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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
製品番号 製品名 製品効果 純度 構造式
  • HY-N6257R
    Cafestol (Standard) Inhibitor
    Cafestol (Standard) is the analytical standard of Cafestol. This product is intended for research and analytical applications. Cafestol is an orally active diterpenoid and an inhibitor of ERK2. Cafestol has elevated blood lipids, anti-inflammatory, anti-angiogenic and anti-diabetic activities. In addition, Cafestol induces tumor cell apoptosis and autophagy, which can be used in the study of cancer.
    Cafestol (Standard)
  • HY-108694R
    γ-Tocotrienol (Standard) Inhibitor
    γ-Tocotrienol (Standard) is the analytical standard of γ-Tocotrienol. This product is intended for research and analytical applications. γ-Tocotrienol is an active form of vitamin E. γ-tocotrienol reverses the multidrug resistance (MDR) of breast cancer cells through the signaling pathway of NF-κB and P-gp. γ-Tocotrienol is also a novel radioprotector agent, can mitigate bone marrow radiation damage during targeted radionuclide treatment.
    γ-Tocotrienol (Standard)
  • HY-B0380S1
    Trimebutine-d5 fumarate Inhibitor
    Trimebutine-d5 fumarate is deuterium labeled Trimebutine fumarate. Trimebutine fumarate is a multi-target inhibitor and opioid receptor agonist with antimuscarinic activity. Trimebutine fumarate inhibits L-type Ca2+ channels and large-conductance calcium-activated potassium channels (BKCa channels), thereby inhibiting extracellular calcium influx and potassium ion efflux. Trimebutine fumarate also targets Toll-like receptors, inhibits Toll-like receptor 2/4/7/8/9 signals, and inhibits LPS-induced IRAK1 activation, as well as ERK1/2, JNK and NF-κB activation, thereby exerting anti-inflammatory effects. Trimebutine fumarate also induces tumor cell apoptosis by inhibiting the AKT/ERK pathway. Trimebutine fumarate also inhibits excessive contraction of smooth muscle and can be used in the study of gastrointestinal disorders such as irritable bowel syndrome (IBS).
    Trimebutine-d<sub>5</sub> fumarate
  • HY-183276
    TLR8 antagonist-2 Inhibitor
    TLR8 antagonist-2 (Compound 35) is a selective TLR8 antagonist with an IC50 of 0.032 μM against hTLR8. TLR8 antagonist-2 potently inhibits TLR8-dependent NF-κB activity in cells stimulated with TL8-506 (HY-20457). TLR8 antagonist-2 can be used in research related to inflammatory and immune diseases.
    TLR8 antagonist-2
  • HY-116052
    p53-MDM2-IN-2 Inhibitor
    p53-MDM2-IN-2 (Compound 5q) is an orally active p53-MDM2 inhibitor with a Ki value of 0.25 μM. p53-MDM2-IN-2 exerts antitumor activity by inhibiting NF-κB pathway.
    p53-MDM2-IN-2
  • HY-128483R
    Fusaric acid (Standard) Inhibitor
    Fusaric acid (Standard) is the analytical standard of Fusaric acid (HY-128483). This product is intended for research and analytical applications. Fusaric acid is an orally active multi-pathway inhibitor with the activity of inducing oxidative stress and apoptosis. Fusaric acid can chelate divalent metal cations, damage mitochondrial membrane structure, and activate apoptosis-related proteases such as Caspase-3/7, -8, and -9. Fusaric acid also regulates Bax/Bcl-2 protein, inhibits fibrosis-related signaling pathways such as NF-κB, TGF-β1/SMADs, and PI3K/AKT/mTOR, and reduces collagen deposition. Fusaric acid is also a dopamine β-hydroxylase inhibitor, which reduces endogenous levels of norepinephrine and epinephrine in the brain, heart, spleen, and adrenal glands. Fusaric acid can play a role in myocardial fibrosis and improve cardiac hypertrophy in heart disease, and can also be used in the study of esophageal cancer and liver cancer.
