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
- Activating mutations in FMS-like tyrosine kinase 3 (FLT3) drive aggressive acute myeloid leukemia (AML) and confer poor prognosis. Although FLT3 inhibitors have improved outcomes, their efficacy is frequently limited by microenvironment-mediated signaling and treatment-emergent resistance. XY0206 is a structurally optimized derivative of sunitinib, an inhibitor approved for multiple solid tumors. Biochemical, multi-omics, and functional analyses showed that XY0206 directly engages FLT3 and suppresses downstream STAT5, AKT, and ERK signaling, resulting in apoptosis in FLT3-ITD AML cells. Across models of FLT3-dependent resistance, XY0206 retained antileukemic activity, including in FLT3-ITD cells harboring the F691L gatekeeper mutation, a recurrent alteration conferring resistance to approved FLT3 inhibitors. In primary AML blasts and xenograft models, XY0206 exhibited enhanced antileukemic activity with favorable tolerability relative to gilteritinib. In a phase I/II trial (NCT04471064) of XY0206 monotherapy in patients with relapsed or refractory (R/R) AML, XY0206 achieved a composite complete remission rate (CRc) of 45.7% overall, with a notable 60.0% CRc rate among patients with FLT3-ITD mutations. Three of eight patients with prior FLT3 inhibitor-exposed R/R AML also achieved CRc. Together, these findings support further clinical evaluation of XY0206 as a FLT3-directed therapeutic in AML, particularly in disease settings with reduced sensitivity to existing FLT3 inhibitors. - Source: PubMed
Publication date: 2026/09/01
Shen LongYang YangXu ChenghuaJiang BoDuan XiaoxiaoShao XianfengLi SimengLiu SiyiHuang ChaoSong LinSun MingyuanFan JintingWang NingZhang DongFang YouyangKang LichunJiang YajunNiu MingmingQi JunyuanCheng TaoWang Hong - Acute myeloid leukemia (AML) is an aggressive and heterogeneous hematological malignancy in which treatment resistance and relapse remain major causes of mortality. Extracellular vesicles (EVs) contribute to AML progression by mediating communication among leukemic blasts, leukemia stem cells, hematopoietic stem and progenitor cells, stromal and endothelial cells, and immune-cell populations. Experimental studies indicate that AML-associated EVs can remodel the bone marrow niche, suppress normal hematopoiesis, impair antileukemic immune responses, promote leukemic-cell survival, and facilitate drug resistance. Their surface markers and molecular cargo, including proteins, miRNAs, mRNAs, DNA, lipids, and metabolites, have also prompted investigation into their use as liquid-biopsy biomarkers. Candidate EV-based markers include particle abundance, blast-associated antigens, TGF-β1, FLT3-ITD and NPM1 alterations, and several circulating miRNAs. However, most biomarker studies remain small, heterogeneous, and insufficiently compared with established measurable residual disease assays. Therapeutic strategies involving inhibition of EV release or uptake, EV-based immunotherapy, and engineered EVs for drug or RNA delivery are also being explored, but current evidence is predominantly preclinical. Clinical translation is further limited by inconsistent terminology, variable isolation and characterization methods, contamination by non-vesicular particles, and a lack of prospective multicenter validation. This review summarizes the biological roles, biomarker potential, therapeutic applications, and methodological challenges of EVs in AML and highlights the priorities required for their future clinical development. - Source: PubMed
Publication date: 2026/08/31
Oriquat GhalebAl-Hasnaawei ShakerMousa Hayjaa MohaisenMalathi HSahoo SamirPrathiba SSingh GurjantSinha AashnaAbdalla Rufaida - Mutations in FLT3 are present in approximately 30% of patients with AML. The addition of midostaurin (MIDO) to intensive chemotherapy (IC) became standard of care following the RATIFY trial, but comprehensive real-world data spanning the full adult age spectrum and including both FLT3-ITD and FLT3-TKD mutations remain limited. We retrospectively analyzed 1658 adults aged 14-85 years with newly diagnosed FLT3-mutated AML from 129 PETHEMA registry centers: 469 received IC + MIDO and 1189 IC alone. Composite complete remission was higher with IC + MIDO than IC (81.4% vs. 71.7%; p < 0.001) and Day 30 mortality was substantially lower (2.1% vs. 7.1%; p < 0.001). Median overall survival was 47.2 versus 19.3 months (HR 0.64; 95% CI, 0.53-0.76; p < 0.001), and the benefit was sustained after multivariable adjustment (HR 0.73; p = 0.017). In 261 propensity score-matched pairs, the effect was attenuated, remaining significant for event-free survival (HR 0.77; p = 0.029) and showing a nonsignificant trend for OS (HR 0.77; p = 0.06). Allogeneic hematopoietic stem cell transplantation in first remission was more frequent in the IC + MIDO cohort (48.9% vs. 41.3%; p = 0.023). Time-dependent analyses showed the largest MIDO effect among autologous and non-transplanted patients (OS HR 0.45; p = 0.138, and HR 0.69; p = 0.014, respectively). The benefit of MIDO was consistent irrespective of FLT3 mutation type, FLT3-ITD allelic burden, cytogenetic risk, and gender, while less improvement occurred among NPM1 wild type and secondary AML patients. This large real-world cohort confirms the survival benefit of MIDO plus IC across the full adult age spectrum, supporting its standard-of-care status in FLT3-mutated AML. - Source: PubMed
