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-N0513R
    Loganic acid (Standard)
    		Inhibitor
    Loganic acid (Standard) is the analytical standard of Loganic acid. This product is intended for research and analytical applications. Loganic acid is an iridoid isolated from cornelian cherry fruits. Loganic acid inhibits NF-κB signaling pathway, activates Nrf2 signaling pathway, exhibits anti-inflammatory activity. Loganic acid can modulate diet-induced atherosclerosis and redox status. Loganic acid has strong free radical scavenging activity and remarkable cyto-protective effect against heavy metal mediated toxicity. Loganic acid is orally active.
    Loganic acid (Standard)
  • HY-174138
    NF-κB degrader 1
    		Degrader
    NF-κB degrader 1 (Compound MD-1) is a NF-κB1 p105 subunit degrader. NF-κB degrader 1 shows anti-inflammatory activity (IC50 for inhibiting TNF-α is 2.02 μM, and for inhibiting NO is 5.40 μM). NF-κB degrader 1 induces p105 degradation dependent on the Cullin-RING ligase (CRL) SCFBTCP, suppressing NF-κB transcriptional activity. NF-κB degrader 1 is promising for research of inflammation-related diseases.
    NF-κB degrader 1
  • HY-162316
    NF-κB-IN-15
    		Inhibitor
    NF-κB-IN-15 (compound 14r) is a potent NF-κB inhibitor. NF-κB-IN-15 decreases the NO levels and inhibits the release of IL-6, TNF-α, and IL-1β in LPS (HY-D1056) -induced cells. NF-κB-IN-15 inhibits LPS-induced phosphorylation of p65 and degradation of IκBα. NF-κB-IN-15 shows anti-inflammatory activity has the potential for the research of acute lung injury (ALI).
    NF-κB-IN-15
  • HY-158311
    Anti-osteoporosis agent-8
    		Inhibitor
    Anti-osteoporosis agent-8 (Compound 4aa) is an inhibitor for RANKL, which inhibits RANKL-induced osteoclastogenesis and osteoclast differentiation (IC50 is 2.41 μM) in cells RAW264.7. Anti-osteoporosis agent-8 ameliorates bone loss in an ovariectomized (OVX) mice model.
    Anti-osteoporosis agent-8
  • HY-174419
    TFSeB
    		Inhibitor
    TFSeB is an orally active neuroprotective agent. TFSeB can reduce Streptozotocin (STZ) (HY-13753) induced MAO-B and AChE activity. TFSeB exerts neuroprotective effects by increasing the expression of BCL-2, BDNF, NRF2, and decreasing the expression of BAX. TFSeB can reduce lipid peroxidation (TBARS) and reactive oxygen species (ROS) levels. TFSeB can reduce neuroinflammation. TFSeB can be used for research on Alzheimer’s disease.
    TFSeB
  • HY-P10462
    SAP15
    		Inhibitor
    SAP15 (Synthetic anti-inflammatory peptide 15) is a synthetic anti-inflammatory peptide consisting of 15 amino acids designed from human beta-defensin 3. SAP15 has the ability to penetrate cells and is able to induce downregulation of intracellular inflammation. SAP15 inhibits inflammation by inhibiting the phosphorylation of HDAC5 and thereby reducing the phosphorylation of NF-κB p65. In LPS-induced macrophages, SAP15 inhibits HDAC5 and NF-κB p65 phosphorylation. In addition, SAP15 treatment increased the expression of aggrecan and type II collagen and decreased the expression of osteocalcin in LPS-induced chondrocytes. SAP15 can be used in the study of inflammation regulation and anti-inflammatory therapy of biomaterials.
    SAP15
  • HY-N7043R
    Isosilybin A (Standard)
    		Inhibitor
    Isosilybin A (Standard) is the analytical standard of Isosilybin A (HY-N7043). Isosilybin A is a PPARγ agonist that can be isolated from silymarin. Isosilybin A activates extrinsic and intrinsic pathways of apoptosis through targeting of the Akt-NF-kB-AR axis. Isosilybin A can relieve the inflammatory response in the rosacea model via inhibiting Erk and p38 signaling pathways and M1 macrophage polarization, with its targets related to RELA and VEGFA. Isosilybin A has anti-prostate cancer (PCA) activity[1][2][3].
    Isosilybin A (Standard)
  • HY-N0460R
    1-Caffeoylquinic acid (Standard)
    		Inhibitor
    1-Caffeoylquinic acid (Standard) is the analytical standard of 1-Caffeoylquinic acid. This product is intended for research and analytical applications. 1-Caffeoylquinic acid is an effective NF-κB inhibitor, shows significant binding affinity to the RH domain of p105 with Ki of 0.007 μM. 1-Caffeoylquinic acid has anti-oxidative stress ability. 1-Caffeoylquinic acid is the inhibitor for PD-1/PD-L1.
    1-Caffeoylquinic acid (Standard)
  • HY-170585
    COX-2-IN-51
    		Inhibitor
    COX-2-IN-51 (E25) is a potent COX-2 inhibitor, with an IC50 of 70.7 nM. COX-2-IN-51 significantly inhibits LPS-induced release of NO and PGE2, expression of COX-2 and iNOS, and activation of NF-κB pathway. COX-2-IN-51 exhibits anti-inflammatory and analgesic effects in diverse murine models through inhibiting NF-κB pathway. COX-2-IN-51 has lower gastrointestinal side effects than Indomethacin (HY-14397).