    Fusaric acid (Standard)
  • HY-162170
    Anti-inflammatory agent 72 Inhibitor
    Anti-inflammatory agent 72 (compound 5) is a novel resveratrol derivative hybrid with benzoylhydrazine. Anti-inflammatory agent 72 shows anti-inflammatory and antioxidant activities by activating Nrf2 and inhibiting NF-κB p65/iNOS and MAPKs signaling pathways.
    Anti-inflammatory agent 72
  • HY-176554
    sEH-IN-21 Inhibitor
    sEH-IN-21 is an orally active sEH inhibitor with IC50s of 0.1 nM for hsEH and msEH. sEH-IN-21 potently inhibits NF-κB signaling pathways. sEH-IN-21 shows a strong anti-inflammatory activity, decreases the release of IL-6 and TNF-α and maintained the integrity of the intestinal barrier. sEH-IN-21 can be used for the study of inflammatory bowel disease (IBD).
    sEH-IN-21
  • HY-N0222R
    Avicularin (Standard) Inhibitor
    Avicularin (Standard) is the analytical standard of Avicularin. This product is intended for research and analytical applications. Avicularin is an orally active flavonoid. Avicularin inhibits NF-κB (p65), COX-2 and PPAR-γ activities. Avicularin has anti-inflammatory, anti-infectious anti-allergic, anti-oxidant, hepatoprotective, and anti-tumor activities.
    Avicularin (Standard)
  • HY-W556870
    OT-551 Inhibitor
    OT-551 is a NF-κB inhibitor with antioxidant and anti-inflammatory effects. OT-551 has the potential for retinal diseases research.
    OT-551
  • HY-123121
    Nargenicin A1 Inhibitor
    Nargenicin A1 is an antibiotic agent against various Gram-positive bacteria. Nargenicin A1 shows anti-inflammatory activity. Nargenicin A1 protects HINAE cells against Tacrolimus (HY-13756)-induced DNA damage and apoptosis. Nargenicin A1 can also be used for the research of acute myeloid leukemia.
    Nargenicin A1
  • HY-N3632
    Methoxycoronarin D Inhibitor
    Methoxycoronarin D can be isolated from Hedychium coronarium J. Koenig and is a potent inhibitor of NF-κB with an IC50 value of 7.3 μM. Methoxycoronarin D is also a selective inhibitor of COX-1 with an IC50 value of 0.9 μM.
    Methoxycoronarin D
  • HY-183357
    GABAAR/5-HT2AR modulator-1 Inhibitor
    GABAAR/5-HT2AR modulator-1 is an orally active and brain-penetrant GABAAR agonist and 5-HT2AR antagonist with Kd values of 0.89 and 0.78 μM. GABAAR/5-HT2AR modulator-1 blocks 5-HT-stimulated IP1 accumulation, inducing a chloride current, reduces LPS (HY-D1056)-induced increases of ROS, NO, TNF-α, IL-6, IL-1β, iNOS, and COX-2 levels. Antidepressant agent 11 dihydrochloride inhibits NF-κB pathway activation by reducing IκBα and p65 phosphorylation and blocking p65 nuclear translocation. GABAAR/5-HT2AR modulator-1 alleviates depression-like behaviors in LPS-challenged and chronic restraint stress-challenged mice, and protects hippocampal neurons against inflammation-mediated damage.
