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-175277
    PIM1-IN-8
    		Inhibitor
    PIM1-IN-8 is a PIM1/p65 pathway inhibitor. PIM1-IN-8 suppresses the expression of α-SMA and collagen I in activated fibroblasts and blocks TGF-β induced migration. PIM1-IN-8 alleviates pulmonary fibrosis in a Bleomycin (BLM) (HY-17565A)-induced pulmonary fibrosis mice model. PIM1-IN-8 can be used for the study of idiopathic pulmonary fibrosis (IPF).
    PIM1-IN-8
  • HY-14621R
    Zingerone (Standard)
    		Inhibitor
    Zingerone (Standard) is the analytical standard of Zingerone. This product is intended for research and analytical applications. Zingerone (Vanillylacetone) is a nontoxic methoxyphenol isolated from Zingiber officinale, with potent anti-inflammatory, antidiabetic, antilipolytic, antidiarrhoeic, antispasmodic and anti-tumor properties. Zingerone alleviates oxidative stress and inflammation, down-regulates NF-κB mediated signaling pathways. Zingerone acts as an anti-mitotic agent, and inhibits the growth of neuroblastoma cells.
    Zingerone (Standard)
  • HY-118668
    ABD-350
    ABD-350 is an antiresorptive agent that inhibits osteoclast activity without affecting osteoblast activity and preventing ovariectomy-induced bone loss. ABD-350 inhibits NF-κB ligand-induced inhibitor of NF-κB phosphorylation, leading to osteoclast apoptosis, but has no inhibitory effect on osteoblast function, effectively preventing bone loss in ovariectomized mice, and does not inhibit parathyroid hormone-induced bone formation.
    ABD-350
  • HY-169630
    DBMB
    		Inhibitor
    DBMB is an inhibitor of spleen tyrosine kinase (Syk), capable of significantly inhibiting the activity of Syk kinase. DBMB exhibits anti-inflammatory activity by suppressing the signaling of NF-κB, which in turn reduces the production of inflammatory mediators such as nitric oxide (NO) and prostaglandin E2 (PGE2). DBMB can be utilized in research on inflammatory diseases.
    DBMB
  • HY-N4314R
    Scutellarein tetramethyl ether (Standard)
    		Inhibitor
    Scutellarein tetramethyl ether (Standard) is the analytical standard of Scutellarein tetramethyl ether. This product is intended for research and analytical applications. Scutellarein tetramethyl ether (4',5,6,7-Tetramethoxyflavone) is a bioactive compound extracted from Eupatorium odoratum. Scutellarein tetramethyl ether exhibits anti-inflammatory, antibacterial, pro-coagulant, and anti-tumor activities. Scutellarein tetramethyl ether exerts its anti-inflammatory effects by modulating the NF-κB pathway and regulates bacterial resistance through the inhibition of efflux pumps. Additionally, Scutellarein tetramethyl ether accelerates coagulation time via the endogenous coagulation pathway. Studies have shown that Scutellarein tetramethyl ether can effectively inhibit the growth of the liver cancer cell line HepG2 (IC50= 20.08 μg/mL).
    Scutellarein tetramethyl ether (Standard)
  • HY-111193
    Declopramide
    		Inhibitor
    Declopramide (3-Chloroprocainamide) is an orally active antitumor agent, which inhibits proliferation of cancer cells HL60 and K562, and inhibits tumor growth of human brain astrocytoma (T24) in mouse model. Declopramide induces apoptosis, inhibits NF-κB through inhibition of IκBα degradation. Declopramide serves also as chemosensitizer in research.
    Declopramide
  • HY-117356A
    MRS2693 ammonium
    		Inhibitor
    MRS2693 ammonium is the ammonium dalt form of MRS2693 (HY-117356). MRS2693 ammonium is a selective agonist for P2Y6 with an EC50 of 0.015 μM. MRS2693 ammonium protects C2C12 skeletal muscle cells from TNFα-induced apoptosis. MRS2693 ammonium reduces the activation of NF-kB, activates the ERK1/2 pathway, and has a cytoprotective effect on mouse ischemia-reperfusion injury model[2].
    MRS2693 ammonium
  • HY-150594
    IRAK4-IN-17
    		Inhibitor
    IRAK4-IN-17 (Compound 5) is a potent IRAK4 inhibitor with the IC50 of 1.3 nM. IRAK4-IN-17 can be used in large B-cell lymphoma (DLBCL) research.
    IRAK4-IN-17
  • 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-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-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-122961
    Dehydromiltirone
    		Inhibitor
    Dehydromiltirone (1,2-Didehydromiltirone) is a diterpenoid quinone with an anti-inflammatory effect. Dehydromiltirone prevents liver injury by modifying the MAPK and NF-κB signaling pathways, reducing neuroinflammatory responses, and inhibiting platelet aggregation. Dehydromiltirone can be used for osteoporosis research.
    Dehydromiltirone
  • 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-B0289S2
    Erdosteine-d4
    Erdosteine-d4 is a deuterium labeled Erdosteine (HY-B0289). Erdosteine has muco-modulatory, anti-bacterial, anti-inflammatory and anti-oxidant effects.
    Erdosteine-d<sub>4</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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