Bay11-7082
/ InvivoGen, Bayer
- LARVOL DELTA
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September 27, 2026
Fusobacteriumnucleatum-Stimulated OSCC Cell-Derived Exosomes Induce a Pro-Adhesive Phenotype in Lymphatic Endothelial Cells via the ROS/NF-κB/ICAM1 Axis.
(PubMed, Microorganisms)
- "N-acetyl-L-cysteine (NAC) attenuated Fn-Exo-induced ROS accumulation and NF-κB activation, and both NAC and the NF-κB inhibitor BAY 11-7082 reduced ICAM1 upregulation and partially attenuated the enhanced adhesion of OSCC cells to Fn-Exo-treated LECs. These pharmacological inhibition experiments support the involvement of ROS/NF-κB/ICAM1 signaling in the Fn-Exo-induced pro-adhesive phenotype. Collectively, these findings indicate that F. nucleatum is associated with increased exosome yield from OSCC cells and that Fn-Exo enhances the adhesive interaction between OSCC cells and LECs."
Journal • Oncology • Oral Cancer • Squamous Cell Carcinoma • ICAM1
September 23, 2026
ACOX1 downregulation contributes to macrophage M1 polarization and neutrophilic airway inflammation in asthma.
(PubMed, Int Immunopharmacol)
- "ACOX1 downregulation contributes to macrophage M1 polarization and neutrophilic airway inflammation through lipid accumulation-upregulated NF-κB signaling in asthma."
Journal • Asthma • Immunology • Inflammation • Pulmonary Disease • Respiratory Diseases • ACOX1 • IL1B
September 17, 2026
Cathelicidin LL-37 inhibits angiogenesis and migration in gastric cancer via inhibition of NF-κB/IL-6 signaling.
(PubMed, Histol Histopathol)
- "LL-37 inhibits angiogenesis, migration, and invasion in GC by suppressing the NF-κB/IL-6 signaling axis. This work provides a rationale for considering LL-37 as a potential therapeutic candidate."
Journal • Gastric Cancer • Oncology • Solid Tumor • IL6
September 12, 2026
Impact of extraction techniques on the structural features and immunomodulatory activity of polysaccharides from Cremastra appendiculata.
(PubMed, Int J Biol Macromol)
- "TAK-242 attenuated all three ACE-P-induced responses, C29 had no significant effect under the conditions tested, and BAY 11-7082 reduced NO and IL-6 but not TNF-α, supporting TLR4-associated activation and differential downstream regulation of these mediators. Exploratory across-fraction correlations suggested that higher activity co-occurred with higher carbohydrate content and lower molecular weight and O-acetylation, although UAE-P showed that low molecular weight alone was insufficient. These findings demonstrate extraction-dependent variation in CAP structure and macrophage-stimulatory activity and identify ACE-P as a candidate for further mechanistic and in vivo evaluation."
Journal • Oncology • IL6 • TLR4 • TNFA
September 11, 2026
Ribes fasciculatum Leaf Water Extract Enhances Macrophage Immune Responses via TLR4-Mediated JNK and NF-κB Activation in RAW264.7 Cells.
(PubMed, J Microbiol Biotechnol)
- "The immunostimulatory effects of RFL-DW20 were strongly inhibited by TAK-242, SP600125, and BAY 11-7082, suggesting the involvement of TLR4, JNK, and NF-κB signaling. Ethanol precipitation further enriched its NO-inducing activity. These findings suggest that RFL-DW20 activates macrophages through the TLR4/JNK/NF-κB signaling axis and may serve as a natural immune-stimulating material."
Journal • IL1B • IL6 • NFKBIA • PTGS2 • TLR4 • TNFA
September 09, 2026
The NET effect on NF- ?B–activation in CF epithelia and the impact of ETI
(NACFC 2026)
- "Elexacaftor/tezacaftor/ivacaftor (ETI) has been shown to reduce the concentrations of several inflammatory cytokines in the lungs of people with CF...Cells were pretreated with the NF- ?B inhibitor, BAY 11-7082 (2.5 ?M) for 24 hours prior to NET exposure... NETs drive proinflammatory cytokine production in CF airway epithelia through NF- ?B activation. Although baseline NF- ?B activation is not altered by the presence of ETI, the extent to which ETI modulates NETdriven cytokine secretion is the focus of our future studies."
Cystic Fibrosis • Genetic Disorders • Immunology • Pulmonary Disease • Respiratory Diseases • CXCL8
August 30, 2026
ε-Viniferin Attenuates LPS-Induced Inflammatory Activation in Canine Macrophages by Regulating NF-κB and MAPK Pathways.
