NF-κB

Nuclear factor-κB; Nuclear factor-kappaB

NF-κB

NF-κB Isoform Specific Products:

NF-κB Isoform Comparison

NF-κB Related Products (1746)
Antibodies (32)
NF-κB Signaling Pathway
NF-κB Isoform Comparison

By Effects:	Inhibitors (1431) Agonists (6) Degraders (3) Controls (7) Ligands (2) Antagonist (1) Activators (131) Modulators (33) Inducers (3)

Cat. No.	Product Name	Effect	Purity	Chemical Structure

HY-P10081

CTP-NBD	Inhibitor
CTP-NBD is a cell permeable specific NFκB peptide inhibitor. CTP-NBD could be used in colitis study

HY-P1847

IKKγ NBD Inhibitory Peptide
IKKγ NBD Inhibitory Peptide is a highly specific inhibitor NF-κB inhibitor. IKKγ NBD Inhibitory Peptide acts by disrupting the interaction between IKKγ/NEMO-binding domain (NBD) with IKKα and IKKβ, thus blocking TNF-α-induced NF-kB activation. IKKγ NBD Inhibitory Peptide could significantly suppresses inflammation and ameliorate the cerebral ischemia-induced neurological deficits.

HY-108659

NF340	Inhibitor
NF340 is a P2Y11 receptor inhibitor with a pIC₅₀ of 7.3-7.7 against human P2Y11 receptor, and it exhibits high selectivity over other P2Y family receptors. NF340 binds to the ATP-binding amino acid residues of the P2Y11 receptor to inhibit its activity, block nociceptive activity, and reduce spinal dorsal horn P2Y11 receptor upregulation induced by spinal nerve injury. NF340 attenuates the NFκB signaling pathway activated by IL-1β by decreasing IκBα phosphorylation, nuclear p65 accumulation, and NFκB promoter activity. NF340 inhibits IL-1β-induced pro-inflammatory cytokine expression, reduces intracellular ROS and 4-HNE levels, and suppresses IL-1β-induced matrix metalloproteinase expression in primary fibroblast-like synoviocytes. NF340 inhibits ATP-induced elevation of intracellular Ca²⁺ concentration and cell migration in human hepatocellular carcinoma cells. NF340 can be used in the research of neuropathic pain, myocardial ischemia/reperfusion injury, inflammatory pain, rheumatoid arthritis, and hepatocellular carcinoma.

HY-Y0332L

Potassium dihydrogen phosphate, meets analytical specification of Ph. Eur., NF, E340	Activator
Potassium dihydrogen phosphate (Potassium phosphate monobasic), meeting the analytical specifications of Ph. Eur., NF, E340, is a reagent with buffering capacity, used for preparing biological buffers. Potassium dihydrogen phosphate downregulates the expression of IκBα in the cytoplasm, increases the expression of p-P65 in the cytoplasm, and upregulates the expression of P65 in the nucleus, thereby activating the NF-κB pathway. Potassium dihydrogen phosphate promotes the proliferation of human periodontal ligament stem cells in the logarithmic growth phase. Potassium dihydrogen phosphate upregulates the expression of odontogenic/osteogenic markers (OCN, DSP/DSPP, OSX, RUNX2, ALP) in human periodontal ligament stem cells and enhances the mineralization capacity of these cells. Potassium dihydrogen phosphate can be used in the research of periodontal diseases.

HY-N0908R

Ginsenoside Rg5 (Standard)	Inhibitor
Ginsenoside Rg5 (Standard) is the analytical standard of Ginsenoside Rg5. This product is intended for research and analytical applications. Ginsenoside Rg5 is the main component of Red ginseng and IGF-1R agonist. Ginsenoside Rg5 compets for the binding site of IGF-1R and blocks the binding of IGF-1 to IGF-1R (IC50 about 90 nM). Ginsenoside Rg5 also inhibits the mRNA expression of COX-2 via suppression of the DNA binding activities of NF-κB p65.

