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-111214
    K-14585
    		Inhibitor
    K-14585 is a peptide competitive PAR2 antagonist. K-14585 inhibits PAR2-dependent IL-8 production, NF-κB phosphorylation, and p38 signaling. K-14585 reduces SLIGKV (PAR2 agonist peptide)-induced Ca2+ mobilisation in primary human keratinocytes.
    K-14585
  • HY-N15653
    Heveadride
    		Inhibitor
    Heveadride is a fungal metabolite and an antifungal agent. Heveadride is active against various filamentous fungi and some human pathogenic yeasts. Heaveadride induces down-regulation of TNFα-induced NF-κB activity in human chronic myeloid leukemia cells with an IC50 of 82.7 μM.
    Heveadride
  • HY-153762
    COX-2-IN-32
    		Inhibitor
    COX-2-IN-32 (Compound 2f) is an iNOS and COX-2 inhibitor. COX-2-IN-32 decreases the expression of NF-κB. COX-2-IN-32 has anti-inflammatory activity by inhibits NO production in LPS-induced RAW264.7 macrophages (IC50: 11.2 μM).
    COX-2-IN-32
  • HY-179432
    Cannabitwinol
    		Inhibitor
    Cannabitwinol is a selective thermosensitive TRP modulator and NF-κB inhibitor. Cannabitwinol inhibits TNFα-induced NF-κB-driven transcription and TNFα-induced IL-8 release, and exhibits anti-inflammatory and antioxidant activities. Cannabitwinol shows selectivity for cold-activated TRP channels, activating TRPA1 (EC50 = 3.0 μM) and antagonizing TRPM8 (IC50 = 3.9 μM), but has no significant affinity for heat-activated TRP channels such as TRPV1 and TRPV2. Cannabitwinol can be used in research related to inflammatory skin diseases, cold allodynia, and hyperalgesia.
    Cannabitwinol
  • HY-76006R
    3-Hydroxybenzaldehyde (Standard)
    		Inhibitor
    3-Hydroxybenzaldehyde (Standard) is the analytical standard of 3-Hydroxybenzaldehyde. This product is intended for research and analytical applications. 3-Hydroxybenzaldehyde (3-HBA) is a precursor compound for phenolic compounds like Protocatechuic aldehyde (PCA) (HY-N0295). 3-Hydroxybenzaldehyde, produced by 3-hydroxybenzyl-alcohol dehydrogenase, is a substrate of aldehyde dehydrogenase (ALDH) in rats and humans. 3-Hydroxybenzaldehyde has vasculoprotective effects in vitro and in vivo. 3-Hydroxybenzaldehyde is proming for research of atherosclerosis[1][2][3][4].
    3-Hydroxybenzaldehyde (Standard)
  • HY-N1928
    Dauricinoline
    		Inhibitor
    Dauricinoline is an orally active NF-κB inhibitor that can significantly inhibit NF-κB activation induced by TNF-α. Dauricinoline exhibits certain anti-inflammatory activity and can be used in the research of inflammatory diseases such as lung inflammation.
    Dauricinoline
  • HY-124995
    BMS-986126
    		Inhibitor
    BMS-986126 is a potent, selective, and orally active IRAK4 inhibitor (IC50 = 5.3 nM). BMS-986126 broadly inhibits MyD88-dependent signaling pathways. BMS-986126 demonstrates robust activity in the MRL/lpr and NZB/NZW murine models of lupus, inhibiting multiple pathogenic responses. BMS-986126 can be used for autoimmune diseases research, such as lupus erythematosus (SLE).
    BMS-986126
  • HY-121632R
    Quinoclamine (Standard)
    		Inhibitor
    Quinoclamine (Standard) is the analytical standard of Quinoclamine. This product is intended for research and analytical applications. Quinoclamine, a naphthoquinone derivative, is a NF-κB inhibitor. Quinoclamine exhibits anti-cancer activity.
    Quinoclamine (Standard)
  • HY-162805
    iNOS/TopoI-IN-1
    		Inhibitor
    iNOS/TopoI-IN-1 (compound AuL9) is a multi-target hybrid molecule with anti-tumor, anti-inflammatory and antioxidant activities. iNOS/TopoI-IN-1 inhibits the growth of breast cancer cells MCF-7 and MDA MB-231 in vitro with IC50 of 3.5 μM and 6.3 μM, respectively, and induces DNA damage and apoptosis of breast cancer cells by inhibiting human topoisomerase I (TopoI) (Ki=2.72 μM). In addition, NOS/TopoI-IN-1 inhibits the expression of iNOS by inhibiting the activation of NF-kB (Ki=1.49 μM).
    iNOS/TopoI-IN-1
  • HY-19356B
    (+)-Rocaglamide
    		Inhibitor
    (+)-Rocaglamide is the dextrorotatory enantiomer of Rocaglamide (HY-19356). Rocaglamide (Roc-A) is isolated from the genus Aglaia and can be used for coughs, injuries, asthma and inflammatory skin diseases. Rocaglamide is a potent inhibitor of NF-κB activation in T-cells. Rocaglamide is a potent and selective heat shock factor 1 (HSF1) activation inhibitor with an IC50 of 50 nM. Rocaglamide inhibits the function of the translation initiation factor eIF4A. Rocaglamide also has anticancer properties in leukemia.
