Bay11-7082 / InvivoGen, Bayer - LARVOL DELTA

Integrated multi-omics study identifies ursolic acid as a novel therapeutic agent targeting the TNF-α/TAK1/IKKβ/NF-κB axis in hepatic sinusoidal obstruction syndrome (ASH 2025) - "The busulfan-cyclophosphamide (BUCY)conditioning regimen induces endothelial injury, thereby initiating a thromboinflammatory cascade.While TNF-α/NF-κB signaling is implicated in this process, its precise role and therapeutic targeting in SOSremain undefined...In vitro: Primary rat HSECswere treated with BUCY ± UA, NF-κB was overexpressed (OE-p65 plasmid) or inhibited (BAY 11-7082).Apoptosis (Annexin V/PI flow cytometry), ROS (DCFH-DA), mRNA (qPCR), and protein (WB) levels of TNF-α/NF-κB pathway components and antioxidants were measured...MD simulations revealed stable binding of BUCYmetabolites (e.g., acrolein, ΔG=-8.2 kcal/mol) and UA to TNF-α (Tyr59/Trp107, ΔG=-9.3 kcal/mol)... TNF-α/NF-κB signaling critically drives BUCY-induced HSEC injury and SOS. UA, a first-in-classnatural TNF-α inhibitor, binds TNF-α with high affinity, thereby blocking downstream TAK1/IKKβ/NF-κBactivation. This mechanism suppresses endothelial inflammation, oxidative stress, and..."

IO biomarker • Bone Marrow Transplantation • Hepatology • Inflammation • ANXA5 • BAX • BCL2 • CASP3 • FASLG • ICAM1 • IL1B • IL6 • MMP9 • NFKBIA • RELA • TNFA • VCAM1

Oncolytic Reovirus-Induced Prostaglandin E2 Production in Human Tumor Cells. (PubMed, Biol Pharm Bull) - "A nuclear factor-kappa B (NF-κB) inhibitor, BAY11-7082, and a cyclooxygenase 2 (COX2) inhibitor, celecoxib, significantly inhibited PGE2 secretion, indicating that NF-κB and COX2 played a crucial role in reovirus-induced PGE2 production. These results indicate that reovirus replication in tumor cells is important for reovirus-induced PGE2 production. Attention should be paid to possible PGE2 production in tumors following reovirus treatment."

Journal • Oncology • CTSS

SUN5 interacts with TRIM28, enhancing IκBα ubiquitination to promote glycolysis in colorectal cancer cells. (PubMed, Acta Biochim Biophys Sin (Shanghai)) - "Mechanistically, SUN5 activates the NF-κB signaling pathway, which can be inhibited by the IKK inhibitor BAY11-7082...Moreover, xenograft transplantation experiments reveal that the knockdown of SUN5 inhibits glycolysis and tumorigenesis in vivo. Taken together, these findings indicate that SUN5 enhances the glycolysis and tumorigenesis of CRC cells via interaction with TRIM28, which provides a potential target for the diagnosis and treatment of CRC."

Journal • Colorectal Cancer • Oncology • Solid Tumor • Targeted Protein Degradation • Transplantation • LDHA • NFKBIA • SLC2A1 • SUN5 • TRIM28

Parthenolide Restores Testosterone Biosynthesis After Nanoplastic Exposure by Blocking ROS-Driven NF-κB Nuclear Translocation. (PubMed, Antioxidants (Basel)) - "In TM3 cells, PS-NPs suppressed testosterone synthesis in a concentration-dependent manner; this effect was fully reversed by pretreatment with N-acetylcysteine (NAC) or Bay 11-7082. Collectively, these data indicate that PS-NPs disrupt testosterone biosynthesis in immature testes through the ROS/NF-κB/p65-SF-1 axis, while PTL emerges as a candidate small molecule to counter nanoplastic-associated reproductive toxicity. These findings underscore translational relevance and support future evaluation under chronic low-dose exposure conditions, including in vivo validation of PTL efficacy, pharmacokinetics, and safety."

Journal

Aspirin Attenuates the Pathogenesis of Amyotrophic Lateral Sclerosis by Inhibiting the Activities of Microglia in a NF-κB-dependent Complement System-deactivating Mechanism. (PubMed, Mol Neurobiol) - "Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease, which is pathologically characterized by impairing the motor neurons, leading to the disorders of motor function. More importantly, Terminal complement complex (TCC) was identified to be the critical component of CS for mediating the effects of SOD1G93A protein or LPS on inducing the apoptosis of neurons, which was inhibited by the ASP or Bay 11-7082. On the basis of these observations, our findings novelly revealed that ASP delayed the progression of ALS via inhibiting the activities of microglia in a NF-κB-dependent CS-deactivating mechanisms."

