Flt3 ligand
- Known as:
- Flt3 ligand
- Catalog number:
- PA056
- Product Quantity:
- 2 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- Flt3 ligand
Related genes to: Flt3 ligand
- 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
&_945;2&_946;1 Integrin Ligand Peptide(1R,2R)_(+)_1,2_Diaminocyclohexane_N, min. 94%rost ligand (na(1S,2S)_(+)_1,2_Cyclohexanediamino_N, (S,S)_Jacobsen ligand(1S,2S)_(_)_1,2_Diaminocyclohexane_N,N min. 94% rost ligand (n(1S,2S)_(_)_1,2_Diaminocyclohexane_N,N Rost ligand24(S)-Hydroxycholesterol Ligand24(S)-Hydroxycholesterol Ligand24(S)-Hydroxycholesterol, LXR ligand, (3β,24S)-Cholest-5-ene-3,24-diol, CAS: 474-73-724(S)-Hydroxycholesterol, LXR ligand, (3β,24S)-Cholest-5-ene-3,24-diol, CAS: 474-73-72B4,CD244,h2B4,Homo sapiens,Human,NAIL,Natural killer cell receptor 2B4,NK cell activation-inducing ligand,NK cell type I receptor protein 2B4,NKR2B42C101 Fas Ligand4-1BB ligand , 71-254aa, Human, His tag, E.coli4-1BB ligand , 71-254aa, Human, His tag, E.coli4-1BB ligand , 71-254aa, Human, His tag, E.coli4-1BB ligand , 71-254aa, Human, His-tag, Recombinant, E.coli Related articles to: Flt3 ligand
- In patients with FLT3-mutated AML who receive frontline azacitidine plus venetoclax, relapses are commonly driven by expansion of the FLT3-mutated clone, providing rationale for "triplet" FLT3 inhibitor-based lower-intensity regimens. Here we report long-term outcomes of a phase II study of azacitidine, venetoclax and gilteritinib in adults with newly diagnosed FLT3-mutated AML who were unfit for intensive chemotherapy. Thirty patients were treated; the median age was 71 years, and 22 (73%) had a FLT3-ITD mutation. The complete remission (CR)/CR with incomplete hematologic recovery rate was 96%, and 14 patients (47%) underwent allogeneic hematopoietic stem cell transplantation (HSCT) in first remission. With a median follow-up of 41.5 months, 11 patients (37%) relapsed; in 67% of evaluable relapses, the FLT3 mutation was not detectable. The median RFS and OS were 23.4 and 29.7 months, respectively, and the 3-year RFS and OS rates were 43% and 46%, respectively. Among patients with FLT3-ITD-mutated AML, the median RFS and OS were 17.0 and 21.8 months, respectively, and the 3-year RFS and OS rates were 32% and 36%, respectively. The presence of a baseline RAS pathway mutation was associated with worse outcomes. Survival rates were similar regardless of HSCT in first remission. Among patients who received at least one consolidation cycle, 68% had a reduction in the dose or duration of at least one of the study drugs. The triplet regimen of azacitidine, venetoclax and gilteritinib is associated with durable remissions and encouraging long-term survival. Randomized studies comparing this regimen to standard of care approaches are warranted. This trial is registered at www.clinicaltrials.gov #NCT04140487. - Source: PubMed
Publication date: 2026/05/27
Short Nicholas JKantarjian Hagop MDaver Naval GAzevedo Roberta SKarrar OmerDiNardo Courtney DKadia Tapan MYilmaz MusaMaroun Manuel MHachem Maria Catherine RitaBorthakur GautamIssa Ghayas CShpall Elizabeth JPopat Uday RHuang XuelinQiao WeiNasr Lewis FadyMacaron WalidAbramova ReginaGarcia-Manero GuillermoKonopleva MarinaRavandi Farhad - Along with the more and more clinical application of various FLT3 inhibitors in acute myeloid leukemia (AML), their real clinical benefits still remain a debated topic. Therefore, this study uses a network meta-analysis method to make comparison on the treatment efficacy and safety situation of different FLT3 inhibitors, hence aiming to offer evidence-based supporting materials for the selection work of clinical treatment strategies. - Source: PubMed
Publication date: 2026/05/11
