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Merck
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SML3370

Sigma-Aldrich

BI605906

≥98% (HPLC)

Sinónimos:

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

Fórmula empírica (notación de Hill):
C17H22F2N4O3S2
Número de CAS:
960293-88-3
Peso molecular:
432.51
MDL number:
MFCD22665698
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

100

assay

≥98% (HPLC)

form

powder

color

, White to very dark gray

solubility

DMSO: 2 mg/mL, clear

storage temp.

−20°C

SMILES string

CCC(F)(C1=C2C(SC(C(N)=O)=C2N)=NC(N3CCC(CC3)S(C)(=O)=O)=C1)F

Biochem/physiol Actions

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.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificados de análisis (COA)

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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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