1. Signaling Pathways
  2. NF-κB
  3. NF-κB

NF-κB

Nuclear factor-κB; Nuclear factor-kappaB

NF-κB (Nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls transcription of DNA. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens. NF-κB plays a key role in regulating the immune response to infection. Incorrect regulation of NF-κB has been linked to cancer, inflammatory, and autoimmune diseases, septic shock, viral infection, and improper immune development. NF-κB has also been implicated in processes of synaptic plasticity and memory. There are five proteins in the mammalian NF-κB family: NF-κB1, NF-κB2, RelA, RelB, c-Rel.

Cat. No. Product Name Effect Purity Chemical Structure
  • HY-175317
    Nogo-B-IN-1
    Inhibitor
    Nogo-B-IN-1 ((S,R)-4v) is a covalent Nogo-B inhibitor. Nogo-B-IN-1 inhibits the progression of osteosarcoma (OS) by suppressing Nogo-B activity and the PI3K/AKT/NF-κB/Bcl-2 signaling pathway. Nogo-B-IN-1 inhibits the proliferation of OS 143B cells (IC50 = 0.28 µM) and induces apoptosis. Nogo-B-IN-1 can be used for OS targeting research.
    Nogo-B-IN-1
  • HY-157809
    Anti-inflammatory agent 74
    Inhibitor
    Anti-inflammatory agent 74 (B5) is an anti-inflammatory agent that can inhibit NO, IL-6, and TNF-α, with IC50 values of 10.88 μM and 4.93 μM for NO and IL-6, respectively. Anti-inflammatory agent 74 alleviates acute lung injury (ALI) by regulating inflammatory mediators and inhibiting the MAPK and NF-κB signaling pathways.
    Anti-inflammatory agent 74
  • HY-172871
    Anti-inflammatory agent 102
    Inhibitor
    Anti-inflammatory agent 102 (Compound 11a) is an orally active anti-inflammatory agent. Anti-inflammatory agent 102 exerts its anti-inflammatory effect by blocking the activation of the ASK1/p38 MAPKs/NF-κB signaling pathway. Anti-inflammatory agent 102 has significant anti-inflammatory activity and can inhibit the release of NO, ROS, and inflammatory factors (such as IL-6, TNF-α, IL-1β). Anti-inflammatory agent 102 can be used in the study of inflammatory diseases such as ulcerative colitis (UC).
    Anti-inflammatory agent 102
  • HY-N0716AR
    Berberine hemisulfate (Standard)
    Inhibitor
    Berberine (hemisulfate) (Standard) is the analytical standard of Berberine (hemisulfate). This product is intended for research and analytical applications. Berberine hemisulfate is the hemisulfate form of Berberine (HY-N0716). Berberine hemisulfate is an alkaloid isolated from the Chinese herbal medicine Huanglian. Berberine hemisulfate exhibits anti-inflammatory, antibiobic, antitumor, cardiovascular protective and neuroprotective activity.
    Berberine hemisulfate (Standard)
  • HY-N16637
    (3R,5R)-3,5-Dihydroxy-1,7-bis(3,4-dihydroxyphenyl)heptane 3-O-β-D-glucopyranoside
    Inhibitor
    (3R,5R)-3,5-Dihydroxy-1,7-bis(3,4-dihydroxyphenyl)heptane 3-O-β-D-glucopyranoside is a diarylheptanol glycoside compound isolated from Tacca plantaginea. (3R,5R)-3,5-Dihydroxy-1,7-bis(3,4-dihydroxyphenyl)heptane 3-O-β-D-glucopyranoside significantly inhibit TNF-α-induced NF-κB transcriptional activity (IC50 = 9.4 μM). (3R,5R)-3,5-Dihydroxy-1,7-bis(3,4-dihydroxyphenyl)heptane 3-O-β-D-glucopyranoside significantly activates PPAR transcriptional activity (EC50 = 9.9 μM) and has a specific activating effect on PPAR β(δ) (EC50 = 23.1 μM). (3R,5R)-3,5-Dihydroxy-1,7-bis(3,4-dihydroxyphenyl)heptane 3-O-β-D-glucopyranoside is non-toxic to cells at the tested concentration. (3R,5R)-3,5-Dihydroxy-1,7-bis(3,4-dihydroxyphenyl)heptane 3-O-β-D-glucopyranoside can be used for research on inflammatory conditions.
    (3R,5R)-3,5-Dihydroxy-1,7-bis(3,4-dihydroxyphenyl)heptane 3-O-β-D-glucopyranoside
  • HY-149816
    Anti-inflammatory agent 41
    Inhibitor
    Anti-inflammatory agent 41 (13a) significantly inhibit lipopolysaccharide (LPS)-induced expression of the proinflammatory cytokines IL-6 and TNF-α on J774A.1, THP-1 and LX-2 cells, and inhibits the activation of the NF-κB pathway.
    Anti-inflammatory agent 41
  • HY-138135
    OP-1118
    Inhibitor
    OP-1118 (Fidaxomicin metabolite OP-1118) is an orally active dual inhibitor of NF-κB and ERK1/2, with low systemic plasma exposure, no accumulation, and primary excretion via feces. By inhibiting the phosphorylation of NF-κB and ERK1/2 and reducing the expression of pro-inflammatory cytokines, OP-1118 exerts significant anti-inflammatory, cytoprotective, anti-apoptotic and antibacterial activities. In Clostridium difficile infection models, OP-1118 effectively blocks toxin-mediated intestinal inflammation, cell rounding, histological damage and apoptosis, and its protective effect can be reversed by PMA (HY-18739).
    OP-1118
  • HY-172201
    NF-κB-IN-19
    Inhibitor
    NF-κB-IN-19 (Compound 8) is an NF-κB inhibitor. NF-κB-IN-19 effectively induces DNA damage, promotes the generation of ROS, and induces autophagy and apoptosis through the NF-κB signaling pathway in tumor cells. In addition, NF-κB-IN-19 can inhibit the levels of VEGF and HIF-1α, and exert antiproliferative activity in tumor cells through the PI3K/AKT and STAT-3 pathways. NF-κB-IN-19 can effectively overcome cisplatin resistance and has anti-tumor activity.
