NF-κB
NF-κB regulates innate and adaptive immunity, inflammatory responses, immune-cell survival, activation, and differentiation[1]. Mechanistically, canonical NF-κB signaling depends on phosphorylation-induced proteasomal degradation of IκB proteins, releasing cytosolic NF-κB dimers for transcriptional control[2]. In inflammation models, NF-κB induces cytokines, chemokines, adhesion molecules, and inflammasome-related responses, linking pathway activation to chronic inflammatory disease and cancer research[1][3][4]. Compared with related isoforms, mammalian NF-κB includes RelA/p65, RelB, c-Rel, p50/NF-κB1, and p52/NF-κB2, and RelA loss causes embryonic lethality with liver apoptosis, whereas p50 loss produces immune-response defects without developmental abnormalities[2][5][6]. For experimental applications, NF-κB inhibitors, including IKK-targeting agents and BAY 11-7082, help test pathway dependence in inflammatory signaling, but broad pathway targeting requires careful interpretation because NF-κB also supports normal immune physiology[4][7].
References:
- [1]. Liu T, et al. NF-κB signaling in inflammation. Signal Transduct Target Ther. 2017;2:17023–. [Content Brief]
- [2]. Oeckinghaus A, et al. The NF-kappaB family of transcription factors and its regulation. Cold Spring Harb Perspect Biol. 2009 Oct;1(4):a000034. [Content Brief]
- [3]. Lawrence T. The nuclear factor NF-kappaB pathway in inflammation. Cold Spring Harb Perspect Biol. 2009 Dec;1(6):a001651. doi: 10.1101/cshperspect.a001651. Epub 2009 Oct 7. PMID: 20457564; PMCID: PMC2882124. et al. The nuclear factor NF-kappaB pathway in inflammation. Cold Spring Harb Perspect Biol. 2009 Dec;1(6):a001651. [Content Brief]
- [4]. Yu H, et al. Targeting NF-κB pathway for the therapy of diseases: mechanism and clinical study. Signal Transduct Target Ther. 2020 Sep 21;5(1):209. [Content Brief]
- [5]. Beg AA, et al. Embryonic lethality and liver degeneration in mice lacking the RelA component of NF-kappa B. Nature. 1995 Jul 13;376(6536):167-70. [Content Brief]
- [6]. Sha WC, et al. Targeted disruption of the p50 subunit of NF-kappa B leads to multifocal defects in immune responses. Cell. 1995 Jan 27;80(2):321-30. [Content Brief]
- [7]. Lee J, et al. BAY 11-7082 is a broad-spectrum inhibitor with anti-inflammatory activity against multiple targets. Mediators Inflamm. 2012;2012:416036. [Content Brief]
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NF-κB Inhibitors
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NF-κB Activators
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NF-κB Modulators
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NF-κB Inducers
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NF-κB Ligand
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NF-κB Related Products (1455)
Related Products (1455)
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Antibodies (24)
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Urocortin II, human TFA
0 ImagesCat. No.: HY-P1752AUrocortin II, human TFA is a selective endogenous peptide agonist of type-2 corticotropin-releasing factor (CRF2) receptor. Urocortin II, human TFA has an effect of promoting satiet and neuroprotective effect. Urocortin II, human TFA also has bactericidal, antiparasitic and pro-inflammation activity. Urocortin II, human TFA can activate NF-κB pathway and ERK1/2 MAP kinase. Urocortin II, human TFA can reduce pulmonary arterial hypertension and shows cardiac protection effect. Urocortin II, human TFA can be used for the researches of infection, inflammation, metabolic, neurological and cardiovascular disease.
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LM9
0 ImagesCat. No.: HY-180336CAS No.: 2249864-11-5LM9 is a potent, orally active MyD88 inhibitor. LM9 blocks TLR4/MyD88 binding, MyD88 homodimer formation, and TLR4/MyD88/NF-κB signaling pathway activation. LM9 prevents atherosclerosis by regulating inflammatory responses and oxidative stress in macrophages. LM9 efficiently mitigates inflammatory responses and fibrosis in obesity-induced cardiomyopathy. LM9 can be used for fibrosis and atherosclerosis research.
