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

NF-κB

Nuclear factor-κB; Nuclear factor-kappaB

NF-κB

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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.

NF-κB Isoform Specific Products:

NF-κB Isoform Comparison
Cat. No. Product Name Effect Purity Chemical Structure
  • HY-U00450
    4-O-Methyl honokiol
    		Inhibitor 98.18%
    4-O-Methyl honokiol is a natural neolignan isolated from Magnolia officinalis, acts as a PPARγ agonist, and inhibtis NF-κB activity, used for cancer and inflammation research.
    4-O-Methyl honokiol
  • HY-Y0148
    10-Hydroxydecanoic acid
    		Inhibitor 98.77%
    10-Hydroxydecanoic acid (10-HDAA) is a saturated fatty acid derived from 10-hydroxy-trans-2-decenoic acid, which can be isolated from royal jelly. 10-Hydroxydecanoic acid exhibits various biological activities, including anti-inflammatory, insecticidal, anti-malarial, and anti-Leishmania properties, as well as enhancing antigen-specific immune responses. The anti-inflammatory effects of 10-Hydroxydecanoic acid are primarily mediated by inhibiting the activation of NF-κB and the translation of interferon regulatory factor 1 (IRF-1), which reduces the production of interleukin 6 (IL-6) and nitric oxide (NO) in inflammatory cells. Additionally, 10-Hydroxydecanoic acid alleviates neuroinflammatory responses through the p53-autophagy pathway and the p53-NLRP3 pathway. Finally, 10-Hydroxydecanoic acid enhances antigen-specific immune responses by promoting the effective uptake of antigens by microfold cells.
    10-Hydroxydecanoic acid
  • HY-N0119
    Naringin Dihydrochalcone
    		Inhibitor 99.65%
    Naringin Dihydrochalcone is an artificial sweetener derived from naringin. Naringin is a major flavanone glycoside obtained from tomatoes, grapefruits, and many other citrus fruits. Naringin exhibits biological properties such as antioxidant, anti-inflammatory, and antiapoptotic activities. Naringin suppresses NF-κB signaling pathway.
    Naringin Dihydrochalcone
  • HY-18976
    UF010
    		99.84%
    UF010 is a selective inhibitor of class I HDAC. UF010 has cytotoxicity to cancer cells and reduces neuroinflammation in the hippocampus. UF010 can be used for the research of neurological diseases.
    UF010
  • HY-N0106
    (Rac)-Salvianic acid A sodium
    		Inhibitor ≥98.0%
    (Rac)-Salvianic acid A sodium is the racemic form of Salvianic acid A (HY-N1913). Salvianic acid A is an orally active phenolic compound that induces Nrf2/HO-1 activation and inhibits the NF-κB pathway, and it also activates the mitochondrial antioxidant defense system (Mitochondrial Metabolism). Salvianic acid A exhibits anti-inflammatory, antioxidant, and anti-apoptotic properties (Apoptosis), demonstrating potential for research into inflammation and cardiovascular diseases.
    (Rac)-Salvianic acid A sodium
  • HY-N1410
    Triacetylresveratrol
    		Inhibitor 99.58%
    Triacetylresveratrol, an acetylated analog of Resveratrol. Triacetylresveratrol decreases the phosphorylation of STAT3 and NF-κB in a dose- and time- dependent manner in PANC-1 and BxPC-3 cells. Anticancer effects.
    Triacetylresveratrol
  • HY-107802
    Breviscapine
    		Inhibitor
    Breviscapine is a crude flavonoid extract of Breviscapine, which is more than 85% of the active ingredient, Breviscapine. Breviscapine has a wide range of cardiovascular pharmacological activities, such as increasing blood flow, improving microcirculation, dilating blood vessels, reducing blood viscosity, promoting fibrinolysis, inhibiting platelet aggregation and thrombosis. Breviscapine has been used in the study of cerebral infarction and its sequelae, cerebral thrombosis, coronary heart disease and angina pectoris.
    Breviscapine
  • HY-N2543
    Damascenone
    		Inhibitor 99.26%
    Damascenone ((E/Z)-Damascenone) is an active compound of?Epipremnum pinnatum with anti-inflammatory activity. Damascenone is a mixture complex of?E-isomer-Damascenone and Z-isomer Damascenone.
    Damascenone
  • HY-P1847A
    IKKγ NBD Inhibitory Peptide TFA
    		98.20%
    IKKγ NBD Inhibitory Peptide TFA is a highly specific inhibitor NF-κB inhibitor. IKKγ NBD Inhibitory Peptide TFA acts by disrupting the interaction between IKKγ/NEMO-binding domain (NBD) with IKKα and IKKβ, thus blocking TNF-α-induced NF-kB activation. IKKγ NBD Inhibitory Peptide TFA could significantly suppresses inflammation and ameliorate the cerebral ischemia-induced neurological deficits.
    IKKγ NBD Inhibitory Peptide TFA
  • HY-N1193
    Sulfuretin
    		Inhibitor 99.36%
