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TargetMol Star Molecule—BAY 11-7082 (Cat. No. T1902, CAS 19542-67-7), A Potent USP7 and USP21 Inhibitor for Ubiquitination Research
Background
BAY 11-7082 (T1902) is a potent inhibitor primarily recognized for its ability to block NF-κB signaling by preventing TNFα-induced phosphorylation of IκBα, with an IC50 of approximately 10 μM. This phosphorylation event is a critical step in the canonical NF-κB pathway, where IκBα phosphorylation by the IκB kinase (IKK) complex leads to its ubiquitination and subsequent proteasomal degradation, thereby releasing NF-κB dimers to translocate into the nucleus and activate transcription of genes involved in inflammation, apoptosis, and autophagy. By inhibiting IκBα phosphorylation, BAY 11-7082 effectively stabilizes IκBα, maintaining NF-κB in its inactive cytoplasmic form and thus suppressing downstream gene expression. Beyond its role in NF-κB inhibition, BAY 11-7082 also targets deubiquitinases (DUBs), specifically USP7 and USP21, with IC50 values of 0.19 μM and 0.96 μM respectively. These ubiquitin-specific proteases regulate protein stability and signaling by removing ubiquitin moieties from substrates, and their inhibition by BAY 11-7082 further modulates ubiquitin-dependent pathways, including those involved in apoptosis and autophagy. This dual activity positions BAY 11-7082 as a valuable tool in dissecting the crosstalk between ubiquitination and NF-κB signaling cascades. In research contexts, BAY 11-7082 is extensively utilized to investigate the molecular mechanisms underlying inflammatory responses, cell death, and autophagic processes by selectively disrupting NF-κB activation and ubiquitin-mediated regulation. Its ability to inhibit both IκBα phosphorylation and DUB activity allows researchers to explore the dynamic interplay between phosphorylation-dependent signaling and ubiquitin editing in cellular homeostasis and stress responses. Moreover, BAY 11-7082’s inhibition of E2-conjugating enzymes and IKK further underscores its multifaceted impact on the ubiquitin-proteasome system and kinase-driven signaling networks. Collectively, BAY 11-7082 serves as a critical biochemical probe for elucidating the regulation of apoptosis, autophagy, and inflammatory signaling pathways, providing insights into the molecular basis of these processes and facilitating the identification of novel therapeutic targets in basic and translational research settings[1,2].
Molecular Structure of BAY 11-7082
Literature review
2.1 C20orf27 Promotes Cell Growth and Proliferation of Colorectal Cancer via the TGFβR-TAK1-NFĸB Pathway
BAY 11-7082(T1902) functioned as an NFĸB pathway inhibitor in this study, demonstrating a pronounced effect on C20orf27 overexpressing colorectal cancer cells. Specifically, BAY 11-7082 suppressed NFĸB pathway activation, as evidenced by the decreased expression of key pathway proteins including p-IĸB, p-p65, CyclinD1, and Bcl-2. This inhibition resulted in a reduced growth viability of cells with C20orf27 overexpression starting from the third day of treatment. Additionally, BAY 11-7082 significantly curtailed the clonal proliferation ability of these cells. The drug also induced a cell cycle arrest indicated by an increased G1 phase percentage in HCT15-C20orf27 and DLD-1-C20orf27 cell lines. Importantly, BAY 11-7082 reversed the anti-apoptotic effect of C20orf27 in the presence of oxaliplatin treatment, leading to enhanced apoptosis after 72 hours. Together, these findings characterize BAY 11-7082 as an effective inhibitor that counteracts the growth-promoting and apoptosis-suppressing effects mediated by C20orf27 via NFĸB signaling in colorectal cancer cells.[3]
2.2 Spring Viremia of Carp Virus Infection Induces Carp IL-10 Expression, Both In Vitro and In Vivo
In this study, BAY 11-7082(T1902), identified as an NF-κB inhibitor, was used to investigate its effect on the expression of carp IL-10 induced by SVCV infection. The results demonstrated that BAY 11-7082 downregulated the upregulated carp IL-10 production that was triggered by SVCV infection. In addition to reducing IL-10 production, BAY 11-7082 inhibited the gene expressions of JAK2, JAK3, and TYK2, which are involved in SVCV-induced IL-10 signaling pathways. These findings indicate that BAY 11-7082 effectively suppressed the NF-κB signaling pathway, thereby hindering the production and regulatory gene expression associated with carp IL-10 in response to viral infection.[4]
2.3 Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression
In this study, BAY 11-7082(T1902) functioned as an inhibitor of the NF-κB signaling pathway in MC3T3-E1 cells undergoing osteogenic differentiation. Specifically, when cells were treated with recombinant MDK protein, there was an up-regulation of inflammatory cytokines IL-6 and IL-1β associated with activation of the NF-κB pathway. Pretreatment with 10 μM BAY 11-7082 partially suppressed the increased expression levels of IL-6 and IL-1β induced by MDK. These results demonstrate that BAY 11-7082(T1902) can mitigate MDK-induced inflammatory cytokine expression by inhibiting NF-κB signaling activity during osteoblast differentiation, thus exerting an inhibitory effect on the inflammatory response triggered in this cellular model.[5]
Reference
[1] 1. Pierce JW, Schoenleber R, Jesmok G, et al. Novel inhibitors of cytokine-induced IκBα phosphorylation and endothelial cell adhesion molecule expression show anti-inflammatory effects in vivo. J Biol Chem. 1997;272(34):21096-21103.
[2] 2. Colland F, Formstecher E, Jacq X, et al. Small-molecule inhibitor of USP7/HAUSP ubiquitin protease stabilizes and activates p53 in cells. Mol Cancer Ther. 2009;8(8):2286-2295.
[3] Gao J, Wang Y, Zhang W, Zhang J, Lu S, Meng K, et al.. C20orf27 Promotes Cell Growth and Proliferation of Colorectal Cancer via the TGFβR-TAK1-NFĸB Pathway. Cancers. 2020;12(2):336.
[4] Ouyang P, Tao Y, Wei W, Li Q, Liu S, Ren Y, et al.. Spring Viremia of Carp Virus Infection Induces Carp IL-10 Expression, Both In Vitro and In Vivo. Microorganisms. 2023;11(11):2812.
[5] Ruze X, Hu Y, Wang X, Lai H, Zhang R, Pan S, et al.. Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression. Genes & Diseases. 2026;13(3):101931.
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