| CAS NO: | 965-52-6 |
| 规格: | ≥98% |
| 包装 | 价格(元) |
| 100mg | 电议 |
| 250mg | 电议 |
| 500mg | 电议 |
| 1g | 电议 |
| 2g | 电议 |
| Molecular Weight (MW) | 275.22 |
|---|---|
| Formula | C12H9N3O5 |
| CAS No. | 965-52-6 |
| Storage | -20℃ for 3 years in powder form |
| -80℃ for 2 years in solvent | |
| Solubility (In vitro) | DMSO: 55 mg/mL (199.8 mM) |
| Water: <1 mg/mL | |
| Ethanol: <1 mg/mL | |
| Other info | 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 |
| Synonyms | Nifuroxazide; Bacifurane; Diafuryl; Ambatrol; Antinal; Diarlidan |
| In Vitro | 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. |
|---|---|
| In Vivo | Compared with the vehicle group, treatment with Nifuroxazide could inhibit tumor growth and tumor weight in a dose-dependent manner, with the inhibition rate of tumor volumes being 43.0% and 62.1% at 25 mg/kg and 50 mg/kg, respectively. It is also shown that Nifuroxazide significantly inhibits the proliferation of nuclear Ki-67-positive cells and induces apoptosis cells of cleaved caspase-3-positive cells. Besides, it is found that treatment with Nifuroxazide could inhibit the expression of MMP-2, MMP-9 and p-Stat3 in A375 tumor tissues. What’s more, Nifuroxazide inhibits the infiltration of MDSCs into the lung, which might be associated with suppression of distant colonization of tumor cells in B16-F10 melanoma metastasis model. |
| Animal model | Mice |
| Formulation & Dosage | 25 mg/kg, 50 mg/kg; i.p. |
| References | Blood. 2008 Dec 15;112(13):5095-102. doi |
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