Journal • Amyotrophic Lateral Sclerosis • CNS Disorders • C1QB

Inhibition of interleukin-1 receptor-associated kinase (IRAK)-4 provides partial rescue of interleukin-1 beta induced functional and gene expression changes in equine tenocytes. (PubMed, Mol Biol Rep) - "Together, this data demonstrates that IL-1β has a broad mechanism of action on tendon cells which cannot be fully mediated by targeting specific parts of the signalling pathway."

Journal • Inflammation • ENPP2 • IL1B • IL1RN • IL6 • IRAK1 • MYD88

Tetramethoxyluteolin, an active constituent in mulberry leaves, promotes osteogenesis of jaw bone marrow mesenchymal stem cells in periodontitis microenvironment via NF-κB inhibition. (PubMed, Arch Oral Biol) - "TML reduces periodontal inflammation and enhances the osteogenic potential of JBMMSCs by inhibiting the NF-κB pathway, providing a novel strategy for periodontitis-related bone regeneration."

Journal • Dental Disorders • Inflammation • Osteoporosis • Periodontitis • IL1B • IL6 • TNFA

Tsugaforrestolide, an Anti-Inflammatory Bisabolane-Type Sesquiterpene Lactone From the Vulnerable Conifer Tsuga forrestii. (PubMed, Chem Biodivers) - "As the first sesquiterpenoid isolated from hemlock species, 1 exhibited pronounced anti-inflammatory activity, effectively inhibiting LPS-induced nitric oxide (NO) production in RAW 264.7 macrophages, with an IC50 value of 7.1 µM, comparable to the known inhibitor BAY11-7082 (IC50 = 8.7 µM). This finding further highlights the importance of conserving and sustainably utilizing this endangered plant species."

Journal

Sublingual immunotherapy suppresses Th2-type immune response in the allergic rhinitis mouse model by inhibiting the activation of the NFκB pathway. (PubMed, Immunotherapy) - "The NFκB inhibitor BAY11-7082 amplified SLIT's therapeutic effects, further suppressing Th2 responses...Collectively, we demonstrated that SLIT inhibits NFκB pathway activation, thereby suppressing the Th2-type immune response and alleviating AR progression. These findings provide new insights into the mechanism of SLIT in the treatment of AR."

Journal • Preclinical • Allergic Rhinitis • Eosinophilia • Immunology • Inflammation • IFNG • IL4 • IL5 • NFKBIA

Cigarette Smoke Extract Induces Inflammation by RELMβ via NF-κB/p65 Signaling in Chronic Obstructive Pulmonary Disease. (PubMed, Ann Clin Lab Sci) - "CSE induces inflammation via RELMβ through NF-κB/p65 signaling pathway in COPD. This study provides new insights into the involvement of CSE in the progression of COPD from the perspective of RELMβ."

Journal • Chronic Obstructive Pulmonary Disease • Immunology • Inflammation • Pulmonary Disease • Respiratory Diseases • CXCL8 • IL1B • IL6 • NFKBIA • RELA • RETN • TNFA

Aloperine Protects Against Cisplatin-Induced Injury in Kidney Cells Via Modulating PI3K/AKT/Nfκb-Mediated NLRP3 Inflammasome. (PubMed, Protein Pept Lett) - "These results suggest that ALO protects against CDDP-induced injury in kidney cells by modulating the PI3K/AKT/NFκB-mediated NLRP3 inflammasome."

Journal • NLRP3

The RPE-derived NF-κB/HO-1/MCP-1 pathway mediated Microglia Recruitment Involved in the Outer Blood-Retinal Barrier Breakdown in Experimental Diabetic Retinopathy. (PubMed, Exp Cell Res) - "Under diabetic condition, microglia are recruited by RPE cells via the NF-κB/HO-1/MCP-1 pathway, which subsequently result in the oBRB breakdown. This study provides a novel mechanistic insight for the interaction between microglia and RPE cells, and implies a potential therapeutic strategy for the treatment of DR."

Journal • Diabetes • Diabetic Retinopathy • Retinal Disorders • OCLN • TJP1

Cardioprotective Effect and Mechanism of Panaxadiol Saponin Component in Radiation-Induced Heart Disease in Mice. (PubMed, Chin J Integr Med) - "PDS-C showed cardioprotective effect in alleviating inflammation and fibrosis through inhibition of the NF-κB signaling pathway."

