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-123870
    MX107
    		Inhibitor
    MX107 is a selective and potent survivin inhibitor that suppresses triple-negative breast cancer (TNBC) cell proliferation. MX107 induces degradation of survivin and inhibitor-of-apoptosis proteins (IAPs), which inhibits nuclear factor κB (NF-κB) activation induced by DNA damage. MX107 enhances tumoricidal efficacy of genotoxic treatments synergized with chemotherapeutic drugs.
    MX107
  • HY-N0390G
    L-Glutamine (GMP)
    		Inhibitor
    L-Glutamine GMP is L-Glutamine (HY-N0390) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. L-Glutamine is an orally active nutritional agent and cellular metabolism regulator. L-Glutamine is taken up in a Na+-dependent manner and targets multiple key molecules including glutaminase, mTORC1, NF-κB, STAT-3 and HIF-1α. L-Glutamine enhances glutaminolytic catabolism, drives the conversion of glutamate to α-ketoglutarate, thereby regulating gene expression, integrating metabolic signals, mediating glutamine flux and maintaining redox homeostasis. L-Glutamine also promotes cell proliferation, osteogenic differentiation and fracture healing, exerts neuroprotective and cardioprotective effects, and inhibits osteoarthritis. L-Glutamine can be applied to research related to osteoporosis, osteoarthritis, ischemic stroke and acute cantharidin-induced cardiotoxicity.
    L-Glutamine (GMP)
  • HY-159144
    Anti-inflammatory agent 91
    		Inhibitor
    Anti-inflammatory agent 91 (Compound 4o) is an anti-inflammatory agent that can reduce inflammatory cytokines by inhibiting the STAT3 and NF-κB signaling pathways. Anti-inflammatory agent 91 can be used in research to improve skin inflammation associated with psoriasis.
    Anti-inflammatory agent 91
  • HY-P992462
    SHR-1806
    		Activator
    SHR-1806 is a OX40 agonist and a NF-κB activator, with antitumor activity. SHR-1806 mediates ADCC and CDC effects, enhances the function and expansion of effector T cells, suppresses regulatory T cells, and increases γ-interferon secretion. SHR-1806 exhibits typical pharmacokinetic characteristics and favorable safety profiles. SHR-1806 can be used in studies related to solid tumors and colon cancer.
    SHR-1806
  • HY-177624A
    Cupabimod sodium
    		Inhibitor
    Cupabimod sodium is a decoy oligodeoxynucleotide for transcription factor NF-κB.
    Cupabimod sodium
  • HY-149331
    TNF-α-IN-11
    		Inhibitor
    TNF-α-IN-11 (Compound 10) is a TNF-α inhibitor with a KD value of 12.06 μM. TNF-α-IN-11 binds to TNF-α and blocks the activation of TNF-α-trigged caspase and NF-κB signaling pathway. TNF-α-IN-11 inhibits the phosphorylation of IκBα, as well as the nuclear translocation of NF κB p65. TNF-α-IN-11 can be used for research of TNF-α-mediated autoimmune diseases.
    TNF-α-IN-11
  • HY-168070
    COX-2-IN-48
    		Inhibitor
    COX-2-IN-48 (5-25), a COX-2 inhibitor with an IC50 of 51.7 nM for human COX-2, exerts anti-inflammatory and analgesic effects in various rodent models by inhibiting NF-κB pathway. COX-2-IN-48 (5-25) inhibits the degradation of IκB, the phosphorylation and nuclear translocation of NF-κB p65, and the expression of COX-2 and iNOS.
    COX-2-IN-48
  • HY-175270
    MAGL-IN-22
    		Inhibitor
    MAGL-IN-22 (Compound 40) is a reversible, competitive, selective and BBB-penetrable MAGL inhibitor with an IC50 of 0.34  μM for hMAGL. MAGL-IN-22 has significant antioxidant and anti-inflammatory activity, and activates the Nrf2 pathway and significantly inhibits NFκB-mediated inflammation, without inducing cytotoxic effects. MAGL-IN-22 can be used for neurodegenerative diseases, chronic pain and cancers research.
