PROTAC IKKβ/NR4A1 degrader-1

PROTAC IKKβ/NR4A1 degrader-1 (Compound A9) (48 h) shows strong AML cell killing activity in Monomac-6 (IC₅₀ = 0.32 µM), NB-4 (IC₅₀ = 0.23 µM), U-937 (IC₅₀ = 0.36 µM), Molm-13 (IC₅₀ = 0.23 µM), and HL-60 cells (IC₅₀ = 0.54 µM)^[1].
PROTAC IKKβ/NR4A1 degrader-1 (0.5-1 µM) dose-dependently increases the levels of caspase 3 and cleaved caspase 3 proteins in NB-4, Monomac-6, and Molm-13 cells, while the necrosis marker RIP kinase remained unchanged, indicating that it can induce apoptosis^[1].
PROTAC IKKβ/NR4A1 degrader-1 (0-1 µM) results in a dose-dependent decrease in IKKβ and NR4A1 protein levels in NB-4, Monomac-6, and Molm-13 cells^[1].
PROTAC IKKβ/NR4A1 degrader-1 (0.5 μM, 16 h)-mediated degradation of IKKβ and NR4A1 can be reversed by the proteasome inhibitor MG132 (HY-13259), the E3 ligase competitor Pomalidomide (HY-10984), or the neddylation inhibitor Pevonedistat (MLN4924) (HY-70062) in A375 melanoma cells, while PROTAC IKKβ/NR4A1 degrader-1 NC has no degradation activity^[1].
PROTAC IKKβ/NR4A1 degrader-1 (10 μM, 3 h) promotes the formation of a ternary complex in HEK293T cells, evidenced by co-immunoprecipitation of IKKβ with exogenous Flag-CRBN and of CRBN with Flag-NR4A1^[1].
PROTAC IKKβ/NR4A1 degrader-1 (0.25-1 μM, 48 h) exhibits reduced efficacy in IKKβ or NR4A1 knockout cells^[1].
PROTAC IKKβ/NR4A1 degrader-1 (0.125-0.25 μM, 72 h) results in overlap of the NF-κB signaling pathway in Molm-13 and Monomac-6 cells with the enrichment pathway in AML cells with high NR4A1 expression^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.