Flt3-Itd and Its Mutant Type-Ii Kinase Inhibitors

Technology #ua15-202

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Neil Shah
Associate Professor, Medicine
Brendan Frett
Postdoctoral Research Associate I, Pharmacology and Toxicology
Hong yu Li
Associate Professor, Pharmacology and Toxicology
Managed By
Rakhi Gibbons
Asst. Director, Life Sciences (520) 626-6695

Title: FLT3 kinase inhibitor to treat acute myeloid leukemia (AML)


Invention: This technology is envisioned to become the first FTL3-ITD kinase inhibitor for the treatment of AML.


Background: Pathological activating mutations in the FLT3 kinase represent the most common genetic alteration in patients with AML occurring approximately in one third of all cases. The most common FLT3 gain of function is the FLT3 internal tandem duplication (ITD) mutation, which is present in 20-25% of all AML patients. In normal karyotype AML, the presence of a FLT3/ITD mutation is associated with poor prognosis, as mirrored by a high risk of relapse even after allogeneic stem cell transplantation. The poor prognostic impact along with the observation that FLT3 is frequently overexpressed in the majority of AML cases has formed the platform for the development of FLT3-targeted strategies. To date, several FLT3 kinase inhibitors have been investigated in preclinical and clinical studies. However, as of yet, none of the studied FLT3 inhibitors have received FDA approval for routine clinical use in AML.


Expert Opin Ther Targets. 2015 Jan;19(1):37-54



  • Treatment for AML by inhibition of FLT3-ITD kinase



  • Potential to attenuate limitations and failures of previous investigational FLT3 agents
  • Demonstrates substantial efficacy and improvement over quizartinib, crenolanib, and ponatinib
  • Broad FLT3 mutant activity
  • Selective for FLT3 and FLT3 mutants
  • Has no identified off-target toxicities
  • Remarkably effective at reducing and eliminating FLT3-driven tumor growth
  • The first in the market to establish mutant activity with favorable drug-like properties
  • Can improve the future of a tailored, molecular-based treatment approach for FLT3-mutated AML


Related Publications:

N. shah et al. Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukemia. Nature 2012, 485, 260-263