PROTAC HDAC3 degrader-1

PROTAC HDAC3 degrader-1 (b22) (20 nM, 200 nM; 12 h) induces HDAC3 degradation in MV4-11 cells, with 24.4% degradation at 20 nM and 81.8% degradation^[1].
PROTAC HDAC3 degrader-1 induces HDAC3 degradation in THP-1 AML cells with a DC₅₀ of 143.1 nM^[1].
PROTAC HDAC3 degrader-1 (0.5-1000 nM; 24 h) induces concentration-dependent HDAC3 degradation in MV4-11 cells, with a DC₅₀ of 30.73 nM and a maximum degradation efficiency of 82% after 24 h of treatment^[1].
PROTAC HDAC3 degrader-1 (200 nM; 0.5-24 h) induces time-dependent HDAC3 degradation in MV4-11 cells, reaching maximum levels within 8 h and sustaining degradation^[1].
PROTAC HDAC3 degrader-1 (8-1000 nM; 12 h) exhibits highly selective degradation of HDAC3 over other HDAC isoforms (HDAC1, HDAC2, HDAC4, HDAC6, HDAC11) in MV4-11 cells at concentrations up to 200 nM, with an effect on HDAC8 only seen at ≥1000 nM after 12 h of treatment^[1].
PROTAC HDAC3 degrader-1 (48 h) exhibits moderate antiproliferative activity against MV4-11 AML cells with an IC₅₀ of 1.26 μM after 48 h of treatment, and significantly reduced cytotoxicity against Kasumi-1, THP-1, HL-7702, and iBMDMs cells^[1].
PROTAC HDAC3 degrader-1 (0.078-2.500 μM; 48 h) synergizes with Venetoclax (HY-15531) to inhibit MV4-11 cell proliferation, with CI values <1 for all tested concentration combinations after 48 h of treatment^[1].
PROTAC HDAC3 degrader-1 (300-600 nM; 48 h) synergizes with Venetoclax to promote apoptosis in MV4-11 cells, with apoptosis rates reaching up to 88.90% after 48 h of combined treatment^[1].
PROTAC HDAC3 degrader-1 (150-600 nM; 24 h) synergizes with Venetoclax in MV4-11 cells to downregulate anti-apoptotic proteins Mcl-1 and Bcl-xL, enhance DNA damage (increased γH2A.X), and activate caspase3 cleavage after 24 h of combined treatment, while b22 alone has no significant effect on these proteins^[1].

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