Table : Cell viability assays against four solid cancer cell lines (A2780, ovarian; U87, malignant glioma; Cal27, head-neck; HepG2, hepatocellular carcinoma) and the non-cancer cell line MRC-5. In addition, selectivity indices for anticancer activity over the non-cancer cell line MRC-5 were calculated (Table ). 9d is clearly superior to quisinostat and SAHA in its selectivity for cancer cells over MRC-5, except for Cal27 cells where 9d and quisinostat gave the same selectivity index. However, in the ovarian cancer cell line A2780, 9d is 10-fold more selective than quisinostat compared to MRC-5 cells. Taken together, although quisinostat is more potent than 9d, compound 9d has the clear advantage of improved selectivity for cancer cells. Docking studies of 9d into human HDAC1. To investigate the possible binding mode of 9d, the most potent anticancer HDAC inhibitor identified in this study, we conducted docking experiments to its main target HDAC1 (Figure ). To this end, 9d was docked into an HDAC1 crystal structure (PDB ID: 5ICN).