AR-42 is an orally available, targeted inhibitor of the Pan-DAC and Akt* pathways. In preclinical studies, AR-42 has demonstrated greater potency and a competitive profile in tumors when compared with vorinostat (SAHA), the leading marketed histone deacetylase inhibitor. Arno plans to initiate Phase I studies of AR-42 in liquid and solid tumors in early 2009.




Publications

• Sargeant AM, Rengel RC, Kulp SK et al., OSU-HDAC42, a Histone Deacetylase Inhibitor, Blocks Prostate Tumor Progression in the Transgenic Adenocarcinoma of the Mouse Prostate Model. Cancer Res 2008; 68: (10). (Include link to Article)
• Chen CS, Wang YC, Yang HC, Huang PH et al., Histone deacetylase inhibitors sensitize prostate cancer cells to agents that produce DNA double-strand breaks by targeting Ku70 acetylation. Cancer Research, 67:5318-27, 2007.
• Lu YS, Kashida Y, Kulp SK, Wang YC et al., Efficacy of OSU-HDAC42, a Novel Histone Deacetylase Inhibitor, in Murine Models of Hepatocellular Carcinoma. Hepatology, Vol. 46, 2007.
• Kulp SK, Chen CS, Wang D, Chen CY and Chen CS. Antitumor effects of a novel phenylbutyrate-based histone deacetylase inhibitor, (S)-HDAC-42, in prostate cancer. Clinical Cancer Research 12:5199-206, 2006.
• *Chen CS, Weng SC, Tseng PH, Lin HP, and Chen CS. Nonepigenetic effects of histone deacetylase inhibitors on Akt through reshuffling protein phosphatase-1 complexes. J Biol Chem, 280:38879-38887, 2005.
• *Chen CS, Weng SC, Tseng PH, Lin HP, and Chen CS, Histone Acetylation-independent Effect on Histone Deacetylase Inhibitors on Akt through the Reshuffling of Protein Phosphatase 1 Complexes. Journal of Biological Chemistry November 18, 2005: Volume 280: Number 46.