NF-κB Inhibitors | Inhibitors | 여러 강력하고, 높은 선택성을 가지며, 잘 인용된

NF-κB controls the 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.

기타 NF-κB 억제제

IκB/IKK AP-1

Cat.No.	제품명	정보	제품 사용 인용
E4686	DCZ0415	DCZ0415는 TRIP13의 강력한 억제제입니다. DCZ0415는 비상동 말단 연결 복구를 손상시키고 NF-κB 활성을 억제합니다. 이는 시험관 내(in vitro) 및 생체 내(in vivo) 환경과 약물 내성 다발성 골수종 환자로부터 얻은 일차 세포 모두에서 항골수종 효과를 유발합니다.	SLAS Discov, 2025, 33:100233 SLAS Discovery, 2025, 100233
S7672	Omaveloxolone (RTA-408)	Omaveloxolone (RTA-408)은 세포 보호 전사 인자인 Nrf2를 활성화하고 NF-κB 신호 전달을 억제하는 합성 트리테르페노이드입니다. 임상 2상.	J Clin Invest, 2025, 135(14)e176655 Redox Biol, 2025, 87:103885 Front Pharmacol, 2025, 16:1539032
S1013	Bortezomib	Bortezomib은 0.6 nM의 K_i 값을 갖는 강력한 20S proteasome 억제제입니다. 이는 정상 세포보다 종양 세포에 대해 유리한 선택성을 나타냅니다. 이 화합물은 NF-κB를 억제하고 ERK 인산화를 유도하여 난소암 및 기타 고형암에서 Cathepsin B를 억제하고 Autophagy의 촉매 과정을 저해합니다.	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	Triptolide는 중국 허브인 Tripterygium wilfordii에서 추출한 디테르펜 트리 에폭사이드이자 면역 억제제입니다. 이것은 p65/CBP 상호작용의 방해와 p65 단백질의 감소라는 이중 작용을 통해 NF-κB 억제제로서 기능합니다. Triptolide(PG490)는 heat shock transcription factor 1 (HSF1)의 전사 활성화 기능을 무효화합니다. Triptolide는 MDM2를 억제하고 p53 비의존적 경로를 통해 apoptosis를 유도합니다.	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)은 UBCH10 E2 티오에스테르 분석에서 1 ± 0.2 nM의 IC50을 가지는 강력한 메커니즘 기반의 ubiquitin activating enzyme (UAE) 저해제입니다. 이 화합물은 다양한 키나아제 및 수용체 분석뿐만 아니라 인간 탄산탈수효소 I형 및 II형에 대해 최소한의 저해 활성을 나타냅니다. TAK-243 (MLN7243)은 ER stress를 유도하고 NFκB 경로 활성화를 차단하며 apoptosis를 촉진합니다.	Mol Cell, 2026, 86(7):1397-1416.e11 J Virol, 2026, e0028526. bioRxiv, 2026, 2026.05.06.723260
S8483	CBL0137 Hydrochloride	CBL0137 Hydrochloride(CBLC137, Curaxin 137)은 세포 기반 p53 및 NF-κB 리포터 분석에서 각각 0.37 μM 및 0.47 μM의 EC50으로 p53을 활성화하고 NF-κB를 억제합니다. 또한 히스톤 샤페론인 FACT(facilitates chromatin transcription complex)를 억제합니다.	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)은 IKK 억제제로서 강력한 세포사멸 촉진 및 항염증 활성을 나타내며, 강력한 Nrf2 활성제이자 NF-κB 억제제이기도 합니다. Bardoxolone Methyl은 Ferroptosis를 제거합니다. Bardoxolone methyl은 암세포에서 Apoptosis related 및 Autophagy를 유도합니다.	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)	Acetylcysteine(N-acetyl-l-cysteine, NAC, N-acetylcysteine)은 ROS(reactive oxygen species) 억제제로 proteasome inhibitors의 활성을 길항합니다. 또한 tumor necrosis factor production 억제제이기도 합니다. Acetylcysteine(N-acetyl-l-cysteine)은 IκB kinases의 억제를 통해 TNF-induced NF-κB 활성화를 억제합니다. Acetylcysteine(N-acetyl-l-cysteine)은 mitochondria-dependent pathway를 통해 Apoptosis를 유도합니다. Acetylcysteine(N-acetyl-l-cysteine)은 Ferroptosis와 virus replication을 억제합니다.용액은 불안정하므로 신선하게 준비해야 합니다.	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)은 NF-κB 억제제로, 종양 세포에서 10 μM의 IC50으로 TNFα 유도 IκBα 인산화를 억제합니다. BAY 11-7082는 각각 0.19 μM 및 0.96 μM의 IC50으로 ubiquitin-specific protease USP7 및 USP21을 억제합니다. BAY 11-7082는 위암 세포에서 apoptosis 및 S기 정지를 유도합니다.	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-23은 NF-κB 전사 활성을 억제하는 억제제로, RAW 264.7 세포에서 7.1 μM의 IC50 값으로 LPS 자극에 의한 핵인자(NF)-κB 전사 활성을 억제하며, IκB 분해에 영향을 주지 않으면서 LPS 유도 NF-κB의 핵 내 이동을 방해합니다.	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]