| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 50mg | 电议 |
Cell lines | U266 myeloma cells |
Preparation method | The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below - 20 ℃ for several months. |
Reacting condition | 0 ~ 10 μM; 0 ~ 24 hrs |
Applications | In U266 myeloma cells, Nifuroxazide significantly inhibited STAT3 tyrosine phosphorylation in a dose-dependent manner, with an IC50 value of 10 μM. The inhibitory effect of Nifuroxazide on STAT3 tyrosine phosphorylation was rapid, occurring as early as 1 hr after treatment and sustained for at least 24 hrs. In addition, Nifuroxazide did not affect STAT3 serine (727) phosphorylation. |
Animal models | 4T1 tumor-bearing mice |
Dosage form | 10 or 50 mg/kg; i.p.; q.d., for 24 days |
Applications | In 4T1 tumor-bearing mice, Nifuroxazide significantly reduced tumor outgrowth and tumor weight, without causing any significant change in body weight. The immunohistochemical staining results of 4T1 tumors collected on day 31 showed that Nifuroxazide substantially reduced Ki-67-positive cells and increased CC-3-positive cells, indicating that Nifuroxazide inhibited cell proliferation and induced apoptosis in breast tumor tissues by inhibiting Ki-67 and activating caspase-3. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
| 产品描述 | Nifuroxazide is an effective inhibitor of STAT3, also exerts potent anti-tumor and anti-metastasis activity. 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[1]. 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[2]. References: |
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