HRG038

HRG038 (0.001-5 μM; 24 h) potently degrades both long and short BRD4 isoforms in MDA-MB-231 breast cancer cells^[1].
HRG038 (1 μM; 24 h) moderately selectively degrades BRD4 and induces a 21% reduction in BRD3 levels in MDA-MB-231 cells, with 89 additional proteins significantly downregulated^[1].
HRG038 (1 μM; 24 h) induces 84% loss of BRD4 with selective degradation of the short isoform over the long isoform in HEK293T cells, without impairing cell viability^[1].
HRG038 (100 nM; 24 h)-mediated BRD4 degradation in HEK293T cells is proteasome- and Cullin E3 ligase-dependent, as pretreatment with 1 μM Bortezomib (HY-10227) or 1 μM Pevonedistat (HY-70062) for 1 h attenuates degradation^[1].
HRG038 (100 nM; 24 h)-mediated BRD4 degradation is fully attenuated in CUL4^DCAF16 knockout HEK293T cells, confirming dependence on CUL4^DCAF16 for degradation^[1].
HRG038 (100 nM; 24 h)-mediated BRD4 degradation in CUL4^DCAF16 knockout HEK293T cells requires the C173 cysteine residue of CUL4^DCAF16, as mutation to serine (C173S) completely attenuates degradation, while C58S, C119S, and C178S mutations do not^[1].
HRG038 exhibits high reactivity with glutathione, with a half-life of 34 min in a cell-free system^[1].

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