    MAGL-IN-22
  • HY-N0044R
    Ginsenoside Re (Standard)
    		Inhibitor
    Ginsenoside Re (Standard) is the analytical standard of Ginsenoside Re. This product is intended for research and analytical applications. Ginsenoside Re (Ginsenoside B2) is an extract from Panax notoginseng. Ginsenoside Re decreases the β-amyloid protein (Aβ). Ginsenoside Re plays a role in antiinflammation through inhibition of JNK and NF-κB.
    Ginsenoside Re (Standard)
  • HY-120657R
    9-PAHSA (Standard)
    		Inhibitor
    Flumethrin (Standard) is the analytical standard of Flumethrin. This product is intended for research and analytical applications. 9-PAHSA is an orally active endogenous GPR120 agonist (EC50=18 μM). 9-PAHSA significantly inhibits LPS-induced inflammatory responses by blocking the NF-κB pathway. 9-PAHSA induces adipocyte browning, enhances glucose uptake and reduces lipid accumulation, while improving mitochondrial function and the survival rate of steatotic hepatocytes. In terms of neuroprotection, 9-PAHSA regulates the expression of REST and BDNF in the prefrontal cortex of diabetic mice, and effectively prevents spatial working memory deficits and abnormal social behaviors. 9-PAHSA does not directly regulate insulin secretion or improve systemic insulin sensitivity, and possesses specific anti-inflammatory, metabolic regulatory and neuroprotective properties. 9-PAHSA can be used in the research of diabetes-related cognitive impairment, obesity and non-alcoholic fatty liver disease.
    9-PAHSA (Standard)
  • HY-175782
    SMU-R39
    		Inhibitor
    SMU-R39 is a TLR7 and TLR8 antagonist with IC50 values of 3.22 μM and 0.24 μM, respectively. SMU-R39 binds to recombinant mTLR7 protein (KD = 2.36 μM) and to recombinant hTLR8 protein (KD = 105 nM). SMU-R39 suppresses downstream NF-κB and MAPK signaling, and reduces secretion/transcription of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) in PBMCs and THP-1 cells. SMU-R39 demonstrates anti-inflammatory efficacy in Imiquimod (IMQ) (HY-B0180)-induced psoriasis mouse model. SMU-R39 can be used for the study of autoimmune diseases such as psoriasis.
    SMU-R39
  • HY-179503
    PDE/TRPA1/CHIT1-IN-1
    		Inhibitor
    PDE/TRPA1/CHIT1-IN-1 is a phosphodiesterases (PDEs), TRPA1, and hCHIT1 (KD of 37.7 μM) inhibitor. PDE/TRPA1/CHIT1-IN-1 is a broad-spectrum PDE inhibitor, potently targeting key isoforms including PDE4B, PDE7A, PDE3A, and PDE8A with IC50s of 15.54, 15.15, 8.39 and 16.46 μM. PDE/TRPA1/CHIT1-IN-1 suppresses NLRP3 inflammasome activation and inhibits NF-κB phosphorylation, downregulating the expression of pro-inflammatory genes (TNF-α and IL-6) in vivo. PDE/TRPA1/CHIT1-IN-1 can be used for chronic obstructive pulmonary disease (COPD) and related inflammatory lung disorders research.
    PDE/TRPA1/CHIT1-IN-1
  • HY-N1474R
    Picfeltarraenin IA (Standard)
    Picfeltarraenin IA (Standard) is the analytical standard of Picfeltarraenin IA (HY-N1474). This product is intended for research and analytical applications. Picfeltarraenin IA is an Acetylcholinesterase inhibitor. Picfeltarraenin IA can be extracted from the plant Picria fel-terrae Lour. Picfeltarraenin IA reduces the production of IL-8 and PGE2. Picfeltarraenin IA inhibits COX2 via the NF-κB pathway. Picfeltarraenin IA can be used in the research of respiratory system diseases.