    COX-2-IN-51
  • HY-N7183
    9-Hydroxycanthin-6-one
    		Inhibitor
    9-Hydroxycanthin-6-one is an alkaloid compound. 9,10-Dimethoxycanthin-6-one exhibits NF-κB inhibitory effects with an IC50 of 3.8 μM.
    9-Hydroxycanthin-6-one
  • HY-172619
    BS-153
    		Inhibitor
    BS-153 is a novel synthetic oxazolidinone agent with anti-inflammatory activities by blocking the activation of the NF-κB/PKCθ pathway. BS-153 inhibits the expression levels of iNOS and COX-2 and pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) on LPS-stimulated RAW264.7 cells.
    BS-153
  • HY-N2497R
    Isoliquiritin apioside (Standard)
    		Inhibitor
    Isoliquiritin apioside (Standard) is the analytical standard of Isoliquiritin apioside. This product is intended for research and analytical applications. Isoliquiritin apioside significantly decreases PMA-induced increases in MMP9 activities and suppresses PMA-induced activation of MAPK and NF-κB. Isoliquiritin apioside auppresseses invasiveness and angiogenesis of cancer cells and endothelial cells.
    Isoliquiritin apioside (Standard)
  • HY-W705168
    Yangonin-d3
    Yangonin-d3 is the deuterium labeled Yangonin (HY-N0919). Yangonin exhibits affinity for the human recombinant cannabinoid CB1 receptor with an IC50 and a Ki of 1.79 μM and 0.72 μM, respectively.
    Yangonin-d<sub>3</sub>
  • HY-N0212R
    Peimine (Standard)
    		Inhibitor
    Peimine (Standard) is the analytical standard of Peimine. This product is intended for research and analytical applications. Peimine (Verticine; Dihydroisoimperialine) is an orally active natural product. Peimine has anti-inflammatory, analgesic and cough relieving effects. Peimine can be used in cancer and inflammation related research.
    Peimine (Standard)
  • HY-N0043R
    Ginsenoside Rd (Standard)
    		Inhibitor
    Ginsenoside Rd (Standard) is the analytical standard of Ginsenoside Rd. This product is intended for research and analytical applications. Ginsenoside Rd inhibits TNFα-induced NF-κB transcriptional activity with an IC50 of 12.05±0.82 μM in HepG2 cells. Ginsenoside Rd inhibits expression of COX-2 and iNOS mRNA. Ginsenoside Rd also inhibits Ca2+ influx. Ginsenoside Rd inhibits CYP2D6, CYP1A2, CYP3A4, and CYP2C9, with IC50s of 58.0±4.5 μM, 78.4±5.3 μM, 81.7±2.6 μM, and 85.1±9.1 μM, respectively.
    Ginsenoside Rd (Standard)
  • HY-173410
    iNOs-IN-6
    		Inhibitor
    iNOs-IN-6 is an anti-inflammatory agent. iNOs-IN-6 inhibits NF-κB, iNOS, and MAPK expression(IC50: 0.2-0.62 μM). iNOs-IN-6 reduces IL-6, TNF-α, and IL-1β pro-inflammatory mediators levels (IC50: 0.4-0.69 μM).
    iNOs-IN-6
  • HY-N15196
    Andrographolide-lipoic acid
    		Inhibitor
    Andrographolide-lipoic acid is an Andrographolide (HY-N0191) analogue, which is formed by the coupling of Andrographolide and Lipoic acid (HY-18733). Andrographolide-lipoic acid inhibits NF-κB and has anti-diabetic and β-cell protective activities.
    Andrographolide-lipoic acid
  • HY-175257
    Theophylline-platinum(IV) prodrug-1
    		Inhibitor
    Theophylline-platinum(IV) prodrug-1 is a PARP-1 inhibitor. Theophylline-platinum(IV) prodrug-1 enhances DNA damage, ROS production, mitochondrial dysfunction, apoptosis and S-phase arrest, along with reducing invasion and metastasis in SKOV3-BRCA1-KD cells. Theophylline-platinum(IV) prodrug-1 exhibits superior antitumor activity in the xenograft SKOV3-BRCA1-KD tumor model. Theophylline-platinum(IV) prodrug-1 can be used for the study of ovarian cancer.
    Theophylline-platinum(IV) prodrug-1
  • HY-170669
    PROTAC XPO1 degrader-1
    		Inhibitor
    PROTAC XPO1 degrader-1 (Compound 2c) is an XPO1 degrader. PROTAC XPO1 degrader-1 exhibits anti-proliferative effects, can induce cell apoptosis, inhibit NF-κB activity, and cause cell cycle arrest in the G1 phase. PROTAC XPO1 degrader-1 can be used in research on hematological malignancies (Pink: Target Protein Ligand (HY-170672); Black: Linker (HY-W010525); Blue: E3 Ligase Ligand (HY-170671); E3 Ligase Ligand-Linker Conjugate (HY-170673)).
    PROTAC XPO1 degrader-1
  • HY-N9971
    Hentriacontane
    		Inhibitor ≥98.0%
    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
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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