Western blot analysis of extracts from HeLa cells, untreated (-) or treated with Human Tumor Necrosis Factor-α (hTNF-α) #8902 (20 ng/ml, 5 min; +) and Calyculin A #9902 (50 nM, 5 min; +) with or without pretreating the cells with BAY 11-7082 (5 μM, 1 hr; +), using Phospho-NF-κB p65 (Ser468) Antibody #3039 (upper), NF-κB p65 (D14E12) XP® Rabbit mAb #8242 (middle), and β-Actin (D6A8) Rabbit mAb #8457 (lower).
Chemical structure of BAY 11-7082.
BAY 11-7082 is supplied as a lyophilized powder. For a 20 mM stock, reconstitute 5 mg of powder in 1.2 ml of DMSO. Working concentrations and length of treatment can vary depending on the desired effect.
Store lyophilized at room temperature, desiccated. In lyophilized form, the chemical is stable for 24 months. Once in solution, store at -20ºC and use within 3 months to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.
|Molecular Weight||207.3 g/mol|
|Solubility||Soluble in DMSO at 25 mg/ml or ethanol at 15 mg/ml.|
BAY 11-7082 is a selective and irreversible inhibitor of cytokine-induced IκBα phosphorylation. Treatment with TNF-α leads to the activation of IκBα resulting in nuclear translocation of NF-κB where it regulates gene expression. Inhibition of IκBα phosphorylation leads to the inactivation of NF-κB (1). The effect that BAY 11-7082 has on proinflammatory cytokine production as it relates to the NF-κB/IκB kinase pathways makes it useful when studying inflammation (2). This compound inhibits IFN-α production and nuclear translocation of interferon regulatory factor 7 (IRF7) in human plasmacytoid dendritic cells, both important factors when studying immunotherapeutic strategies as they relate to autoimmune disorders (3). BAY 11-7082 inhibits TNF-α-induced surface expression of ICAM-1, VCAM-1, and E-Selectin in human endothelial cells with an IC50 value between 5–10 μM (1).