Etomoxir treats heart failure by switching the heart's energy supply from fatty acids to pyruvate, which is more efficiently converted to energy by the mitochondria.

Mouse model experiments showed that combining etomoxir with the apoptosis-inducing drug ABT-737 or with cytarabine, a frontline drug for acute myeloid leukemia, reduced the leukemia burden and increased median survival time by 33 percent and 67 percent respectively compared to control group mice.

Additionally, etomoxir was found to decrease the number of quiescent leukemia progenitor cells in half of blood samples taken from acute myeloid leukemia patients. These quiescent cells are important, the researchers note, because they are capable of initiating leukemia and are highly resistant to traditional chemotherapy.

"Our findings suggest that mitochondrial function and resistance to apoptosis in leukemia cells are intimately linked with the entry of fatty acids into mitochondria," said first author Ismael Samudio, M.D., a fellow in Stem Cell Transplantation and Cellular Therapy. "For many years it has been apparent that leukemia cells are addicted to glucose for the generation of cellular energy (ATP). Now our results suggest that leukemia cells are addicted to fatty acids for the function of the Krebs cycle and the prevention of cell death."