dBRD9

dBRD9 is a BRD9 PROTAC degrader. dBRD9 reduces the binding of the ISGF3 complex to ISG promoters, decreases the level of ISG induction downstream of IFNAR signaling, and reduces the chromatin binding of BRD4 at BRD9 co-binding sites. dBRD9 can be used in research related to acute myeloid leukemia^[1]. In Vitro:dBRD9 (0.5-5000 nM; 4 h) induces dose-dependent degradation of BRD9 in MOLM-13 cells, with no off-target degradation of BRD4 or BRD7 detected^[1].
dBRD9 (7 days potently inhibits the proliferation of EOL-1 and MOLM-13 acute myeloid leukemia (AML) cells, with an efficacy 10 to 100 times higher than that of non-degradable BRD9 probes^[1].
dBRD9 (3 μM; 24 h) selectively reduces the induction of IFNAR-dependent secondary response genes (including interferon-stimulated genes) in Lipid A-stimulated mouse bone marrow-derived macrophages, without affecting primary response genes or IFN-β production^[2].
dBRD9 (3 μM; 24 h) induces widespread loss of BRD9 chromatin binding as well as partial loss of BRD4 binding in Lipid A-stimulated mouse bone marrow-derived macrophages, which correlates with reduced ISGF3 complex binding and downregulation of interferon-stimulated genes^[2].
dBRD9 (3 μM; 24 h) does not impair the induction of IRF9 and STAT2 proteins in Lipid A-stimulated mouse bone marrow-derived macrophages^[2].