Bay11-7082 / InvivoGen, Bayer - LARVOL DELTA

Kaempferol alleviates ferroptosis in melanocytes via NF-?B-mediated downregulation of PTGS2 (AAD 2026) - " Primary human melanocytes were exposed to RSL3 to induce ferroptosis, with kaempferol or ferrostatin-1 administered as protective agents...Validation of NF-κB/PTGS2 signaling was performed by qPCR, Western blotting, and p65 nuclear translocation assays; pharmacological inhibition with Bay11-7082 was used to substantiate causality... Kaempferol exerts a robust cytoprotective effect against melanocyte ferroptosis through suppression of the NF-κB-driven PTGS2 axis and downstream arachidonic acid/prostaglandin signaling. These findings establish NF-κB/PTGS2 as a mechanistic hub and nominate kaempferol as a potential therapeutic candidate for vitiligo."

Immunology • Vitiligo • ANXA5 • IL7 • PACERR • PTGS2

Two-step mechanism of plexiform neurofibroma formation: Role of the NF-κB pathway in neurofibroma formation (AACR 2026) - "A two-step process to PNF formation is proposed, with Nf1 loss in Schwann cells an initiating step and the formation of an inflammatory microenvironment via activation of the NF-κB pathway and Schwann cell reprogramming as a second step. (Supported by DOD-HT9425-1-0435 (to NR and JS), NIH NS115438R01 (to DAL and NR) and a Children's Tumor Foundation Young Investigator Award to RR)"

Oncology • Solid Tumor • CD44 • IL1B • ITGA6 • ITK • NF1 • TNFA

Endoplasmic reticulum stress mediates oxidative stress-driven endothelial impairment and atherogenesis induced by sodium perfluorononenoxybenzene sulfonate exposure. (PubMed, Environ Res) - "Pharmacological inhibition with N-acetylcysteine (NAC, an antioxidant), 4-phenylbutyric acid (4-PBA, an ERS inhibitor), and BAY 11-7082 (an inhibitor for NF-κB signaling pathway) revealed a sequential pathogenic cascade, in which oxidative stress acts upstream to initiate ERS and compromise endothelial barrier function, leading to NF-κB activation, which drives inflammatory responses, monocyte adhesion, and impaired endothelial migration. Consistent with these findings, in vivo experiments in ApoE-/- mice showed that OBS exposure caused endothelial impairment, collagen deposition, and oxidative stress in aortic tissues, accompanied by upregulating the expression of ERS and inflammation-related markers. These findings suggest that ERS serves as a key mediator linking oxidative stress to inflammation in OBS-induced endothelial dysfunction, highlighting the potential cardiovascular hazards of OBS as an emerging PFOS alternative."

Journal • Atherosclerosis • Cardiovascular • Inflammation • APOE • ATF4

HIF-1-MEDIATED MACROPHAGE METABOLIC REPROGRAMMING PROMOTES AKI TO CKD TRANSITION (ISN-WCN 2026) - "Macrophage depletion was performed with clodronate liposomes. To investigate molecular mechanisms, myeloid-specific HIF-1α knockout mice and the NF-κB inhibitor BAY11-7082 were employed in vivo, while in vitro studies included co-culture of TECs and bone marrow–derived macrophages under prolonged hypoxia–reoxygenation. Glycolysis was modulated with 2-deoxy-D-glucose, and chromatin immunoprecipitation combined with database analysis was used to confirm transcriptional regulation of HIF-1α by NF-κB.Results Both I/RI and UUO models exhibited impaired recovery with tubular injury and interstitial fibrosis...The NF-κB–HIF-1α signaling axis governs this process and represents a critical pathogenic pathway in AKI to CKD transition. Targeting macrophage metabolism by disrupting NF-κB–HIF-1α signaling provides a promising therapeutic strategy to mitigate maladaptive repair and slow CKD progression following AKI."

