Acute myeloid leukemia (AML) is the most common acute leukemia in adults and has the lowest survival rate.  AML accounts for approximately 25% of all adult leukemias worldwide, with the highest incidence rates occurring in the United States, Europe and Australia. In the US, there are about 20,000 people each year that are diagnosed with AML.

AML is an aggressive cancer of the blood and bone marrow which prevents white blood cells from maturing, resulting in an accumulation of "blasts" which do not allow room for the normal blood cells. But AML is a heterogeneous condition with a diverse set of genetic mutations. This heterogeneity extends to the leukemic stem cells (LSCs), which evolve to overcome selection pressures during disease progression. This results in multiple pools of LSCs within individual patients which may differ both phenotypically and molecularly. Leukemic stem cells are relatively resistant to current chemotherapeutic regimens and may be responsible for disease progression in AML.  As with CML LSCs, AML LSCs also are dependent on an over expression of β-catenin, which makes ES-3000 a therapeutic candidate for AML. Our objective is to develop ES-3000 for use with the current standard of care therapeutics in the treatment of AML to provide more durable remissions and a reduction in relapses.