Chemical Structure
BAY 11-7082 [19542-67-7]
AG-CR1-0013
Overview
- SupplierAdipoGen Life Sciences
- Product NameBAY 11-7082
- Delivery Days Customer10
- CAS Number19542-67-7
- CertificationResearch Use Only
- Estimated Purity>99%
- Molecular FormulaC10H9NO2S
- Molecular Weight207.3
- Scientific DescriptionChemical. CAS: 19542-67-7. Formula: C10H9NO2S. MW: 207.3. IkappaBalpha kinase inhibitor. NF-kappaB inhibitor. Potential anti-inflammatory agent. Apoptosis inducer. Inhibits the release of proinflammatory cytokines. NLRP3 inflammasome inhibitor. Reduces ATPase activity of the NLRP3 inflammasome. Inhibits platelet aggregation. - IkappaBalpha kinase inhibitor. NF-kappaB inhibitor. Potential anti-inflammatory agent. Apoptosis inducer. Inhibits the release of proinflammatory cytokines. NLRP3 inflammasome inhibitor. Reduces ATPase activity of the NLRP3 inflammasome. Inhibits platelet aggregation. RBR E3 ligase inhibitor. Effects by inactivating the E2-conjugating enzymes Ubc13 and UbcH7 and the E3 ligase LUBAC, preventing the formation of Lys63-linked and linear polyubiquitin chains.
- SMILESCC(C)(C)C1=CC=C(C=C1)S(=O)(=O)\C=C\C#N
- Storage Instruction-20°C,2°C to 8°C
- UNSPSC12352200
References
- Novel inhibitor of cytokine-induced IkBa phosphorylation and endothelial cell adhesion molecule expression show anti-inflammatory effects in vivo: J.W. Pierce, et al.; J. Biol. Chem. 272, 21096 (1997)
- Bay 11-7082 inhibits transcription factor NF-kappaB and induces apoptosis of HTLV-I-infected T-cell lines and primary adult T-cell leukemia cells: N. Mori, et al.; Blood 100, 1828 (2002)
- Sulfasalazine and BAY 11-7082 interfere with the nuclear factor-kappa B and I kappa B kinase pathway to regulate the release of proinflammatory cytokines from human adipose tissue and skeletal muscle in vitro: M. Lappas et al.; Endocrinology 146, 1491 (2005)
- Anti-inflammatory compounds parthenolide and Bay 11-7082 are direct inhibitors of the inflammasome: C. Juliana, et al.; J. Biol. Chem. 285, 9792 (2010)
- A noble function of BAY 11-7082: Inhibition of platelet aggregation mediated by an elevated cAMP-induced VASP, and decreased ERK2/JNK1 phosphorylations: H.S. Lee, et al.; Eur. J. Pharmacol. 627, 85 (2010)