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-N7700
    Guluronic acid
    		Inhibitor 98.90%
    Guluronic acid (G2013) is an orally active oxidative stress regulator and anti-inflammatory agent that exerts pharmacological effects by down-regulating various pro-inflammatory and oxidative stress-related genes (such as TLR4, NF-κB, iNOS, etc.) and inhibiting the activities of COX-2, MMPs and VEGF. Low-dose Guluronic acid up-regulates the expression of immunoregulatory genes SHIP1 and SOCS1, thereby effectively inhibiting cancer-related inflammation, tumor angiogenesis, cell adhesion and metastasis, while reducing the accumulation of immunosuppressive cells. Guluronic acid significantly prolongs the survival time of tumor-bearing hosts within a concentration range without direct cytotoxicity, demonstrating favorable safety. Guluronic acid has involved in the research of multiple sclerosis, ankylosing spondylitis, breast cancer and other inflammatory diseases.
    Guluronic acid
  • HY-160222
    HSV-60mer sodium
    		Activator 98.11%
    HSV-60mer sodium is a 60 bp double-stranded DNA oligonucleotide derived from the HSV-1 genome, and also an IFNβ inducer. HSV-60mer sodium colocalizes with endogenous cytoplasmic IFI16 in immune cells. HSV-60mer sodium activates the transcription factors IRF3 and NF-κB, induces the production of proinflammatory cytokines, and inhibits HSV-1 replication in immune cells. HSV-60mer sodium can be used in studies related to herpes simplex virus type 1 infection.
    HSV-60mer sodium
  • HY-P99579
    Tamtuvetmab
    		Inhibitor
    Tamtuvetmab (AT-005) is a caninised blontuvetmab against CD52. Tamtuvetmab increases progression-free survival (PFS), exhibits in vivo efficacy in dogs with naïve T-cell lymphoma (LSA). Tamtuvetmab has been approved by veterinary.
    Tamtuvetmab
  • HY-176192
    SMU-14a
    		Inhibitor
    SMU-14a is a selective Toll-like receptor 3 (TLR3) inhibitor wirh an IC50 of 0.18 μM. SMU-14a reduces phosphorylation of p65, ERK, and TBK1 via NF-κB, MAPK, and IRF3 signaling pathways. SMU-14a inhibits IL-6 secretion in mouse peritoneal macrophages, downregulates TNF-α in human peripheral blood monocytes and decreases serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. SMU-14a can be used for the research of acute hepatitis.
    SMU-14a
  • HY-178041
    BRD4-BD1/2-IN-3
    		Inhibitor 99.52%
    BRD4-BD1/2-IN-3 (Compound B6) is a selective BRD4 BD2 inhibitor with an IC50 of 0.41  nM for BRD4 BD2 over BRD4 BD1. BRD4-BD1/2-IN-3 significantly inhibits the LPS (HY-D1056)-induced expression of IL-6. BRD4-BD1/2-IN-3 shows anti-inflammatory activities by modulating the TNF and NF-κB signaling pathway. BRD4-BD1/2-IN-3 can be used for inflammatory diseases research.
    BRD4-BD1/2-IN-3
  • HY-107665
    Ro 106-9920
    		Inhibitor ≥99.0%
    Ro 106-9920 is a potent inhibitor of NF-kappaB. Ro 106-9920 has the potential for the research of tumor and cancer diseases.
    Ro 106-9920
  • HY-N1965
    Gaultherin
    		Inhibitor 99.44%
    Gaultherin is an orally active non-steroidal anti-inflammatory agent. Gaultherin selectively inhibits NF-κB, MAPK, COX-2 (IC50 = 0.35 mg/mL), LOX (IC50 = 0.56 mg/mL) and HYAL (IC50 = 28.58 μg/mL) to exert anti-inflammatory, antipyretic and analgesic effects. Gaultherin exhibits modest direct antioxidant capacity, greater in cell-based models. Gaultherin does not affect COX-1 so that avoids the common gastrointestinal side effects of Aspirin (HY-14654).
    Gaultherin
  • HY-135808
    BIZ 114
    		Inhibitor 98.0%
    BIZ 114 (Example 11) is a fatty acid derivative and potent inhibits the TNF-α activated NF-κΒ pathway. BIZ 114 has the potential to prevent and / or treat ophthalmic disorders such as retinal degenerative disorders and ocular inflammatory diseases.
    BIZ 114
  • HY-B0185G
    Lidocaine (GMP)
    		Inhibitor
    Lidocaine (GMP) is Lidocaine (HY-B0185) produced by using GMP guidelines. GMP small molecules work appropriately as an auxiliary reagent for cell therapy manufacture. Lidocaine inhibits sodium channels involving complex voltage and using dependence. Lidocaine decreases growth, migration and invasion of gastric carcinoma cells via up-regulating miR-145 expression and further inactivation of MEK/ERK and NF-κB signaling pathways. Lidocaine is an amide derivative and has potential for the research of ventricular arrhythmia.
    Lidocaine (GMP)
  • HY-P2670
    SN50M
    		Control
    SN50M, a mutant peptide of SN50 (HY-P0151), is a cell membrane-permeable inactive control peptide.
    SN50M
  • HY-W744739
    Betulinic acid-d3
    		99.9%
    Betulinic acid-d3 (Lupatic acid-d3) is a deuterium labeled Betulinic acid (HY-10529). Betulinic acid is a natural pentacyclic triterpenoid, acts as a eukaryotic topoisomerase I inhibitor, with an IC50 of 5 μM, and possesses anti-HIV, anti-malarial, anti-inflammatory and anti-tumor properties. Betulinic acid can cross the blood-brain barrier.
