CX-4945 [Silmitasertib]，≥99% (HPLC)

Application

一种选择性的有效的CK2(酪蛋白激酶2)抑制剂。

CX-4945 (Silmitasertib) is an ATP-competitive CK2 protein kinase inhibitor with a Ki and an IC50 of 0.38 and 1 nM for recombinant human CK2α, respectively. CX-4945 has broad-spectrum anti-proliferative activity in multiple cancer cell lines. The anti-proliferative activity of CX-4945 against cancer cells correlated with expression levels of the CK2α catalytic subunit. Attenuation of PI3K/Akt signaling by CX-4945 was evidenced by dephosphorylation of Akt on the CK2-specific S129 site and the canonical S473 and T308 regulatory sites. CX-4945 suppresses Akt signaling and inhibits proliferation of HUVEC Cells. CX-4945 causes cell-cycle arrest and selectively induced apoptosis in certain cancer cells. In models of angiogenesis, CX-4945 inhibited human umbilical vein endothelial cell migration, tube formation, and blocked CK2-dependent hypoxia-induced factor 1 alpha (HIF-1α) transcription in cancer cells. Collectively, CX-4945 inhibits pro-angiogenic CK2 signaling in vitro and in vivo. CX-4945 is an inhibitor of Flt-3/Flk-2 and Pim-1.

CX-4945（Silmitasertib）是一种具有ATP竞争性的CK2蛋白激酶抑制剂，对于重组人CK2α，Ki和IC50分别为0.38和1 nM。 CX-4945在多种癌细胞系中具有广谱抗增殖活性。 CX-4945对癌细胞的抗增殖活性与CK2α催化亚基的表达水平相关。 CX-4945使PI3K / Akt信号减弱，这是通过CK2特异性S129位点以及规范的S473和T308调控位点上Akt的去磷酸化来证明的。 CX-4945抑制Akt信号传导并抑制HUVEC细胞的增殖。 CX-4945导致细胞周期停滞并选择性诱导某些癌细胞的凋亡。在血管生成模型中，CX-4945抑制人脐静脉内皮细胞迁移，管形成，并阻断癌细胞中CK2依赖性缺氧诱导的因子1α（HIF-1α）的转录。集体地，CX-4945在体外和体内抑制促血管生成的CK2信号传导。 CX-4945是Flt-3 / Flk-2和Pim-1的抑制剂。

性质

安全信息