    Sulfuretin inhibits the inflammatory response by suppressing the NF-κB pathway. Sulfuretin can be used for the research of allergic airway inflammation. Sulfuretin reduces oxidative stress, platelet aggregation, and mutagenesis. Sulfuretin is a competitive and potent inhibitor of monophenolase and diphenolase activities with the IC50 of 13.64 μM.
    Sulfuretin
  • HY-N0631
    Cornuside
    		Inhibitor 99.99%
    Cornuside is a secoiridoid glucoside isolated from the fruit of Cornus officinalis Sieb. et Zucc., which is a traditional oriental medicine for treating inflammatory diseases and invigorating blood circulation. Cornuside inhibits mast cell-mediated allergic response by down-regulating MAPK and NF-κB signaling pathways. Cornuside has anti-allergic effects in vivo and in vitro which suggests a therapeutic application of this agent in inflammatory allergic diseases.
    Cornuside
  • HY-N0716A
    Berberine hemisulfate
    		Inhibitor 99.63%
    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
  • HY-N0231
    Bavachalcone
    		Inhibitor 99.95%
    Bavachalcone is a potent inducer of apoptosis. Bavachalcone exerts anticancer activity by promoting autophagy and apoptosis in HepG2 cells. Bavachalcone acts as an anti-neuroinflammatory and antidepressant through the NF-κB pathway. Bavachalcone inhibits osteoclasts by interfering with ERK and Akt signaling pathways and the expression of c-Fos and NFATc1. Bavachalcone exhibits a significant inhibitory effect on baculovirus-expressed BACE-1 in vitro.
    Bavachalcone
  • HY-123984
    LTβR-IN-1
    		Activator 99.79%
    LTβR-IN-1 is a potent, selective lymphotoxin β receptor (LTβR) inhibitor. LTβR-IN-1 also selectively inhibits the nuclear translocation of p52 depended on TNF12A, instead of the nuclear translocation of p65 mediated by TNF-α receptor. LTβR-IN-1 regulates the NF-kB signaling pathway IN a ligand-independent manner.
    LTβR-IN-1
  • HY-B1278
    D-α-Tocopherol acetate
    		Inhibitor 98.32%
    D-α-Tocopherol acetate (D-Vitamin E acetate) can be hydrolyzed to d-alpha-tocopherol (VE) and absorbed in the small intestine.
    D-α-Tocopherol acetate
  • HY-B0072
    Tropisetron
    		Inhibitor 98.72%
    Tropisetron (SDZ-ICS-930 free base) is an orally active anti-inflammatory and antiemetic agent. Tropisetron is 5-HT3R antagonists with a Ki of 5.3 nM. Tropisetron is also a partial agonist of α7 nicotinic receptor (α7 nAChR) with an EC50 of 1.3 μM. In addition, Tropisetron has antitumor and neuroprotective effects.
    Tropisetron
  • HY-N0592A
    Demethyleneberberine chloride
    		Inhibitor 98.93%
    Demethyleneberberine chloride is a natural mitochondria-targeted antioxidant. Demethyleneberberine chloride alleviates mice colitis and inhibits the inflammatory responses by inhibiting NF-κB pathway and regulating the balance of Th cells. Demethyleneberberine chloride could serve as a AMPK activator for researching non-alcoholic fatty liver disease (NAFLD).
    Demethyleneberberine chloride
  • HY-147972
    NF-κB/MAPK-IN-1
    		Inhibitor 98.42%
    NF-κB/MAPK-IN-1 (compound 11a) is a potent inhibitor of NF-κB and MAPK pathway. NF-κB/MAPK-IN-1 shows inhibitory activity against NO production, with an IC50 of 6.96 µM. NF-κB/MAPK-IN-1 suppresses LPS-induced iNOS, COX-2, ERΚ and P38 signaling activation. NF-κB/MAPK-IN-1 can prevent LPS induced inflammatory response in macrophages. NF-κB/MAPK-IN-1 can be used for rheumatoid arthritis (RA) research.
    NF-κB/MAPK-IN-1
  • HY-N0589
    Dehydrodiisoeugenol
    		Inhibitor 99.98%
    Dehydrodiisoeugenol is isolated from Myristica fragrans Houtt, shows anti-inflammatory and anti-bacterial actions. Dehydrodiisoeugenol inhibits LPS- stimulated NF-κB activation and cyclooxygenase (COX)-2 gene expression in murine macrophages.
    Dehydrodiisoeugenol
  • HY-112671
    CDDO-dhTFEA
    		Inhibitor 99.71%
    CDDO-dhTFEA (RTA dh404) is a synthetic oleanane triterpenoid compound which potently activates Nrf2 and inhibits the pro-inflammatory transcription factor NF-κB. CDDO-dhTFEA restores hypertension (MAP), increases Nrf2 and expression of its target genes, attenuates activation of NF-κB and transforming growth factor-β pathways, and reduces glomerulosclerosis, interstitial fibrosis and inflammation in the chronic kidney disease (CKD) rats.
    CDDO-dhTFEA
Cat. No. Product Name / Synonyms Application Reactivity
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Download NF-κB Signaling Pathway Map.

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.

NF-κB Isoform Comparison

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