    (+)-Rocaglamide
  • HY-149043
    NIK-IN-1
    		Inhibitor
    NIK-IN-1 (Compound 2) is an inhibitor of NF-κB-inducing kinase (NIK). NIK-IN-1 is used for research on hepatic inflammatory diseases and acute liver injury.
    NIK-IN-1
  • HY-175521
    HIF-1α-IN-8
    		Inhibitor
    HIF-1α-IN-8 is an orally active HIF-1α inhibitor, with an IC50 of 2.02 μM. HIF-1α-IN-8 significantly suppresses the expression of inflammation factors of IL-6 and NO, reduces hypoxia-induced ROS production and apoptosis in C8-D1A cells. HIF-1α-IN-8 inhibits HIF-1α/IKKα/NF-κB signaling pathway and reduces the expression of blood-brain barrier permeability-related proteins. HIF-1α-IN-8 reduces brain water content and oxidative stress level in mice with high altitude cerebral edema (HACE) model. HIF-1α-IN-8 can be used for the study of high altitude cerebral edema (HACE).
    HIF-1α-IN-8
  • HY-139718
    IMD-biphenylB
    		Modulator
    IMD-biphenylB is a potent imidazoquinolinone-NF-κB immunomodulator dimer that inhibits tumor proliferation while induces low systemic inflammation and reduces adjuvant toxicity.
    IMD-biphenylB
  • HY-N17600
    Pterocenoid C
    		Inhibitor
    Pterocenoid C is an inhibitor of the NF-κB pathway and can be used for research on diseases related to the NF-κB pathway.
    Pterocenoid C
  • HY-111172
    Inotilone
    		Inhibitor
    Inotilone is an inhibitor of matrix metalloproteinase MMP-2 and MMP-9, to against metastatic in lung cancer cells. Inotilone enhances the activity of the antioxidant enzymes to support its anti-metastatic activity. Inotilone also inhibits IκBα phosphorylation and NFκB p65 nuclear translocation, involving in FAK, PI3K/AKT, MAPKs and NFκB pathways.
    Inotilone
  • HY-N7128R
    Flavanone (Standard)
    		Inhibitor
    Flavanone (Standard) is the analytical standard of Flavanone. This product is intended for research and analytical applications. Flavanone is a naturally occurring flavone. Flavanone has inhibitory activity for human estrogen synthetase (aromatase). lavanone is the inhibitor for ERK/p38/NF-κB signaling pathway. Flavanone exhibits oral activity and antitumor efficacy.
    Flavanone (Standard)
  • HY-161850
    ULK1-IN-3
    		Agonist
    ULK1-IN-3 (Compound 8) is a novel chromone-based as a potential inhibitor of ULK1. ULK1-IN-3 inhibits cell cycle, autophagy and induces apoptosis, oxidative stress in colon cancer cell lines.
    ULK1-IN-3
  • HY-128447R
    Allyl methyl sulfide (Standard)
    		Inhibitor
    Allyl methyl sulfide (Standard) is the analytical standard of Allyl methyl sulfide (HY-128447). This product is intended for research and analytical applications. Allyl methyl sulfide is an orally active organic sulfide. Allyl methyl sulfide is one of the main active ingredients in garlic volatile metabolites. Allyl methyl sulfide can be extracted from garlic. Allyl methyl sulfide enhances SOD activity, inhibits NF-κB signaling pathway, and upregulates pancreatic GLUT2 expression. Allyl methyl sulfide has significant antioxidant, anti-inflammatory and hypoglycemic activities. Allyl methyl sulfide can be used in the research of diabetes and its complications.
    Allyl methyl sulfide (Standard)
  • HY-N2453R
    Convallatoxin (Standard)
    		Inhibitor
    Convallatoxin (Standard) is the analytical standard of Convallatoxin. This product is intended for research and analytical applications. Convallatoxin is a cardiac glycoside isolated from Adonis amurensis Regel et Radde. Convallatoxin ameliorates colitic inflammation via activation of PPARγ and suppression of NF-κB. Convallatoxin is a P-glycoprotein (P-gp) substrate and recognized Val982 as an important amino acid involved in its transport. Convallatoxin is an enhancer of ligand-induced MOR endocytosis with high potency and efficacy. Anti-inflammatory and anti-proliferative properties.
    Convallatoxin (Standard)
  • HY-W754303
    Dihydroartemisinin-13C,d5
    Dihydroartemisinin-13C,d5 (Dihydroqinghaosu-13C,d5) is the deuterium labeled and 13C-labeled Dihydroartemisinin (HY-N0176). Dihydroartemisinin is a potent anti-malaria agent.
    Dihydroartemisinin-<sup>13</sup>C,d<sub>5</sub>
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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