BRD4/FKBP12 ligand 1

BRD4/FKBP12 ligand 1 (compound a1dj) (0.09-103 nM; 6 h, 5 days) potently reduces MV4-11 acute myeloid leukemia cell viability (IC₅₀ = 0.09 nM) in a FKBP12-dependent manner, with a 1144-fold loss of potency when FKBP12 is depleted^[1].
BRD4/FKBP12 ligand 1 (10-100 nM; 6 h, 6 h) represses MYC gene expression in MV4-11 acute myeloid leukemia cells at 10 nM and 100 nM, with this effect being dependent on FKBP12 expression^[1].
BRD4/FKBP12 ligand 1 (0.4->480 nM; 5 days) potently reduces wild-type INA-6 human myeloma cell viability (IC₅₀ = 0.4 nM), with nearly complete loss of cytotoxic activity in FKBP1A knock-out INA-6 cells^[1].
BRD4/FKBP12 ligand 1 (1-1000 nM; 5 days) selectively reduces the population of PC3 prostate carcinoma cells in co-culture with non-transformed PNT1-A prostate epithelial cells at concentrations from 1 nM to 1000 nM, leaving PNT1-A cell numbers largely unaffected^[1].
BRD4/FKBP12 ligand 1 binds to purified FKBP12 with high affinity (K_d = 0.4 nM) and exhibits >25-fold positive cooperative binding to purified BRD4 BD1 (K_d = 32 nM) and 7-fold positive cooperative binding to purified BRD4 BD2 (K_d = 70 nM) in the presence of 15 μM FKBP12, compared to weaker binding to BRD4 domains alone^[1].
BRD4/FKBP12 ligand 1 induces ternary complex formation between eGFP-FKBP12 and His-BRD4 BD1 and between eGFP-FKBP12 and His-BRD4 BD2 in a purified protein system^[1].
BRD4/FKBP12 ligand 1 potently occupies intracellular FKBP12 (IC₅₀ = 2.6 nM) and weakly occupies intracellular BRD4 (IC₅₀ = 653 nM) in intact HEK293T cells^[1].

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