G5-7 |
| Catalog No.GC62246 |
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.
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Cas No.: 939681-36-4
Sample solution is provided at 25 µL, 10mM.
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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.
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