Acute Kidney Injury • Cardiovascular • Chronic Kidney Disease • Fibrosis • Immunology • Nephrology • Reperfusion Injury • HIF1A • HK1 • IL1B • TNFA

NF-κB modulates ROS/JNK signaling to attenuate apoptosis in largemouth bass hepatocytes during recovery from heat stress. (PubMed, J Therm Biol) - "JNK inhibitor SP600125 had no effect on ROS accumulation, whereas the ROS inhibitor N-acetylcysteine significantly reduced JNK activation, suggesting that ROS is functionally associated with JNK activation in this context. Furthermore, inhibition of either JNK or ROS significantly suppressed NF-κB activation, whereas the NF-κB inhibitor BAY11-7082 led to increased ROS accumulation and JNK activation, indicating a possible compensatory mechanism...In contrast, NF-κB inhibition enhanced apoptosis. Collectively, our findings indicate that NF-κB may plays a protective role during HS recovery in fish by attenuating apoptosis through modulation of ROS/JNK signaling."

Journal • CASP3 • MAPK8

NLRP3 inflammasome as a therapeutic target in oral squamous cell carcinoma: implications for tumorigenesis and immunomodulation. (PubMed, Int Immunopharmacol) - "Emerging strategies to modulate NLRP3 include small-molecule inhibitors (e.g., MCC950, BAY-117082), plant-derived compounds (e.g., oridonin, Bacopa monnieri), and immunotherapy approaches, including intratumoral NLRP3 agonists combined with checkpoint blockade. This review synthesizes the multifaceted roles of NLRP3 in OSCC, highlighting its centrality in inflammation-driven tumor biology and its promise as a therapeutic target. Understanding the contextual duality of NLRP3 activation is critical for developing precision therapies that disrupt its tumor-supportive effects while preserving or enhancing its immunogenic functions."

Journal • Review • Immunology • Oncology • Oral Cancer • Squamous Cell Carcinoma • IL18 • IL1B • IL6 • MIR22 • NLRP3 • PRDX1

Cyanidin-3-O-glucoside chloride inhibits cartilage degeneration and inflammation in TMJOA via YAP/NF-κB signaling pathway. (PubMed, Food Funct) - "Pharmacological inhibitors of YAP (verteporfin) and NF-κB (BAY 11-7082) were applied to confirm pathway involvement. Moreover, intra-articular administration of C3G significantly downregulated MMP13 and IL-1β expression, enhanced COL2A1 expression, and increased cartilage thickness in vivo. Collectively, these findings indicate that C3G confers protection against TMJOA by inhibiting cartilage matrix degradation, promoting extracellular matrix deposition, and suppressing inflammation through blockade of the YAP/NF-κB signaling axis, thereby highlighting C3G as a promising therapeutic candidate for the management of TMJOA."

Journal • Immunology • Inflammation • Osteoarthritis • Pain • Rheumatology • COL2A1 • IL1B • MMP13 • SOX9

ETS1 potentiates pancreatic Pyroptosis in mice with acute pancreatitis by regulating the NKIRAS1/NF-κB Axis. (PubMed, Int Immunopharmacol) - "This study reveals that ETS1 transcriptionally suppresses NKIRAS1, activating NF-κB signaling and promoting pyroptosis and pancreatic injury in AP. Targeting ETS1 may represent a promising therapeutic strategy."

Journal • Preclinical • Inflammation • Oncology • Pancreatitis • ETS1

Glycoprotein non-metastatic melanoma protein B promotes pyroptosis of macrophages induced by homocysteine associated with the upregulation of the NOX-2/ NF-κB signaling pathway. (PubMed, Cell Signal) - "Importantly, the pro-pyroptotic effect of GPNMB overexpression in Hcy-treated THP-1-derived macrophages was counteracted by either inhibition of NADPH oxidase 2 (NOX2) using the specific inhibitor gp91ds-tat or blockade of NF-κB activation with the inhibitor BAY11-7082. Moreover, serum GPNMB levels were correlated with serum Hcy levels and lipid profiles in both healthy individuals and HHcy patients. Collectively, these findings demonstrate that GPNMB facilitates Hcy-induced macrophage pyroptosis associated with the upregulation of the NOX2/NF-κB signaling pathway, highlighting the potential relevance of GPNMB as a candidate target for the clinical management of HHcy-related atherosclerotic cardiovascular disease."

