1. Signaling Pathways
  2. NF-κB
  3. NF-κB

NF-κB

Nuclear factor-κB; Nuclear factor-kappaB

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.

Cat. No. Product Name Effect Purity Chemical Structure
  • HY-179214
    DEL-C1
    Inhibitor
    DEL-C1 is a CHI3L1 inhibitor. DEL-C1 can restore the ability to clear Amyloid-β and repair lysosomal function of astrocytes. DEL-C1 can inhibit NF-κB signaling and IL-6 secretion. DEL-C1 can be used for the researches of inflammation and neurological disease, such as Alzheimer's disease.
    DEL-C1
  • HY-172620
    LIB3S0280
    Inhibitor 99.89%
    LIB3S0280 is a potent TBK1 inhibitor with an IC50 value of 493.9 nM. LIB3S0280 exhibits better anticancer effects in pancreatic cancer cell lines with high TBK1 expression. LIB3S0280 inhibits TBK1 downstream signaling pathways, including PI3K/AKT and NF-κB. LIB3S0280 induces G2/M arrest, apoptosis and cellular senescence. LIB3S0280 can be used for pancreatic ductal adenocarcinoma (PDAC) research.
    LIB3S0280
  • HY-147770
    NF-κB-IN-6
    Inhibitor
    NF-κB-IN-6 (Compound 3d) is an anti-inflammatory agent through the mechanism of decreasing the protein expressions of iNOS and COX-2 by suppressing NF-κB signaling pathway. NF-κB-IN-6 inhibits NO production in LPS-induced RAW264.7 cells with an IC50 of 23.1 μM.
    NF-κB-IN-6
  • HY-116474R
    Viridicatol (Standard)
    Inhibitor
    Viridicatol (Standard) is the analytical standard of Viridicatol (HY-116474). This product is intended for research and analytical applications. Viridicatol is a quinolone alkaloid with anti-inflammatory, antibacterial, antifungal, osteogenic and chondrogenic activities. Viridicatol reduces the phosphorylation levels of ERK, JNK, p38 and STAT6; inhibits MMP-2, MMP-9, NF-κB signaling pathway and PTP1B; downregulates genes related to mast cell activation; and binds to SHN3 to activate the Wnt/SHN3 signaling pathway. Viridicatol inhibits the expression of pro-inflammatory mediators and cytokines, and promotes osteogenic/chondrogenic differentiation. Viridicatol can be used in studies related to fibrosarcoma, allergy, bacterial infection, fungal infection and osteoporosis.
    Viridicatol (Standard)
  • HY-163888
    NO-IN-1
    Inhibitor
    NO-IN-1 (Compound 7a) inhibits the production of NO (IC50 = 3.13 μΜ). NO-IN-1 has anti-inflammatory effects. NO-IN-1 downregulates the expression of COX-2 and iNOS by inhibiting the NF-κB signaling pathway.
    NO-IN-1
  • HY-N18091
    Tovophyllin A
    Inhibitor
    Tovophyllin A is an orally active xanthonoid compound. Tovophyllin A exerts neuroprotective effects against Parkinson's disease by activating the Akt/GSK3β signaling pathway. Tovophyllin A protects mouse models of liver injury by activating Nrf2. Tovophyllin A exhibits protective anti-inflammatory activity in mouse models of acute lung injury. Tovophyllin A inhibits the activation of NF-κB and subsequent release of pro-inflammatory cytokines. Tovophyllin A reduces apoptotic cell death (Apoptosis). Tovophyllin A has antiplasmodial activity. Tovophyllin A shows cytotoxic activity against lung epithelial cancer cells and breast cancer cells. Tovophyllin A can be used in research related to Parkinson's disease, liver injury, acute lung injury, lung epithelial cancer, and breast cancer.
    Tovophyllin A
  • HY-175841
    Tau Protein Phosphorylation-IN-1
    Inhibitor