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NUCC-0227579
0 ImagesCat. No.: HY-184969NUCC-0227579 is a VHL-recruiting PROTAC degrader targeting CD73, with a DC50 of 0.32 μM. NUCC-0227579 synergistically mediates CD73 degradation through the ubiquitin-proteasome pathway and the lysosomal pathway. NUCC-0227579 inhibits the conversion of AMP to adenosine, abrogates adenosine-mediated immunosuppression, upregulates the activities of the NF-κB and NFAT pathways, and enhances the secretion, activation and proliferation levels of IFN-γ and TNF-α. NUCC-0227579 downregulates NAD+ synthesis in tumor cells, and inhibits the proliferation, migration and adhesion abilities of tumor cells under glutamine-deficient conditions. NUCC-0227579 significantly suppresses tumor growth in a humanized NSG mouse model of triple-negative breast cancer.
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β-Funaltrexamine
0 ImagesCat. No.: HY-160938CAS No.: 72782-05-9Synonyms: β-FNAβ-Funaltrexamine (β-FNA) is a blood-brain barrier-permeable, selective and irreversible μ-opioid receptor antagonist with immunomodulatory, anti-inflammatory and neuroprotective activities. β-Funaltrexamine inhibits p38 MAPK and TLR4 signaling by blocking μ-opioid receptors, and reduces the transcriptional activities of NF-κB, AP-1, CREB and Stat. Furthermore, β-Funaltrexamine inhibits iNOS activation and pro-inflammatory microglial polarization, converting microglia to an anti-inflammatory phenotype, thereby downregulating neuroinflammation and ameliorating neuronal degeneration. β-Funaltrexamine is widely applicable to research related to stroke, cerebral ischemia/reperfusion injury and neurodegenerative diseases.
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STAT3/NF-κB-IN-2
0 ImagesCat. No.: HY-184734STAT3/NF-κB-IN-2 is a dual STAT3/NF-κB inhibitor that exhibits antiproliferative, antimigratory and anti-invasive activities in cancer cells. STAT3/NF-κB-IN-2 inhibits the transcriptional activities of NF-κB and STAT3, binds to the STAT3-SH2 domain, and blocks STAT3 dimerization. STAT3/NF-κB-IN-2 can be used in studies related to triple-negative breast cancer.
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Mesalamine impurity P
0 ImagesCat. No.: HY-131265CAS No.: 887256-40-8Mesalamine impurity P is an impurity of Mesalamine (HY-15027). 5-Aminosalicylic acid (Mesalamine) acts as a specific PPARγ agonist and also inhibits p21-activated kinase 1 (PAK1) and NF-κB.
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Leupeptin hemisulfate (Standard)
0 ImagesLeupeptin hemisulfate (Standard) is the analytical standard of Leupeptin hemisulfate (HY-18234A ). This product is intended for research and analytical applications. Leupeptin hemisulfate is a broad-spectrum protease inhibitor. By inhibiting the activation of the PTEN/PI3K/Akt/NF-κB/ERK1/2/p38 signaling pathway, Leupeptin hemisulfate significantly reduces LPS-induced NO and ROS production, mitochondrial membrane potential hyperpolarization, phagocytic activity, pro-inflammatory cytokine release, and M1 polarization in mouse peritoneal macrophages, and reverses autophagic flux impairment. It also decreases Concanavalin A (HY-P2149)-induced proliferation index of mouse splenic lymphocytes and the Th1/IL-10 and Th2/IL-10 cytokine ratios, thereby modulating innate and adaptive immune responses. Leupeptin hemisulfate inhibits blood coagulation and tumorigenesis in mouse skin. Leupeptin hemisulfate can be used in research on chronic inflammatory diseases and skin tumorigenesis.
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DA5-CH
0 ImagesCat. No.: HY-P12141CAS No.: 2227651-65-0Synonyms: KP405DA5-CH (KP405) is a blood-brain barrier-permeable GLP-1/GIP receptor agonist. DA5-CH activates GLP-1 and GIP receptors, inhibits the NF-κB inflammatory pathway, reduces α-synuclein (α-synuclein) levels, restores the expression of tyrosine hydroxylase and neurotrophic factors, improves motor function, decreases amyloid plaques and phosphorylated tau protein levels in the hippocampus, restores synaptic plasticity, regulates the PI3K/AKT/GSK3β and CREB signaling pathways, and alleviates mitochondrial stress. DA5-CH can be used for research on Parkinson's disease and Alzheimer's disease.
