Acute myelogenous leukemia (AML) is one of the most common and aggressive forms of acute leukemia affecting 30,000 people per year.  The limits of current treatment modalities indicate a need for innovative therapies directed against relevant biological targets in AML to improve the clinical outcome in AML.  Heat shock protein 90 (Hsp90) and Histone deacetylase isozyme 6 (HDAC6) are required for the maintenance of AML oncogenic signaling and the stabilization of oncogenic factors.  Hsp90 and HDAC6 are constitutively active and over-expressed in AML.  We have identified a novel class of selective HDAC6/Hsp90 inhibitors, which preferentially inhibit HDAC6 at low �M concentrations and rapidly induce inactive acetylated Hsp90 thereby resulting in Hsp90 client protein depletion.  Our overarching hypothesis is that a functional HDAC6/Hsp90 complex is an essential part of AML pathogenesis.

Unique HDAC6 inhibitors targeting Hsp90 complexes

243rd National Meeting (2012)

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