Flt3 Ligand Blocking Peptide
- Known as:
- Flt3 Ligand Blocking Peptide
- Catalog number:
- 33r-9360
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- Flt3 Ligand Blocking Peptide
Related genes to: Flt3 Ligand Blocking Peptide
- 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 Blocking Peptide
α - Calcitonin Gene Related Peptide, α - CGRP, rat&_945;2&_946;1 Integrin Ligand Peptide&_946;_catenin 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 ligand(Ala92)-Peptide 6 98% C93H155N31O26 CAS:(Arg)9 Peptide (Arg8)-Vasopressin Biotin peptide This is (Arg8)-Vasopressin Biotin peptide. For research use only.(Asn5)-Delta-Sleep Inducing Peptide
(Asn5)-Delta-Sleep Inducing Peptide (rabbit), (Asn5)-DSIP (rabbit) 98% C35H49N11O14 CAS: 80064-67-1(Asn5)_Delta_Sleep Inducing Peptide Salt _ Binding _ Synonym (Asn5)_Delta_Sleep Inducing Peptide (rabbit), (Asn5)_DSIP (rabbit) SumFormula C35H49N11O14(Asn5)_Delta_Sleep Inducing Peptide Salt _ Binding _ Synonym (Asn5)_Delta_Sleep Inducing Peptide (rabbit), (Asn5)_DSIP (rabbit) SumFormula C35H49N11O14(Biotin Conjugates) Dopamine D2 Receptor Immunogen: peptide Host: Rabbit(Biotin Conjugates) Glucose Transporter 1 Immunogen: peptide Host: Rabbit Related articles to: Flt3 Ligand Blocking Peptide
- Mutations in Fms-like tyrosine kinase 3 (FLT3) are strongly associated with relapse and resistance in acute myeloid leukemia (AML) patients, and the treatment of relapsed or refractory AML (R/R AML) remains a major clinical challenge. We previously conducted a prospective clinical trial on R/R AML with chemotherapy regimen BHA (bortezomib, homoharringtonine and cytarabine), which demonstrated promising efficacy in patients with FLT3-mutated R/R AML. However, the therapeutic mechanism remains unclear. In this study, we aim to elucidate the therapeutic mechanism of BHA regimen on the basis of its efficacy for FLT3-mutated R/R AML. We retrospectively analyzed twenty-nine patients with R/R AML, after one course of therapy, patients harboring FLT3 mutations had a significantly higher complete remission/complete remission with incomplete hematologic recovery rate than those without FLT3 mutations (46.67% vs. 7.14%, respectively; P = 0.035). To further explore the underlying mechanisms, we conducted combination index analysis, inhibition of proliferation and apoptosis assays. Compared with 293 T-FLT3 cells, 293 T-FLT3-ITD cells were more sensitive to bortezomib, with significantly lower IC50 values. Bortezomib in combination with homoharringtonine had a synergistic effect on FLT3-ITD cells. Moreover, compared with monotherapy, the combination of bortezomib (4 nM) and homoharringtonine (1 nM) markedly increased total cell death in FLT3-ITD cell lines (MV4-11 and Molm-13). Mechanistically, bortezomib promoted the degradation of FLT3-ITD protein, and the degradation of FLT3-ITD protein was further enhanced by homoharringtonine. Notably, this degradation effect was partially reversed by chloroquine. These findings demonstrate that bortezomib and homoharringtonine have synergistic effects and lead to degradation of FLT3-ITD oncoprotein, potentially contributing to a higher complete remission rate in FLT3-ITD R/R AML. - Source: PubMed
Publication date: 2026/05/20
Wei MingWang FurongHuang DanKang ZhijieYang YanZhang ChengtaoLou JiachengYan Jinsong - Acute myeloid leukemia (AML) is a hematological malignancy with a high mortality rate and heterogeneous prognosis. Traditional risk stratification is based on the genetic classification in the 2022 guidelines of the European Leukemia Net. However, the risks of some patients remain unclear, and other prognostic assessment methods are required to improve the risk assessment of these patients. Apoptosis-related genes (ARGs) play critical roles in regulating the survival and drug resistance of AML cells. Therefore, we collected gene expression and clinical data from patients with AML from The Cancer Genome Atlas Acute Myeloid Leukemia (TCGA-LAML) datasets to develop a risk assessment model based on 5 ARGs. Using the least absolute shrinkage and selection operator Cox regression (LASSO-Cox) model, we identified 5 key ARGs (, , , , and ) and constructed a 5-ARG prognostic model. Using this model, we successfully stratified patients in both TCGA-LAML training and independent external validation cohorts, with high-risk patients consistently exhibiting significantly poorer clinical outcomes. In addition, high-risk patients exhibited significant enrichment in pathways related to dysfunction, mechanistic target of rapamycin complex 1 (mTORC1) signaling activation, and pro-inflammatory responses, which were closely correlated with co-mutations. Decitabine, sunitinib, and MK-1775 were identified as potential therapeutic agents. In summary, we established a 5-ARG prognostic model that may facilitate risk stratification and inform therapeutic decision-making in AML. - Source: PubMed
Publication date: 2026/05/15
Pei XiangLiu WenbingLi YishuangWei HuiWang MinWang Jianxiang - 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