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-183573
    PTPRO-IN-1
    		Inhibitor
    PTPRO-IN-1 is a selective, orally active PTPRO inhibitor with an IC50 of 0.16 μM. PTPRO-IN-1 exhibits IC50 values of 2.4 μM, 2.33 μM and 2.13 μM against PTPN22, PTP1B and PTPRT, respectively, and shows almost no inhibitory activity against STEP/SSH2. PTPRO-IN-1 inhibits the TLR4/NF-κB signaling pathway in macrophages, ameliorates colonic pathological conditions and suppresses the secretion of pro-inflammatory cytokines by T cells. PTPRO-IN-1 can be used for the research of inflammatory bowel disease.
    PTPRO-IN-1
  • HY-160938
    β-Funaltrexamine
    		Inhibitor
    β-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.
    β-Funaltrexamine
  • HY-150587
    Anti-inflammatory agent 31
    		Inhibitor
    Anti-inflammatory agent 31 (enone 17) is a kind of andrographolide derivatives, is a anti-inflammatory agent. Anti-inflammatory agent 31 inhibits NF-κB activation by upstream blockade of PI3K/Akt and ERK1/2 MAPK activation. Anti-inflammatory agent 31 shows recovery effective of the intracellular GSH levels and protective effect on liver.
    Anti-inflammatory agent 31
  • HY-N0603R
    20(S)-Ginsenoside Rg3 (Standard)
    		Inhibitor
    20(S)-Ginsenoside Rg3 (Standard) is the analytical standard of 20(S)-Ginsenoside Rg3. This product is intended for research and analytical applications. 20(S)-Ginsenoside Rg3 is the main component of Panax ginseng C. A. Meyer. Ginsenoside Rg3 inhibits Na+ and hKv1.4 channel with IC50s of 32.2±4.5 and 32.6±2.2 μM, respectively. 20(S)-Ginsenoside Rg3 also inhibits Aβ levels, NF-κB activity, and COX-2 expression.
    20(S)-Ginsenoside Rg3 (Standard)
  • HY-161329
    NLRP3-IN-32
    		Inhibitor
    NLRP3-IN-32 (compound 7a), a 3, 4-dihydronaphthalene-1(2H)-one derivative, is a potential NLRP3 inflammatory vesicles inhibitor. NLRP3-IN-32 can block the assembly and activation of NLRP3 inflammasome by down-regulating the expression of NLPR3 and apoptosis-associated speck-like protein containing a CARD (ASC), and inhibiting the production of reactive oxygen species (ROS) and other inflammatory mediators. NLRP3-IN-32 inhibits the phosphorylation of IκBα and NF-κB/p65 and the nuclear translocation of p65, thereby inhibiting NF-κB signaling.
    NLRP3-IN-32
  • HY-N2515R
    Ginsenoside Rk1 (Standard)
    		Inhibitor
    Ginsenoside Rk1 (Standard) is the analytical standard of Ginsenoside Rk1. This product is intended for research and analytical applications. Ginsenoside Rk1 is a unique component created by processing the ginseng plant (mainly Sung Ginseng, SG) at high temperatures. Ginsenoside Rk1 has anti-inflammatory effect, suppresses the activation of Jak2/Stat3 signaling pathway and NF-κB. Ginsenoside Rk1 has anti-tumor effect, antiplatelet aggregation activities, anti-insulin resistance, nephroprotective effect, antimicrobial effect, cognitive function enhancement, lipid accumulation reduction and prevents osteoporosis. Ginsenoside Rk1 induces cell apoptosis by triggering intracellular reactive oxygen species (ROS) generation and blocking PI3K/Akt pathway.
    Ginsenoside Rk1 (Standard)
  • HY-163607
    SpiD3
    		Inhibitor 98.24%
    SpiD3, a spirocyclic dimer, is an anticancer agent. SpiD3 markedly inhibits malignant B-cell proliferation and suppressed NF-κB activation independent of TME-associated stimuli. SpiD3 induces apoptosis and inhibits protein synthesis in chronic lymphocytic leukemia cells. SpiD3 can be used for study of chronic lymphocytic leukemia (CLL).
    SpiD3
  • HY-129085
    5-Methyl cromolyn disodium
    		Inhibitor
    5-Methyl cromolyn (C5OH) disodium, an analog of Cromolyn (HY-B1619), is a S100P inhibitor. 5-Methyl cromolyn disodium inhibits the binding of S100P to its receptor RAGE, NF-κB activity and cell proliferation, and promotes Gemcitabine (HY-17026)-induced apoptosis. 5-Methyl cromolyn disodium reduces tumor growth and metastasis, and prolongs survival in mouse models of syngeneic PDAC. 5-Methyl cromolyn disodium can be used for pancreatic cancer like pancreatic ductal adenocarcinoma (PDAC) research.