Journal • Preclinical • Cardiovascular • Fibrosis • Heart Failure • Immunology • Inflammation • CTGF • IL6 • SMAD2

Effects of NF-κB Inhibition on Chronic Airway Epithelial Inflammation and Cell Migration (OGP-OGTC 2025) - "NF-kB inhibition by BAY11-7082 suppresses airway epithelial inflammatory responses, mucus hypersecre tion, and cell migration in vitro. Targeting NF-kB signaling may represent a promising therapeutic approach, reducing both inflammation and aberrant epithelial remodeling."

Asthma • Immunology • Inflammation • Respiratory Diseases • IL4 • IL6 • MUC4 • MUC5AC

Estrogen Alleviates Myocardial Ischemia-Reperfusion Injury by Inhibiting NLRP3 Inflammasome-Mediated Pyroptosis. (PubMed, Cardiol Res Pract) - "Conversely, coadministration of the estrogen receptor antagonist ICI 182780 reversed the protective effects of E2. Additionally, treatment with the NLRP3 inhibitor Bay11-7082 and the Caspase-1 inhibitor AC-YVAD-CMK also attenuated pyroptosis. Collectively, these results suggest that estrogen may alleviate myocardial I/R injury by inhibiting pyroptosis through the ER/TXNIP/NLRP3/Caspase-1 pathway, offering insights into potential therapeutic strategies for cardiac ischemic injury."

Journal • Cardiovascular • Inflammation • Myocardial Ischemia • Reperfusion Injury • IL1B • NLRP3 • TXNIP

HEPATOCYTE-SPECIFIC HAF DEFICIENCY PROMOTES LIPID DYSREGULATION THROUGH MAPK PATHWAY ACTIVATION IN A MURINE MODEL OF MASH-HCC (AASLD 2025) - "To assess the involvement of NF-κB in these signaling events, hepatocytes were treated with the inhibitor BAY11-7082, and subsequent p38/JNK activation was analyzed... Our findings reveal that hepatocyte-specific HAF deficiency induces non-canonical activation of p38 and JNK, contributing to lipid dysregulation through FGF21 resistance, impaired autophagy, and LDLR suppression. These mechanisms may play a role in lean-MASH pathogenesis."

Preclinical • Hepatocellular Cancer • Hepatology • Liver Cancer • Metabolic Disorders • Metabolic Dysfunction-Associated Steatohepatitis • Metabolic Dysfunction-Associated Steatotic Liver Disease • Solid Tumor • FGF21 • LDLR • MAP1LC3A • TNFA

Peripheral nerve injury-induced remodeling of the tumor-associated macrophages promotes immune evasion in breast cancer. (PubMed, J Exp Clin Cancer Res) - "These findings underscore the critical role of peripheral nerve injury in reshaping the interplay between TAMs and antitumor immunity, via NFL-driven NF-κB activation and T cell dysfunction. Suggesting that neuroprotection could serve as a promising strategy to restore anticancer immunosurveillance."

Journal • Breast Cancer • Oncology • Solid Tumor • CD8 • NEFL

Inflammatory reprogramming of human brain endothelial cells compromises blood-brain barrier integrity in Alzheimer's disease. (PubMed, bioRxiv) - "In our perfusable iPSC-derived BBB-Chip that recapitulates human BBB signatures, single-cell profiling reveals inflammatory endothelial state-specific programs reflecting those in AD brains and demonstrates that BAY11-7082 suppresses cytokine-triggered dysfunction and reverses inflammation-associated gene activation. Together, these findings position cerebrovascular inflammation as a therapeutic target to preserve BBB integrity in AD."

Journal • Alzheimer's Disease • CNS Disorders • Inflammation

Periodontitis-induced Systemic Multi-organ Aging Mediated by the NF-κB Signalling Pathway. (PubMed, Chin J Dent Res) - "This study provides direct experimental evidence that periodontitis can promote systemic multi-organ aging via activation of the NF-κB signalling pathway, establishing a theoretical basis for developing therapeutic interventions."

Journal • Dental Disorders • Periodontitis • CDKN1A • CDKN2A • IL1B • IL6 • MMP13

Trimethylamine-N-oxide damages astrocytes and lymphatic endothelial cells in the cerebral lymphatic system. (PubMed, IBRO Neurosci Rep) - "However, NF-κ B signaling pathway inhibitor BAY11-7082 improved the above indicators. Animal studies revealed that TMAO induced intracranial inflammation, affected the expression of functional proteins in the cerebral lymphatic system, and intensified SNCA aggregation in the mouse brain. TMAO can activate the NF-κB signaling pathway and damage the cellular function of brain glymphatic system and meningeal lymphatic vessels, and promote intracranial inflammation and SNCA deposition in mice, which may be a potential mechanism for TMAO involvement in neurodegenerative diseases."