    GABAAR/5-HT2AR modulator-1
  • HY-B0678S1
    Metaxalone-d6 Inhibitor
    Metaxalone-d6 is deuterium labeled Metaxalone. 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-d<sub>6</sub>
  • HY-B0516A
    Articaine Inhibitor
    Articaine (Hoe-045) is a selective inhibitor of voltage-gated sodium channels (such as rNav1.4, hNav1.7, and rNav1.8), with an IC50 of 15.8 μM for open-state Na+ channels, and IC50 of 40.6 μM and 378 μM for inactivated and resting-state Na+ channels, respectively. Articaine exerts local anesthetic activity by inhibiting Na+ influx to block nerve impulse conduction, and can also inhibit NF-κB activation and NLRP3 inflammasome pathways, exhibiting anti-inflammatory function. Articaine can be used in the study of dental local anesthesia and inflammatory-related diseases (such as acute kidney injury).
    Articaine
  • HY-15027S
    5-Aminosalicylic Acid-d3 hydrochloride Inhibitor 99.00%
    5-Aminosalicylic Acid-d3 (hydrochloride) is the deuterium labeled 5-Aminosalicylic Acid. 5-Aminosalicylic acid (Mesalamine) hydrochloride acts as a specific PPARγ agonist and also inhibits p21-activated kinase 1 (PAK1) and NF-κB.
    5-Aminosalicylic Acid-d<sub>3</sub> hydrochloride
  • HY-P11093
    Papiliocin Inhibitor
    Papiliocin is a potent peptide antibiotic with both anti-inflammatory and antibacterial activities. Papiliocin is primarily active against Gram-negative bacteria. Papiliocin exhibits strong anti-inflammatory activity against cell, exerting its anti-inflammatory activity by inhibiting the production of NO and the secretion of TNF-α and MIP-2. Papiliocin participates in the innate defense response mechanism by inhibiting the Toll-like receptor pathway and NF-κB. Papiliocin induces apoptosis in fungal cells and increases the total level of intracellular ROS. Papiliocin acts as an effective antiseptic peptide in sepsis models. Papiliocin is useful in anti-inflammatory and antibacterial research.
    Papiliocin
  • HY-143243
    Antioxidant agent-5 Inhibitor
    Antioxidant agent-5 (compound D-6) is a potent antioxidant agent. Antioxidant agent-5 can inhibit oxLDL (oxidized low-density lipoprotein)-induced apoptosis and the expression of ICAM-1 and VCAM-1 in VECs. Antioxidant agent-5 suppresses oxLDL-induced increase of ROS level and nuclear translocation of NF-κB. Antioxidant agent-5 protects against oxLDL-induced endothelial injury by activating Nrf2/HO-1 anti-oxidation pathway.
    Antioxidant agent-5
  • HY-175833
    NF-κB-IN-20 Inhibitor
    NF-κB-IN-20 is an orally active NF-κB inhibitor. NF-κB-IN-20 directly binds to the Keap1 protein, activating the Keap1/Nrf2/HO-1 antioxidant pathway, and simultaneously inhibiting the NF-κB inflammatory pathway, thereby synergistically reducing oxidative stress and inflammatory responses. NF-κB-IN-20 M11 inhibits the expression of IL-6, IL-1β, and TNF-α, significantly reduces the level of ROS, and restores the mitochondrial membrane potential. NF-κB-IN-20 can be used for the study of acute lung injury (ALI).
    NF-κB-IN-20
  • HY-B1773AS2
    Sodium propionate-13C2 Inhibitor
    Sodium propionate-13C-2 is the 13C-labeled Propionate sodium (HY-B1773A). Sodium propionate is an orally active short-chain fatty acid. Sodium propionate can be produced by intestinal bacteria from the metabolism of dietary fiber. Sodium propionate increases PPAR-γ, inhibits NF-κB activation, and reduces COX-2 expression and NO production. Sodium propionate also induces Apoptosis and Autophagy. Sodium propionate reduces HSV-1-induced keratitis. Sodium propionate has anticancer effects against glioblastoma. Sodium propionate exhibits neuroprotective, antioxidant, and anti-inflammatory activities. Sodium propionate can be used in the research of spinal cord injury and Alzheimer's disease.
    Sodium propionate-<sup>13</sup>C<sub>2</sub>
製品番号 製品名 / 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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