-treated with 10 nM TCDD); 0.1 nM, 1 nM, 10 nM, 100 nM, 1000 nM (treated alone)
-
Incubation Time:6 h
-
Result:Decreased TCDD-induced Akt serine phosphorylation at 1 nM.
Induced complete inhibition of TCDD-induced Akt serine phosphorylation at 100 nM.
Caused a slight increase in TCDD-induced Akt phosphorylation at 10 nM.
Had minimal effect on basal Akt phosphorylation when treated alone.\nInhibited TCDD-dependent Erk1,2 phosphorylation at 10 nM, 100 nM, and 1000 nM.
Significantly increased basal Erk1,2 activation alone at 1 nM.
-
Cell Line:MCF-10A human mammary epithelial cells
-
Concentration:0.1 nM, 1 nM, 10 nM, 100 nM (co-treated with 10 nM TCDD); 0.1 nM, 1 nM, 10 nM, 100 nM (treated alone)
-
Incubation Time:6 h
-
Result:Completely reversed the TCDD-induced 2-fold increase in TGFα mRNA at concentrations as low as 1 nM.
Increased TGFα mRNA over basal levels alone at 0.1 nM.
-
Cell Line:HaCaT cells
-
Concentration:0.05 μM
-
Incubation Time:0, 10, 20 and 30 h
-
Result:Significantly induced CYP1A1 mRNA expression in cells cultured in commercial DMEM, with no significant induction observed in cells cultured in DMEM with recrystallized tryptophan.
Chemical Information
-
CAS No. 145370-39-4
-
Molecular Weight 297.26
-
Formula C16H11NO5
-
SMILES
O=C1C=C(C2=CC(OC)=C([N+]([O-])=O)C=C2)OC3=C1C=CC=C3
-
Synonyms
MNF
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
[1]. Davis JW Jr, et al. The aryl hydrocarbon receptor antagonist, 3'methoxy-4'nitroflavone, attenuates 2,3,7,8-tetrachlorodibenzo-p-dioxin-dependent regulation of growth factor signaling and apoptosis in the MCF-10A cell line. Toxicol Appl Pharmacol. 2003;188(1):42-49. [Content Brief]
[2]. Wincent E, et al. Inhibition of cytochrome P4501-dependent clearance of the endogenous agonist FICZ as a mechanism for activation of the aryl hydrocarbon receptor. Proc Natl Acad Sci U S A. 2012;109(12):4479-4484. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
3'-Methoxy-4'-nitroflavone Related Classifications
HY-20888 Related Classifications
Powered by Bioz