PROTAC sEH degrader-1

PROTAC sEH degrader-1 (compound 8) exhibits an IC₅₀ of 3.8 nM for the inhibition of recombinant human sEH, and an IC₅₀ of 210 nM for the inhibition of recombinant mouse sEH^[1].
PROTAC sEH degrader-1 (1 μM; 24 h) induces 78% sEH degradation in HepG2 cells^[1].
PROTAC sEH degrader-1 (0.01-1000 nM; 24 h) induces concentration-dependent degradation of sEH in HepG2 cells, with a DC₅₀ of approximately 0.5 nM and a maximum degradation level of 79% at a concentration of 100 nM^[1].
PROTAC sEH degrader-1 (50 nM; 2-48 h) induces more than 50% degradation of sEH in HepG2 cells within 4 h, and achieves the maximum degradation effect at 24 h^[1].
PROTAC sEH degrader-1 (50 nM; 1 μM t-TUCB (HY-114266); 1 μM Lenalidomide (HY-A0003); 1 μM MLN4924 (HY-70062); 10/40 μM MG-132 (HY-13259)) induces sEH degradation in HepG2 cells via a PROTAC mechanism dependent on sEH binding, E3 ligase recruitment, and the ubiquitin-proteasome system^[1].
PROTAC sEH degrader-1 (100 nM; 48 h) selectively degrades cytosolic sEH but does not degrade peroxisomal sEH in HepG2 cells^[1].
PROTAC sEH degrader-1 effectively degrades sEH in HEK293T, MDA-MB-231 and SH-SY5Y human cell lines; it significantly reduces sEH protein levels in HepG2 cells, and quantitative proteomic analysis identifies sEH as one of the most significantly downregulated proteins^[1].
PROTAC sEH degrader-1 (100 nM-1 μM; 12 h pretreatment) effectively reduces endoplasmic reticulum stress induced by Thapsigargin (HY-13433) in HEK293T cells^[1].

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