PROTAC sEH degrader-3

PROTAC sEH-degrader-3 (compound 1a) (1 μM; 24 h) alleviates endoplasmic reticulum stress in HepG2 and 293T cells by inhibiting the IRE1α-XBP1 signaling pathway, and partially rescues Thapsigargin (HY-13433)-induced cell death; its efficacy is stronger when used in combination with Thapsigargin at a concentration of 1 μM for 24 h^[1].
PROTAC sEH-degrader-3 (1 μM; 24 h) induces lysosome-dependent, proteasome-independent degradation of sEH in HepG2 and 293T cells when treated at 1 μM for 24 h^[1].
PROTAC sEH-degrader-3 (250 nM; 24-48 h) reduces sEH protein levels in HepG2 cells after 24 h and 48 h, and this degradation effect is partially reversed by Bortezomib (BTZ) (HY-10227), and significantly reversed by Thalidomide (HY-14658), 1a' or compound 1^[1].
PROTAC sEH-degrader-3 (250 nM; 24 h) reduces sEH protein levels in wild-type HEK293T cells, and this degradation effect is significantly reversed after co-treatment with 10 nM, 25 nM or 50 nM MG132 (HY-13259)^[1].
PROTAC sEH-degrader-3 (250 nM; 24 h) does not reduce sEH protein levels after a 24-h treatment in CRBN-knockout HEK293T cells, and no significant effect is observed even when combined with 10 nM, 25 nM, or 50 nM MG132^[1].
PROTAC sEH-degrader-3 (250 nM; 24 h) reduces sEH protein levels in 293T cells, and combined treatment with 5 nM, 10 nM, or 25 nM Bafilomycin A1 (BafA1) (HY-100558) fails to sustainably reverse this degradation effect^[1].
PROTAC sEH-degrader-3 (250 nM; 24 h) reduces sEH protein levels in wild-type 293T cells and ATG2A/ATG2B-knockout 293T cells^[1].
PROTAC sEH-targeted protein degrader-3 (250 nM; 24 h) reduces sEH protein levels in 293T cells transfected with negative control siRNA, siATG5 or siTSG101 (after 24 h of treatment), and transfection with siATG5 or siTSG101 does not impair the activity of this degrader^[1].
PROTAC sEH-degrader-3 (250 nM; 24 h) reduces sEH protein levels in HepG2 cells, and this degradation effect is partially reversed upon co-treatment with 5 μM, 10 μM, 20 μM or 50 μM VER155008 (HY-10941)^[1].
PROTAC sEH-degrader-3 (250 nM; 24 h) significantly increases the viability of HepG2 cells treated with 1 μM Thapsigargin for 24 h^[1].
PROTAC sEH-degrader-3 (5-1000 nM; 24 h) induces significant degradation of sEH in HepG2 cells, with the maximum degradation effect observed at 250 nM after 24 h, while reducing its hydrolase activity, phosphatase activity and sEH protein level^[1].
PROTAC sEH-degrader-3 (250 nM; 24 h) effectively degrades sEH in 293T cells^[1].
PROTAC sEH-degrader-3 (1 μM; 24 h) selectively degrades cytosolic sEH, but does not degrade peroxisomal sEH, when HepG2 cells are treated with 1 μM of the agent for 24 h^[1].
PROTAC sEH-degrader-3 (1 μM; 24 h) selectively reduces sEH protein levels in HepG2 cells, while also downregulating a small number of identified off-target proteins^[1].

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