Compared with the hydroxamic acid SAHA (IC50 = 20 nM), the mainstay of HDAC-targeting anticancer therapy, the pan-HDAC-inhibitory potency of the novel compounds is distinctly weaker, yet still in a clinically meaningful range (Figure 4a) [12].Their HDAC-inhibitory efficacy was further evaluated in prostate cancer cells by immunodetection of the increased portion of acetylated histone H3, which is part of the cellular nucleosome. The gene discussed is HDAC9; the disease is prostate cancer.