SML3370
BI605906
≥98% (HPLC)
别名:
3-Amino-4-(1,1-difluoro-propyl)-6-(4-methanesulfonyl-piperidin-1-yl)-thieno[2,3-b]pyridine-2-carboxylic acid amide, 3-Amino-4-(1,1-difluoropropyl)-6-[4-(methylsulfonyl)-1-piperidinyl]-thieno[2,3-b]pyridine-2-carboxamide, BI 605906, BI-605906
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About This Item
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质量水平
方案
≥98% (HPLC)
表单
powder
颜色
, White to very dark gray
溶解性
DMSO: 2 mg/mL, clear
储存温度
−20°C
SMILES字符串
CCC(F)(C1=C2C(SC(C(N)=O)=C2N)=NC(N3CCC(CC3)S(C)(=O)=O)=C1)F
InChI
1S/C17H22F2N4O3S2/c1-3-17(18,19)10-8-11(23-6-4-9(5-7-23)28(2,25)26)22-16-12(10)13(20)14(27-16)15(21)24/h8-9H,3-7,20H2,1-2H3,(H2,21,24)
InChI key
IYHHRZBKXXKDDY-UHFFFAOYSA-N
生化/生理作用
BI605906 is a selective, ATP-competitive IκB kinase β (IKK2, IKKβ, IKK-beta) inhibitor (IC50 = 380 nM, [ATP] = 0.1 mM) with no potency toward 100 other kinases, including IKKα, IKKε, TBK1, and IGF1R (IC50 ≥7.6 µM). BI605906 (10 µM) effectively blocks IKK-β-dependent phosphorylation of IKKε and TBK1 in IKKα-/- MEFs upon IL-1α (5 ng/mL) induction.
Sective, ATP-competitive IκB kinase β (IKK2, IKKβ, IKK-beta) inhibitor with no potency toward 100 other kinases, including IKKα, IKKε, TBK1, and IGF1R.
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
新产品
Amy R Cameron et al.
Circulation research, 119(5), 652-665 (2016-07-16)
The diabetes mellitus drug metformin is under investigation in cardiovascular disease, but the molecular mechanisms underlying possible benefits are poorly understood. Here, we have studied anti-inflammatory effects of the drug and their relationship to antihyperglycemic properties. In primary hepatocytes from
Kristopher Clark et al.
The Biochemical journal, 434(1), 93-104 (2010-12-09)
Members of the IKK {IκB [inhibitor of NF-κB (nuclear factor κB)] kinase} family play a central role in innate immunity by inducing NF-κB- and IRF [IFN (interferon) regulatory factor]-dependent gene transcription programmes required for the production of pro-inflammatory cytokines and
Raid B Nisr et al.
Cellular and molecular life sciences : CMLS, 76(24), 4887-4904 (2019-05-19)
Sustained nutrient (fuel) excess, as occurs during obesity and diabetes, has been linked to increased inflammation, impaired mitochondrial homeostasis, lipotoxicity, and insulin resistance in skeletal muscle. Precisely how mitochondrial dysfunction is initiated and whether it contributes to insulin resistance in
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