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ChemGenex’s Omacetaxine Kills Leukemic Stem Cells in Human CML Models

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ChemGenex Pharmaceuticals Limited has announced that the results of pre-clinical research that demonstrated that omacetaxine kills model human leukemic stem cells were presented at the 14th Congress of the European Hematology Association (EHA) in Berlin, Germany on Sunday.

Human leukemic stem cells are known to be insensitive to tyrosine kinase inhibitors (TKIs), the drug family currently approved to treat Chronic Myeloid Leukemia (CML). The work was carried out in collaboration with Professor Tessa Holyoake at the University of Glasgow, Scotland, UK.

Ms. Elaine Allan, Clinical Scientist of the Scottish National Blood Transfusion Service working at the Paul O'Gorman Leukaemia Research Centre, University of Glasgow in Scotland, UK delivered the oral presentation. Ms Allan said, “Currently licensed drugs target and disable the diseased cells in the blood stream and bone marrow, but they have little, if any, effect on the primitive leukemic stem cells that are at the “root” of this blood cancer. In contrast, we have shown omacetaxine to be not only anti-proliferative, but also to induce apoptosis in human CML stem cells.”

Hagop M. Kantarjian, M.D., Chairman and Professor, Department of Leukemia, at the University of Texas M. D. Anderson Cancer Center, described the study results as exciting. Dr. Kantarjian added, “These results raise the possibility of eradicating the dormant malignant stem cells that are thought to be responsible for relapse in CML patients who discontinue TKIs. I look forward to working with ChemGenex in future trials to evaluate the clinical application of this research."

Dr. Greg Collier, Chief Executive Officer and Managing Director of ChemGenex, said, “The data presented today is entirely consistent with our strategic plans to investigate omacetaxine in combination with selected TKIs in an attempt to eradicate this form of leukemia. In the meantime ChemGenex remains focused on our primary objective of developing omacetaxine as a therapeutic option for CML patients who have developed the T315I mutation. This is one of the most pressing unmet medical needs in the field of CML management.”
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