Nifuroxazide是硝基呋喃类化合物抑制剂，有效地抑制细胞内STAT1/3/5转录活性的激活，IC50为3 µM。Nifuroxazide通过减少Jak激酶自身磷酸化阻碍了STAT3组成型磷酸化，从而降低骨髓瘤细胞存活性，而不影响正常的外周血单核细胞。硝呋齐特能够降低Jak和TYK2的酪氨酸磷酸化，而对EGF受体酪氨酸激酶或Src激酶没有影响，表明硝呋齐特对Jak2和TYK2的相对特异性。Nifuroxazide会引起包含STAT3活化的初级骨髓瘤细胞和骨髓瘤细胞系的存活性降低，但不影响正常外周血单核细胞。

>98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

硝呋齐特

黄色结晶性粉末

DMSO ：51 mg/mL (185.3 mM)

STAT1,STAT3,STAT5

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.