Ask about this productRelated genes to: Flt3 Ligand antibody
- Gene:
- FLT3 NIH gene
- Name:
- fms related tyrosine kinase 3
- Previous symbol:
- -
- Synonyms:
- STK1, FLK2, CD135
- Chromosome:
- 13q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-30
- Date modifiied:
- 2019-04-23
Related products to: Flt3 Ligand antibody
Related articles to: Flt3 Ligand antibody
- Cutting edge protein kinase inhibitors are often plagued by unpredicted off target binding that can limit their therapeutic window, impacting clinical outcomes. However, such off-target binding may provide in vivo clinical evidence supporting therapeutic avenues in nonrelated diseases. We have recently identified off target transforming growth activated kinase beta-1 (TAK1) affinity in FDA approved FLT3 inhibitors. The receptor tyrosine kinase Fms-like tyrosine kinase 3 (FLT3) serves as a key regulator of hematopoietic stem cell survival and proliferation. Unlike FLT3, TAK1 is a serine threonine kinase involved in inflammatory signaling in the MAPK pathway. Despite very little sequence homology between the TAK1 and FLT3, through targeted inhibitor development and kinome wide screening we identified a strong structural homology between the active sites of these two kinases that leads to cross reactivity of several FLT3 inhibitors in clinical use with TAK1. Enzymatic and in silico modeling confirmed binding and affinity of many common FLT3 inhibitors against TAK1. Furthermore, we explored the in vitro implications of off target TAK1 inhibition by FLT3 inhibitors in human PBMCs stimulated with lipopolysaccharides (LPS) on downstream cytokine production. Our results confirm intracellular inhibition of TAK1 by several FLT3 inhibitors in clinical use. Given that FLT3 inhibitors are administered chronically to treat AML, the nonharmful unintended off target inhibition of TAK1 in vivo by current FLT3 inhibitors provides some insight into the safety and tolerability of chronic TAK1 inhibition in patients. - Source: PubMed
Publication date: 2026/05/18
Haystead TimothyFreeze RobertLiu GraceChen JiegenHughes PhilipScarneo Scott - In Mexico, FMS-like tyrosine kinase 3 (FLT3) inhibitors have been approved for newly diagnosed or relapsed/refractory (R/R) FLT3-positive (FLT3)acute myeloid leukemia (AML). This retrospective, physician panel-based chart review study evaluated the real-world treatment landscape, clinical outcomes, and healthcare resource utilization (HRU) in patients with FLT3 R/R AML in Mexico. - Source: PubMed
Publication date: 2026/04/22
De León Andrés GómezAn Jamie Jung-HeeGourgioti GeorgiaXie YanwenZhong JiaWu Eric QAriza Juan GuillermoCheng Li-Jen - Current genetic risk stratification systems for acute myeloid leukemia (AML), including the 2017 European Leukemia Network (ELN), 2022 ELN, and 2023 China (CN) stratifications, inconsistently categorize key genetic variants such as and . These systems also demonstrate limited applicability to Chinese patients, complicating clinical decision-making. This study optimized genetic stratification for Chinese AML patients and developed a multi-omics prognostic model by integrating immunophenotypic and clinical characteristics to enhance outcome prediction. - Source: PubMed
Publication date: 2026/05/01
Li FengliDing YangyangFeng ShanglongJin YingzhaoXie BeibeiZhang QingJiao XunyiZhu JinliZhang WanqiuTao QianshanWang HuipingWu DepeiLiu XinZhai Zhimin - FLT3 inhibitors have improved outcomes in acute myeloid leukemia (AML) with -like tyrosine kinase 3 internal tandem duplication (FLT3-ITD), but responses are not durable. Notably, FLT3 inhibitors clear blasts from the blood, but not the bone marrow, a hypoxic niche. We investigated effects of hypoxia and the key nutrient glutamine on FLT3 inhibitor response. FLT3-ITD AML cell lines and patient blasts were cultured with FLT3 inhibitors under normoxia (21%) or hypoxia (<1% O ) with or without glutamine or the glutaminase inhibitor telaglenastat (CB-839). Cytotoxicity was measured in WST-1 assays and drug combination effects by Chou-Talalay analysis. Protein expression was measured by immunoblotting, turnover and proteasomal degradation by cycloheximide chase with and without MG-132, and mRNA expression by RT-qPCR. Effect of the ubiquitin ligase c-CBL was tested by siRNA knockdown. FLT3 inhibitor IC s were 3-5-fold higher in hypoxia than normoxia, associated with FLT3-ITD and p-STAT5 downregulation and accelerated FLT3-ITD proteasomal degradation (half-life, 1.0 vs. 2.5 hours). c-CBL expression increased in hypoxia, and c-CBL knockdown restored FLT3-ITD expression and FLT3 inhibitor sensitivity. Glutamine deprivation or telaglenastat treatment abrogated c-CBL upregulation in hypoxia and preserved FLT3-ITD and p-STAT5 expression and FLT3 inhibitor sensitivity. Telaglenastat synergized with FLT3 inhibitors in hypoxia, supporting clinical testing. - Source: PubMed
Publication date: 2026/05/06
Silvestri GiovanninoChatterjee AditiRendina Blair PBar Eli EBaer Maria R - Gene mutations identified through next-generation sequencing (NGS) have been increasingly recognised for their clinical significance in myeloid malignancies. However, data concerning Chinese populations remain limited. This study aimed to characterise mutation profiles in Chinese patients with myeloid malignancies and to evaluate the associations of genetic alterations with clinical features, disease progression, and prognosis. - Source: PubMed
Publication date: 2026/04/30
Liao PengjunXu RuohaoGeng SuxiaDeng ChengxinHuang XinWu PingLi MinmingZeng LingjiLai PeilongWeng JianyuDu Xin