    Picfeltarraenin IA (Standard)
  • HY-N12527
    Hyperelamine A
    Hyperelamine A (compound 5) is a polycyclic polyprenylated acylphloroglucinols (PPAPs). Hyperelamine A exhibits inhibitory activity against LPS-activated NO production in BV-2 cells via TLR-4/NF κB signaling.
    Hyperelamine A
  • HY-N19847
    LYRM03
    		Inhibitor
    LYRM03 is a derivative of Ubenimex (HY-B0134) and a Aminopeptidase N inhibitor. LYRM03 is isolated from Streptomyces HCCB10043. LYRM03 inhibits TLR4, MyD88, NLRP3, ASC, NF-κB and p38 MAPK, stabilizes IκB, and suppresses LPS-induced expression of iNOS and COX-2. LYRM03 reduces the levels of inflammatory cytokines and oxidative stress markers, and alleviates pulmonary edema. LYRM03 exhibits anticancer activity against breast cancer. LYRM03 has anti-inflammatory activity. LYRM03 can be used in the research of acute lung injury and breast cancer.
    LYRM03
  • HY-N17413
    (-)-γ-Cuparenol
    		Inhibitor
    (-)-γ-Cuparenol is a sesquiterpene compound with an IC50 of 23.6 μg/mL against porcine Na+/K+-ATPase. (-)-γ-Cuparenol reduces phytohemagglutinin (PHA)-induced activation of NF-AT and NF-κB in Jurkat cells. (-)-γ-Cuparenol inhibits the growth of Gram-positive bacteria and some Gram-negative bacteria. (-)-γ-Cuparenol exhibits weak inhibitory activity against Candida albicans. (-)-γ-Cuparenol is applicable for research related to immunoregulation, cardiovascular diseases and bacterial infections.
    (-)-γ-Cuparenol
  • HY-B0808A
    Oxaprozin potassium
    		Inhibitor
    Oxaprozin potassium is an orally active and potent COX inhibitor, with IC50 values of 2.2 μM for human platelet COX-1 and and 36 μM for IL-1-stimulated human synovial cell COX-2, respectively. Oxaprozin potassium also inhibits the activation of NF-κB. Oxaprozin potassium induces cell apoptosis. Oxaprozin potassium shows anti-inflammatory activity. Oxaprozin potassium-mediated inhibition of the Akt/IKK/NF-κB pathway contributes to its anti-inflammatory properties.
    Oxaprozin potassium
  • HY-N0375R
    18α-Glycyrrhetinic acid (Standard)
    		Inhibitor
    18α-Glycyrrhetinic acid (Standard) is the analytical standard of 18α-Glycyrrhetinic acid. This product is intended for research and analytical applications. 18α-Glycyrrhetinic acid, a diet-derived compound, is an inhibitor of NF-kB and an activator of proteasome, which serves as pro-longevity and anti-aggregation factor in a multicellular organism. 18α-Glycyrrhetinic acid induces apoptosis.
    18α-Glycyrrhetinic acid (Standard)
  • HY-N9699
    8α-Hydroxyhirsutinolide
    		Inhibitor
    8α-Hydroxyhirsutinolide is a sesquiterpene lactone. 8α-Hydroxyhirsutinolide inhibits TNF-α-induced NF-κB activity (IC50: 1.9 μM) and NO production. 8α-Hydroxyhirsutinolide can be isolated from Vernonia cinerea.
    8α-Hydroxyhirsutinolide
  • HY-N15691
    Tadehaginoside
    Tadehaginoside, a phenylpropanoid glycoside, is a regulator of lipogenesis and glucose consumption. Tadehaginoside has antioxygenic property. Tadehaginoside mediates liver protection against oxidative stress injury and inflammation by regulating Nrf2 and NF-κB signaling pathways in hepatocytes. Tadehaginoside can be used for the study of obesity and diabetes.
    Tadehaginoside
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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