    Tau Protein Phosphorylation-IN-1 is a tau protein phosphorylation inhibitor that potently protects PC12 cells against Aβ25–35-induced cytotoxicity (EC50 = 1.93 μM), and can penetrate the blood-brain barrier (BBB).Tau Protein Phosphorylation-IN-1 reverses the hyperphosphorylation of tau, significantly inhibits the expression of certain immune-related cytotoxic factors, suppresses the MAPK and NF-κB signaling pathways, and significantly inhibits the expression of RAGE and the apoptosis factors Bax/Bcl-2, both in vitro and in vivo. Tau Protein Phosphorylation-IN-1 relieves nerve damage, and improves learning and memory in an Alzheimer’s disease (AD) mouse model. Tau Protein Phosphorylation-IN-1 can be used for AD research.
    Tau Protein Phosphorylation-IN-1
  • HY-N3552
    Catalposide
    Inhibitor 98.0%
    Catalposide, an iridoid glycoside that could be isolated from Catalpa ovate G. Don (Bignoniaceae), inhibits TNF-α, IL-1β, and IL-6 productions and NF-κB (p65) activation in lipopolysaccharide-activated RAW 264.7 macrophages.
    Catalposide
  • HY-147682
    NF-κB-IN-5
    Inhibitor
    NF-κB-IN-5 (compound 4d) is an orally active and potent NF-κB inhibitor by interacting directly with NF-κB. NF-κB-IN-5 shows antitumor activity against human cancer cell lines (HCT116, U87-MG, HepG2, BGC823, PC9), with IC50 values of 5.35, 2.81, 2.83, 2.02 and 3.90 μM, respectively. NF-κB-IN-5 induces apoptosis in U87-MG tumor cell and cell cycle arrest in G0/G1 phase.
    NF-κB-IN-5
  • HY-P11214
    Hydrostatin-TL1
    Inhibitor
    Hydrostatin-TL1 (H-TL1), a nine-amino-acid peptide, is a TNF-α antagonist. Hydrostatin-TL1 can be isolated from the venom gland of sea snake Hydrophis cyanocinctus. H-TL1 competitively inhibits the interaction between TNF-α/TNFR1 and attenuates the cytotoxicity and inflammation of TNF-α. Hydrostatin-TL1 can be used for TNF-α-associated inflammatory diseases, such as rheumatoid arthritis, osteoporosis and inflammatory bowel disease (IBD) research.
    Hydrostatin-TL1
  • HY-N8529
    Eupalestin
    Inhibitor
    Eupalestin is an anti-inflammatory agent. Eupalestin reduces the levels of p-p65 NF-κB and p-p38 MAPK. Eupalestin inhibits MPO and adenosine deaminase. Eupalestin decreases the levels of pro-inflammatory cytokines including IL-17A, IL-6, TNF and IFN-γ. Eupalestin exerts anti-inflammatory activity in a carrageenan (HY-125474)-induced mouse pleurisy model.
    Eupalestin
  • HY-P11502
    COG112
    Inhibitor
    COG112 is an antennapedia-linked apoE-mimetic peptide. COG112 attenuates induction of NO production, inhibits CXC chemokines KC and MIP-2. COG112 reduces nuclear translocation of NF-κB. COG112 inhibits phosphorylation of IκB-α and prevents the degradation of IκB-α. COG112 inhibits the inflammatory response to Citrobacter rodentium .
    COG112
  • HY-N1490R
    14-Deoxy-11,12-didehydroandrographolide (Standard)
    Inhibitor
    14-Deoxy-11,12-didehydroandrographolide (Standard) is the analytical standard of 14-Deoxy-11,12-didehydroandrographolide. This product is intended for research and analytical applications. 14-Deoxy-11,12-didehydroandrographolide is an analogue of Andrographolide. 14-Deoxy-11,12-didehydroandrographolide inhibits NF-κB activation.
    14-Deoxy-11,12-didehydroandrographolide (Standard)
  • HY-14592R
    Tectochrysin (Standard)
    Inhibitor
    Tectochrysin (Standard) is the analytical standard of Tectochrysin. This product is intended for research and analytical applications. Tectochrysin (Techtochrysin) is one of the major flavonoids of Alpinia oxyphylla Miquel. Tectochrysin inhibits activity of NF-κB.
    Tectochrysin (Standard)
  • HY-N18025
    Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside
    Inhibitor
    Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside is an anti-inflammatory agent. Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside exerts significant anti-inflammatory effects in LPS (HY-D1056)-induced RAW 264.7 macrophages by inhibiting the NF-κB, MAPK and Akt signaling pathways, thereby reducing the production of inflammatory mediators (NO, PGE2) and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6).
    Kaempferol 3-O-(2G-glucosylrutinoside)-7-O-glucoside
  • HY-N19801
    N-Palmitoyl-D-glucosamine
    Inhibitor
    N-Palmitoyl-D-glucosamine is an orally active TLR4 antagonist. N-Palmitoyl-D-glucosamine stably binds MD-2 with, preventing LPS-induced NF-κB signaling, decreases pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), increases anti-inflammatory IL-10 and IL-1rα, and normalizes miR-20a-5p, miR-106a-5p, and miR-27a-3p levels. N-Palmitoyl-D-glucosamine decreases allodynia and prevents myelino-axonal degeneration of peripheral nerves. N-Palmitoyl-D-glucosamine can be used for the researches of keratitis and peripheral neuropathy.
    N-Palmitoyl-D-glucosamine
  • HY-N0732R
    Jolkinolide B (Standard)
    Inhibitor
    Jolkinolide B (Standard) is the analytical standard of Jolkinolide B (HY-N0732). This product is intended for research and analytical applications. Jolkinolide B is a bioactive diterpene isolated from the roots of Euphorbia fischeriana Steud with oral activity. Jolkinolide B downregulates XIAP, cIAP1, cIAP2, and phosphorylated Akt, upregulates Smac, activates caspase-3 and caspase-9, and inhibits NF-κB, TGFβ/smad3 and JAK/STAT3 pathways. Jolkinolide B exerts comprehensive biological effects including inducing cancer cell apoptosis, suppressing inflammatory responses, improving lung function, alleviating hepatic steatosis and eliminating intracellular Mycobacterium tuberculosis. Jolkinolide B can be used for the research of leukemia, histiocytic lymphoma, asthma, metabolic dysfunction-associated steatotic liver disease and tuberculosis.
    Jolkinolide B (Standard)
  • HY-168567
    RIPK2-IN-6
    Inhibitor
    RIPK2-IN-6 (Compound 15a) is an inhibitor for RIPK, that inhibits the phosphorylation of RIPK2, and thus inhibits the NF-κB and MAPK signaling pathways. RIPK2-IN-6 exhibits anti-inflammatory and anti-fibrotic activities in Dextran sodium sulfate (HY-116282C)-induced mice colitis models.
    RIPK2-IN-6
  • HY-B0380S2
    Trimebutine-d3 hydrochloride
    Inhibitor
    Trimebutine-d3 hydrochloride is deuterium labeled Trimebutine hydrochloride. Trimebutine hydrochloride is a multi-target inhibitor and opioid receptor agonist with antimuscarinic activity. Trimebutine hydrochloride inhibits L-type Ca2+ channels and large-conductance calcium-activated potassium channels (BKCa channels), thereby inhibiting extracellular calcium influx and potassium ion efflux. Trimebutine hydrochloride 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 hydrochloride also induces tumor cell apoptosis by inhibiting the AKT/ERK pathway. Trimebutine hydrochloride 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>3</sub> hydrochloride
  • HY-155753
    Anti-inflammatory agent 50
    Inhibitor
    Anti-inflammatory agent 50 (compound a1) is a Fusidic acid derivative with anti-inflammatory effects. Anti-inflammatory agent 50 inhibits inflammatory factor NO, IL-6 and TNF-α. Anti-inflammatory agent 50 alleviates acute lung injury by regulating inflammatory mediators and suppressing the MAPK, NF-κB and NLRP3 inflammasome signaling pathways.
    Anti-inflammatory agent 50
Cat. No. Product Name / Synonyms Application Reactivity

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.

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