BAY 11-7082 Chemical Properties

Melting point:

133-135℃

Boiling point:

397.6±42.0 °C(Predicted)

Density 

1.237±0.06 g/cm3(Predicted)

storage temp. 

Keep in dark place,Inert atmosphere,2-8°C

solubility 

DMSO: 25 mg/mL, soluble

form 

solid

color 

white

Stability:

Stable for 1 year from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20° for up to 3 months.

Safety Information

WGK Germany 

3

RTECS 

UD1430000

HS Code 

2926907090

MSDS

• Language:English Provider:SigmaAldrich

BAY 11-7082 Usage And Synthesis

Description

BAY 11-7082 (19542-67-7)?inhibits cytokine-induced IκB-α phosphorylation via inhibition of IκB Kinase which results in inhibition of NFκB .1 Inhibits anchorage-independent growth of mammary epithelial cells induced with 4-hydroxyestradiol via inhibition of NFκB activation.2 Inhibits IFNα production and blocks nuclear translocation of IRF7 in plasmacytoid dendritic cells.3? Facilitates wound healing by inhibiting TNFα-induced MMP expression.4 A useful tool for probing the involvement of NFκB in physiological and pathophysiological processes.5? Cell permeable.

Uses

Bay 11-7082 has been used as:

• a nuclear factor-kappa B (NF-kB) inhibitor to verify the action of the NF-kB signaling pathway in the production of interleukin (IL)-8
• a nuclear factor-kappa B (NF-kB) inhibitor to study the role of NF-kB activation in Mycoplasma hyorhinis -induced epithelial-mesenchymal transition (EMT) and cell migration
• a nod-like receptor family pyrin domain containing 3 (NLRP3) selective inhibitor to examine its effects on liver inflammation in mice after hematopoietic stem cell transplantation

Definition

ChEBI: A nitrile that is acrylonitrile in which the hydrogen located beta,trans to the cyano group is replaced by a tosyl group. It is an inhibitor of cytokine-induced IkappaB-alpha phosphorylation i cells.

General Description

Potential anti-inflammatory agent that selectively and irreversibly inhibits the TNF-α-inducible phosphorylation of IκBα (IC₅₀ = 10 μM), resulting in a decreased expression of NF-κB and of adhesion molecules. Does not affect constitutive IκBα autophosphorylation. Inhibits TNF-α-induced surface expression of the endothelial-leukocyte cell adhesion molecules E-selectin, VCAM-1, and ICAM-1. A 100 mM (10 mg/483 μl) solution of BAY 11-7082 (Cat. No. 196871) in DMSO is also available is also available.

Biological Activity

Irreversible inhibitor of TNF- α -stimulated I κ B α phosphorylation (IC 50 ~ 10 μ M); leads to decreased NF- κ B and subsequent decreased expression of adhesion molecules. Also reversibly activates MAP kinases and stimulates apoptosis.

Biochem/physiol Actions

Bay 11-7082 acts as a selective inhibitor for nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome pathway. In addition, to the inhibition of nuclear factor-kappa B (NF-kB), Bay 11-7082 also triggers apoptosis in anucleated erythrocytes, human T-cell leukemia virus type I (HTLV-I)-infected T-cell lines and primary adult T-cell leukemia cells.

Enzyme inhibitor

This protein kinase inhibitor (FW = 207.31 g/mol; CAS 19542-67-7; lmax = 251 nm), also named 3-[(4-methylphenyl)sulfonyl]-(2E)-propenenitrile, targets NF-κB activation, selectively and irreversibly blocking TNF-α- induced phosphorylation of IκB-α without affecting phosphorylation of constitutive IκB-α. Mechanism of Inhibitory Action: NF-κB transcription factor regulates expression of inflammatory cytokines, various chemokines and immunoreceptors, as well as cell adhesion molecules. When stationed within the cytoplasm, NF-κB is kept inactive through its binding to the inhibitory factor IκB; however, certain stimuli result in IκB phosphorylation and ubiquitin-mediated degradation, freeing NF-κB for translocation to the nucleus. In endothelial cells, IκB-α phosphorylation and degradation occur within 15 min of TNFα treatment, allowing NF-κB to translocate to the nucleus to activate gene expression. Treatment of humnan vascular endothelial cells (HUVEC) with TNFα results in rapid loss of IκB-α from the cytoplasm. BAY11-7082 stabilizes IκB-α in a dose-dependent manner (IC50 ≈ 10 μM). There is a clear correlation between the concentration of drug that stabilizes IκB-α, the concentration that inhibits nuclear levels of NF-κB, and the concentration that inhibits adhesion molecule expression. More recent studies demonstrate that BAY 11- 7082 prevents ubiquitin conjugation to Ubc13 and UbcH7 by forming a covalent adduct with their cysteine residues via Michael addition at the C-3 atom of BAY 11-7082, followed by the release of 4-methylbenzenesulfinate. BAY 11-7082 stimulated Lys48-linked polyubiquitin chain formation in cells and protected Hypoxia-Inducible Factor-1α (HIF1α) from proteasomal degradation, suggesting it inhibits the proteasome. These results indicate that the anti-inflammatory effects of BAY 11-7082, its ability to induce B-cell lymphoma and leukemic T-cell death and to prevent the recruitment of proteins to sites of DNA damage are exerted via inhibition of components of the ubiquitin system– not by inhibiting NF-κB. BAY11-7082 also inhibits proliferation and promotes apoptosis in breast carcinoma MCF-7 cells by inhibiting phosphorylation of ATP citrate lyase.

storage

+4°C

References

1) Pierce et al. (1997) Novel inhibitor of cytokine-induced IkBα phosphorylation and endothelial cell adhesion molecule expression show anti-inflammatory effects in vivo; J. Biol. Chem., 272 21096 2) Park et al. (2009) 4-hydroxyestradiol induces anchorage-independent growth of human mammary epithelial cells via activation of IkappaB kinase: potential role of reactive oxygen species; Cancer Res., 69 2416 3) Miyamoto et al. (2010) Inhibitor of IkappaB kinase activity, BAY 11-7082, interferes with interferon regulatory factor 7 nuclear translocation and type I interferon production by plasmacytoid dendritic cells; Arthritis Res. Ther., 12 R87 4) Xu et al. (2019) Bay 11-7082 facilitates wound healing by antagonizing mechanical injury – and TNF-α-induced expression of MMPs in posterior cruciate ligament; Connect. Tissue Res. 60 311 5) Kim et al. (2018) TNF-α induces human neural progenitor cell survival after oxygen-glucose deprivation by activating the NFκB pathway; Exp. Mol. Med., 50 14

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