Erikson et al. from the Department of Medical Science in Uppsala, Sweden, have performed a second study in order to characterize the effects of AKN-028 on AML cells. The results are interesting: the inhibitor showed an arrest in AML cell line MV4-11. Treatment with this compound caused significantly altered gene expression in all AML cell types tested. Subsequent gene set enrichment analysis revealed that Myc associated gens were downregutated. On top of that, AKN-028 inhibited tyrosine kinase activity, but not serine/threonine kinase activity, in a dose dependent manner in all samples tested.
AML is a life-threatening neoplastic disease characterized by several acquired genetic abnormalities and with multiple signaling pathways involved in the pathogenesis. Treatment in AML is still based on cytotoxic chemotherapy, but much effort is now being put in the identification of molecular drug targets, allowing more specific therapeutic approaches in this disease. However, progress in AML treatment has been slow and the long-term survival remains poor.