Catalog No.S2913 Synonyms: BAY 11-7821
Molecular Weight(MW): 207.25
BAY 11-7082 is a NF-κB inhibitor, inhibits TNFα-induced IκBα phosphorylation with IC50 of 10 μM in tumor cells. Also inhibiting components of the ubiquitin system.
Cited by 9 Publications
6 Customer Reviews
The inhibition of IκBα phosphorylation by BAY11-7082 (10 µM) was confirmed using western blotting, and GAPDH was used as an internal reference.
Cancer Lett, 2016, 378(2):131-41. BAY 11-7082 purchased from Selleck.
Immunofluorescence images of Ishikawa cells showing the increase in the nuclear colocalization of ERa (red) and p65 (green) after E2 incubation. Nuclear colocalization is yellow. Treatment with ICI 182,780, PDTC or Bay inhibited the nuclear localization of both ERa and p65. Blue, DAPI-stained nuclei. All pictures were obtained the same day using the same microscope settings. Original magnification 3200, bar =50 um. Arrows, cytoplasmic ERa and p65 staining. ICI, ICI 182,780; Bay, Bay 11-7082.
Int J Cancer 2014 135(2), 282-94. BAY 11-7082 purchased from Selleck.
Shown are Western blot analysis of Wnt5a expression in HDPCs treated with TNF-a (n=3–4). The gene expression level was normalized to GAPDH (n = 3–6). HDPCs were preincubated with pyrrolidinedithiocarbamic acid (PDTC, an NF-κB inhibitor), BAY11-7082 (an NF-κB inhibitor), SP600125 (a JNK inhibitor), SB203580 (a p38 inhibitor), or U0126 (an ERK inhibitor) before treatment with TNF-a.
J Biol Chem 2014 289(30), 21028-21039. BAY 11-7082 purchased from Selleck.
The effect of vaspin on TNF α -induced THP-1 cell adhesion to HAECS measured staining with VibrantDiO® Cell-Labeling Solution. The level of THP-1 cell adhesion to HAECs was measured at 4 hr after treatment with 25 -100 ng/mL vaspin in the presence or absence of 10 ng/mL TNF α . BAY11-7082 (10 uM, S2913, Selleckchem, USA), an inhibitor of NF- κ B, was used as a positive control.
Cardiovasc Diabetol 2014 13, 41. BAY 11-7082 purchased from Selleck.
The irradiated Beas-2B cells were further co-cultured with U937 cells for 24 h after irradiation. In some experiments, Beas-2B cells were pretreated with 10 μM of U0126, SB203580, or necrostatin-1 for 1 h before irradiation, U937 cells were pretreated with 10 μM BAY 11-7082 1 h prior to cell co-culture, or 1 μg/ml anti-TNF-a antibody, 2 μg/ml anti-IL-8 antibody,40 nM SB225002 were added to the medium in the cell co-culture period. ***P < 0.001 compared with the non-irradiation control. #P < 0.05 ##P < 0.01 compared with cor-responding -irradiated cells.
Mutation Research, 2016, 789:1-8. BAY 11-7082 purchased from Selleck.
Reverse transcription-quantitative polymerase chain reaction assays revealed the effect of atorvastatin on visfatin-induced inflammation. Human coronary artery endothelial cells were incubated in the absence or presence of 50 ng/ml visfatin, with or without 50 nM FK866, 50 µM BAY11-0782 or 10 µM atorvastatin, for 24 h. (A) Atorvastatin downregulated visfatin-induced IL-6 gene expression (P-values from left to right vs. control: 0.0081, 0.0045, 0.0233 and 0.0057). (B) Atorvastatin decreased visfatin-induced IL-8 gene expression (P-values from left to right vs. control: 0.0096, 0.0037, 0.0043 and 0.0031). (C) Atorvastatin downregulated visfatin-induced IL-6 release (P-values from left to right vs. control: 0.0078, 0.0022, 0.0783 and 0.0382). (D) Atorvastatin inhibited visfatin-induced IL-8 release (P-values from left to right vs. control: 0.0094, 0.0032, 0.0039 and 0.0035). Significant differences were determined using Student's t-test; *P<0.05, **P<0.01 vs. visfatin control. IL-6, interleukin-6; IL-8, interleukin-8.
Oncol Lett, 2016, 12(2):1438-1444. BAY 11-7082 purchased from Selleck.
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Choose Selective IκB/IKK Inhibitors
|Description||BAY 11-7082 is a NF-κB inhibitor, inhibits TNFα-induced IκBα phosphorylation with IC50 of 10 μM in tumor cells. Also inhibiting components of the ubiquitin system.|
BAY 11-7082 completely and specifically abrogates NF-κB DNA binding, downregulating the NF-κB-inducible cytokine IL-6 and inducing apoptosis.  BAY 11-7082 (< 8 μM) is able to effectively inhibit both basal and TNFα stimulated NFκB luciferase activity in a dose dependent manner. BAY 11-7082 (8 μM) strongly inhibits the rate of proliferation in NCI-H1703 cells.  Bay 11-7082 (5 μM) rapidly and efficiently reduces the DNA binding of NF-kappaB in HTLV-I-infected T-cell lines and down-regulates the expression of the antiapoptotic gene, Bcl-x(L), whereas it has little effect on the DNA binding of another transcription factor, AP-1. Bay 11-7082-induced apoptosis of primary ATL cells is more prominent than that of normal peripheral blood mononuclear cells, and apoptosis of these cells is also associated with down-regulation of NF-kappaB activity. Bay 11-7082 (5 μM) selectively induces apoptosis of HTLV-I–infected T-cell lines associated with down-regulation of the expression of cyclin D1, cyclin D2, and Bcl-xL.  BAY 11-7082 (100 μM) prevents the nuclear translocation of p65 elicited by NMDA and the NMDA-induced increase of NF-κB binding in mouse hippocampal slices. BAY 11-7082 prevents NMDA toxicity occurring in CA1 region of hippocampal slices with 40% neuroprotection at 20 μM and 70% neuroprotection at 100 μM.  BAY 11-7082 at all concentrations tested significantly inhibits NF-κB p65 DNA-binding activity in adipose tissue, whereas in skeletal muscle, BAY 11-7082 at 50 μM and 100 μM significantly inhibits NF-κB p65 DNA-binding activity. BAY 11-7082 (100 μM) reduces IKK-β protein in human adipose tissue and skeletal muscle. BAY 11-7082 (100 μM) significantly decreases the release of TNF-α from adipose tissue, whereas the release of IL-6 and IL-8 is significantly inhibited at all concentrations of BAY 11-7082 tested. BAY 11-7082 (50 μM) significantly decreases the release of TNF-α, IL-6, and IL-8 in skeletal muscle.  BAY 11-7082 is also found to inactivate the E2-conjugating enzymes Ubc (ubiquitin conjugating) 13 and UbcH7 and the E3 ligase LUBAC (linear ubiquitin assembly complex), and thus induces B-cell lymphoma and leukaemic T-cell death. 
-  Melisi D, et al. Expert Opin Ther Targets, 2007, 11(2), 133-144.
-  Gastonguay A, et al. Cancer Biol Ther, 2012, 13(8), 647-656.
-  Miwatashi S, et al. J Med Chem, 2005, 48(19), 5966-5979.
|In vitro||DMSO||41 mg/mL (197.82 mM)|
|Ethanol||10 mg/mL (48.25 mM)|
|In vivo||Add solvents to the product individually and in order:
5% DMSO+corn oil
For best results, use promptly after mixing.
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