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Ruxolitinib

CAS No. : 941678-49-5

MCE 国际站：Ruxolitinib

产品活性：Ruxolitinib (INCB18424) 是具有口服活性的，选择性的 JAK1/2 抑制剂， IC₅₀ 值分别为 3.3 nM 和 2.8 nM，选择性是 JAK3 的 130 多倍。Ruxolitinib 诱导自噬 (autophagy)，通过毒性线粒体自噬 (mitophagy) 杀死肿瘤细胞。

研究领域：Epigenetics  |  Protein Tyrosine Kinase/RTK  |  JAK/STAT Signaling  |  Stem Cell/Wnt  |  Autophagy  |  Apoptosis

作用靶点：JAK  |  Autophagy  |  Mitophagy  |  Apoptosis

In Vitro: Ruxolitinib potently and selectively inhibits JAK2V617F-mediated signaling and proliferation, markedly increases apoptosis in a dose dependent manner, and at 64 nM results in a doubling of cells with depolarized mitochondria in Ba/F3 cells. Ruxolitinib demonstrates remarkable potency against erythroid colony formation with IC₅₀ of 67 nM, and inhibits proliferating of erythroid progenitors from normal donors and polycythemia vera patients with IC₅₀ values of 407 nM and 223 nM, respectively.

In Vivo: Ruxolitinib (180 mg/kg, orally, twice a day) results in survive rate of greater than 90% by day 22 and markedly reduces splenomegaly and circulating levels of inflammatory cytokines, and preferentially eliminated neoplastic cells, resulting in significantly prolonged survival without myelosuppressive or immunosuppressive effects in a JAK2V617F-driven mouse model. In the Ruxolitinib group, the primary end point is reached in 41.9% of patients, as compared with 0.7% in the placebo group in the double-blind trial of myelofibrosis. Ruxolitinib results in maintaining of reduction in spleen volume and improvement of 50% or more in the total symptom score.

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