    NF-κB-IN-19
  • HY-170836
    NLRP3-IN-69
    Inhibitor
    NLRP3-IN-69 (Compound 23) inhibits the activation of NF-κB p65 and the formation of NLRP3 inflammasome. NLRP3-IN-69 inhibits LPS (HY-D1056)-induced overexpression of IL-1β, iNOS and COX-2, inhibits NO generation (IC50=5.66 μM), thereby exhibiting anti-inflammatory activity.
    NLRP3-IN-69
  • HY-159516
    Sabialimon P
    Inhibitor
    Sabialimon P (compound 16) is a NO release inhibitor (IC50=18.12 μM) with anti-inflammatory activity. Sabialimon P significantly reduces the secretion of TNF-α, iNOS, IL-6 and NF-κB and inhibits the expression of COX-2 and NF-κB/p65 in RAW264.7 cells induced by LPS (HY-D1056).
    Sabialimon P
  • HY-115385R
    Lumichrome (Standard)
    Inhibitor
    Lumichrome (Standard) is the analytical standard of Lumichrome. This product is intended for research and analytical applications. Lumichrome, a photodegradation product of Riboflavin, is an endogenous compound in humans. Lumichrome inhibits human lung cancer cell growth and induces apoptosis via a p53-dependent mechanism. Lumichrom is the inhibitor for AKT/β-catenin signaling pathway. Lumichrom is the inhibitor for AKT/β-catenin signaling pathway.
    Lumichrome (Standard)
  • HY-138284
    Avenanthramide-C methyl ester
    Inhibitor
    Avenanthramide-C methyl ester is an anti-inflammatory agent and NF-κB inhibitor that inhibits the secretion of pro-inflammatory factors. Avenanthramide-C methyl ester inhibits NF-κB activation by inhibiting IKK and IκB phosphorylation and inhibiting proteasome activity.
    Avenanthramide-C methyl ester
  • HY-146419
    Anti-inflammatory agent 20
    Inhibitor
    Anti-inflammatory agent 20 (compound 5a) is a potent inhibitor of NO activity. Anti-inflammatory agent 20 shows anti-inflammatory activity. Anti-inflammatory agent 20 suppresses LPS-induced inflammation via inhibiting the activation of NF-κB and MAPK signaling and thereby reducing IL-6, TNF-α, iNOS, and COX-2 upregulation.
    Anti-inflammatory agent 20
  • HY-N2477R
    Taraxerol (Standard)
    Inhibitor
    Taraxerol (Standard) is the analytical standard of Taraxerol. This product is intended for research and analytical applications. Taraxerol is isolated from Taraxacum mongolicum, and has anti-inflammtory and anti-cancer effects. Taraxerol attenuates acute inlammation through inhibition of NF-κB signaling pathway. Taraxerol induces cell apoptosis.
    Taraxerol (Standard)
  • HY-149472
    Anti-osteoporosis agent-4
    Inhibitor
    Anti-osteoporosis agent-4 (Compound 11h) inhibits differentiation of primary osteoclasts. Anti-osteoporosis agent-4 attenuates RANKL-induced osteoclastogenesis. Anti-osteoporosis agent-4 inhibits osteoclast formation with an IC50 value of 358.29 nM. Anti-osteoporosis agent-4 inhibits PI3K/AKT and IκBα/NF-κB signaling pathway activation.
    Anti-osteoporosis agent-4
  • HY-N3625
    Coronalolic acid
    Inhibitor
    Coronalolic acid, extract from the apical bud of Gardenia sootepenesis Hutch, inhibits TNF-α-induced NF-κB activity and NO production.
    Coronalolic acid
  • HY-182064
    EGFR-IN-206
    Inhibitor
    EGFR-IN-206 is an orally active EGFR inhibitor. EGFR-IN-206 inhibits the phosphorylation of the key tumor growth protein EGFR, and suppresses the proliferation, migration and invasion of EGFR triple-mutant tumor cell lines. EGFR-IN-206 downregulates the expression of inflammation-related proteins iNOS, COX-2 and NF-κB (p65). EGFR-IN-206 promotes the secretion of NO. EGFR-IN-206 reduces the secretion of IL-6. EGFR-IN-206 induces apoptosis (apoptosis) of EGFR triple-mutant tumor cells. EGFR-IN-206 exerts antitumor activity in EGFR triple-mutant mice. EGFR-IN-206 is applicable to the research of non-small cell lung cancer.
    EGFR-IN-206
  • HY-180952
    Zaltoprofen sulfoxide
    Inhibitor
    Zaltoprofen sulfoxide (Compound M2) is the main metabolite of Zaltoprofen (HY-B0619). Zaltoprofen sulfoxide is an efficient and selective COX-2 inhibitor (IC50 = 45.38 nM) and a PPAR-γ activator. Zaltoprofen sulfoxide effectively inhibits NF-κB and MAPK inflammatory signaling pathways and alleviates acute lung injury induced by LPS (HY-D1056B3). Zaltoprofen sulfoxide can be used for the study of acute lung injury.
    Zaltoprofen sulfoxide
  • HY-P10850
    PIYLGGVFQ
    Inhibitor
    PIYLGGVFQ is a peptide inhibitor for TNF-α. PIYLGGVFQ inhibits TNF-α-mediated apoptosis, NF-κB nuclear translocation and activation. PIYLGGVFQ exhibits anti-arthritic activity in the CIA mouse model.
    PIYLGGVFQ
  • HY-163778
    ZM600
    Inhibitor
    ZM600 is a potent and orally active antihepatic fibrosis agent. ZM600 decreases the LPS (HY-D1056) induced protein expression of collagen I, α-SM, p-p65. ZM600 has the potential for the research of liver fibrosis.
    ZM600
Cat. No. Product Name / Synonyms Application Reactivity

