dCBP-30

dCBP-30 (0.01-1000 nM; 1-24 h) potently degrades both CBP and p300 in HAP1 cells, with DC₅₀ values of 0.05 nM (CBP) and 0.04 nM (p300) at 4 hours, and maximum degradation rates of 0.79 (CBP) and 0.81 (p300) at 1 nM after 1 hour^[1].
dCBP-30 (10 nM; 4 h) selectively decreases only CBP and p300 protein levels in MM1.S multiple myeloma cells after 4 hours of 10 nM treatment^[1].
dCBP-30 (10 nM; 0.5-24 h) potently reduces acetylation of CBP/p300 histone substrates (H3K18ac, H3K27ac, H2BK5ac, H2BK20ac) in MM1.S multiple myeloma cells after 10 nM treatment^[1].
dCBP-30 potently inhibits viability across 25 multiple myeloma cell lines (median AUC_0-t lower than dCBP-1, GNE-781, and A-485), induces complete cell killing in MM1.S cells at 10 nM within 72 hours, and triggers apoptosis in a time-dependent manner, with ~80% of cells apoptotic after 24 hours of 10 nM exposure^[1].
dCBP-30 (10 nM; 2-24 h) treatment of MM1.S multiple myeloma cells at 10 nM rapidly downregulates critical myeloma dependency genes (MYC, IRF4, MAF, PRDM1, PIM2) within 2 hours, induces modest chromatin accessibility decreases at CBP/p300 binding sites, and alters transcription factor motif accessibility in a time-dependent manner, disrupting essential myeloma signaling nodes^[1].
dCBP-30 (10 μM; 4 h) has significantly greater membrane permeability than dCBP-1 in a cell-free PAMPA assay at 10 μM, contributing to its enhanced in vitro degradation potency^[1].
dCBP-30 (multiple doses; 48-120 h) acts synergistically with Dexamethasone (HY-14648) to reduce viability in MM1.S and NCI-H929 multiple myeloma cells, while showing antagonism with other standard anti-myeloma agents^[1].

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