IκB/IKK

Otro NF-κB Inhibidores

Productos selectivos de isoformas

• Inhibidores destacados
• Inhibidores (38)
• Moduladores (2)

Nº Cat.	Nombre del producto	Información	Citas de uso del producto	Validaciones del producto
S8922	TBK1/IKKε-IN-5	TBK1/IKK -IN-5 (compuesto 1) es un inhibidor dual de la TANK-binding kinase 1 (TBK1) y la I B kinase- (IKK /IKK-i) con una IC50 de 1,0 nM y 5,6 nM para TBK1 e IKK , respectivamente. La inhibición de TBK1/IKK mejora la respuesta al bloqueo de PD-1, lo que predice eficazmente la respuesta tumoral in vivo.	Autophagy, 2025, 1-23. Cancer Res, 2025, 10.1158/0008-5472.CAN-25-1791 Sci Adv, 2024, 10(6):eadk2285
S9042	Wedelolactone	Wedelolactone, un compuesto natural derivado de plantas medicinales, es un inhibidor de IKK que es crítico para la activación de NF-κB al mediar la fosforilación y degradación de IκBα. Este compuesto también es un inhibidor de la caspase-11.	Int J Ophthalmol, 2024, 17(4):616-624 PeerJ, 2022, 10:e13766 Exp Eye Res, 2021, 211:108750
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.	J Clin Invest, 2025, 135(14)e176655 Redox Biol, 2025, 87:103885 Research (Wash D C), 2025, 8:0980
S1396	Resveratrol (trans-Resveratrol)	El Resveratrol tiene un amplio espectro de dianas, incluyendo las ciclooxigenasas (es decir, COX, IC50=1.1 μM), las lipooxigenasas (LOX, IC50=2.7 μM), las quinasas, las sirtuinas y otras proteínas. Tiene efectos anticancerígenos, antiinflamatorios, hipoglucemiantes y otros efectos cardiovasculares beneficiosos. El Resveratrol induce la mitofagia/autofagia y la apoptosis dependiente de la autofagia.	Aging Cell, 2025, e70075 Biomed Pharmacother, 2025, 190:118393 Breast Cancer Res, 2025, 27(1):186
S2882	IKK-16	IKK-16 es un inhibidor selectivo de IκB quinasa (IKK) para IKK-2, IKK complex e IKK-1 con una IC50 de 40 nM, 70 nM y 200 nM en ensayos sin células, respectivamente. IKK-16 también inhibe la fosforilación de LRRK2 Ser935 en células y la actividad quinasa de LRRK2 in vitro con una IC50 de 50 nM.	Ann Rheum Dis, 2025, S0003-4967(25)04453-X Nucleic Acids Res, 2025, 53(17)gkaf891 Cell Commun Signal, 2025, 23(1):274
S2824	TPCA-1	TPCA-1 (GW683965) es un inhibidor de IKK-2 con una IC50 de 17,9 nM en un ensayo sin células, inhibe la vía de NF-κB y exhibe una selectividad 22 veces mayor sobre IKK-1. TPCA-1 también es un inhibidor de STAT3 y mejora la apoptosis.	Nat Genet, 2025, 10.1038/s41588-025-02221-2 EMBO J, 2025, 10.1038/s44318-025-00412-5 EMBO J, 2025, 10.1038/s44318-025-00561-7
S8044	BMS-345541	BMS-345541 es un inhibidor altamente selectivo de las subunidades catalíticas de IKK-2 e IKK-1 con IC50 de 0,3 μM y 4 μM en ensayos sin células, respectivamente.	Cell Death Dis, 2025, 16(1):124 Mol Med, 2025, 31(1):197 Cancer Med, 2025, 14(5):e70047
S7352	Bay 11-7085	BAY 11-7085 (Bay 11-7083) es un inhibidor irreversible de la fosforilaci n de I B inducida por TNF con una IC50 de 10 M.	JCI Insight, 2025, e186456 J Am Soc Nephrol, 2024, 35(8):998-1015 Theranostics, 2024, 14(2):861-878
S2864	IMD 0354	IMD-0354 (IKK2 Inhibitor V) es un inhibidor de IKKβ y bloquea la fosforilación de IκBα en la vía NF-κB.	Nat Commun, 2025, 16(1):5387 Iran J Basic Med Sci, 2023, 26(8):912-918 Blood, 2022, blood.2021014304
S7948	MRT67307 HCl	MRT67307 es un potente inhibidor dual de IKKϵ y TBK1 con IC50 de 160 y 19 nM, respectivamente. MRT67307 inhibe potentemente ULK1 y ULK2 y bloquea la autophagy.	EMBO Rep, 2025, 10.1038/s44319-025-00444-2 EMBO J, 2024, 10.1038/s44318-024-00244-9 mBio, 2023, 10.1128/mbio.02506-23
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IκB (Inhibitor of κB) functions as a primary inhibitor of NF-κB activation, with an N-terminal regulatory domain, followed by six or more ankyrin repeats and a PEST domain near their C terminus. ^[1] IκB family contains eight known members, IκBα, IκBβ, IκBε, Bcl-3 (B-cell lymphoma 3), IκBζ, and IκBns (NF-κBδ), as well as the precursor Rel proteins p100 (NF-κB2) and p105 (NF-κB1) due to the presence of multiple ankyrin repeats in their C-terminal halves. IκBα and IκBβ are broadly expressed in all type of cells, whereas IκBε is expressed only in hematopoietic cells. Bcl-3, IκBζ and IkBNS are atypical IκB proteins that exhibit limited expression following NF-κB activation. The regulation of IκB proteins varies by protein type, and each IκB moiety exhibits a unique affinity for NF-κB complexes. ^[2]