NF-κB transcription factors are critical regulators of immunity, stress responses, apoptosis and differentiation. In mammals, there are five members of the transcription factor NF-κB family: RELA (p65), RELB and c-REL, and the precursor proteins NF-κB1 (p105) and NF-κB2 (p100), which are processed into p50 and p52, respectively. NF-κB transcription factors bind as dimers to κB sites in promoters and enhancers of a variety of genes and induce or repress transcription. NF-κB activation occurs via two major signaling pathways: the canonical and the non-canonical NF-κB signaling pathways[1]

 

The canonical NF-κB pathway is triggered by signals from a large variety of immune receptors, such as TNFR, TLR, and IL-1R, which activate TAK1. TAK1 then activates IκB kinase (IKK) complex, composed of catalytic (IKKα and IKKβ) and regulatory (NEMO) subunits, via phosphorylation of IKKβ. Upon stimulation, the IKK complex, largely through IKKβ, phosphorylates members of the inhibitor of κB (IκB) family, such as IκBα and the IκB-like molecule p105, which sequester NF-κB members in the cytoplasm. IκBα associates with dimers of p50 and members of the REL family (RELA or c-REL), whereas p105 associates with p50 or REL (RELA or c-REL). Upon phosphorylation by IKK, IκBα and p105 are degradated in the proteasome, resulting in the nuclear translocation of canonical NF-κB family members, which bind to specific DNA elements, in the form of various dimeric complexes, including RELA-p50, c-REL-p50, and p50-p50. Atypical, IKK-independent pathways of NF-κB induction also provide mechanisms to integrate parallel signaling pathways to increase NF-κB activity, such as hypoxia, UV and genotoxic stress.

 

The non-canonical NF-κB pathway is induced by certain TNF superfamily members, such as CD40L, BAFF and lymphotoxin-β (LT-β), which stimulates the recruitment of TRAF2, TRAF3, cIAP1/2 to the receptor complex. Activated cIAP mediates K48 ubiquitylation and proteasomal degradation of TRAF3, resulting in stabilization and accumulation of the NFκB-inducing kinase (NIK). NIK phosphorylates and activates IKKα, which in turn phosphorylates p100, triggering p100 processing, and leading to the generation of p52 and the nuclear translocation of p52 and RELB[2][3].

 

Reference:

[1]. Oeckinghaus A, et al. The NF-kappaB family of transcription factors and its regulation.Cold Spring Harb Perspect Biol. 2009 Oct;1(4):a000034. 
[2]. Taniguchi K, et al. NF-κB, inflammation, immunity and cancer: coming of age. Nat Rev Immunol. 2018 May;18(5):309-324.
[3]. Perkins ND,et al. Integrating cell-signalling pathways with NF-kappaB and IKK function. Nat Rev Mol Cell Biol. 2007 Jan;8(1):49-62.

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