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Triphala
0 ImagesCat. No.: HY-114335CAS No.: 857906-76-4Triphala, an Ayurvedic polyherbal formulation comprising of equiproportional fruit parts of Terminalia chebula, Terminalia bellerica, and Phyllanthus emblica. Triphala inhibits NF-κB activation. Triphala exerts antifungal action. Anti-adipogenic, anti-inflammatory, and anti-neoplastic activities.
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HDAC6-IN-71
0 ImagesCat. No.: HY-180829CAS No.: 3062867-16-4HDAC6-IN-71 (Compound 24) is a HDAC6 inhibitor with IC50 values for HDAC6 and HDAC1 of 13.68 and 443.12 nM respectively. HDAC6-IN-71 effectively inhibits the production of NO by mouse macrophages, with its IC50 being 2.31 μM. HDAC6-IN-71 inhibits the HDAC6-NF-κB signaling pathway, reduces the levels of phosphorylated IκB-α and IKK-α/β, and suppresses the expression of downstream inflammatory proteins COX-2 and iNOS. HDAC6-IN-71 significantly alleviates ulcerative colitis in mice.
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NIK-IN-3
0 ImagesCat. No.: HY-179701NIK-IN-3 is a potent and orally active NF-κB-inducing kinase (NIK) inhibitor with an IC50 of 5.2 nM. NIK-IN-3 suppresses non-canonical NF-κB pathway activation and inhibits the secretion of pro-inflammatory cytokines, such as TNF-α, IL-6, IL-1β and chemokine CXCL12. NIK-IN-3 shows significant anti-inflammatory effects in LPS (HY-D1056)-induced sepsis mice model and DSS (HY-116282)-induced colitis model. NIK-IN-3 can be used for the research of inflammation, such as colitis.
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GUT-70
0 ImagesCat. No.: HY-120923CAS No.: 161633-75-6GUT-70, a tricyclic coumarin, is a Hsp90 inhibitor. GUT-70 activates the caspase 2, 3, 8 and 9, and induces the apoptosis in leukemic cells. GUT-70 inhibits HIV-1 replication in chronically infected cells via suppression of the NF-κB pathway. GUT-70 can be used for the study of leukemic, mantle cell lymphoma (MCL) and HIV-1 infection.
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CAY10512
0 ImagesCat. No.: HY-120269CAS No.: 139141-12-1CAY10512 is a NF-κB inhibitor. CAY10512 can suppress the upregulation of NF-κB-sensitive proinflammatory miRNAs (miRNA-9, miRNA-125b, miRNA-146a, miRNA-155) in cerebrospinal fluid and extracellular fluid. CAY10512 significantly reduces the release of pro-inflammatory cytokines (such as TNF-α, MCP-1, IL-8, IL-6). CAY10512 can be used for researchs on neuroinflammation, islet transplantation and microRNA regulation.
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Triflusal-d3
0 ImagesCat. No.: HY-B0531SCAS No.: 2748541-63-9Triflusal-d3 is deuterium labeled Triflusal (HY-B0531). Triflusal is an orally bioavailable, blood-brain barrier-permeable dual Cyclooxygenase-1 (COX-1)/cAMP phosphodiesterase inhibitor. Triflusal inhibits platelet aggregation, NF-κB activation, iNOS activity, and prostaglandin synthesis in ischaemic tissue. Triflusal stimulates neutrophil nitric oxide production, eNOS protein expression, and cNOS activity. Triflusal alleviates cerebral ischemic injury in rats and ameliorates pathological lesions and related gene expression in transgenic Alzheimer’s disease models. Triflusal can be used for the research of thromboembolic/ischemic cardiovascular and cerebrovascular diseases, and Alzheimer’s disease.