    Betulinic acid-d<sub>3</sub>
  • HY-N11011
    Withaphysalin A
    		Inhibitor 98%
    Withaphysalin A is a withanolide compound with anti-inflammatory and antioxidant activities. Withaphysalin A inhibits LPS (HY-D1056)-induced nuclear translocation of NF-κB p65, as well as phosphorylation of STAT3, ERK, JNK and p38 MAPK. Withaphysalin A upregulates the expression of HO-1. Withaphysalin A inhibits LPS-induced production of NO, PGE2, IL-1β, IL-6 and TNF-α. Withaphysalin A downregulates LPS-induced expression of iNOS and COX-2. Withaphysalin A interacts with B-cell activating factor protein (BAFF) to exert inhibitory effects. Withaphysalin A exhibits ELOVL6 inhibitory activity. Withaphysalin A can be used in the research of inflammatory diseases, nephrotic syndrome and chronic myeloid leukemia.
    Withaphysalin A
  • HY-B0130R
    Perindopril (Standard)
    Perindopril (Standard) is the analytical standard of Perindopril. This product is intended for research and analytical applications. Perindopril (S-9490) is an orally available, long-acting angiotensin-converting enzyme (ACE) inhibitor. Perindopril inhibits inflammatory cell influx and intimal thickening, preserving elastin on the inside of the aorta. Perindopril effectively inhibits experimental abdominal aortic aneurysm (AAA) formation in a rat model and reduces pulmonary vasoconstriction in rats with pulmonary hypertension.
    Perindopril (Standard)
  • HY-W012349
    2′-Hydroxychalcone
    		Inhibitor
    2′-Hydroxychalcone is a hydroxyl derivative of chalcones with anticancer activities. 2'-Hydroxychalcone inhibits NF-κB pathway and induces autophagy and apoptosis in breast cancer cells. 2′-Hydroxychalcone shows a better antifungal activity against the complex Paracoccidioides spp.
    2′-Hydroxychalcone
  • HY-B1773AS5
    Sodium propionate-d3
    		Inhibitor 98.38%
    Sodium propionate-d3 is the deuterium 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-d<sub>3</sub>
  • HY-B1272R
    Desipramine hydrochloride (Standard)
    Desipramine hydrochloride (Standard) is the analytical standard of Desipramine hydrochloride (HY-B1272). This product is intended for research and analytical applications. Desipramine hydrochloride is a first-generation tricyclic antidepressant. Desipramine hydrochloride selectively binds to norepinephrine transporter and blocks neuronal norepinephrine reuptake. Desipramine hydrochloride activates MAPK signaling via ERK1/2, JNK, and p38, represses NF-κB and AP-1 activity, and induces apoptosis via ROS elevation, mitochondrial membrane potential reduction, and intracellular calcium increase. Desipramine hydrochloride also shows anyi-inflammatory activity, inhibiting TNF-α production. Desipramine hydrochloride can be used for the research of hepatocellular cancer, inflammation, and neurological diseases.
    Desipramine hydrochloride (Standard)
  • HY-W041608
    Methylchloroisothiazolinone
    		Activator
    Methylchloroisothiazolinone is a widely used fungicide and also an aquatic pollutant with pro-inflammatory activity and neurotoxicity. Methylchloroisothiazolinone induces the production of pro-inflammatory cytokines (such as IL-1β, TNF-α, IL-6) by activating the NF-κB signaling pathway and upregulating TLR4 expression, thereby triggering allergic contact dermatitis. Methylchloroisothiazolinone reduces cholinesterase activity and exacerbates oxidative stress by impairing catalase activity and disrupting redox balance. Methylchloroisothiazolinone poses significant harm to Mediterranean mussels, reducing the viability of hemocytes and digestive gland cells, inhibiting immune phagocytic function, and disrupting osmoregulatory capacity. Methylchloroisothiazolinone is used in studies on allergic contact dermatitis and related immunotoxicity mechanisms.
    Methylchloroisothiazolinone
  • HY-141582S
    Ceramide 3-d3
    		Inhibitor 98.0%
    Ceramide 3-d3 (N-Stearoyl phytosphingosine-d3) is deuterium labeled Ceramide 3. Ceramide 3 is an orally active major component of intercellular lipids in the stratum corneum of the skin, and belongs to the ceramide family. Ceramide 3 inhibits c-jun and NF-κB activation induced by Histamine (HY-B1204), and suppresses the expression of IL-4 and TNF-α. Ceramide 3 inhibits scratching behavior and vascular permeability in mice, and exhibits antihistamine effects in guinea pig ileum. Ceramide 3 improves skin barrier function, reduces transepidermal water loss, erythema and the number of circulating epidermal cells, and accelerates barrier repair of irritated or dysfunctional skin.
    Ceramide 3-d<sub>3</sub>
  • HY-N2149R
    Tomatidine (Standard)
    		Inhibitor
    Tomatidine acts as an anti-inflammatory agent by blocking NF-κB and JNK signaling. Tomatidine activates autophagy either in mammal cells or C elegans.
    Tomatidine (Standard)
  • HY-13010S
    Laquinimod-d5
    		Inhibitor 98.25%
    Laquinimod-d5 (ABR-215062-d5) is deuterium labeled Laquinimod. Laquinimod (ABR-215062), an orally available carboxamide derivative, is a potent immunomodulator that prevents neurodegeneration and inflammation in the central nervous system. Laquinimod reduces astrocytic NF-κB activation to protect from Cuprizone-induced demyelination. Laquinimod has the potential for relapsing-remitting (RR) and chronic progressive (CP) forms of multiple sclerosis (MS; RRMS or CPMS) as well as neurodegenerative diseases research.
    Laquinimod-d<sub>5</sub>
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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