(PubMed, Prev Nutr Food Sci)
- "BAY 11-7082, a pharmacological inhibitor of NF-κB activation, produced similar effects, suggesting that ε-viniferin exerts its anti-inflammatory action partly through the inhibition of the NF-κB pathway. Collectively, these findings demonstrated that ε-viniferin attenuates LPS-induced inflammatory responses in canine macrophages via the suppression of the NF-κB and MAPK signaling pathways, highlighting its potential as a nutraceutical for the management of chronic inflammatory conditions in companion animals."
Journal • Dermatitis • Dermatology • Gastrointestinal Disorder • Immunology • Inflammation • Oncology • Rheumatology • IL10 • IL1B • IL6 • MAPK8 • TNFA
August 28, 2026
NO-Responsive Oleanolic Acid Self-Assembled Micelles Co-Loaded with BAY 11-7082 for Synergistic Chondroprotection and Anti-Osteoarthritis Therapy.
(PubMed, Bioengineering (Basel))
- "At mRNA and protein levels, the supramolecular micelle formulation remarkably suppressed NF-κB p65 phosphorylation, downregulated cartilage-degrading ADAMTS5, and upregulated ACAN compared with free BAY or blank OA-Der. Collectively, this natural bioactive self-assembled NO-responsive delivery platform achieves synergistic anti-inflammatory and matrix-protective effects by precisely releasing drugs at NO-overexpressed osteoarthritis inflammatory sites and offers an in vitro design strategy for osteoarthritis responsive delivery systems."
Journal • Immunology • Inflammation • Osteoarthritis • Pain • Rheumatology • ACAN • ADAMTS5
August 26, 2026
Early-life oxidative stress programs persistent NFκB activation and neuroinflammation in autism spectrum disorder.
(PubMed, Front Immunol)
- "The mechanistic relationship between oxidative stress and NFκB signaling was investigated in prenatal valproic acid (VPA)-exposed mice using antioxidant intervention (N-acetylcysteine, NAC), NFκB inhibition (Bay 11-7082), pro-oxidant challenge, behavioral assays, and primary amygdala neuron models. NFκB primarily mediates inflammatory signaling, while oxidative stress likely contributes to ASD-related behaviors through additional downstream pathways. These findings highlight early redox modulation as a potential therapeutic strategy."
Journal • Autism Spectrum Disorder • CNS Disorders • Genetic Disorders • Inflammation
August 25, 2026
cGAS-STING Modulates the NF-κB Pathway to Influence the Occurrence of Ulcerative Colitis-Associated Colorectal Cancer.
(PubMed, Dig Dis Sci)
- "This study suggests that the cGAS-STING signaling pathway plays an important promoting role in the malignant transformation from UC to CAC by activating NF-κB signaling, providing experimental evidence for elucidating the pathogenesis of CAC."
Journal • Colorectal Cancer • Gastroenterology • Gastrointestinal Disorder • Immunology • Inflammation • Inflammatory Bowel Disease • Oncology • Solid Tumor • Ulcerative Colitis • CASP3 • CGAS • NFKBIA • STING
August 12, 2026
Photobiomodulation mitigates DAMP signaling to improve odontoblast survival.
(PubMed, Arch Oral Biol)
- "PBM treatments evoked context-dependent, wavelength-specific odontoblast survival that could guide precision clinical protocols for pulp-dentin regeneration."
Journal • Infectious Disease • Inflammation • BCL2 • CASP3 • TGFB1 • TNFA
August 12, 2026
LCN2 knockout protects endothelial barrier function in mice with sepsis-induced acute lung injury by regulating the NF-κB signaling pathway
(PubMed, Nan Fang Yi Ke Da Xue Xue Bao)
- "LCN2 knockout alleviates sepsis-induced ALI and vascular endothelial dysfunction in mice by inhibiting NF-κB signaling."
Journal • Preclinical • Acute Lung Injury • Infectious Disease • Inflammation • Respiratory Diseases • Septic Shock • CD31 • CDH5 • ICAM1 • IL6 • LCN2 • PECAM1 • RELA • TNFA • VCAM1
July 22, 2026
BIRC3 activates NF-κB to drive TNF-α-induced endothelial dysfunction in atherosclerosis.
(PubMed, Biochem Biophys Res Commun)
- "Importantly, the deleterious effects of BIRC3 overexpression were largely reversed by co-treatment with the NF-κB inhibitor BAY 11-7082, indicating that BIRC3 drives TNF-α-mediated endothelial dysfunction in a strictly NF-κB-dependent manner. Collectively, our results identify BIRC3 as a positive regulator of TNF-α-induced endothelial injury and suggest that targeting BIRC3 may offer a novel avenue for alleviating endothelial dysfunction and hindering atherosclerotic progression."
