NF-κB Inhibitors

Övrigt NF-κB Inhibitorer

• Utvalda inhibitorer
• Inhibitorer (127)
• Modulatorer (8)
• Kemikalier (4)
• Aktivatorer (4)

Kat.nr.	Produktnamn	Information	Citeringar av produktanvändning	Produktvalideringar
E4686	DCZ0415	DCZ0415 är en potent hämmare av TRIP13. DCZ0415 försämrar icke-homolog sammanslagning av DNA-ändar (nonhomologous end joining) och hämmar NF-κB-aktivitet. Det utlöser anti-myelom-effekter både in vitro och in vivo, samt i primära celler erhållna från myelompatienter som är resistenta mot läkemedel.	SLAS Discov, 2025, 33:100233 SLAS Discovery, 2025, 100233
S7672	Omaveloxolone (RTA-408)	Omaveloxolone (RTA-408) är en syntetisk triterpenoid som aktiverar den cytoprotektiva transkriptionsfaktorn Nrf2 och hämmar NF-κB-signalering. Fas 2.	J Clin Invest, 2025, 135(14)e176655 Redox Biol, 2025, 87:103885 Front Pharmacol, 2025, 16:1539032
S1013	Bortezomib	Bortezomib är en potent 20S proteasomhämmare med Ki på 0,6 nM. Den uppvisar fördelaktig selektivitet mot tumörceller framför normala celler. Denna förening hämmar NF-κB och inducerar ERK-fosforylering för att undertrycka Cathepsin B och hämma den katalytiska processen av Autophagy i äggstockscancer och andra solida tumörer.	Mol Cell, 2026, S1097-2765(26)00238-8 Cancer Res, 2026, 10.1158/0008-5472.CAN-25-4114. J Cell Mol Med, 2026, 30(4):e71053
S3604	Triptolide	Triptolide är en diterpen triepoxid, immunsuppressivt medel extraherat från den kinesiska örten Tripterygium wilfordii. Den fungerar som en NF-κB-hämmare med dubbla åtgärder genom störning av p65/CBP-interaktion och genom minskning av p65-protein. Triptolide (PG490) upphäver transaktiveringsfunktionen hos heat shock transcription factor 1 (HSF1). Triptolide hämmar MDM2 och inducerar apoptos genom en p53-oberoende väg.	Mol Cell, 2025, S1097-2765(25)00316-8 Mol Cell, 2025, 85(15):2839-2853.e8 Chin Med, 2025, 20(1):122
S8341	TAK-243 (MLN7243)	TAK-243 (MLN7243) är en potent, mekanismbaserad småmolekylär hämmare av ubiquitin activating enzyme (UAE) med ett IC50-värde på 1 ± 0,2 nM i UBCH10 E2-tioesteranalys. Den har minimal hämmande aktivitet i en panel av kinas- och receptoranalyser, samt på humant karbanhydras typ I och typ II. TAK-243 (MLN7243) inducerar ER stress, häver aktivering av NFκB-vägen och främjar apoptosis.	Mol Cell, 2026, 86(7):1397-1416.e11 J Virol, 2026, e0028526. bioRxiv, 2026, 2026.05.06.723260
S8483	CBL0137 Hydrochloride	CBL0137 (CBLC137, Curaxin 137) HCl aktiverar p53 och hämmar NF-κB med EC50-värden på 0,37 μM respektive 0,47 μM i cellbaserade p53- och NF-kB-reporteranalyser. Det hämmar också histonchaperonet FACT (facilitates chromatin transcription complex).	Oncogene, 2025, 893-908 Oncogene, 2025, 44(13):893-908 Cancer Biology & Therapy, 2025, 2511301
S8078	Bardoxolone Methyl (RTA 402)	Bardoxolone Methyl (RTA 402, TP-155, NSC 713200, CDDO Methyl Ester, CDDO-Me) är en IKK-hämmare, som uppvisar potenta proapoptotiska och antiinflammatoriska aktiviteter; även en potent Nrf2-aktivator och nuclear factor-κB (NF-κB)-hämmare. Bardoxolone Methyl upphäver ferroptosis. Bardoxolone methyl inducerar apoptosis och autophagy i cancerceller.	J Clin Invest, 2025, 135(14)e176655 Redox Biol, 2025, 87:103885 Research (Wash D C), 2025, 8:0980
S1623	N-Acetylcysteine (NAC chemical, N-Acetyl-L-Cysteine)	Acetylcystein (N-acetyl-L-cystein, NAC, N-acetylcystein) är en ROS (reaktiva syreradikal)-hämmare som motverkar aktiviteten hos proteasomhämmare. Det är också en hämmare av tumörnekrosfaktorproduktion. Acetylcystein (N-acetyl-L-cystein) hämmar TNF-inducerad NF-κB-aktivering genom att hämma IκB-kinaser. Acetylcystein (N-acetyl-L-cystein) inducerar apoptos via den mitokondrieberoende vägen. Acetylcystein (N-acetyl-L-cystein) hämmar ferroptosis och virusreplikation.Lösningar är instabila och bör beredas färskt.	Cell Death Dis, 2026, 17(1):227 Int Immunopharmacol, 2026, 181:116687 Curr Res Toxicol, 2026, 10:100281
S2913	BAY 11-7082 (BAY 11-7821)	BAY 11-7082 (BAY 11-7821) är en NF-κB-hämmare, hämmar TNFα-inducerad IκBα-fosforylering med en IC50 på 10 μM i tumörceller. BAY 11-7082 hämmar ubiquitin-specifik proteas USP7 och USP21 med en IC50 på 0,19 μM respektive 0,96 μM. BAY 11-7082 inducerar apoptos och S-fasarrest i magsäckscancerceller.	Research (Wash D C), 2026, 9:1190 J Dairy Sci, 2026, 109(3):2890-2903 Transl Androl Urol, 2026, 15(2):55
S7351	JSH-23	JSH-23 är en hämmare av NF-κB transkriptionell aktivitet, som hämmar LPS-stimulerad nukleär faktor (NF)-κB transkriptionell aktivitet i RAW 264.7-celler med ett IC50-värde på 7,1 μM, och stör LPS-inducerad NF-κB nukleär translokation utan att påverka IκB-nedbrytning.	Nat Commun, 2026, 17(1)3228 Transl Oncol, 2026, 65:102681 Nat Commun, 2025, 16(1):5912
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NF-κB (nuclear factor-kappa B) is a highly regulated, homo- or hetero-dimeric transcription factor, present in almost all cell types. The NF-κB proteins are composed of five different subunits, RelA (p65), RelB, c-Rel (Rel), NF-κB1, and NF-κB2, all of which share a Rel homology domain (RHD) in their N-termini, and have a transactivation domain in their C-termini, except for NF-κB1 and NF-κB2. The NF-κB1 and NF-κB2 proteins are synthesized as longer precursors, p105, and p100, which undergo selective degradation of their C-terminal region containing ankyrin repeats to generate the active NF-κB subunits, p50 and p52, respectively. [i] Different dimer combinations act as transcriptional activators or repressors, respectively. The p50 and p52 NF-κB members play critical roles in modulating the specificity of NF-κB function by forming heterodimers with RelA, RelB, or c-Rel. The NF-κB RelA-p50 and RelB-p50 heterodimeric complexes are transcriptional activators. The NF-κB p50/p50 and p52/p52 homodimers are generally transcriptional repressors, but can function as transcriptional activators when bound to nuclear protein Bcl-3. ^[2]