Journal • Atherosclerosis • Cardiovascular • Melanoma • Metabolic Disorders • Oncology • Solid Tumor • GPNMB

Transfer Factor Alleviates Bovine Mastitis and Protects Mammary Epithelial Barrier via the TAK1/NF-κB/MLCK Signaling Axis. (PubMed, J Anim Sci) - "It also mitigated LPS-induced changes via inhibiting the nuclear factor κB (NF-κB) pathway, similar to NF-κB inhibitor Bay 11-7082, and blocked NF-κB activation by inhibiting the transforming growth factor-β-activated kinase 1 (TAK1) pathway, comparable to TAK1 inhibitor Takinib. Our findings demonstrate that TF, by concurrently eliciting anti-inflammatory and barrier-repair effects via inhibition of the TAK1/NF-κB/MLCK axis, effectively alleviates bovine mastitis. This study furnishes a robust molecular framework for deploying TF as a non-antibiotic tool in the sustainable control of mastitis."

Journal • IL1B • IL6 • MYLK • NECTIN4 • OCLN • TJP1

PLS3-AS1 promotes colorectal cancer progression and radioresistance by sustaining NF-κB signaling. (PubMed, Biochem Biophys Res Commun) - "Inhibition of NF-κB with BAY 11-7082 suppressed PLS3-AS1 expression and reversed its pro-tumorigenic effects. These findings identify PLS3-AS1 as a critical mediator of NF-κB-driven radioresistance in CRC and a potential therapeutic target to improve radiotherapy efficacy."

Journal • Colorectal Cancer • Oncology • Solid Tumor • NFKBIA • PLS3

Phorbol Myristate Acetate Inhibits Senecavirus A Replication by Activating IKBKE-Mediated IFN Pathway and NF-κB Signal. (PubMed, Transbound Emerg Dis) - "However, the PMA-mediated detrimental effect on SVA is reversed in IKBKE-deficient cells or when the NF-κB pathway blocked by BAY-117082, implying that IKBKE is the target for the antiviral effect of PMA...Overall, our findings offer that PMA inhibits SVA replication by activating IKBKE-mediated IFN pathway and NF-κB signal. And it might be a promising candidate for further broad-spectrum therapeutic development."

Journal • Cardiovascular • CNS Disorders • Infectious Disease • Respiratory Diseases • IKBKE

Canonical and noncanonical NF-κB signaling in uveal melanoma: mechanisms, microenvironment, and therapeutic modulation. (PubMed, Med Hypothesis Discov Innov Ophthalmol) - "Canonical NF-κB signaling is mechanistically related to UM cell survival, proliferation, and migration, as shown by pharmacologic inhibition like BAY11-7082, and niclosamide and genetic modulation like microRNA-9. NF-κB signaling, particularly the canonical branch, is required for UM malignancy, while noncanonical signaling is linked with high-risk features. Branch-specific genetic manipulations and clinically relevant models should be employed in future research to maximize therapeutic strategies."

Journal • Review • Eye Cancer • Melanoma • Ocular Melanoma • Oncology • Solid Tumor • Targeted Protein Degradation • Uveal Melanoma • BAP1 • TNFA

Activation of NF-κB signaling pathway in GSDME-low esophageal squamous cell carcinoma cells enhances radioresistance. (PubMed, J Transl Med) - "GSDME functions as a tumor suppressor by enhancing radiosensitivity and inhibiting proliferation and migration in ESCC, through the suppression of the NF-κB signaling pathway. These findings nominate GSDME as a promising biomarker and the NF-κB signaling pathway as a therapeutic target for overcoming radioresistance in ESCC."

IO biomarker • Journal • Esophageal Squamous Cell Carcinoma • Oncology • Squamous Cell Carcinoma • GSDME • SLAMF7 • TNFA • TRAF6

Disruption of goat airway epithelial barrier function by caprine parainfluenza virus type 3 infection in an ALI model. (PubMed, Vet Microbiol) - "Treatment with the NF-κB inhibitor BAY 11-7082 partially restored the expression of TJ proteins and proinflammatory cytokines. Collectively, the activation of the NF-κB pathway and subsequent production of proinflammatory cytokines is responsible for CPIV3-induced TJ disruption. In addition, the developed ALI-GAECs model provides a valuable in vitro tool for investigating the pathogenesis of CPIV3 and other caprine respiratory pathogens."

