FLT3 (Ab_591) Antibody
- Known as:
- FLT3 (Ab_591) Antibody
- Catalog number:
- E021187-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- FLT3 (Ab_591) Antibody
Related genes to: FLT3 (Ab_591) 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 (Ab_591) Antibody
Related articles to: FLT3 (Ab_591) Antibody
- Clonal hematopoiesis of indeterminate potential (CHIP) is a precursor condition characterized by the expansion of mutant hematopoietic stem and progenitor cell (HSPC) clones that increases the risk of hematologic malignancies. Although genome-wide association studies have identified multiple non-coding loci associated with CHIP susceptibility, their mechanisms remain unclear. We hypothesized that CHIP risk variants alter enhancer activity in HSPCs. To test this, we screened 1,374 non-coding variants from 51 CHIP-associated loci using a Massively Parallel Reporter Assay (MPRA) in the CD34+ fraction of MUTZ-3 cells. We identified 87 regulatory variants across 32 loci. Targeted genome editing in hematopoietic cells and complementary reporter assays in primary human HSPCs validated enhancer activity for variants regulating NKD2, FLT3, and MSI2. Functional studies demonstrated that increased MSI2 expression, modeling the effect of the CHIP risk allele, promotes clonal expansion of TET2-deficient HSPCs, providing a mechanistic link between inherited non-coding variation and CHIP clonal expansion. - Source: PubMed
Publication date: 2026/09/03
Nguyen TrieuJeejan JessicaIwasaki TakeshiKales SusanChakraborty JoyeetaYanase ChieShekhar ArunaKwasniak DominikaHegde AditiVoit RichardWeinstock JoshuaStengel Kristy RIto KeisukeTewhey RyanNandakumar Satish K - Not available. - Source: PubMed
Publication date: 2026/09/03
Marvin-Peek JenniferDiNardo Courtney D - The phase 3, open-label LACEWING study evaluated efficacy and safety of the FMS-like tyrosine kinase 3 (FLT3) inhibitor gilteritinib (GIL) plus azacitidine (AZA) in newly diagnosed (ND) FLT3-mutated (FLT3mut+) acute myeloid leukemia (AML) ineligible for intensive induction chemotherapy (IIC). Patients were enrolled into a safety cohort (n=15) or randomized (n=168) to GIL+AZA, GIL, or AZA. We present final (6.5-year) outcomes and additional data on mutational subgroups, measurable residual disease (MRD), and pharmacokinetics. Median overall survival (OS) was 9.82 versus 9.23 months (GIL+AZA vs AZA, p=0.182) and 5.24 months (GIL). Corresponding two-year OS rates were 18.8%, 12.9%, and 4.5%. Overall response rates were 70.2% versus 36.8% (GIL+AZA vs AZA, nominal p. - Source: PubMed
Publication date: 2026/09/03
Wang Eunice SMontesinos PauMinden Mark DSibai HassanLee Je-HwanHeuser MichaelNaoe TomokiChou Wen-ChienLaribi KamelEsteve JordiAltman Jessica KHavelange ViolaineWatson Anne-MarieFumagalli MonicaPatkowska ElzbietaHill Jason EGill Stanley CPandya Bhavik JChen CarolineHasabou Nahla - Feline McDonough sarcoma (FMS)-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD) mutations are clinically important in acute myeloid leukaemia (AML). We developed and validated a machine learning model using routine laboratory tests to estimate the probability of FLT3-ITD mutations in newly diagnosed AML to prioritise rapid molecular testing. Consecutive patients treated at Ruijin Hospital during 2021-2024 were included. Those diagnosed in 2021-2023 comprised the training cohort, and those in 2024 formed the internal temporal validation cohort, and the BeatAML2 cohort served as external validation. Following Boruta feature selection, seven machine learning algorithms were evaluated via area under the receiver operating characteristic curve (AUC). The optimal model was interpreted using SHapley Additive exPlanations (SHAP) and deployed as a web-based calculator. Overall, 514 patients were included (training, n = 254; validation, n = 84; external validation, n = 176). Boruta algorithm selected five candidate features, and a simple four-feature model was constructed. Gradient boosting machine (GBM) performed best, with AUCs of 0.847, 0.772 and 0.760 in the training, internal validation and external validation cohorts respectively. SHAP analysis showed absolute blast count contributed most to the model. The GBM model may help identify patients with newly diagnosed AML who should be prioritised for rapid molecular testing for FLT3-ITD mutations. - Source: PubMed
Publication date: 2026/09/02
Song JunjunGu ZhichaoHan JinZhang YuqingZhao LinglingYan HanLu JingShen YangZhu Yongmei - Acute myeloid leukemia (AML) driven by FLT3-ITD mutations remains a therapeutic challenge with limited treatment options. Herein, we report the design, synthesis, and biological evaluation of a series of 4-(2-fluorophenoxy)pyridine derivatives featuring an imidazolidinone carboxamide linker as potent FLT3-ITD inhibitors. Systematic structure-activity relationship exploration identified compound 18p as the optimal candidate, which displayed exceptional enzymatic potency against FLT3-ITD (IC = 1.1 nM) and single-digit nanomolar antiproliferative activity against FLT3-ITD driven AML cell lines (BaF-FLT3-ITD IC = 5.7 nM; MOLM-13 IC = 1.6 nM). Compound 18p demonstrated a marked selectivity profile, discriminating FLT3-ITD from FLT3-WT and sparing normal PBMCs and a broad panel of solid tumor cells. Kinome profiling revealed that 18p maintained high selectivity over c-Kit, CDKs, FGFRs, and the majority of 60 tested kinases, with PDGFRβ identified as the principal off-target liability. Mechanistically, 18p suppressed FLT3 autophosphorylation and downstream STAT5, AKT, and ERK signaling more effectively than gilteritinib at equimolar concentrations, and induced potent G-phase arrest and apoptosis in MOLM-13 cells. In the MV4-11 xenograft model, oral administration of 18p at 10 mg/kg achieved 80% tumor growth inhibition, comparable to gilteritinib at 2.5 mg/kg, with concomitant suppression of Ki67 and p-STAT5 and induction of cleaved caspase-3 and γH2AX in tumor tissues. Histopathological examination of major organs confirmed an absence of overt toxicity. These findings position 18p as a promising FLT3-ITD inhibitor and provide valuable insights for further development of mutation-selective AML therapeutics. - Source: PubMed
Publication date: 2026/09/01
Wang ZhongyuanZhang YiweiLi LinWang YunfengYang DanSong QingmeiFu QingqingZhao DongshengTang LeiOuyang WeiweiChai Yue'eLiao Weike