rHuman FLt3 Active, Human cytokinesand growth factors
- Known as:
- rHuman FLt3 Active, Human cytokinesand growth factors
- Catalog number:
- RF0039-500
- Product Quantity:
- 500
- Category:
- -
- Supplier:
- Agren
- Gene target:
- rHuman FLt3 Active Human cytokinesand growth factors
Related genes to: rHuman FLt3 Active, Human cytokinesand growth factors
- 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: rHuman FLt3 Active, Human cytokinesand growth factors
Related articles to: rHuman FLt3 Active, Human cytokinesand growth factors
- To explore the status of peripheral blood immunological markers and gene mutations in patients with myelodysplastic syndrome (MDS) and the correlation between them. - Source: PubMed
Sun Da-XiangMa YunHan Qiu-HongChen ZhuoLiu Wei-YiWang De-XiuLi Rui-BaiLyu YanXiao Hai-YanLiu ChiLi LiuTang Xu-Dong - The FMS-like tyrosine kinase 3- internal tandem duplication (FLT3-ITD) subtype of acute myeloid leukemia (AML) is associated with poor clinical outcomes. Homoharringtonine (HHT), a natural protein inhibitor, has shown strong activity against FLT3-ITD AML. However, its clinical use is limited by rapid clearance and systemic toxicity. To address these limitations, a CD71-targeted, ROS-responsive micelle (TDTP/HHT) was developed for precise and efficient HHT delivery. - Source: PubMed
Publication date: 2026/05/27
Tang YuqianLi JiaxinYe WuDu YiwenZhang YingYang YankunYe YunxiaGong Yuping - Bulk sequencing of relapsed tumors reveals mutations associated with resistance to cancer therapy but is insufficient to fully assess all causes of relapse. Due to inherent tumor heterogeneity, on-treatment tumor evolution may select for genetically distinct clones or shifts in malignant transcriptional states not resolvable by bulk sequencing. We performed multiomic single cell (SC) DNA/protein and RNA/protein profiling of a clinical trial cohort of acute myeloid leukemia (AML) patients treated on the Phase 1b clinical trial of the BCL2 inhibitor venetoclax and the FLT3 inhibitor gilteritinib (Ven/Gilt) to characterize immunophenotypic, transcriptional, and genetic clonal evolution driving resistance. We found that while Ven/Gilt effectively eliminated FLT3 mutant clones, resistance was associated with RAS activation via multiple mechanisms including selection for RAS mutant clones, non-mutational upregulation of RAS transcriptional programs and a shift to RAS-associated monocytic AML differentiation. In an in vitro model of monocytic differentiation associated with non-mutational RAS transcriptional activation, we demonstrated that RAS pathway inhibition re-sensitized to Ven/Gilt. These data illustrate that convergent resistance pathways in patients can be activated via diverse genetic and non-genetic mechanisms. These results underscore that RAS signaling is central to FLT3 and BCL2 inhibitor resistance, is tightly coupled to AML monocytic differentiation and highlight RAS pathway inhibition as a viable clinical strategy to combat resistance. CT# NCT03625505. - Source: PubMed
Publication date: 2026/06/01
Kennedy Vanessa EPeretz Cheryl A CWalia AnushkaChyla BrendaSun YanHill Jason ETran ElaineKoh Andrew DFerng Timothy TPintar SamanthaJones MatthewPopescu BogdanLomeli IsabelleChehab FaridMurad NataliaJohn AugustRoy Ritu ParnaOlshen Adam BBerryhill Christine ADavis ChristopherAngus Steven PatrickRivera Jose MMeshulam AliciaStieglitz ElliotJoshi Sunil KumarTraer ElieDail MoniqueHamidi HabibAltman Jessica KDaver Naval GLevis Mark JMcCloskey JamesPerl Alexander ESmith Catherine C - Acute myeloid leukemia (AML) remains a therapeutic challenge due to its aggressive nature and poor prognosis in relapsed/refractory cases. This study explores novel MNK (MAP kinase-interacting kinase) inhibitors derived from the marine natural product phorbazole C. Through systematic structure-activity relationship studies, compound (YTB53) was identified as a potent MNK1/2-targeting compound with IC values of 0.037 and 0.009 μM, respectively. Kinase profiling further revealed that also significantly inhibits PDGFRα, TRKB and FLT3, indicating that its antiproliferative activity in MV4-11 cells arises from multikinase engagement rather than selective MNK inhibition alone. Mechanistically, induced cell cycle arrest, apoptosis, pyroptosis, and mitochondrial dysfunction. It also exhibited antiangiogenic effects and suppressed tumor growth in a xenograft model without overt toxicity. These findings support as a promising multimechanistic lead for AML therapy, warranting further medicinal chemistry optimization to improve its pharmacokinetic properties and advance its development potential. - Source: PubMed
Publication date: 2026/06/01
Chen XiangZhang LitingHan YuqiangWang YongkunLiu JinliHan GuiyanZhang ZixuanYin RuijuanYu RileiJiang TaoGuo Yue-WeiSu MingzhiJin Xin - Mutations in FLT3 are found in around one third of acute myeloid leukemia (AML) cases and contribute significantly to disease progression, making this kinase a key therapeutic target. In this study, flavonoids from Artemisia campestris L. were investigated as potential FLT3 inhibitors. Among the screened compounds, apigenin, chrysin, and sakuranetin showed the highest binding affinities toward FLT3, with docking scores of - 10.1, - 9.8, and - 9.9 kcal/mol, respectively, compared with - 8.7 kcal/mol for Quizartinib. molecular dynamics simulations confirmed the stability of these complexes over 600 ns. ADMET analysis indicated favorable pharmacokinetic profiles, with high intestinal absorption (93.25%, 93.76%, and 92.60%) and no predicted AMES toxicity or hepatotoxicity. DFT calculations revealed improved electronic stability and reactivity of the selected flavonoids, while ELF and MEP analyses highlighted charge distribution patterns supporting strong interactions within the FLT3 binding site. Overall, these compounds represent promising scaffolds for FLT3 inhibitor development. - Source: PubMed
Publication date: 2026/06/01
Belghalia EtibariaElbamtari FaridBouamrane SoukainaKhaldan AyoubGuendouzi AbdelkrimSbai AbdelouahidLakhlifi TaharBouachrine Mohammed