title: Emergence of crenolanib for FLT3-mutant AML.
abstract: In this issue of Blood, Zimmerman and colleagues demonstrate that the tyrosine kinase inhibitor (TKI) crenolanib effectively suppresses growth of leukemic cells harboring both FLT3-ITD and FLT3-TKD mutations, the latter of which are increasingly seen to emerge as resistant mutations after FMS-like tyrosine kinase 3 (FLT3) inhibitor therapy.
authors.affiliation: HARVARD MEDICAL SCHOOL.
authors.forename: Amir T
authors.initials: AT
authors.lastname: Fathi
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001562:Benzimidazoles / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000188:drug therapy* / Q000201:enzymology*; D008297:Male; D010880:Piperidines / Q000627:therapeutic use*; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D051941:fms-Like Tyrosine Kinase 3 / Q000037:antagonists & inhibitors* / Q000235:genetics*
chemical_list: D000970:Antineoplastic Agents; D001562:Benzimidazoles; D010880:Piperidines; D047428:Protein Kinase Inhibitors; C497970:FLT3 protein, human; D051941:fms-Like Tyrosine Kinase 3; C577197:crenolanib