NF-κB is a rapidly acting primary transcription factor, and is controlled by subcellular compartmentalization and post-translational modifications (PTMs) including phosphorylation, acetylation, methylation and ubiquitylation. NF-κB dimers are primarily sequestered as an inactive form in the cytoplasm by a protein complex called inhibitor of kappa B (IκB) among unstimulated cells. Activation of NF-κB occurs via the degradation of IκB, a process initiated by IκB kinase (IKK). A variety of stimuli such as cytokines and cellular stress can activate the IKK, resulting in ubiquitination and dissociation of the IκB from NF-κB. The activated NF-κB is then translocated into the nucleus to regulate gene expression. NF-κB regulates a broad range of genes involved in various biological processes including inflammation, immunity, differentiation, development, as well as genes regulating cell proliferation, apoptosis, cell adhesion and the cellular microenviroment. In addition, NF-κB activates its own repressor IκBα and IκBε, as well as the TNFAIP3 (A20) a negative regulator of IKK activation, forming a negative feedback loop. ^[1]

NF-κB has been found to be constitutively active in a number of diseases, including arthritis, chronic inflammation, asthma, neurodegenerative diseases, and heart disease, as well as in many types of human tumors. [ii] NF-κB has long been linked with cancer, primarily through aberrant constitutive NF-κB activation that suppresses apoptosis or promotes tumor growth, metastasis, and angiogenesis by inducing the expression of anti-apoptotic genes, proto-oncogenes, matrix metalloproteinase, cell adhesion genes, and genes associated with the growth of new blood vessels. Additionally, NF-κB promotes a metabolic switch in cancer cells from oxidative phosphorylation to glycolysis (the Warburg effect) by inducing the expression of glycolytic enzymes and inhibiting the expression of mitochondrial gene. Constitutive activation of NF-κB can result from continuous exposure to NF-κB activating stimuli, such as cytokine release by tumor-associated macrophages (TAMs), or from mutations in NF-κB subunits and genes involved in regulating NF-κB function. Inhibiting NF-κB activation can prevent tumor cell proliferation and induce cell death. Given the importance of NF-κB in initiating or enhancing cell survival, NF-κB is therefore considered as a promising target for anticancer therapies. ^[1]