NBE5

NBE5 (1.0 μM; 12 h) induces potent Keap1 degradation in HCT116, RKO, and BEAS-2B cells, with the highest activity (92.5% degradation) observed in BEAS-2B cells^[1].
NBE5 (0.1-10.0 μM; 12 h) induces concentration-dependent Keap1 degradation in HCT116 and RKO cells over 12 h, with higher potency (lower DC₅₀, higher D_max) in HCT116 cells^[1].
NBE5 (1.0 μM; 1.5-24 h) induces time-dependent Keap1 degradation in HCT116 and RKO cells, with faster degradation kinetics (shorter DT₅₀) observed in HCT116 cells^[1].
NBE5 (2.0 μM; 6-18 h, plus washout culture) mediates Keap1 degradation in HCT116 and RKO cells that depends on both the ubiquitin-proteasome system and autophagy-lysosome system, involves enhanced Keap1-Hsp90 interaction, and produces sustained degradation after washout^[1].
NBE5 (0.5-2.5 μM; 12 h) activates the Nrf2 pathway in HCT116, RKO, and BEAS-2B cells via Keap1 degradation, leading to increased nuclear Nrf2, upregulated downstream antioxidant enzyme protein and mRNA levels, with no effect on Keap1 transcription^[1].
NBE5 (2.0 μM; 12 h) selectively induces Keap1 degradation in HCT116 cells, activates the Nrf2 antioxidant pathway, upregulates autophagy-related and HSP70 family proteins, and shows no significant effect on off-target proteins IKKβ and SLC30A1^[1].
The DC₅₀ values ​​of NBE5 for Keap1 degradation in HCT116 and RKO cells were 0.82 μM and 1.72 μM, respectively; furthermore, at a concentration of 1 μM, the maximum degradation rate of Keap1 in BEAS-2B cells reached 92.5%^[1].

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