1. Immunology/Inflammation Metabolic Enzyme/Protease Apoptosis PI3K/Akt/mTOR Stem Cell/Wnt MAPK/ERK Pathway TGF-beta/Smad
  2. Aryl Hydrocarbon Receptor Cytochrome P450 Apoptosis Akt ERK TGF-beta/Smad
  3. 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.

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3'-Methoxy-4'-nitroflavone

3'-Methoxy-4'-nitroflavone Chemical Structure

CAS No. : 145370-39-4

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Description

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[1][2].

In Vitro

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.

Apoptosis Analysis[1]

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.

Western Blot Analysis[1]

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.

Real Time qPCR[1]

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.

Real Time qPCR[2]

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.
Molecular Weight

297.26

Formula

C16H11NO5

CAS No.
SMILES

O=C1C=C(C2=CC(OC)=C([N+]([O-])=O)C=C2)OC3=C1C=CC=C3

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3'-Methoxy-4'-nitroflavone
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