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-N0492A
    α-Lipoic Acid sodium
    		Inhibitor 99.95%
    α-Lipoic Acid (Thioctic acid) sodium is an antioxidant, which is an essential cofactor of mitochondrial enzyme complexes. α-Lipoic Acid sodium inhibits NF-κB-dependent HIV-1 LTR activation. α-Lipoic Acid sodium induces endoplasmic reticulum (ER) stress-mediated apoptosis in hepatoma cells. α-Lipoic Acid sodium can be used with CPUL1 (HY-151802) to construct the self-assembled nanoaggregate CPUL1-LA NA, which has improved antitumor efficacy than CPUL1.
    α-Lipoic Acid sodium
  • HY-N0732
    Jolkinolide B
    		Inhibitor 99.65%
    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
  • HY-133987
    AP-1/NF-κB activation inhibitor 1
    		Inhibitor 98.08%
    AP-1/NF-κB activation inhibitor 1 is a potent AP-1 and NF-κB mediated transcriptional activation inhibitor (IC50=1 μM), without blocking basal transcription driven by the β-actin promoter. AP-1/NF-κB activation inhibitor 1 has a similar inhibitory effect on the production of IL-2 and IL-8 levels in stimulated cells.
    AP-1/NF-κB activation inhibitor 1
  • HY-171579
    RS47
    		Inhibitor 98.0%
    RS47 is a selective RelB inhibitor with a Kd value of 1.1 μM. RS47 also acts as an inhibitor of HCV replication. RS47 can block the non-canonical NF-κB signaling pathway without affecting the canonical pathway. RS47 exerts anti-tumor effects of inhibiting proliferation and promoting apoptosis on colorectal cancer, B-cell lymphoma and other related tumors both in vitro and in vivo by disrupting the binding of RelB to target DNA. RS47 can be used for the research of tumors and infectious diseases.
    RS47
  • HY-N0668
    Rubusoside
    		Inhibitor 98.05%
    Rubusoside is a diterpene glycoside that is also a sweetener and solubilizer with anti-angiogenic, anti-cancer, anti-obesity, anti-allergic and anti-asthmatic effects. Rubusoside attenuates airway hyperresponsiveness and reduces inflammatory cells in bronchoalveolar lavage fluid (BALF), reducing OVA (HY-W250978)-induced airway inflammation. Rubusoside also prevents palmitic acid-induced lipotoxicity in pancreatic INS-1 cells, reduces the transport of human glucose transporters GLUT-1 and fructose GLUT-5, and inhibits NF-κB and α-amylase (α-amylase).
    Rubusoside
  • HY-N0559
    Kirenol
    		Inhibitor 99.82%
    Kirenol is a diterpenoid compound, an orally active apoptosis inducer and signaling pathway regulator, with a Kd value of 5.47 μM against the target CK2. Kirenol promotes the cleavage of Bid into tBid, regulates the protein levels/phosphorylation of Bax, Bcl-2, p53 and p21, and induces caspase-independent apoptosis, S-phase cell cycle arrest, ROS accumulation and cytotoxicity in cancer cells. Kirenol activates the CK2/AKT and AMPK-mTOR-ULK1 pathways, inhibits the signaling of NF-κB, TGF-β/Smads and NLRP3 inflammasome, and regulates the GSK3β, BMP and Wnt/β-catenin pathways. Kirenol induces autophagy, mitophagy and osteoblast differentiation, promotes mitochondrial fusion, and exerts antioxidant, anti-inflammatory, antifibrotic, renoprotective, cardioprotective, neuroprotective and analgesic effects. Kirenol is applicable to research related to chronic myeloid leukemia, ischemic stroke, diabetic nephropathy, heart failure, acute lung injury and osteoporosis.
    Kirenol
  • HY-122778
    δ-Tocotrienol
    		Inhibitor 98.10%
    δ-Tocotrienol is a Vitamin E in vegetables, fruits, seeds, nuts, grains and oils. Vitamin E has become well known for its role as an antioxidant, in lowering cholesterol and other lipids, as a neuroprotective and anticancer agent, and in cardiovascular disease protection.
    δ-Tocotrienol
  • HY-N0231
    Bavachalcone
    		Inhibitor 99.90%
    Bavachalcone is a potent inducer of apoptosis. Bavachalcone exerts anticancer activity by promoting autophagy and apoptosis in HepG2 cells. Bavachalcone acts as an anti-neuroinflammatory and antidepressant through the NF-κB pathway. Bavachalcone inhibits osteoclasts by interfering with ERK and Akt signaling pathways and the expression of c-Fos and NFATc1. Bavachalcone exhibits a significant inhibitory effect on baculovirus-expressed BACE-1 in vitro.
    Bavachalcone
  • HY-124179
    IT-901
    		Inhibitor 99.32%
    IT-901 is an orally active and potent NF-κB subunit c-Rel inhibitor with an IC50 of 0.1 μM, 3 μM for NF-κB DNA binding and c-Rel DNA binding, respectively. IT-901, a bioactive naphthalenethiobarbiturate derivative, has the potential for human lymphoid tumors and ameliorate graft-versus-host disease (GVHD).
