The derivatives 133 and 134 (Scheme 9) showed potent cytotoxicity against four cancer cell lines (PC-3, MCF-7, A549, and HL-60) and better HDAC inhibition than psammaplin A. Molecular docking simulation showed that the hydrogen atom of the oxime group could interact with the active site of Asp 99 of HDAC1 via hydrogen bonding, and the hydroxyl group which could interact with Glu 203 at the entrance to the active site tunnel was optimally attached on the para-position of the benzene ring. The gene discussed is HDAC9; the disease is cancer.