Journal • Infectious Disease • Respiratory Diseases • CLDN1 • IL1B • IL4 • IL6 • OCLN • TJP1 • TNFA

AQP3-mediated H₂O₂ Transport Drives Macrophage M1 Polarization and Cervical Matrix Remodeling in Cervical Insufficiency†. (PubMed, Biol Reprod) - "Both H₂O₂ scavenging with PEG-catalase and NF-κB inhibition with Bay 11-7082 prevented macrophage-mediated matrix degradation. These findings suggest that AQP3 may serve as an important mediator linking oxidative stress to inflammatory cervical remodeling through facilitation of H₂O₂ influx, NF-κB activation, and M1 macrophage polarization. Targeting AQP3 or its downstream signaling may represent a potential therapeutic approach that requires preclinical validation to prevent CI-associated pregnancy complications."

Journal • AQP3 • CAT • MMP9

Tumor-Associated Macrophage-Derived CXCL1 Promotes Endometrial Cancer Progression Through the CXCR2/NF-κB Pathway. (PubMed, Cancer Sci) - "This mechanism can be effectively inhibited by silencing CXCR2 or by employing the NF-κB inhibitor BAY 11-7082...Additionally, in EC tissue samples, CXCL1 and CXCR2 expression, as well as the extent of macrophage infiltration, exhibited a significant positive relationship with disease progression, suggesting an unfavorable prognosis. In conclusion, targeting the CXCL1/CXCR2 axis is a potential therapeutic approach for EC treatment."

Journal • Endometrial Cancer • Oncology • Solid Tumor • CXCL1 • CXCR2

Overexpression of TFPI-2 Suppresses Colorectal Cancer Progression by Inducing Ferroptosis via NF-κB Signaling. (PubMed, J Biochem Mol Toxicol) - "To investigate the involvement of the NF-κB signaling pathway, HCT116 cells were treated with the NF-κB inhibitor Bay 11-7082...Mechanistically, TFPI-2 knockdown inhibited ferroptosis by promoting NF-κB pathway activity. This study reveals that TFPI-2 suppresses CRC progression by inducing ferroptosis through NF-κB signaling, providing new insights for future CRC therapy."

Journal • Colorectal Cancer • Oncology • Solid Tumor • AIFM2 • GPX4 • NFKBIA • TFRC

Basic Science and Pathogenesis. (PubMed, Alzheimers Dement) - "Ghrelin binds to its receptor GHSR-1a and inhibits the activation of NF-κB, thereby inhibiting the expression of BACE1, reducing Aβ deposition, attenuating oxidative stress, and improving the learning and memory ability of diabetic rats."

Journal • Diabetes • Metabolic Disorders • BACE1 • NFKBIA

Excessive lipolysis and inflammatory response in adipose tissue are associated with elevated serum growth hormone in dairy cows with clinical ketosis. (PubMed, J Dairy Sci) - "Differentiated adipocytes were used for (1) treatment with 0, 5, 10, or 15 ng/mL of GH for 8 h, or 15 ng/mL of GH for 0, 4, 8 or 12 h; (2) co-treatment with 15 ng/mL GH and 0.1 ng/mL tumor necrosis factor α (TNF-α); (3) pretreatment with 10 μM BAY 11-7082, a nuclear factor kappa B (NF-κB) inhibitor, and then treatment with 15 ng/mL GH...Furthermore, TNF-α exacerbated GH-induced lipolysis and inflammation, whereas inhibition of NF-κB signaling pathway partially reverses these metabolic alterations of GH-treated adipocytes. These findings suggested that GH promote lipolysis in bovine adipocytes by activating inflammatory pathways."

Journal • Inflammation • Oncology • DFFA • IL18 • IL1B • NFKBIA • NLRP3 • TNFA

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