About: Lestaurtinib is a research topic. Over the lifetime, 127 publications have been published within this topic receiving 6774 citations. The topic is also known as: CEP-701 & KT-5555.
TL;DR: Results show that FLT3 inhibition is associated with clinical activity in AML patients harboringFLT3-activating mutations and indicate that CEP-701 holds promise as a novel, molecularly targeted therapy for this disease.
TL;DR: The data reveal that the combination of excellent potency, selectivity, and pharmacokinetic properties is unique to AC220, which therefore is the first drug candidate with a profile that matches the characteristics desirable for a clinical FLT3 inhibitor.
TL;DR: The results suggest that midostaurin has hematologic activity in both patients with FLT3-mutant and wild-type AML, and the degree of clinical activity observed supports additional studies that combine midosturin and other agents such as chemotherapy especially in FLT 3-Mutant AML.
Abstract: Purpose Mutations leading to constitutive activation of the FMS-like tyrosine kinase 3 receptor (FLT3) occur in blasts of 30% of patients with acute myeloid leukemia (AML). Midostaurin (PKC412; N-benzoylstaurosporin) is a multitargeted tyrosine kinase inhibitor, with demonstrated activity in patients with AML/myelodysplastic syndrome (MDS) with FLT3 mutations. Patients and Methods Ninety-five patients with AML or MDS with either wild-type (n = 60) or mutated (n = 35) FLT3 were randomly assigned to receive oral midostaurin at 50 or 100 mg twice daily. The drug was discontinued in the absence of response at 2 months, disease progression, or unacceptable toxicity. Response was defined as complete response, partial response (PR), hematologic improvement, or reduction in peripheral blood or bone marrow blasts by ≥ 50% (BR). Results The rate of BR for the population in whom efficacy could be assessed (n = 92) was 71% in patients with FLT3-mutant and 42% in patients with FLT3 wild-type. One PR occurred in a pati...
TL;DR: A phase 2 trial of the FLT3-selective tyrosine kinase inhibitor lestaurtinib (CEP701) used as monotherapy in untreated older patients with acute myeloid leukemia (AML) was conducted in this article.
TL;DR: Overall, lestaurtinib treatment after chemotherapy did not increase response rates or prolong survival of patients withFLT3 mutant acute myeloid leukemia in first relapse, and any conclusions regarding the efficacy of combining FLT3 inhibition with chemotherapy are limited.