FLT3 (FMS-like tyrosine kinase 3) is a class III receptor tyrosine kinase critical for hematopoiesis, particularly in the survival, proliferation, and differentiation of hematopoietic stem and progenitor cells. Aberrant FLT3 signaling, often due to mutations like internal tandem duplications (FLT3-ITD) or tyrosine kinase domain (FLT3-TKD) mutations, is implicated in acute myeloid leukemia (AML). These mutations drive constitutive activation of FLT3. promoting leukemogenesis and poor prognosis.
FLT3 antibodies are essential tools in research and diagnostics. They detect FLT3 expression and mutation status in AML patients via techniques like flow cytometry, immunohistochemistry, or Western blot. Clinically, therapeutic FLT3 inhibitors (e.g., midostaurin, gilteritinib) are small-molecule tyrosine kinase inhibitors (TKIs), but FLT3-targeting monoclonal antibodies (mAbs) are emerging as investigational therapies. These mAbs aim to block ligand binding or induce antibody-dependent cellular cytotoxicity (ADCC) against FLT3-expressing leukemia cells.
Current challenges include overcoming resistance to FLT3-targeted therapies and improving specificity. Combination strategies with chemotherapy or other targeted agents are under investigation. FLT3 antibodies also aid in monitoring minimal residual disease (MRD) and predicting therapeutic responses. Despite progress, further research is needed to optimize antibody-based approaches for AML treatment and biomarker-driven precision medicine.