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^[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].