IO biomarker • Journal • Atherosclerosis • Cardiovascular • BAX • BCL2 • BIRC3 • IL1B • IL6 • NFKBIA • TNFA • VCAM1
July 07, 2026
ANXA11 recruits tumor-associated neutrophils to promote the progression of colorectal cancer.
(PubMed, Int Immunopharmacol)
- "ANXA11 establishes a pro-tumorigenic positive feedback loop in the CRC microenvironment by regulating the NF-κB/CXCL5/CXCR2 signaling axis. Targeting the ANXA11/CXCR2 axis represents a potential therapeutic strategy for CRC intervention."
Journal • Colorectal Cancer • Oncology • Solid Tumor • ANXA1 • ANXA11 • CDH1 • CXCL5 • CXCR2 • MMP9
July 08, 2026
Interleukin-38 promotes alveolar bone repair in periodontitis by suppressing the nuclear factor kappa B pathway.
(PubMed, Stem Cell Res Ther)
- "Collectively, these findings suggest that IL-38 mitigates periodontitis progression by limiting inflammation and promoting osteogenic differentiation through NF-κB pathway inhibition, highlighting its potential as a therapeutic target in periodontal disease management."
Journal • Dental Disorders • Inflammation • Osteoporosis • Periodontitis • COL1A1 • IL10 • IL17A • IL1B • IL1F10 • IL23A • IL6 • RUNX2
May 25, 2026
Epigenetic memory in vascular smooth muscle cells drives increased tissue factor expression in abdominal aortic aneurysms
(ISTH 2026)
- "TF gene upregulation in response to hemin was abolished by the NF-kB inhibitor BAY 11-7082...This epigenetic response establishes a phenotypic memory following exposure to heme, driving increased TF expression and consequently heightening the prothrombotic profile of VSMCs. DOI*10.1016/j.rpth.2026.105284"
Cardiovascular • Hematological Disorders • Thrombosis • DNMT1 • HDAC3 • SUV39H1
June 19, 2026
Integrated network toxicology and transcriptomics reveal NF-κB signaling as a key mediator of TDCPP-induced inflammatory responses in human microglia.
(PubMed, Environ Int)
- "Pharmacological blockade using BAY 11-7082 and siRNA-mediated knockdown of p65 effectively reversed these pro-inflammatory alterations, establishing a causal link. Collectively, this study demonstrates that TDCPP disrupts microglial homeostasis by hijacking the NF-κB signaling axis. These findings indicate that TDCPP alters microglial immune homeostasis and triggers inflammatory responses, which may serve as a mechanistic link to OPFR-associated neurotoxicity, providing a potential target for mitigation."
Journal • CNS Disorders • Developmental Disorders • Inflammation • Psychiatry • IL10 • IL1B • IL6 • NFKBIA • PACERR • PTGS2
June 14, 2026
Rosavin alleviates COPD via inhibition of IL-17-enriched NET formation and NF-κB signaling.
(PubMed, Biol Direct)
- "Rosavin ameliorates COPD-associated pathology through integrated mechanisms involving NF-κB inhibition, reduction of IL-17-enriched NET formation, and modulation of lung microbiota composition. These findings identify Rosavin as a promising multi-target therapeutic candidate for COPD."
Journal • Chronic Obstructive Pulmonary Disease • Immunology • Inflammation • Pulmonary Disease • Respiratory Diseases • IL17A
June 11, 2026
The Deficiency of USP20 Alleviates Pressure Overload-Induced Cardiac Hypertrophy via the NF-κB Signaling Pathway.
(PubMed, FASEB J)
- "Mechanistically, USP20 elevated the phosphorylation level of P65, and the protective effect of USP20 knockdown against AngII-induced cellular hypertrophy was further enhanced by co-treatment with the NF-κB inhibitor Bay11-7082. USP20 exacerbates cardiac hypertrophy by promoting P65 phosphorylation, which subsequently enhances the release of inflammatory cytokines and apoptotic proteins."
IO biomarker • Journal • Inflammation • Targeted Protein Degradation • BCL2 • IL1B • IL6 • TNFA • USP20
June 02, 2026
Lipid droplet accumulation mediated by Acsl1 is DRP1 dependent
(WPC 2026)
- "LPS-induced neuroinflammation was modeled in vivo (1 mg/kg/day, 4 days) and in vitro using primary microglia treated with LPS (100 ng/mL) ± DRP1 inhibitor (P110) or NF-κB inhibitor (BAY 11-7082)... These results demonstrate that DRP1 plays a critical role in microglial metabolic reprogramming and LDs accumulation. As an upstream regulator of both LD accumulation and inflammation via the NF-κB-Acsl1 axis, DRP1 represents a good target for therapeutic development conditions involving lipid dysregulation."
