G5-7 是具有口服活性的 JAK2 变构抑制剂，可通过结合到 JAK2，选择性的抑制 JAK2 介导的 EGFR 和 STAT3 的磷酸化和激活。G5-7 诱导细胞周阻滞和诱导凋亡、具有抗血管生成活性。G5-7 有用于胶质瘤研究的潜能。
货号:ajcx33342
CAS:939681-36-4
分子式:C22H19F2NO3
分子量：383.39
溶解度:DMSO : 83.33 mg/mL (217.35 mM; Need ultrasonic)
纯度：98%
存储：Store at -20°C
库存：现货

Background:

G5-7, an orally active and allosteric JAK2 inhibitor, selectively inhibits JAK2 mediated phosphorylation and activation of EGFR (Tyr1068) and STAT3 by binding to JAK2. G5-7 induces cell cycle arrest, apoptosis and possesses antiangiogenic effect. G5-7 has the potential for glioma study[1].

G5-7 (0-5 μM) inhibits EGFR tyrosine phosphorylation and downstream mTOR signaling and arrests the cell cycle at G2 phase[1].G5-7 does not directly inhibit EGFR activation[1].G5-7 (0-10 μM) comparably increases the abundance of markers (cleved-PARP and caspase 3) of apoptosis in parental LN229 cells and U87MG/EGFRvIII cells[1].G5-7 interacts with full-length JAK2[1].G5-7 significantly inhibits EGFR Tyr1068 phosphorylation but had no effect on EGFR Tyr1045 phosphorylation[1].G5-7 downregulates the downstream signaling of JAK by mTOR[1].

G5-7 (10 and 50 mg/kg, oral gavege) decreases VEGF secretion and exerts a potent antiangiogenic effect[1].

[1]. Kunyan He, et al. Blockade of glioma proliferation through allosteric inhibition of JAK2. Sci Signal. 2013 Jul 9;6(283):ra55.