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-N0436
    Engeletin
    		Inhibitor 99.88%
    Engeletin is a flavanonol glycoside isolated from Smilax glabra Roxb. , inhibits NF-κB signaling-pathway activation, and possesses anti-inflammatory, analgesic, diuresis, detumescence, and antibiosis effects.
    Engeletin
  • HY-13755A
    (R)-Sulforaphane
    		Inhibitor 99.48%
    (R)-Sulforaphane (L-Sulforaphane) is a orally active, potent inducer of the Keap1/Nrf2/ARE pathway, exhibiting antioxidant and anticancer activities. (R)-Sulforaphane primarily functions by upregulating phase II detoxifying enzymes in cells, aiding in the removal of carcinogens and combating oxidative stress. (R)-Sulforaphane is capable of modulating gene expression, influencing various signaling pathways, including Nrf2, NF-κB, and AP-1. (R)-Sulforaphane can be used in studies of tumor biology, antioxidant defense mechanisms, as well as inflammation and immune responses.
    (R)-Sulforaphane
  • HY-N6966
    Ethyl Caffeate
    		Inhibitor 98.06%
    Ethyl Caffeate is a natural phenolic compound isolated from Bidens pilosa. Ethyl caffeate suppresses NF-κB activation and its downstream inflammatory mediators, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and prostaglandin E2 (PGE2) in vitro or in mouse skin.
    Ethyl Caffeate
  • HY-100581
    CORM-3
    CORM-3, a carbon monoxide-releasing molecule, attenuates NF-κB p65 nuclear translocation, reduces ROS generation and enhances intracellular glutathione and superoxide dismutase levels. CORM-3 reduces NLRP3 inflammasome activation.
    CORM-3
  • HY-14806B
    Teneligliptin hydrobromide hydrate
    		Inhibitor 99.87%
    Teneligliptin (MP-513) hydrobromide hydrate is an orally active and selective dipeptidyl peptidase 4 (DPP-4) inhibitor (IC50s: 0.37 and 0.29 nM for the human and rat DPP-4, respectively). Teneligliptin hydrobromide hydrate improves blood glucose levels and can be used in researches related to type 2 diabetes mellitus.
    Teneligliptin hydrobromide hydrate
  • HY-N0634
    Cimifugin
    		Inhibitor 99.95%
    Cimifugin (Cimitin) is a bioactive component of Cimicifuga racemosa, a Chinese herb. Cimifugin suppresses allergic inflammation by reducing epithelial derived initiative key factors via regulating tight junctions. Cimifugin reduces the migration and chemotaxis of RAW264.7 cells and inhibits the release of inflammatory factors and activation of MAPKs and NF-κB signaling pathways induced by LPS.
    Cimifugin
  • HY-N7088
    Raffinose
    		Inhibitor ≥98.0%
    Raffinose (Melitose) regulates intestinal flora, inhibits TLR4-MyD88-NF-κB signaling pathway, and activates Nrf2 signaling pathway. Raffinose exhibits anti-inflammatory, antioxidant, and immunomodulatory activities. Raffinose is orally active.
    Raffinose
  • HY-110177
    SP-100030
    		Inhibitor 99.86%
    SP-100030 is a potent NF-κB and activator protein-1 (AP-1) double inhibitor (IC50s=50 and 50 nM, respectively). SP-100030 inhibits IL-2, IL-8, and TNF-alpha production in Jurkat and other T cell lines. SP-100030 decreases murine collagen-induced arthritis (CIA).
    SP-100030
  • HY-16172
    DMAPT
    		Inhibitor ≥98.0%
    DMAPT (Dimethylamino Parthenolide), an analogue of Parthenolide (PTL), is an oral active NF-κB inhibitor, with a LD50 of 1.7 μM for cell population in AML cells. Has potential anti-cancer and anti-metastatic effect.
    DMAPT
  • HY-N6257
    Cafestol
    		Inhibitor 99.91%
    Cafestol is an orally active diterpenoid and an inhibitor of ERK2. Cafestol has elevated blood lipids, anti-inflammatory, anti-angiogenic and anti-diabetic activities. In addition, Cafestol induces tumor cell apoptosis and autophagy, which can be used in the study of cancer.
    Cafestol
  • HY-N2350
    Cynaropicrin
    		Inhibitor 99.79%
    Cynaropicrin is a sesquiterpene lactone which can inhibit tumor necrosis factor (TNF-α) release with IC50s of 8.24 and 3.18 μM for murine and human macrophage cells, respectively. Cynaropicrin also inhibits the increase of cartilage degradation factor (MMP13) and suppresses NF-κB signaling.
    Cynaropicrin
  • HY-B0612A
    Lercanidipine hydrochloride
    		Inhibitor 99.80%
    Lercanidipine is a third-generation, lipophilic, brain-penetrant, vascular-selective and orally active dihydropyridine-calcium channel blocker with a pIC50 of 7.74 (converts from μM). Lercanidipine has long lasting antihypertensive action as well as reno- and neuro-protective effect. Lercanidipine also shows anti-oxidant, anti-inflammatory and anti-apoptotic properties. Lercanidipine can be used in cardiovascular and neurological research.