    IT-901
  • HY-N0218
    Benzoylmesaconine
    		Inhibitor 99.56%
    Benzoylmesaconine is a monoester-type alkaloid and is the most abundant component of Wutou decoction, which is widely used in China for rheumatoid arthritis. Benzoylmesaconine exhibits potent anti-inflammatory properties by inhibiting NF-κB. Benzoylmesaconine can suppress NLRP3 inflammasome activation by inhibiting IL-1β secretion and GSDMD-N protein expression. Benzoylmesaconine reduces intracellular K+ efflux and disrupts NLRP3 inflammasome assembly.
    Benzoylmesaconine
  • HY-W009274
    N-Acetylmuramic acid
    		Inhibitor 99.9%
    N-acetylmuramic acid is a component of the bacterial cell wall peptidoglycan, essential for maintaining cell shape and integrity. N-acetylmuramic acid inhibits spore germination by inhibiting a coat-associated hexosaminidase and a core enzyme. N-acetylmuramic acid is required by Bacteroides forsythus for proliferation and the maintenance of its cell shape. N-Acetylmuramic acid inhibits the p38 MAPK/NF-κB signaling pathway, and exhibits anti-inflammatory activity. N-Acetylmuramic acid is orally active.
    N-Acetylmuramic acid
  • HY-P1633
    Protegrin-1
    		Activator 99.87%
    Protegrin-1 is an orally active antibacterial peptide. Protegrin-1 activates ERK, COX2, NFκB, inhibits Apoptosis, and NO production. Protegrin-1 has antibacterial activity against S. aureus, E. faecium, E. coli, P. aeruginosa and K. Pneumoniae, with MBC values between 10 and 20 µM. Protegrin-1 has antiviral activity against dengue NS2B-NS3. Protegrin-1 has anti-inflammatory activity. Protegrin-1 is used in the study of inflammatory diseases and infections.
    Protegrin-1
  • HY-N0253
    Hederacoside C
    		Inhibitor 99.92%
    Hederacoside C (Kalopanaxsaponin B) is an ingredient that can be obtained mainly from ivy leaves. Hederacoside C mediates inflammation by inhibiting activation of MAPK/NF-κB and its downstream signaling pathway. Hederacoside C has anti-inflammatory and antibacterial activity.
    Hederacoside C
  • HY-113772
    Inflachromene
    		Inhibitor 99.76%
    Inflachromene, a microglial inhibitor, binds to HMGB1 and HMGB2 and exerts anti-inflammatory effects. Inflachromene effectively downregulates proinflammatory functions of HMGB and reduces neuronal damage. Inflachromene can be used for the research of neuroinflammatory disorders.
    Inflachromene
  • HY-N0592A
    Demethyleneberberine chloride
    		Inhibitor 98.90%
    Demethyleneberberine chloride is a blood-brain barrier-permeable antioxidant. Demethyleneberberine chloride exerts antioxidant effects by targeting mitochondria, activates the AMPK signaling pathway to regulate lipid metabolism, and inhibits inflammation-related pathways such as NF-κB and MAPK. Demethyleneberberine chloride can be used in the research of inflammatory and other diseases.
    Demethyleneberberine chloride
  • HY-N2389
    Formosanin C
    		Inhibitor 99.28%
    Formosanin C is a diosgenin saponin with multiple biological activities. Formosanin C possesses multiple anti-tumor mechanisms, including inducing apoptosis and autophagy, blocking the cell cycle, inhibiting metastasis and inducing ferroptosis. Formosanin C can inhibit the NF-κB signaling pathway to exert anti-inflammatory effects, and enhance the activity of immune cells. Formosanin C exhibits the inhibiting effect against C. albicans. Formosanin C can be used for the study of anti-inflammation, antifungal anti and anti-cancer (including lung cancer, liver cancer, breast cancer and colorectal cancer, etc.).
    Formosanin C
  • HY-16172
    DMAPT
    		Inhibitor 98.95%
    DMAPT (Dimethylamino Parthenolide), an analogue of Parthenolide (PTL), is an oral active NF-κB inhibitor, with a LD50 of 1.7 μM for cell population in AML cells. Has potential anti-cancer and anti-metastatic effect.
    DMAPT
  • HY-N2119
    Sciadopitysin
    		Inhibitor 99.0%
    Sciadopitysin is a type of biflavonoids in leaves from ginkgo biloba. Sciadopitysi inhibits RANKL-induced osteoclastogenesis and bone loss by inhibiting NF-κB activation and reducing the expression of c-Fos and NFATc1.
    Sciadopitysin
  • HY-153368
    Zomiradomide
    		Inhibitor 98.04%
    Zomiradomide is an orally active PROTAC degrader for IRAK4 (DC50=6 nM), thereby inhibiting the NF-κB signaling pathway. Zomiradomide acts also as a molecular glue, recruiting Ikaros and Aiolos, and mediating their degradation (DC50 for Ikaros is 1 nM), thereby activating the type I IFN signaling pathway. (Pink: target protein ligand PROTAC IRAK4 ligand-5 (HY-168311), Blue: E3 ligase ligand Thalidomide-4-Br (HY-W039116), Black: linker (HY-168313))
    Zomiradomide
  • HY-152177
    JS6
    		Inhibitor 99.4%
    JS6 is a Bcl3 inhibitor, and inhibits Bcl3-NF-kB1 binding. JS6 inhibits tumor cell growth in vitro and in vivo.
    JS6
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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