Xu YaoyaoLi JiamingGao YaoHuang GanZeng Yingjian - : Acute myeloid leukemia (AML) is a hematological malignancy frequently driven by mutations in the FLT3 gene, particularly internal tandem duplications (FLT3-ITD), which contribute to aberrant cell proliferation and resistance to tyrosine kinase inhibitors (FLT3i). The limitations of current FLT3i therapies, including drug resistance, off-target effects, and poor selectivity, necessitate the development of novel therapeutic strategies. Proteolysis-targeting chimeras (PROTACs) represent a promising approach to achieving degradation of oncogenic proteins. : We developed FLT3-targeting PROTACs based on the previously described compound , with a focus on linker modifications to improve degradation efficiency and pharmacokinetic properties. : Among these, compounds and , containing rigid cyclohexyl-piperidine/piperazine linkers, demonstrate superior degradation of FLT3-ITD in MV4-11 AML cells at nanomolar concentrations, achieving >95% reduction in FLT3-ITD levels, outperforming . In addition to improved kinase selectivity, good solubility, and plasma stability, and also exhibit excellent metabolic stability, whereas the predecessor PROTAC was unstable in microsomal assays. In cellular assays, and induce potent apoptosis in FLT3-ITD AML cells but have minimal effects on cells with wild-type FLT3. Proteomics reveal that also degrades MAPK14 (p38α), a kinase upregulated in leukemia, in addition to FLT3. : Dual targeting of FLT3-ITD and MAPK14 enhances proapoptotic signaling without any cytotoxic effect on normal human HEK293 cells. The co-inhibition using or a combination of doramapimod (a MAPK14 inhibitor) with a non-degrading FLT3 inhibitor result in greater caspase-3 activation than either treatment alone. This synergistic effect can be a therapeutic advantage, as several oncogenic drivers are switched off simultaneously by . - Source: PubMed
Publication date: 2026/05/12
Abdelsalam MohamedHalilovic MelisaAshry RamyNassar HusamErdmann FrankSchmidt MatthiasKrämer Oliver HSippl Wolfgang - Acute myeloid leukemia (AML) is a hematologic malignancy of substantial genetic heterogeneity that exhibits clonal growth and blocked differentiation of myeloid progenitor cells in the bone marrow (BM). Genetic alterations play a vital role in the progression, initiation, and recurrence of AML. The aim of this study was to identify the somatic mutational landscape, pathway perturbations, mutational signatures, and druggability of baseline (at diagnosis) and relapsed AML to determine possible treatment options. - Source: PubMed
Publication date: 2026/05/09
Goel HarshPandey Avanish KumarArya AnshulKumar RahulKumar RakeshMakkar HarshitaMajhi Ravi KumarBhattacharya SujataSingh JayDivakar Mohit KumarVasudeva PayalKumar SaranChopra AnitaRanjan AmarMeena Jagdish PrasadGupta Aditya KumarViswanathan Ganesh KumarBatra AtulRath Goura KishorHussain ShowketJain GarimaMisra AroonimaRahul EktaBakhshi SameerTanwar Pranay - After many years of stagnation in the treatment of acute myeloid leukemia (AML), there is currently a rapid move towards personalized medicine. Improvements in molecular diagnostics, risk assessment tools, targeted therapies, overall patient fitness assessments, and quality-of-life assessments have significantly changed how patients are treated. Genetic and molecular analyses, risk and health assessments, and measurable residual disease (MRD) monitoring are now integral to the treatment plan for evaluating patient responses and recurrence. In this regard, lower-intensity treatments are provided to older or unfit individuals. On the other hand, younger patients are usually subjected to curative therapies such as intensive chemotherapy to induce remission. Depending on their fitness and disease risk, they can be considered for hematopoietic cell transplantation, which is done after close observation for MRD. In addition, newer therapeutic drugs and immunotherapy techniques are being applied for patient management. Tremendous strides have been made in improving the efficiency of treatment programs in the relatively new area of personalized AML therapy, with a focus on functionality. - Source: PubMed
Publication date: 2026/05/15
Niscola PasqualeGianfelici ValentinaGiovannini MarcoMazzone CarlaPrincipe Maria Ilaria Del