In unstimulated cells, the IκBα proteins mask the nuclear localization signals (NLS) of NF-κB proteins, keeping them sequestered in an inactive state in the cytoplasm. In response to stimuli, IκB kinase (IKK) phosphorylates IκBα leading to the degradation of IκBα, and subsequent NF-κB activation. IκBα expression can be activated by NF-κB to generate a negative feedback loop. Similar to IκBα, IκBβ acts by sequestering p65- and c-Rel-containing complexes in the cytoplasm. However, nuclear localized IκBβ also binds to p65:c-Rel heterodimers, promoting continued binding to specific κB sites, and augmenting late transcription of select target genes (i.e. TNF and IL-1β). IκBε is induced slowly, and selectively regulates p65 homodimers and c-Rel:p65 heterodimers. Bcl-3 functions as a transcriptional co-activator that may both inhibit and facilitate NF-κB-dependent transcription in a context-specific manner. Like Bcl-3, IκBζ can enhance transcription in association with p50 NF-κB dimmers despite the prescence of distinct mechanisms. IκBns selectively inhibits NF-κB-dependent pro-inflammatory gene expression by stabilizing p50 homodimers at κB sites. In addition to exclusively stabilizing RelB dimers, p100 itself can act more broadly in inhibiting NF-κB dimers. The p105 also acts like a typical IκB protein, and is additionally associated with the activation of the MAPK-ERK signaling pathway through the binding of MAP3K8 (TPL2). Moreover, the functions of individual IκB family members are quite heterogeneous and are not limited to this particular role in regulating NF-κB signaling. ^[2]

In oncology, the direct activation of NF-κB complexes through the loss of the inhibitory proteins IκBα and IκBε has been observed in Hodgkin’s lymphoma. Since the NF-κB signal pathway plays a critical role in tumorigenesis bv way of abberant IκB activity, a variety of compounds targeting IKK and its associated enzymes are in clinical development. ^[3] For instance, the proteasome inhibitor Bortezomib (Velcade®) has been approved by the FDA for use in haematological malignancies. ^[4] In addition, Bortezomib is currently being explored in clinical development for its efficacy against solid tumors (clinicaltrials.gov; NCT00479128).