Nifuroxazide

Research use only, not for human use.

Nifuroxazide is a cell-permeable and orally available nitrofuran-based antidiarrheal agent that effectively suppresses the activation of cellular STAT1/3/5 transcription activity .

Nifuroxazide is a cell-permeable and orally available nitrofuran-based antidiarrheal agent that effectively suppresses the activation of cellular STAT1/3/5 transcription activity .(In Vitro):When U266 cells are incubated with Nifuroxazide, a significant dose-dependent decrease in STAT3 tyrosine phosphorylation is observed. This inhibition of STAT3 tyrosine phosphorylation is rapid, occurring as early as 1 h after treatment, and is sustained for at least 24 h. Treatment of U266 or INA6 cells with Nifuroxazide for 48 hours result in a dose-dependent loss of cell viability with an EC50 of approximately 4.5 μM in both cell types. Notably, the MM cells lacking constitutive STAT3 activation show little toxicity to Nifuroxazide.(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.

When U266 cells are incubated with Nifuroxazide, a significant dose-dependent decrease in STAT3 tyrosine phosphorylation is observed. This inhibition of STAT3 tyrosine phosphorylation is rapid, occurring as early as 1 h after treatment, and is sustained for at least 24 h. Treatment of U266 or INA6 cells with Nifuroxazide for 48 hours result in a dose-dependent loss of cell viability with an EC50 of approximately 4.5 μM in both cell types. Notably, the MM cells lacking constitutive STAT3 activation show little toxicity to Nifuroxazide.

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.

Nifuroxazide | Ambatrol | Antinal | Bacifurane | Diafuryl | Diarlidan

JAK/STAT Signaling

STAT

STAT1| STAT3| STAT5

Infection

——

965-52-6

275.22

C12H9N3O5

>98% (HPLC)

DMSO: 55 mg/mL (199.84 mM)

O=C(N/N=C/C1=CC=C([N+]([O-])=O)O1)C2=CC=C(O)C=C2

4-Hydroxy-N-[(E)-(5-nitrofuran-2-yl)methylideneamino]benzamide

(-20℃)

With Ice Pack

≥ 2 years