FLT3 is a Type III tyrosine kinase cell surface receptor found on primitive bone marrow stem cells. The FLT3 ligand is a hematopoietic growth factor that stimulates cells via a set of structurally related tyrosine kinase receptors. This FLT3 Ligand promotes the differentiation of multiple hematopoietic cell lineages and is expressed as a non-covalently-linked dimer by T-cells, bone marrow, and thymic fibroblasts. Downstream events in the FLT3 pathway include the expansion of monocytes and immature dendritic cells, B-cell differentiation, natural killer (NK) cell development, and myeloid differentiation of hematopoietic stem cells.
Because FLT3 overexpression and mutations are highly associated with acute myeloid leukemia (AML) and a poor outcome, significant effort has been into developing FLT3-targeted therapies. Johns Hopkins researchers have published a comprehensive overview of FLT3 inhibitors and leukemia – their review details the current pipeline of drugs, treatment approaches, and best strategies for success1. Port et al performed a systematic review and meta-analysis of FLT3 internal tandem duplication (ITD) mutations - as well as those also found in the proteins mutated nucleophosmin NPM1 and CEBPA2. This was done across a set of almost 2000 patient samples in order to assess the prognostic value of these markers. Leading hematologists recently reviewed preclinical and early clinical trials of both first- and second-generation FLT3 inhibitors3. While first-generation compounds like sunitinib, midostaurin, and lestuartinib only produced transient results, second-generation compounds like quizartinib are more promising because of their more targeted specificity and better tolerance. FLT3 also appears to play a role in other physiological processes, as FLT3 signaling drives dendritic cell (DCs) formation and development in different organs as part of the autoimmune inflammation response4.
Novus Biologicals offers FLT3 reagents for your research needs including:
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