Recombinant Human Flt3 protein

**Background of FLT3 Recombinant Protein**

FLT3 (FMS-like tyrosine kinase 3), also known as CD135. is a member of the class III receptor tyrosine kinase (RTK) family, which includes receptors like KIT, PDGFR, and CSF1R. It plays a critical role in hematopoiesis, particularly in the development, survival, and differentiation of hematopoietic stem cells (HSCs) and progenitor cells. FLT3 is predominantly expressed in bone marrow, lymphoid tissues, and the placenta. Its activation occurs upon binding to its ligand, FLT3 ligand (FLT3L), leading to dimerization, autophosphorylation, and downstream signaling through pathways such as PI3K/AKT, RAS/MAPK, and STAT5. These pathways regulate cell proliferation, apoptosis resistance, and lineage commitment.

Dysregulation of FLT3 signaling is strongly linked to hematologic malignancies. Activating mutations in FLT3. particularly internal tandem duplications (FLT3-ITD), are found in ~30% of acute myeloid leukemia (AML) cases and correlate with poor prognosis. These mutations cause constitutive kinase activity, driving uncontrolled cell growth. Consequently, FLT3 has emerged as a therapeutic target, with inhibitors like midostaurin and gilteritinib approved for AML treatment.

Recombinant FLT3 protein is engineered *in vitro* using expression systems (e.g., mammalian, insect, or bacterial cells) to produce soluble forms, often comprising the extracellular domain or kinase domain. This protein serves as a vital tool for *in vitro* studies, including ligand-receptor interaction assays, structural analysis, and drug screening. It also aids in developing monoclonal antibodies or targeted therapies. By enabling precise investigation of FLT3’s function and inhibition, recombinant FLT3 protein supports both basic research and translational efforts to combat FLT3-driven malignancies.

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