| Identification | Back Directory | [Name]
BAY 11-7082 | [CAS]
19542-67-7 | [Synonyms]
BAY E
CS-608
100824
BAY 11-7082
BAY 11-7821
BAY 11-7082, >=98%
BAY11-7082/BAY117082
BAY11-7082,BAY 117821
BAY 11-7082 USP/EP/BP
(E)-3-tosylacrylonitrile
Bay 11-7821(BAY 11-7082)
(E)-3-(p-Toluenesulfonyl)acrylonitrile
(E)-3-(p-tolylsulfonyl)prop-2-enenitrile
BAY 11-7082 - CAS 19542-67-7 - Calbiochem
BAY11-7082;BAY11-7082;BAY 11-7082;BAY117082
(E)-3-(4-METHYLPHENYLSULFONYL)-2-PROPENENITRILE
(e)-3-(4-methylphenyl)sulfonylprop-2-enenitrile
(2E)-3-[(4-METHYLPHENYL)SULFONYL]-2-PROPENENITRILE
BAY11-7082 (E)-3-(p-Toluenesulfonyl)acrylonitrile
(2E)-3-[(4-Methylbenzene)sulfonyl]prop-2-enenitrile
2-Propenenitrile, 3-[(4-methylphenyl)sulfonyl]-, (2E)-
Bay 11-7821 (2E)-3-[(4-Methylphenyl)sulfonyl]-2-propenenitrile | [Molecular Formula]
C10H9NO2S | [MDL Number]
MFCD00712162 | [MOL File]
19542-67-7.mol | [Molecular Weight]
207.25 |
| Chemical Properties | Back Directory | [Melting point ]
133-135℃ | [Boiling point ]
397.6±42.0 °C(Predicted) | [density ]
1.237±0.06 g/cm3(Predicted) | [storage temp. ]
Store at +4°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. |
| Hazard Information | Back Directory | [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]
Inhibitor of cytokine induced IκBα phosphorylation resulting thereby in a decreased expression of NF-κB and adhesion molecules. Potential anti-inflammatory agent. | [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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