    5-Methyl cromolyn disodium
  • HY-B0678R
    Metaxalone (Standard)
    		Inhibitor
    Metaxalone (Standard) is the analytical standard of Metaxalone. This product is intended for research and analytical applications. Metaxalone (AHR438; NSC170959) is an FDA-approved muscle relaxant. Metaxalone acts mainly on the central nervous system and achieves muscle relaxation by inhibiting polysynaptic reflex arcs. In addition, Metaxalone is an inhibitor of MAO-A, which has anti-inflammatory and antioxidant effects. Metaxalone inhibits IL-1β-induced inflammatory phenotype, modulates NF-κB and other related signaling pathways, and decreases MAO-A expression and activity in IL-1β-treated microglia.
    Metaxalone (Standard)
  • HY-E70291
    N-Acetylgalactosaminyltransferase 4
    		Inhibitor
    N-Acetylgalactosaminyltransferase 4 (GALNT4) is a glycosyltransferase capable of inhibiting the activation of ASK1. By directly binding to ASK1, N-Acetylgalactosaminyltransferase 4 suppresses its N-terminal dimerization and subsequent phosphorylation, leading to robust inactivation of downstream JNK/p38 and NF-κB signals, and thereby improving the prognosis of liver surgery.
    N-Acetylgalactosaminyltransferase 4
  • HY-121038
    Chamazulene
    		Inhibitor 98.96%
    Chamazulene, a natural compound, is an antioxidant-type inhibitor of leukotriene B4 formation.
    Chamazulene
  • HY-174382
    ROR1-IN-3
    		Inhibitor
    ROR1-IN-3 (Compound 24d) is a potent and highly selective ROR1 kinase inhibitor (IC50 = 17.6 nM). ROR1-IN-3 demonstrates robust antitumor activity and inhibitory effect against ROR1 both in vitro and in vivo. ROR1-IN-3 has robust antiproliferative efficacy in vitro and in vivo. ROR1-IN-3 induces apoptosis in cancer cell lines. ROR1-IN-3 inhibits ROR1 downstream AKT/mTOR and NF-κB signaling pathway. ROR1-IN-3 can be studied in antitumor research.
    ROR1-IN-3
  • HY-131265
    Mesalamine impurity P
    		Inhibitor
    Mesalamine 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.
    Mesalamine impurity P
  • HY-N2526R
    Nervonic acid (Standard)
    		Inhibitor
    Nervonic acid (Standard) is the analytical standard of Nervonic acid. This product is intended for research and analytical applications. Nervonic acid is a monounsaturated fatty acid with oral activity. Nervonic acid exerts anti-inflammatory activity by inhibiting NF-κB signaling. Nervonic acid can be used in the study of neurodegenerative diseases[1][2][3].
    Nervonic acid (Standard)
  • HY-N11892
    7-O-Methylaloesinol
    		Inhibitor
    7-O-Methylaloesinol is a chromone derivative. 7-O-Methylaloesinol shows significant inhibitory effects against TNFα-induced NF-κB transcriptional activity with an IC50 value of 29.07 μM.
    7-O-Methylaloesinol
  • HY-149838
    NF-κB-IN-9
    		Inhibitor
    NF-κB-IN-9 is a nuclear factor kappa B (NF-κB) targeting sonosensitizer (λex/λem=489/628 nm). NF-κB-IN-9 exhibits strong inhibition on NF-κB signaling due to its two resveratrol units in one molecule. NF-κB-IN-9 has anti-tumor activity and shows remarkable sonocytotoxicity against cancer cells. NF-κB-IN-9 has biosafety in eenograft mice model.
    NF-κB-IN-9
  • HY-114335
    Triphala
    		Inhibitor
    Triphala, 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.
    Triphala
  • HY-180829
    HDAC6-IN-71
    		Inhibitor
    HDAC6-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.
    HDAC6-IN-71
  • HY-180890
    PPARγ agonist-21
    		Inhibitor
    PPARγ agonist-21 (Compound 9a) is a PPARγ agonist with an EC50 of 3.12 μM. PPARγ agonist-21 activates PPAR-γ to inhibit NF-κB and attenuate NLRP3 inflammasome assembly. PPARγ agonist-21 blocks NLRP3-ASC and NLRP3-NEK7 interaction. PPARγ agonist-21 attenuates the severity of gouty arthritis.
    PPARγ agonist-21
  • HY-162538
    LC-MI-3
    		Inhibitor
    LC-MI-3 is an orally active and potent interleukin-1 receptor-associated kinase 4 (IRAK4) PROTAC degrader, with a DC50 of 47.3 nM. LC-MI-3 effectively inhibits the activation of downstream NF-κB signaling. LC-MI-3 can be used for the research of acute and chronic inflammatory skin. (Blue: VHL ligand, Black: linker, Pink: CRBN ligand (HY-14658)).
    LC-MI-3
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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