FLT3 (CD135) Antibody (N_term)
- Known as:
- FLT3 (CD135) Antibody (N_term)
- Catalog number:
- AP7644a
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- FLT3 (CD135) Antibody (N_term)
Related genes to: FLT3 (CD135) Antibody (N_term)
- 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 (CD135) Antibody (N_term)
Related articles to: FLT3 (CD135) Antibody (N_term)
- 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 - An internal tandem duplication in the gene encoding Fms-like tyrosine kinase 3 (FLT3-ITD) is associated with high relapse risk and poor prognosis in acute myeloid leukemia (AML) and plays a crucial role in treatment decisions. Measurable residual disease (MRD) analysis of FLT3-ITD during and after treatment has shown prognostic value in adults, but its clinical value in children remains unexplored. - Source: PubMed
Publication date: 2026/05/18
Alm Sofie JohanssonTornberg BeaMalmberg Erik DelsingHasle HenrikJuul-Dam Kristian LøvvikPalmqvist LarsSaeed Borhan RBarkhordar Giti ShahSoboli AnastasiaStaffas AnnaAbrahamsson JonasFogelstrand Linda - FLT3 is a critical therapeutic target for acute myeloid leukemia (AML), and its inhibition remains a key strategy in AML management. In this study, we optimized the known compound CHEMBL4444839 to design a novel analogue, CHEMBL4444839-Analogue, showing improved pharmacological and structural characteristics. Pharmacokinetic profiling evaluation revealed that the analogue had enhanced drug-likeness, metabolic stability, and intestinal permeability, along with reduced predicted toxicity. Molecular docking revealed that CHEMBL4444839-Analogue exhibited a binding energy of -10.4 kcal/mol versus -8.7 kcal/mol for the parent compound, forming additional hydrogen bonds and hydrophobic contacts with GLU661, CYS694, LEU818, and PHE830 in the ATP binding pocket. Molecular dynamics simulation over 100 ns demonstrated lower average RMSD (1.78 Å vs 2.34 Å) and reduced RMSF fluctuations at the activation loop and DFG-out region, indicating enhanced conformational stability. Free energy calculations confirmed higher thermodynamic stability of the analogue versus CHEMBL4444839. The analogue also restricted domain motion and improved residue correlation, indicating better stabilization of FLT3 in its inactive conformation. Incorporation of a fluorocyclobutane moiety significantly contributed to enhanced rigidity and optimized interaction geometry, collectively establishing CHEMBL4444839-Analogue as a more promising and selective FLT3 inhibitor for AML therapy. - Source: PubMed
Publication date: 2026/05/18
Das UddalakRegati DheemanthSowdhamini RKumar Jitendra