DNA-PK/HDAC6-IN-1

DNA-PK/HDAC6-IN-1 (Compound DH-1) potently and balancedly inhibits recombinant DNA-PK (IC₅₀ = 84.2 nM) and HDAC6 (IC₅₀ = 64.8 nM) enzymes in biochemical assays^[1].
DNA-PK/HDAC6-IN-1 forms a stable, high-affinity complex with DNA-PK, as confirmed by molecular docking (binding energy = -10.5 kcal/mol) and 100 ns molecular dynamics simulations, with a calculated binding free energy of -10.605 kcal/mol^[1].
DNA-PK/HDAC6-IN-1 forms a stable, high-affinity complex with HDAC6, as confirmed by molecular docking (binding energy = -9.6 kcal/mol) and 100 ns molecular dynamics simulations, with a calculated binding free energy of -9.635 kcal/mol^[1].
DNA-PK/HDAC6-IN-1 (compound DH-1) (0.1-1 μM) selectively inhibits HDAC6 in HL-60 cells, as shown by concentration-dependent upregulation of acetylated-α-tubulin without affecting acetylated-H3 or acetylated-SMC3 levels^[1].
DNA-PK/HDAC6-IN-1 (48 h) potently inhibits the proliferation of Jurkat (IC₅₀ = 0.72 μM) and HL-60 (IC₅₀ = 0.41 μM) cancer cells, while exhibiting minimal toxicity against normal HEK-293 cells (IC₅₀ >20 μM)^[1].
DNA-PK/HDAC6-IN-1 (10 μM; 24 h) impairs DNA damage repair in LoVo cells, resulting in elevated γ-H2AX levels^[1].
DNA-PK/HDAC6-IN-1 (compound DH-1) (1 μM; 24 h) arrests HL-60 cells in the G2/M phase of the cell cycle^[1].
DNA-PK/HDAC6-IN-1 (1 μM; 24 h) induces significant early and late apoptosis in HL-60 cells^[1].
DNA-PK/HDAC6-IN-1 (1 μM; 24 h) decreases the mitochondrial membrane potential in HL-60 cells^[1].

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