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Afimkibart
0 ImagesCat. No.: HY-P990876ASynonyms: PF-06480605; RVT-3101Afimkibart (PF-06480605; RVT-3101) is a humanized monoclonal antibody targeting TL1A (TNFSF15). Afimkibart blocks the TL1A‑DR3 signaling axis by neutralizing the TL1A ligand, inhibits the release of pro-inflammatory cytokines, suppresses NF-κB activation and IFN-γ production, and simultaneously attenuates fibroblast activation and fibrosis progression associated with this pathway. Afimkibart is applicable to research on immune inflammation-related conditions, such as ulcerative colitis.
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Jolkinolide B (Standard)
0 ImagesCat. No.: HY-N0732RCAS No.: 37905-08-1Jolkinolide B (Standard) is the analytical standard of Jolkinolide B (HY-N0732). This product is intended for research and analytical applications. Jolkinolide B is a bioactive diterpene isolated from the roots of Euphorbia fischeriana Steud with oral activity. Jolkinolide B downregulates XIAP, cIAP1, cIAP2, and phosphorylated Akt, upregulates Smac, activates caspase-3 and caspase-9, and inhibits NF-κB, TGFβ/smad3 and JAK/STAT3 pathways. Jolkinolide B exerts comprehensive biological effects including inducing cancer cell apoptosis, suppressing inflammatory responses, improving lung function, alleviating hepatic steatosis and eliminating intracellular Mycobacterium tuberculosis. Jolkinolide B can be used for the research of leukemia, histiocytic lymphoma, asthma, metabolic dysfunction-associated steatotic liver disease and tuberculosis.
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Anti-inflammatory agent 107
0 ImagesCat. No.: HY-179502Anti-inflammatory agent 107 is an orally active anti-inflammatory agent. Anti-inflammatory agent 107 inhibits and NF-κB with a superior binding affinity of -9.4578 kcal/mol. Anti-inflammatory agent 107 reduces levels of inflammatory biomarkers (TNF-α, IL-6, INF-γ, NF-κβ, C-reactive protein and Erythrocyte Sedimentation Rate) and enhances the endogenous antioxidant defense system by elevating SOD (Superoxide Dismutase), CAT (Catalase) and GSH (Glutathione) activities. Anti-inflammatory agent 107 not induces liver toxicity and demonstrates hepatoprotective effects. Anti-inflammatory agent 107 dose-dependently ameliorates leukocyte infiltration and tissue edema. Anti-inflammatory agent 107 can be used for anti-inflammatory research.
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Cudraflavone B
0 ImagesCat. No.: HY-N10009CAS No.: 19275-49-1Cudraflavone B is a prenylated flavonoid with anti-inflammatory and anti-tumor properties. Cudraflavone B is also a dual inhibitor of COX-1 and COX-2. Cudraflavone B blocks the translocation of nuclear factor κB (NF-κB) from the cytoplasm to the nucleus in macrophages. Thus, Cudraflavone B inhibits tumor necrosis factor α (TNFα) gene expression and secretion. Cudraflavone B also triggers the mitochondrial apoptotic pathway, activates NF-κB, the MAPK p38, and ERK, and induced the expression of SIRT1. Thus Cudraflavone B inhibits the growth of human oral squamous cell carcinoma cells.
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CLP-d2
0 ImagesCat. No.: HY-P11617CLP-d2 is a multi-target anti-inflammatory agent, osteoclastogenesis inhibitor and immunomodulator with superior pharmacokinetic properties to Daptomycin (HY-B0108) and good safety profiles. CLP-d2 inhibits the NF-κB and MAPK signaling pathways by reducing the expression levels of c-Fos and NFATc1, and decreasing the phosphorylation levels of IκBα, p65, ERK and JNK, thereby reducing the secretion of pro-inflammatory cytokines such as IL-6, TNF-α and IL-1β to exert anti-inflammatory activity. CLP-d2 inhibits intra-articular osteoclastogenesis in mice, alleviates bone erosion and joint swelling, reduces synovial hyperplasia and inflammatory cell infiltration, and decreases serum rheumatoid factor (RF) levels. CLP-d2 is applicable to related research on rheumatoid arthritis.