Publication date: 2026/08/31
Romero Riquelme Mónica AlejandraAspas Requena GasparLloret-Madrid PilarGil CristinaAguiar ElianaTormo MarDel Bernal Del Castillo TeresaRodríguez Arbolí EduardoSerrano JosefinaSánchez-García JoaquínRodríguez-Medina CarlosMariz José MárioAyala RosaMartínez-López JoaquínAmigo María LuzVives SusanaAlgarra Algarra LorenzoGarcía Boyero RaimundoBrioso JoanaCastaño TamaraBergua Burgués Juan MSalamero OlgaBass Maturana María FranciscaColorado MercedesGarcía Fortes MaríaSayas Lloris María JoséVicente Belén VidrialesChillón CarmenPérez Santaolalla EstherMadrigal María DoloresLabrador Gómez JorgeGarcía Pérez María JoséCasado Calderón SoledadPérez Encinas ManuelBalerdi Malcorra AmaiaRodríguez María SoléGómez García Lara MaríaHerrera Puente PilarArce Fernández OlgaBarrios García ManuelNoriega VíctorFernández RosaMateos MamenLacalzada CarolinaAlmela Gallego ÁgataGarcía Garay María CarmenCouto CarmenPérez-Simón José AntonioBarragán González EvaMontesinos Pau - Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is an established curative treatment for acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). Advances in supportive care, infection control, and graft-versus-host disease management have substantially reduced non-relapse mortality, leading to improved transplant outcomes. However, post-transplant relapse remains the leading cause of treatment failure, particularly in patients with adverse genetic abnormalities or active disease at transplantation. Post-transplant maintenance therapy has emerged as a strategy to prevent relapse by providing a "third anti-leukemic effect" that complements the cytotoxic effect of conditioning regimens and the graft-versus-leukemia immune response. Maintenance approaches can be broadly categorized into prophylactic therapy administered during molecular remission and preemptive therapy initiated upon detection of measurable residual disease (MRD). This review summarizes the current concepts of post-transplant maintenance therapy in AML/MDS, with a particular focus on hypomethylating agents such as azacitidine and FLT3 inhibitors. It also discusses emerging evidence supporting MRD-guided treatment strategies and molecularly targeted maintenance approaches, highlighting future perspectives for optimizing relapse prevention after allo-HSCT. - Source: PubMed
Najima Yuho - This post hoc pooled analysis of ADMIRAL and COMMODORE trials aimed to determine if response kinetics differ for gilteritinib monotherapy in relapsed/refractory (R/R) -like tyrosine kinase 3 ()-mutated acute myeloid leukemia (AML). In total, 205 patients achieved composite complete remission (CRc). This analysis only included the 166 patients (81.0%) who achieved CRc before on-study hematopoietic stem cell transplantation (HSCT). Of these, 148 patients (89.2%) achieved CRc within 6 gilteritinib cycles, 60 patients (36.1%) after cycle 2, and 119 patients (71.7%) after cycle 4. We defined early responders (ERs; n = 60) and later responders (LRs; n = 106) as those who achieved CRc within 2 cycles and after cycle 3, respectively. Multivariate logistic regression analysis indicated that female patients and patients with nucleophosmin 1 comutations were more likely to be ERs than LRs. Median CRc duration was 2.7 months (range, 0-66) for ERs and 3.5 months (range, 0-61) for LRs. More LRs (41 of 106 patients [38.7%]) had best response of CR vs ERs (13 of 60 patients [21.7%]). Median overall survival indexed at CRc date was 9 months for ERs and 10 months for LRs. In ERs and LRs, 14 of 60 patients (23.3%) and 20 of 106 patients (18.9%) underwent HSCT respectively. The rate of drug-related grade ≥3 adverse events was 11.4 events per patient-years in ERs and 7.8 events per patient-years in LRs. Patients with R/R -mutated AML should continue gilteritinib monotherapy, if tolerated, for a minimum of 6 cycles because later responses can occur. These trials were registered at www.clinicaltrials.gov as NCT02421939 (ADMIRAL) and NCT03182244 (COMMODORE). - Source: PubMed
Publication date: 2026/07/13
Perl Alexander ELevis Mark JWei Andrew HKim Hee-JeCheong June-WonLi JianBondarenko SergeyYokoyama HisayukiHosono NaokoHasabou NahlaElsouda DinaAriza JuanAn Jamie Jung-HeeWang Jianxiang