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Description: Nifuroxazide (Bacifurane; Diafuryl; Ambatrol; Antinal; Diarlidan) is a potent, cell-permeable and orally bioavailable nitrofuran-based antidiarrheal agent that effectively suppresses the activation of cellular STAT1/3/5 transcription activity with IC50 of 3 μM against IL-6-induced STAT3 activation in U3A cells. It is a nitrofuran antibiotic that has been approved for treating colitis and diarrhea. Nifuroxazide is described to block constitutive phosphorylation of STAT3 by reducing Jak kinase autophosphorylation, decreasing the viability of myeloma cells depending on constitutive STAT3 activity for survival while not affecting normal peripheral blood mononuclear cells.
References: Blood. 2008 Dec 15;112(13):5095-102.
Chemical Name: 4-Hydroxy-N-[(E)-(5-nitrofuran-2-yl)methylideneamino]benzamide
InChi Key: YCWSUKQGVSGXJO-NTUHNPAUSA-N
InChi Code: InChI=1S/C12H9N3O5/c16-9-3-1-8(2-4-9)12(17)14-13-7-10-5-6-11(20-10)15(18)19/h1-7,16H,(H,14,17)/b13-7+
SMILES Code: O=C(N/N=C/C1=CC=C([N+]([O-])=O)O1)C2=CC=C(O)C=C2
Nifuroxazide; Bacifurane; Diafuryl; Ambatrol; Antinal; Diarlidan
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2
In vitro activity: Nifuroxazide is a nitrofuran compound inhibitor of STAT transcription factor signaling. Nifuroxazide is described to block constitutive phosphorylation of STAT3 by reducing Jak kinase autophosphorylation, decreasing the viability of myeloma cells depending on constitutive STAT3 activity for survival while not affecting normal peripheral blood mononuclear cells. Nifuroxazide produces decreases in tyrosine phosphorylation of Jak2 and Tyk2, and showed no effects on EGF receptor tyrosine kinase or Src kinase, indicating a relative specificity of Nifuroxazide for Jak2 and Tyk2. Nifuroxazide shows no inhibition of Akt or MAPK phosphorylation. Nifuroxazide inhibits the constitutive phosphorylation of STAT3 in MM cells by reducing Jak kinase autophosphorylation, and leads to down-regulation of the STAT3 target gene Mcl-1. Nifuroxazide causes a decrease in viability of primary myeloma cells and myeloma cell lines containing STAT3 activation, but not normal peripheral blood mononuclear cells. Although bone marrow stromal cells provide survival signals to myeloma cells, nifuroxazide can overcome this survival advantage. Reflecting the interaction of STAT3 with other cellular pathways, nifuroxazide shows enhanced cytotoxicity when combined with either the histone deacetylase inhibitor depsipeptide or the MEK inhibitor UO126.
Blood. 2008 Dec 15;112(13):5095-102. doi
Purity ≥98%
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