HY-N17888

Ephemeranthol A	Inhibitor
Ephemeranthol A is a phenanthrene compound with anticancer and anti-inflammatory activities. Ephemeranthol A exerts significant anti-inflammatory effects in macrophages by inhibiting the NF-κB and MAPK signaling pathways. Ephemeranthol A induces apoptosis and inhibits metastasis of lung cancer cells by suppressing the FAK/Akt signaling and EMT processes. Ephemeranthol A can be used for the research of acute and chronic inflammatory diseases and non-small cell lung cancer.

HY-N0608A

(Rac)-Myrislignan	Inhibitor	99.0%
(Rac)-Myrislignan is the racemate of Myrislignan. Myrislignan, a lignan isolated from Myristica fragrans Houtt, possesses anti-inflammatory activities. Myrislignan attenuates LPS-induced inflammation reaction in murine macrophage cells through inhibition of NF-kB signalling pathway activation.

HY-155646

Anti-inflammatory agent 48	Inhibitor
Anti-inflammatory agent 48 is an anti-inflammatory agent based on its role in inhibiting the NF-κB signaling pathway and activating HO-1 expression.

HY-121239

Lemnalol	Modulator
Lemnalol is a potent agent for neuropathic pain. Lemnalol possesses potent anti-inflammatory, analgesic and anti-tumor activities. Lemnalol has the capacity to attenuate hyperalgesia and allodynia by modulation of neuroinflammatory processes in neuropathy. Lemnalol modulates LPS-induced alterations of left atrial (LA) calcium homeostasis and blocks the NF-κB pathways, which may contribute to the attenuation of lipopolysaccharide (LPS)-induced arrhythmogenesis and neuropathic pain. Lemnalolis a ylangene-type sesquiterpenoid compound, isolated from Lemnalia cervicorni.

HY-N0559R

Kirenol (Standard)	Inhibitor
Kirenol (Standard) is the analytical standard of Kirenol (HY-N0559). This product is intended for research and analytical applications. Kirenol is a diterpenoid compound, an orally active apoptosis inducer and signaling pathway regulator, with a K_d 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.

HY-111024R

2,2,5,7,8-Pentamethyl-6-Chromanol (Standard)	Inhibitor
2,2,5,7,8-Pentamethyl-6-Chromanol (Standard) is the analytical standard of 2,2,5,7,8-Pentamethyl-6-Chromanol. This product is intended for research and analytical applications. 2,2,5,7,8-Pentamethyl-6-Chromanol (PMC) is the anti-oxidant moiety of vitamin E (α-tocopherol). 2,2,5,7,8-Pentamethyl-6-Chromanol has potent androgen receptor (AR) signaling modulation and anti-cancer activity against prostate cancer cell lines[1].

HY-N11739

Helenalin isobutyrate	Inhibitor
Helenalin isobutyrate is an NF-κB (p65 subunit) inhibitor with anti-inflammatory activity. Helenalin isobutyrate irreversibly alkylates cysteine sulfhydryl groups in the p65 subunit to inhibit NF-κB complex DNA binding activity.

HY-B1640S

Ethacrynic acid-¹³C₂,d₅
Ethacrynic acid-13C2,d5 is the deuterium and 13C labeled Ethacrynic acid.

HY-N11775

Eudebeiolide B	Inhibitor
Eudebeiolide B is a compound that can be isolated from Salvia plebeia R. Br. Eudebeiolide B inhibits osteoclastogenesis by regulating RANKL-induced NF-κB, c-Fos and calcium signaling. Eudebeiolide B can be used for osteoclast-related diseases research.

HY-175037

DNH28	Inhibitor
DNH28 is a potent NF-κB and MAPK inhibitor with an IC₅₀ of 0.93 μM against HepG2 cells. DNH28 promotes apoptosis by down-regulating the expression of Bcl-2, up-regulating the expression of BAX and Cleaved-caspase-3. DNH28 blocks the cell cycle and inhibits migration. DNH28 can be used for the study of hepatocellular carcinoma (HCC).

HY-124281

9(R)-PAHSA	Inhibitor
9(R)-PAHSA is a R-enantiomer of 9-PAHSA. 9-PAHSA is an orally available anti-inflammatory lipid that lowers blood sugar and reduces inflammation.