CNS Disorders • Inflammation • Metabolic Disorders • Movement Disorders • Parkinson's Disease • ACSL1 • DNM3 • IL1B • IL6 • RELA • TNFA
May 29, 2026
CMPK2 promotes M1 macrophage polarization in sepsis-induced acute lung injury via NLRP3/NF-κB signalling.
(PubMed, Int Immunopharmacol)
- "CMPK2 exacerbates SALI, at least in part, by promoting M1-skewed alveolar macrophage responses and enhancing NF-κB/NLRP3-associated inflammatory signalling. Mechanistically, CMPK2 associates with IKKα/β through its C-terminal domain, whereas the canonical N-terminal mitochondrial targeting sequence is not strictly required for its pro-inflammatory activity in this context. These findings highlight CMPK2 as a novel therapeutic target for alleviating SALI, offering potential for precision interventions to improve the clinical management of sepsis-related lung injury."
Journal • Acute Lung Injury • Infectious Disease • Inflammation • Pneumonia • Respiratory Diseases • Septic Shock • IL1B • IL6 • NLRP3 • TNFA
May 27, 2026
Zearalenone (ZEA)-Induced Intestinal Epithelial Cell (IPEC-J2) Damage: Role of Oxidative Stress and Inflammation.
(PubMed, Food Chem Toxicol)
- "Notably, NAC pretreatment alleviated ZEA-induced inflammation, and BAY11-7082 reduced oxidative stress, indicating pathway crosstalk. ZEA disrupts intestinal homeostasis by suppressing Nrf2-mediated antioxidant defense and triggering NF-κB-driven inflammation. These insights enhance understanding of ZEA toxicity and support the development of targeted protective strategies."
Journal • Inflammation • CXCL8 • IL1B • IL6 • NQO1 • TNFA
March 13, 2026
Di-n-butyl Phthalate induces senescence associated secretory phenotype via NF-?B activation, promoting proliferation and epithelial mesenchymal transition in epithelial cells and facilitating the development of benign prostatic hyperplasia
(AUA 2026)
- "NF-κB inhibitor BAY 11-7082 and CXCR2 antagonist Danirixin were used to validate pathway involvement in vivo and in vitro. DBP activates NF-κB to induce SASP in prostatic epithelial cells, releasing IL-8 that binds to CXCR2 in adjacent cells, driving proliferation and EMT to facilitate BPH progression. Targeting the IL-8/CXCR2 axis may serve as a therapeutic strategy for DBP-related BPH, providing mechanistic insights into environmental pollutant-induced prostate diseases."
Benign Prostatic Hyperplasia • CDKN1A • CXCL8 • IL6
May 21, 2026
Advanced Oxidation Protein Products Aggravate Inflammation of Henoch-Schönlein Purpura Nephritis Through the RAGE-NF-κB Pathway.
(PubMed, Clin Lab)
- "Collectively, these results implicated that AOPPs may be related to the pathogenesis of HSPN, AOPPs might induce or aggravate inflammation of HSPN through regulating RAGE-NF-κB signaling pathway. Above all, it has important clinical guiding significance for the prognosis judgment of HSPN, and can also provide new therapeutic targets for the HSPN."
Journal • Chronic Kidney Disease • Inflammation • Nephrology • Oncology • Renal Disease • IL1B • IL6 • TNFA
May 21, 2026
Impaired NF-κB/Nrf2 Crosstalk in Rett Syndrome.
(PubMed, FASEB J)
- "To mechanistically study the NF-κB/Nrf2 crosstalk, LPS-stimulated cells were treated with the Nrf2 activator sulforaphane (SFN), alone or combined with the NF-κB inhibitor BAY-117082...Taken together, our findings provide preliminary evidence that RTT exhibits a dysfunctional NF-κB/Nrf2 regulatory axis characterized by basal inflammatory activation and impaired antioxidant compensation. Modulation of NF-κB signaling, in combination with Nrf2 activation, may represent a promising strategy to counteract the persistent OxInflammatory milieu associated with RTT and warrants further investigation."
Journal • CNS Disorders • Developmental Disorders • Inflammation • Metabolic Disorders • Movement Disorders • Psychiatry • HMOX1 • SIRT1
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