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.
NF-κB Inhibitors
| Nº Cat. | Nombre del producto | Información | Citas de uso del producto | Validaciones del producto |
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| E4686 | DCZ0415 | DCZ0415 es un potente inhibidor de TRIP13. DCZ0415 altera la reparación por unión de extremos no homólogos e inhibe la actividad de NF-κB. Desencadena efectos anti-mieloma tanto in vitro como in vivo, y en células primarias obtenidas de pacientes con mieloma resistentes a fármacos. |
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| S7672 | Omaveloxolone (RTA-408) | Omaveloxolone (RTA-408) es un triterpenoide sintético que activa el factor de transcripción citoprotector Nrf2 e inhibe la señalización de NF-κB. Fase 2. |
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| S1013 | Bortezomib | Bortezomib es un potente inhibidor del 20S proteasome con un Ki de 0,6 nM. Exhibe una selectividad favorable hacia las células tumorales sobre las células normales. Este compuesto inhibe NF-κB e induce la fosforilación de ERK para suprimir la Cathepsin B e inhibir el proceso catalítico de la autophagy en el cáncer de ovario y otros tumores sólidos. |
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| S3604 | Triptolide | Triptolide es un triepóxido diterpénico, un agente inmunosupresor extraído de la hierba china Tripterygium wilfordii. Funciona como un inhibidor de NF-κB con doble acción al interrumpir la interacción p65/CBP y al reducir la proteína p65. Triptolide (PG490) anula la función de transactivación del factor de transcripción de choque térmico 1 (HSF1). Triptolide inhibe MDM2 e induce la apoptosis a través de una vía independiente de p53. |
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| S8341 | TAK-243 (MLN7243) | TAK-243 (MLN7243) es un potente inhibidor de molécula pequeña, basado en el mecanismo, de la ubiquitin activating enzyme (UAE) con una IC50 de 1 ± 0,2 nM en el ensayo de tioéster UBCH10 E2. Tiene una actividad inhibidora mínima en un panel de ensayos de quinasas y receptores, así como en la anhidrasa carbónica humana tipo I y tipo II. TAK-243 (MLN7243) induce ER stress, anula la activación de la vía NF-κB y promueve la apoptosis. |
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| S8483 | CBL0137 Hydrochloride | CBL0137 (CBLC137, Curaxin 137) HCl activa p53 e inhibe NF-κB con EC50 de 0,37 μM y 0,47 μM en los ensayos reporteros de p53 y NF-kB basados en células, respectivamente. También inhibe la chaperona de histonas FACT (facilitates chromatin transcription complex). |
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| S8078 | Bardoxolone Methyl (RTA 402) | Bardoxolone Methyl (RTA 402, TP-155, NSC 713200, CDDO Methyl Ester, CDDO-Me) es un inhibidor de la IKK, mostrando potentes actividades proapoptóticas y antiinflamatorias; también un potente activador de Nrf2 y un inhibidor del factor nuclear-κB (NF-κB). Bardoxolone Methyl abroga la ferroptosis. El metil bardoxolona induce apoptosis y autofagia en células cancerosas. |
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| S1623 | N-Acetylcysteine (NAC chemical, N-Acetyl-L-Cysteine) | La acetilcisteína (N-acetil-L-cisteína, NAC, N-acetilcisteína) es un inhibidor de las ROS (especies reactivas de oxígeno) que antagoniza la actividad de los inhibidores del proteasoma. También es un inhibidor de la producción del factor de necrosis tumoral. La acetilcisteína (N-acetil-L-cisteína) suprime la activación de NF-κB inducida por TNF a través de la inhibición de las cinasas IκB. La acetilcisteína (N-acetil-L-cisteína) induce la apoptosis a través de la vía dependiente de mitocondrias. La acetilcisteína (N-acetil-L-cisteína) inhibe la ferroptosis y la replicación viral.Las soluciones son inestables y deben prepararse frescas. |
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| S2913 | BAY 11-7082 (BAY 11-7821) | BAY 11-7082 (BAY 11-7821) es un inhibidor de NF-κB, que inhibe la fosforilación de IκBα inducida por TNFα con una IC50 de 10 μM en células tumorales. BAY 11-7082 inhibe la proteasa específica de ubiquitina USP7 y USP21 con una IC50 de 0,19 μM y 0,96 μM, respectivamente. BAY 11-7082 induce apoptosis y detención de la fase S en células de cáncer gástrico. |
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| S7351 | JSH-23 | JSH-23 es un inhibidor de la actividad transcripcional de NF-κB, que inhibe la actividad transcripcional del factor nuclear (NF)-κB estimulada por LPS en células RAW 264.7 con un valor de IC50 de 7,1 μM, e interfiere con la translocación nuclear de NF-κB inducida por LPS sin afectar la degradación de IκB. |
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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]
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