CUDC-907 inhibits markers of HDAC and PI3K inhibition in vitro and in vivo and acts as a network disrupting agent that directly targets multiple nodes of genetic and epigenetic dysregulation. For instance, CUDC-907 induces acetylation of p53 in hematological cancer cells by stabilizing this tumor suppressor protein, durably reducing the levels of the key PI3K effector phospho-Akt, inhibiting compensatory pathways often utilized in hematological cancer cells during the emergence of resistance to standard-of-care agents and inducing apoptosis in treated cancer cells.As a consequence of its dual molecular activity and network-targeted mechanism, CUDC-907 is an extremely potent inhibitor of cell proliferation in a variety of hematological cancer cells, including cell lines with KRAS mutations, Flt3 amplification and PTEN null status. It outperforms both the combination of the commercially available HDAC inhibitor vorinostat plus the investigational pan-PI3K inhibitor GDC-0941, and the investigational delta isoform-specific inhibitor CAL-101 in all cell lines tested.
Curis Presents Data On PI3K And HDAC Inhibitor CUDC-907 At The 2011 AACR-NCI-EORTC Symposium
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