Journal • Alzheimer's Disease • CNS Disorders • Movement Disorders • Oncology • Parkinson's Disease • AQP4 • CLDN5 • FAP • GFAP • IL1B • IL6 • NLRC5 • NLRP3 • OCLN • SNCA • TNFA

Ginkgolide B Alleviates LPS-Induced Inhibition of Osteogenic Differentiation in Human Periodontal Ligament Stem Cells by Suppressing the p-IκBα/NF-κB Pathway. (PubMed, Drug Des Devel Ther) - "To verify the role of the NF-κB (nuclear factor kappa-B) pathway in this mechanism, the expression level of NF-κB pathway-related protein was detected by Western blot analysis after using BAY-11-7082 (a NF-κB signaling pathway inhibitor)...In vivo, GB mitigated alveolar bone loss and inflammatory tissue destruction in periodontitis rats. GB can mitigate periodontitis by blocking the NF-κB pathway, offering dual anti-inflammatory and bone-protective effects."

Journal • Dental Disorders • Inflammation • Osteoporosis • Periodontitis • NFKBIA

Neuroinflammatory crosstalk between microglia and astrocytes increases viral replication in an iPSC-derived model of CNS HIV infection. (PubMed, bioRxiv) - "Addition of exogenous TNFα to iMg during HIV infection is also sufficient to increase rates of replication, and neutralization of TNFα via adalimumab/Humira treatment in iMg/iAst cocultures reduces replication. Blocking NF-kB signaling with iKK inhibitor Bay-11-7082 (Bay-11) demonstrates that increased HIV replication in iMg/iAst cocultures is due to increased NF-kB activity. Finally, we show that in HIV-infected iMg there is movement of lysosomes to the periphery of the cell membrane and release of lysosomal content into the extracellular space, suggesting that this dysregulated lysosomal flux could further contribute to the pro-inflammatory microenvironment. We propose that this altered lysosomal trafficking and increased cytokine production drives a pro-inflammatory phenotype in glia and represents a potential source of unresolved neuroinflammation in people living with HIV."

Journal • Alzheimer's Disease • Cognitive Disorders • Human Immunodeficiency Virus • Infectious Disease • Inflammation • TNFA

Cross-linked genes analysis of programmed cell death and network pharmacological validation after spinal cord injury. (PubMed, Biochem Biophys Res Commun) - "This study unveiled cross-linked genes and miRNA‒mRNA networks critical to PCD in SCI through integrative bioinformatics analyses. Furthermore, it identified BAY 11-7082 as a promising therapeutic agent for modulating PCD, offering a novel strategy for spinal cord injury repair."

Journal • CNS Disorders • Orthopedics

Protective effects of paederoside in rotenone-induced cellular models of Parkinson's disease. (PubMed, Front Cell Dev Biol) - "When the nuclear factor-κB (NF-κB) inhibitor BAY11-7082 was added 2 h before rotenone exposure, no statistically significant difference in NO levels was observed between the paederoside-treated and untreated groups...Furthermore, pretreatment with 10 μM paederoside markedly enhanced cell viability in rotenone-treated N2A cells. In summary, these findings demonstrate the neuroprotective potential of paederoside through modulation of the NF-κB/NOS/NO/nitrated α-Syn nitration signaling pathway."

Journal • CNS Disorders • Movement Disorders • Parkinson's Disease

DNA hypomethylated modified lncRNA MALAT1 promotes atherosclerotic cardiovascular disease progression through NF-κB signaling pathway regulating cholesterol metabolism and inflammatory response. (PubMed, Biochem Biophys Rep) - "Notably, when NF-κB was inhibited (BAY11-7082) alongside MALAT1 overexpression, the reversal effect was abolished. Taken together, our findings suggest that decreased DNA hypomethylation mediated by DNMT1 leads to increased MALAT1 expression, subsequently activating the NF-κB pathway in ASCVD."

Journal • Atherosclerosis • Cardiovascular • Dyslipidemia • Inflammation • Lung Adenocarcinoma • Lung Cancer • Non Small Cell Lung Cancer • Oncology • Solid Tumor • APOE • DNMT1 • MALAT1