204001
BX-795
BX-795, also referenced under CAS 702675-74-9, modulates the biological activity of multiple kinases. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.
别名:
BX-795, AMPK相关激酶5抑制剂I,ARK5抑制剂I,NUAK激酶抑制剂I,NUAK1抑制剂I,SnF1类激酶-1抑制剂I,N-(3-((5-碘-4-((3-(2-噻吩基羰基)氨基)丙基)氨基)-2-嘧啶基)氨基)苯基)-1-吡咯烷甲酰胺,极光激酶
登录查看公司和协议定价
所有图片(1)
About This Item
推荐产品
品質等級
化驗
≥95% (HPLC)
形狀
solid
製造商/商標名
Calbiochem®
儲存條件
OK to freeze
protect from light
顏色
pale yellow
溶解度
DMSO: 50 mg/mL
運輸包裝
ambient
儲存溫度
2-8°C
InChI
1S/C23H26IN7O2S/c24-18-15-27-22(30-20(18)25-9-5-10-26-21(32)19-8-4-13-34-19)28-16-6-3-7-17(14-16)29-23(33)31-11-1-2-12-31/h3-4,6-8,13-15H,1-2,5,9-12H2,(H,26,32)(H,29,33)(H2,25,27,28,30)
InChI 密鑰
VAVXGGRQQJZYBL-UHFFFAOYSA-N
一般說明
一种可渗透细胞的氨基嘧啶化合物,可作为有效的,ATP竞争性和可逆的多激酶抑制剂(在≤ 10 µM ATP下,PDK1的IC50=11 nM;对于NUAK1,TBK1,MARK4,Aurora B,IKKε和PDK1,在100 µM ATP下,IC50=5、6、19、31、41和111 nM),并且显示出比Cdk2/E、EGFR、GSK-3β、IR、c-Kit、PKA、PKC、TAK1和VEGFR高50倍的选择性。显示可阻断PDK1/Akt信号传导,诱导PC-3和MDA-468细胞的生长停滞和凋亡(IC50分别为0.25和0.75 µM);此外,抑制IRF3的磷酸化(pSer396),核转位和转录活性,并减少刺激的巨噬细胞中IFN-β的产生。
包裝
用惰性气体包装
警告
毒性:标准处理(A)
重構
复溶后,等分并冷冻保存(-20°C)。储备液在-20°C条件下可稳定保存3个月。
其他說明
Clark, K., et al. 2009.J. Biol. Chem.284, 14136.
Tamgumcy, T., et al. 2008.Exp.Cell Res.314, 2299.
Feldman, R.I., et al. 2005.J. Biol. Chem.280, 19867.
Tamgumcy, T., et al. 2008.Exp.Cell Res.314, 2299.
Feldman, R.I., et al. 2005.J. Biol. Chem.280, 19867.
法律資訊
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
儲存類別代碼
11 - Combustible Solids
水污染物質分類(WGK)
WGK 2
閃點(°F)
Not applicable
閃點(°C)
Not applicable
Oncology research, 28(7), 779-790 (2021-03-21)
Glioma are common malignant brain tumors, among which glioblastoma multiforme (GBM) has the worst prognosis. Different studies of GBM revealed that targeting nuclear factor B (NF-B) induced an attenuation tumor proliferation and prolonged cell survival. TBK1 {TANK [TRAF (TNF (tumor-necrosis-factor)
Cancer discovery, 10(3), 460-475 (2019-12-08)
TANK binding kinase 1 (TBK1) is an important kinase involved in the innate immune response. Here we discover that TBK1 is hyperactivated by von Hippel-Lindau (VHL) loss or hypoxia in cancer cells. Tumors from patients with kidney cancer with VHL
我们的科学家团队拥有各种研究领域经验,包括生命科学、材料科学、化学合成、色谱、分析及许多其他领域.
联系技术服务部门