HDAC-IN-53 is an orally active, selective inhibitor of HDAC1-3, demonstrating IC50 values of 47 nM, 125 nM, and 450 nM, respectively. It exhibits no inhibitory effects on class II HDACs (HDAC4, 5, 6, 7, 9; IC50 >10 μM). The compound induces caspase-dependent apoptosis and significantly hampers the growth of human tumor xenografts in nude mice, as well as murine tumor growth in immune-competent mice with MC38 colon cancer [1].

HDAC1:47 nM, HDAC2:125 nM, HDAC3:450 nM, HDAC4:>10 μM, HDAC5:>10 μM, HDAC6:>10 μM, HDAC7:>10 μM, HDAC8:>10 μM, HDAC9:>10 μM

HDAC-IN-53（化合物19h）对包括MC38（IC50=0.66μM）、HCT116细胞（IC50=0.56μM）在内的多个癌细胞系显示出强效的抗增殖作用[1]。在剂量为0.1-1μM并处理24小时的情况下，HDAC-IN-53在MC38细胞中导致G0/G1期细胞周期阻滞，而在HCT116细胞中则引发G2/M期细胞周期延迟[1]。同样条件下，该化合物还能剂量依赖性地增加cleaved caspase-3和cleaved PARP的表达水平[1]。

HDAC-IN-53（60或120 mg/kg；灌胃给药；每日一次；连续15天）展现了通过直接抑制肿瘤生长及间接促进免疫细胞介导的抗肿瘤活性的抗癌效果[1]。小鼠中HDAC-IN-53的药代动力学参数如下[1]：IV (5 mg/kg)与PO (20 mg/kg)的T max (h)分别为0.42和0.42；C max (ng/mL)分别为8129和9558；AUC 0-t (ng/mL∗h)分别为5864和15278；t 1/2 (h)分别为0.85和2.49；F (%)为65.1%。