SK1-I is the Limit in AML
A paper published in Blood suggests that going upstream of the known cancer target sphingosine 1-phosphate could be a better approach than hitting site-1 protease (S1P) itself. By specifically hitting one of the two sphingosine kinase isoenzymes that produce S1P, researchers at Virginia Commonwealth University School of Medicinethink they have a small molecule cancer lead-dubbedSK1-I-with broader effects than S1P inhibitors and more selective effects than compounds that inhibit both isoenzymes.1 The upshot could be a compound for acute myelogenous leukemia with increased efficacy and fewer off-target effects.
S1P is a sphingolipid mediator involved in calcium metabolism, cytoskeletal reorganization, immune cell trafficking, cell growth, differentiation, motility, angiogenesis and survival.2 It is produced by a pair of sphingosine kinase isoenzymes-sphingosine kinase 1 (SphK1) and SphK2-that have opposite functions.3...