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. 상품명 효과 Purity Chemical Structure
  • HY-N17383
    Ligusticum cycloprolactam
    		Inhibitor
    Ligusticum cycloprolactam is a potent, orally active, and CNS-penetrant TLR4/NF-κB inhibitor, exhibiting anti-inflammatory and neuroprotective activity. Ligusticum cycloprolactam reduces FPR1 expression, inhibits NLRP3 inflammasome, TLR4/NF-κB, hepatic MAPK and TGF-β signaling, and selectively activates hepatic FXR. Ligusticum cycloprolactam attenuates pro-inflammatory mediator production, enhances anti-inflammatory cytokine secretion, regulates renal uric acid transporters, and preserves intestinal microbiota composition. Ligusticum cycloprolactam can be used for the research of ischemic stroke, hyperuricemic nephropathy, neuroinflammation, and metabolic dysfunction-associated fatty liver disease.
    Ligusticum cycloprolactam
  • HY-180580
    SMU-C409
    		Inhibitor
    SMU-C409 is a TLR1/2 agonist with an EC50 of 65 nM in HEK-Blue hTLR2 Cells. SMU-C409 activates the TLR1/2–MyD88–NF-κB pathway, inducing TNF-α/IL-1β secretion and robust immune cell activation for antitumor immunomodulation. SMU-C409 shows low toxicity in virto. SMU-C409 can be used for cancer immunotherapy research.
    SMU-C409
  • HY-182006
    TNF-α-IN-28
    		Inhibitor
    TNF-α-IN-28 (compound 4ea) is a TNF-α and NF-κB inhibitor with anti-inflammatory activity. TNF-α-IN-28 inhibits TNF-α and NF-κB expression. TNF-α-IN-28 interacts with TNF-α dimer.
    TNF-α-IN-28
  • HY-142570S1
    Nalmefene-d4
    Nalmefene-d4 is the deuterium labeled Nalmefene (HY-107744). Nalmefene is a BBB-penetrable?opioid receptor?modulator. Nalmefene is an antagonist of?MOR?and?DOR, and a partial agonist of?KOR. Nalmefene has anti-inflammatory and neuroprotective activities. Nalmefene can be used in the research of reducing alcohol-dependent disorders.
    Nalmefene-d<sub>4</sub>
  • HY-W971442
    Moniliphenone
    		Inhibitor
    Moniliphenone (Compounds 5) is a secondary metabolite. Moniliphenone can be isolated from the endophytic fungus Penicillium chrysogenum. Moniliphenone has an anti-inflammatory activity and significantly inhibits TNF-α-stimulated NF-κB activation.
    Moniliphenone
  • HY-119731
    Antidesmone
    		Inhibitor
    Antidesmone is a isoquinoline alkaloid that can be isolated from Antidesma membranaceum. Antidesmone can prevent acute lung injury in vivo via inhibiting MAPK and NF-κb activities.
    Antidesmone
  • HY-N11726
    Ageconyflavone B
    		Modulator
    Ageconyflavone B is a flavonoid. Ageconyflavone B can be separated from AC-AgNPs. Ageconyflavone B reduces inflammation by interfering with IκBα phosphorylation.
    Ageconyflavone B
  • HY-10227G
    Bortezomib (GMP)
    		Inhibitor
    Bortezomib (GMP) (PS-341 (GMP)) is Bortezomib (HY-10227) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Bortezomib (PS-341) is a reversible and selective proteasome inhibitor, and potently inhibits 20S proteasome (Ki=0.6 nM) by targeting a threonine residue. Bortezomib disrupts the cell cycle, induces apoptosis, and inhibits NF-κB. Bortezomib is the first proteasome inhibitor anticancer agent. Bortezomib can be used for the study of multiple myeloma (MM). Bortezomib effectively inhibits TREM2 expression in tumor-associated macrophages (TAMs).
    Bortezomib (GMP)
  • HY-142958
    NF-κB-IN-2
    NF-κB-IN-2 inhibits TNF-α-induced canonical NF-κB signaling in PC-3 cells.
