Discovery of a Highly Potent and Selective Indenoindolone Type 1 Pan-FLT3 Inhibitor.

Comprehensive analysis of kinase inhibitor selectivity. Nat Biotechnol (2011) 5.65

Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies. Blood (2001) 5.17

Internal tandem duplication of the flt3 gene found in acute myeloid leukemia. Leukemia (1996) 5.06

Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia. Nature (2012) 4.01

The role of FLT3 in haematopoietic malignancies. Nat Rev Cancer (2003) 3.97

FLT3 internal tandem duplication mutations associated with human acute myeloid leukemias induce myeloproliferative disease in a murine bone marrow transplant model. Blood (2002) 3.86

Patients with acute myeloid leukemia and an activating mutation in FLT3 respond to a small-molecule FLT3 tyrosine kinase inhibitor, PKC412. Blood (2004) 3.84

Single-agent CEP-701, a novel FLT3 inhibitor, shows biologic and clinical activity in patients with relapsed or refractory acute myeloid leukemia. Blood (2004) 3.76

CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. Cancer Cell (2011) 2.88

Compassionate use of sorafenib in FLT3-ITD-positive acute myeloid leukemia: sustained regression before and after allogeneic stem cell transplantation. Blood (2009) 2.82

A phase 1 study of SU11248 in the treatment of patients with refractory or resistant acute myeloid leukemia (AML) or not amenable to conventional therapy for the disease. Blood (2004) 2.77

A FLT3-targeted tyrosine kinase inhibitor is cytotoxic to leukemia cells in vitro and in vivo. Blood (2002) 2.76

Results from a randomized trial of salvage chemotherapy followed by lestaurtinib for patients with FLT3 mutant AML in first relapse. Blood (2011) 2.66

A phase 2 trial of the FLT3 inhibitor lestaurtinib (CEP701) as first-line treatment for older patients with acute myeloid leukemia not considered fit for intensive chemotherapy. Blood (2006) 2.55

FLT3-mutant allelic burden and clinical status are predictive of response to FLT3 inhibitors in AML. Blood (2009) 2.44

Internal tandem duplication of the FLT3 gene is a novel modality of elongation mutation which causes constitutive activation of the product. Leukemia (1998) 2.35

An innovative phase I clinical study demonstrates inhibition of FLT3 phosphorylation by SU11248 in acute myeloid leukemia patients. Clin Cancer Res (2003) 1.87

Sorafenib in combination with intensive chemotherapy in elderly patients with acute myeloid leukemia: results from a randomized, placebo-controlled trial. J Clin Oncol (2013) 1.46

Identification of a novel activating mutation (Y842C) within the activation loop of FLT3 in patients with acute myeloid leukemia (AML). Blood (2004) 1.33

Identifying and characterizing a novel activating mutation of the FLT3 tyrosine kinase in AML. Blood (2004) 1.27

Sensitivity toward sorafenib and sunitinib varies between different activating and drug-resistant FLT3-ITD mutations. Exp Hematol (2007) 1.09

Characterizing and Overriding the Structural Mechanism of the Quizartinib-Resistant FLT3 "Gatekeeper" F691L Mutation with PLX3397. Cancer Discov (2015) 1.01

High-throughput cellular assays for regulated posttranslational modifications. Anal Biochem (2007) 0.97

FLT3 D835 mutations confer differential resistance to type II FLT3 inhibitors. Leukemia (2015) 0.93

Advances in understanding the biology and genetics of acute myelocytic leukemia. Clin Lab Sci (2005) 0.93

Implications of FLT3 mutations in the therapy of acute myeloid leukemia. Rev Recent Clin Trials (2007) 0.87

Crystal structure of the FLT3 kinase domain bound to the inhibitor Quizartinib (AC220). PLoS One (2015) 0.84

FLT3 INHIBITORS: RECENT ADVANCES AND PROBLEMS FOR CLINICAL APPLICATION. Nagoya J Med Sci (2015) 0.83