    Lercanidipine hydrochloride
  • HY-N5142
    α-Terpineol
    		Inhibitor 99.47%
    α-Terpineol (with oral activity) can be found in Eucalyptus globulus Labill. α-Terpineol exhibits strong antimicrobial activity against periodontopathic and cariogenic bacteria.α-Terpineol possesses antifungal activity against T. mentagrophytes, and the activity might lead to irreversible cellular disruption. In addition, α-Terpineol exhibits antineuropathic and anti-inflammatory activities. α-Terpineol can be utilized in research related to diarrhea, neuropathic pain, infections, and inflammation.
    α-Terpineol
  • HY-101364A
    CHPG sodium salt
    		Activator 99.25%
    CHPG sodium salt is a selective mGluR5 agonist, and attenuates SO2-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells. CHPG sodium salt protects against traumatic brain injury (TBI) in vitro and in vivo by activation of the ERK and Akt signaling pathways..
    CHPG sodium salt
  • HY-N0602
    Ginsenoside Rg2
    		Inhibitor 98.11%
    Ginsenoside Rg2 is one of the major active components of ginseng. Ginsenoside Rg2 inhibits VCAM-1 and ICAM-1 expressions stimulated with lipopolysaccharide (LPS). Ginsenoside Rg2 also reduces Aβ1-42 accumulation.
    Ginsenoside Rg2
  • HY-B0185R
    Lidocaine (Standard)
    		Inhibitor 99.85%
    Lidocaine (Standard) is the analytical standard of Lidocaine. This product is intended for research and analytical applications. Lidocaine (Lignocaine) inhibits sodium channels involving complex voltage and using dependence. Lidocaine decreases growth, migration and invasion of gastric carcinoma cells via up-regulating miR-145 expression and further inactivation of MEK/ERK and NF-κB signaling pathways. Lidocaine is an amide derivative and has potential for the research of ventricular arrhythmia.
    Lidocaine (Standard)
  • HY-P9928A
    Alirocumab (anti-PCSK9)
    		98.24%
    Alirocumab (anti-PCSK9) is an anti-PCSK9 human monoclonal antibody. Alirocumab (anti-PCSK9) inhibits PCSK9. Alirocumab (anti-PCSK9) reduces NLRP3 inflammasome, regulates Nrf2/HO-1, HMGB1/NF-κB and Fractalkine/CX3CR1. Alirocumab (anti-PCSK9) increases the ability of the liver to bind LDL-cholesterol (LDL-C) and reduces levels of LDL-C in blood. Alirocumab (anti-PCSK9) improves atherosclerosis and inflammation.
    Alirocumab (anti-PCSK9)
  • HY-N2922
    β-Amyrin
    		Inhibitor 99.95%
    β-Amyrin shows effectively counteract amyloid β (Aβ)-induced impairment of long-term potentiation (LTP). β-Amyrin is a promising candidate for Alzheimer's disease (AD) research. β-Amyrin exhibits anti-inflammatory effects, protective activity against pulmonary fibrosis, and notable antibacterial capabilities. β-Amyrin is an orally active natural triterpenoid compound.
    β-Amyrin
  • HY-N2609
    7,4'-Dihydroxyflavone
    		Inhibitor 99.68%
    7,4'-Dihydroxyflavone (7,4'-DHF) is a flavonoid, which can be isolated from Glycyrrhiza uralensis. 7,4'-Dihydroxyflavone is eotaxin/CCL11 inhibitor and CBR1 inhibitor (IC50=0.28 μM). 7,4'-Dihydroxyflavone has the ability to consistently suppress eotaxin production and prevent dexamethasone (Dex)‐paradoxical adverse effects on eotaxin production. 7,4'-Dihydroxyflavone (7,4'-DHF) inhibits MUC5AC gene expression, mucus production and secretion via regulation of NF-κB, STAT6 and HDAC2.7,4'-Dihydroxyflavone (7,4'-DHF) decreases phorbol 12-myristate 13-acetate (PMA) stimulated NCI-H292 human airway epithelial cell MUC5AC gene expression and mucus production with IC50 value of 1.4 µM.
    7,4'-Dihydroxyflavone
  • HY-N1365
    Isoscopoletin
    		Inhibitor 99.94%
    Isoscopoletin (6-Hydroxy-7-methoxycoumarin) is an active constituent in Artemisia argyi leaves. Isoscopoletin shows substantial inhibition against cell proliferation, with IC50s of 4.0 μM and 1.6 μM for human CCRF-CEM leukaemia cells and multidrug resistant subline CEM/ADR5000, respectively. Isoscopoletin (6-Hydroxy-7-methoxycoumarin) possesses inhibitory activity against HBV replication. Isoscopoletin exhibits anti-inflammatory activity through inhibition of MAPK/NF-κB/STAT/AKT signaling pathway.
    Isoscopoletin
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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