    NF-κB-IN-2
  • HY-181073
    Apoptosis/necroptosis inducer 1
    		Activator
    Apoptosis/necroptosis inducer 1 is an orally active and brain-penetrant apoptosis and necroptosis inducer. Apoptosis/necroptosis inducer 1 induces mitochondria-dependent (intrinsic pathway) apoptosis. Apoptosis/necroptosis inducer 1 induces necroptosis by activating the TNF-α/NF-κB/MAPK signaling pathway. Apoptosis/necroptosis inducer 1 exhibits antiproliferative activity in glioblastoma cell lines and multiple solid tumor types. Apoptosis/necroptosis inducer 1 inhibits growth of orthotopic glioblastoma in animal models and improves survival rate. Apoptosis/necroptosis inducer 1 can be used for the research of glioblastoma.
    Apoptosis/necroptosis inducer 1
  • HY-N2350R
    Cynaropicrin (Standard)
    		Inhibitor
    Cynaropicrin (Standard) is the analytical standard of Cynaropicrin. This product is intended for research and analytical applications. 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 (Standard)
  • HY-N8903
    Mumefural
    		Inhibitor
    Mumefural is a bioactive component of the processed fruit of Prunus mume Sieb. Mumefural inhibits platelet aggregation. Mumefural shows anti-thrombotic effects and ameliorates cognitive impairment.
    Mumefural
  • HY-139719
    IMD-biphenylC
    		Modulator
    IMD-biphenylC is a novel imidazoquinolinone-NF-κB immunomodulator dimer that inhibits tumor proliferation while induces low systemic inflammation and reduces adjuvant toxicity.
    IMD-biphenylC
  • HY-N9971R
    Hentriacontane (Standard)
    		Inhibitor
    Hentriacontane (Standard) is the analytical standard of Hentriacontane. This product is intended for research and analytical applications. Hentriacontane is a long-chain alkane. Hentriacontane exerts anti-inflammatory effects by inhibiting the NF-κB pathway. Hentriacontane has anti-inflammatory, antitumor and antibacterial activities.
    Hentriacontane (Standard)
  • HY-176127
    JX10
    		Inhibitor
    JX10 is a senomorphic agent. JX10 suppresses the expression of p38 MAPK and NF-κB. JX10 exhibits competent antiaging effects in C. elegans, senescent cells, and aged mice.
    JX10
  • HY-N13798
    ADHPE
    		Inhibitor
    ADHPE is a stabilizer of 14-3-3σ and p65 protein complex. ADHPE inhibits NF-κB (p65) signaling pathway and reduces the inflammatory response. ADHPE can be used for pediatric pneumonia-related acute lung injury and acute respiratory distress syndrome study.
    ADHPE
  • HY-144744
    NF-κB-IN-3
    		Inhibitor
    NF-κB-IN-3 (Compound 2) is a NF-κB inhibitor with an IC50 of 0.70 µM. NF-κB-IN-3 can be used as an antitumor agent.
    NF-κB-IN-3
  • HY-149696
    IR-Crizotinib
    		Inhibitor
    IR-Crizotinib is a NF-κB-inducing kinase (NIK) inhibitor that crosses the blood-brain barrier and fluorescently localizes intracranial glioblastoma (GBM) in mice (IC50=3.381 μM). IR-Crizotinib is conjugated from the near-infrared dye IR-786 and the NF-κB-inducing kinase (NIK) inhibitor Crizotinib. IR-Crizotinib can effectively inhibit the growth and invasion of glioma in vitro and in vivo and can be used in cancer research.
    IR-Crizotinib
  • HY-122019
    ABD56
    ABD56 is a compound that induces osteoclast apoptosis and has the activity of inhibiting osteoclast formation and inducing apoptosis. ABD56 can inhibit osteoclast formation and induce apoptosis, and its mechanism is related to the inhibition of NFκB and ERK pathways.
    ABD56
  • HY-180291
    Anti-inflammatory agent 109
    		Inhibitor
    Anti-inflammatory agent 109 (Compound 2m) is an anti-inflammatory agent. Anti-inflammatory agent 109 directly interacts with p65, attenuates aberrant activation of the NF-κB pathway. Anti-inflammatory agent 109 significantly suppresses the release of key pro-inflammatory mediators, including IL-1β, COX-2, and iNOS. Anti-inflammatory agent 109 conferres robust protection against LPS-induced acute liver injury in septic mice.
    Anti-inflammatory agent 109
Cat. No. 상품명 / 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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