The binding of E-selectin to leukemic cells has been shown to promote cell survival and chemotherapy resistance in acute myeloid leukemia (AML). In this interview, Daniel DeAngelo, MD, PhD, of Dana-Farber Cancer Institute, Boston, MA, discusses a novel therapeutic that is antagonistic towards E-selectin, GMI-1271. Dr DeAngelo discusses the rationale behind the mechanism of action of this drug and the results of the trial investigating this agent (NCT02306291), which he presented at the American Society of Hematology (ASH) 2017 Annual Meeting and Exposition in Atlanta, GA.
Rationale and results behind the use of breakthrough therapy-designated E-selectin antagonist for AML