HY-137315S

TML-6-d₃
TML-6-d₃ is the deuterium labeled TML-6. TML-6, an orally active curcumin derivative, inhibits the synthesis of the β-amyloid precursor protein and β-amyloid (Aβ). TML-6 can upregulate Apo E, suppress NF-κB and mTOR, and increase the activity of the anti-

HY-N17736

Chikusetsusaponin IVa methyl ester	Inhibitor
Chikusetsusaponin IVa methyl ester (CME) is a natural triterpenoid saponin compound. Chikusetsusaponin IVa methyl ester induces G0/G1 cell cycle arrest and apoptosis in colon cancer cells by inhibiting the Wnt/β-catenin signaling pathway. By inhibiting the NF-κB and AP-1 signaling pathways, Chikusetsusaponin IVa methyl ester significantly reduces the production of NO, PGE₂ and pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), and downregulates the levels of iNOS and COX-2. Chikusetsusaponin IVa methyl ester can be used in researches on colorectal cancer and inflammation.

HY-N8719

Pratol	Inhibitor	99.16%
Pratol is a potent inhibitor of NF-κB. Pratol significantly reduces NO and prostaglandin PGE2 production without any cytotoxic in LPS-stimulated RAW 264.7 cells. Pratol reduces proinflammatory cytokines. Pratol can be used in study inflammatory diseases and cancer.

HY-P11183

Cathelicidin-PY	Inhibitor
Cathelicidin-PY is an antimicrobial peptide exhibiting strong antimicrobial property. Cathelicidin-PY inhibits the activation of TLR4 inflammatory response pathways induced by lipopolysaccharide (LPS) (HY-D1056). Cathelicidin-PY possesses strong antimicrobial and anti-inflammatory activities and low cytotoxic ability against RAW 264.7 cells. Cathelicidin-PY can be used for antimicrobial and anti-inflammatory research.

LAT TCR CD3 BCR PLCγ1 ZAP70 PKC ELKs NEMO ATM NEMO PIASy PIDD RIP1 PARP1 NEMO ATM cIAP1 NEMO ATM c-IAP1/2, c-FLIP, XIAP, Bcl-XL, Bcl-2, gadd45β,
TRAF1/2, A1/Bfl-1, p100, IL-1, IL-6, IL8, IL-1β, TNF-α, A20,
IκBα, COX2, MIP-1β, MIP-2, VCAM-1,GM-CSF, CCL2, etc. IκBα TRAF6 ATM Tyr kinase LYN SYK BLK BLNK PLCγ2 BTK CARMA1 MALT1 BCL-10 IκBα CK2 p50 RELA IL-1 IL-1R MyD88 IRAK1 IRAK4 TRAF6 TNF TNFR1 TRADD RIPK1 TRAF2/5 cIAP1/2 TAB2 or
TAB3 TAK1 NEMO IKKα IKKβ p105 p50 p105 REL p50 p50 p50 REL p50 RELA p50 c-REL p50 p50 IκBα REL p50 REL p50 CREB TRIM25 RNF135 IPS1 TRAF3 TRAF2/6 Virus MKK3 or
MKK6 MKK4 or
MKK7 p38 JNK CREB AP1 AP1 LPS LBP CD14 TLR4 MD2 MD2 MD2 TLR4 MyD88 TIRAP TRAM TRIF IRAK1 IRAK4 TRAF6 RIP1 TRAF3 CD40L, RANKL CD40,
RANK LTα1β2, LIGHT,
BAFF LTβR,
BAFFR TRAF6 IKKε TBK1 IRF7 IRF3 IRF3 IRF7 BLC, ELC, SLC, SDF-1α, BAFF,
ICAM, CXCL12, CXCL13, CCL19, CCL21, etc. TRAF3 TRAF2 cIAP1/2 NIK TBK1 IKKα p100 RELB p52 RELB p52 RELB

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.

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NF-κB

NF-κB

NF-κB Isoform Specific Products:

NF-κB Isoform Specific Products:

NF-κB Related Products (1746)

Antibodies (32)

NF-κB Signaling Pathway

NF-κB Isoform Comparison

NF-κB Related Products (1746):