BRD4 RIMTAC-1

BRD4 RIMTAC-1 (compound 10) (4-1000 nM; 4-48 h) potently induces concentration- and time-dependent degradation of endogenous and exogenous BRD4 in HEK-293T cells, with a DC₅₀ of 54.12 nM and a D_max of 83.3% after 24 h of treatment^[1].
BRD4 degradation induced by BRD4 RIMTAC-1 (500 nM; 24 h) in HEK-293T cells depends on the ubiquitin-proteasome system, as co-treatment with the proteasome inhibitor MG132 (HY-13259) or the ubiquitination-like inhibitor MLN4924 (HY-70062) blocks this degradation process^[1].
BRD4 RIMTAC-1 (200 nM; 24 h) induces ubiquitination of FLAG-BRD4 in HEK-293T cells, supporting ubiquitin-proteasome system-mediated degradation^[1].
BRD4 RIMTAC-1 (125-500 nM; 24 h) does not affect the mRNA expression of BRD4 in HEK-293T cells, confirming that the depletion of BRD4 occurs at the post-translational level^[1].
The BRD4-degrading effect of BRD4 RIMTAC-1 (500 nM; 24 h) on HEK-293T cells is reversible, and the BRD4 protein level recovers to baseline within 36 h after removal of the compound^[1].
Degradation of BRD4 induced by BRD4 RIMTAC-1 (500 nM; 24 h) in HEK-293T cells requires simultaneous binding to BRD4 and RIPK1, as co-treatment with the competitive inhibitor JQ1 or a RIPK1 inhibitor blocks this degradation process^[1].
BRD4 degradation in HEK-293T cells mediated by BRD4 RIMTAC-1 (250-1000 nM; 24 h) requires functional VHL and RIPK1, as knockout of VHL or knockdown of RIPK1 blocks this degradation^[1].
BRD4 degradation induced by BRD4 RIMTAC-1 (500 nM; 24 h) in HEK-293T cells depends on functional VHL, as co-treatment with the VHL inhibitor VH298 abolishes this degradation effect^[1].
The BRD4-degrading effect of BRD4 RIMTAC-1 (10 μM; 24 h) in HEK-293T cells depends on the RIPK1-VHL interaction under normoxic conditions, as the hypoxia mimetic FG-4592 (HY-13426) blocks this degradation process^[1].
BRD4 RIMTAC-1 (10 μM; 2 h) promotes the formation of the BRD4-RIMTAC-1-RIPK1-VHL quaternary complex in HEK-293T cells expressing FLAG-BRD4^[1].
BRD4 RIMTAC-1 (500 nM; 24 h) selectively induces BRD4 degradation in HEK-293T cells, with minimal effects on other BET family proteins and the broader proteome^[1].
BRD4 RIMTAC-1 (63-1000 nM; 3-48 h) potently induces concentration- and time-dependent degradation of endogenous BRD4 in RAW264.7 cells, with a DC₅₀ of 179.1 nM and a D_max of 65.63% after 24 h of treatment^[1].
The BRD4-degrading effect of BRD4 RIMTAC-1 (500 nM; 24 h) on RAW264.7 cells is reversible, and the BRD4 protein level recovers to the baseline level within 24 h after removal of the compound^[1].

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