FLT3基因突变主要包括两种类型：近膜结构域的内部串联重复突变（FLT3-ITD）和酪氨酸激酶结构域的点突变或缺失（FLT3-TKD）。ITD突变是FLT3最常见的一类突变，占65%左右，是指在基因近膜结构域(JMD)插入了一段串联重复序列，通常发生在JMD的精氨酸残基595附近，位于14和15号外显子上，插入的位点和序列多种多样，...
Galinsky I, Coleman M, Fechter L. Midostaurin: Nursing perspectives on managing treatment and adverse events in patients with FLT3 mutation–positive acute myeloid leukemia and advanced systemic mastocytosis. Clin J Oncol Nursing. 2019;23(6), 599–...
用于靶向治疗这类患者的小分子FLT3抑制剂种类也在不断扩充,目前AML的FLT3抑制剂根据对FLT3的选择性可分为两代: 第1代FLT3抑制剂是多激酶抑制剂,产品包括米哚妥林、舒尼替尼、来他替尼和索拉非尼。该类药物除靶向FLT3外,对其他酪氨酸激...
FLT3 mutationAMLFLT3 inhibitorsFLT3 ligandFLT3 receptorFMS-like tyrosine kinase 3 (FLT3) receptor and its ligand play a significant role in human hematopoiesis and the proliferation and malignant transformation of primitive hematopoietic cells. FLT3 mutations are observed in approximately 30% of adult ...
ofFLT3mutation (FLT3-ITD; approximately 25% of all AML cases).FLT3-ITD is a common driver mutation that presents with a high leukemic burden and confers a poor prognosis in patients with AML. The prognostic value of aFLT3mutation in the tyrosine kinase domain (FLT3-TKD), which has a ...
香港济民药业指出，复发/难治性FLT3突变阳性的AML患者预后差、生存期短，直到最近以前他们几乎都没有治疗选择，而ADMIRAL研究的结果改变了这一患者群体的治疗模式。参考来源：1.Phase 3 ADMIRAL Trial Data Show XOSPATA? (gilteritinib) Significantly Prolongs Overall Survival in Adult Patients with FLT3 Mutation-...
研究显示,Quizartinib可显著抑制其AML细胞中FLT3磷酸化,对复发/难治性AML细胞的IC50值达0.3 nM,目前已成为临床上首选FLT3抑制剂。在III期QuANTUM*-First试验中,将口服FLT3抑制剂奎扎替尼(quizartinib)加入一线化疗后,新诊断的FLT3-ITD阳性急性髓系白血病(AML)患者的总生存期(OS)延长了1倍以上。与单独化疗相比,奎扎替...
2022年6月,发表在《Blood》的一项研究,呈现了III期ADMIRAL临床试验使用吉瑞替尼治疗复发性/难治性FLT3突变阳性急性髓系白血病患者的2年长期随访结果。 背景和目的:III 期ADMIRAL(NCT02421939;研究ID:2215-CL-0301)试验显示,以2:1的比例随机至接受口服 FMS 样酪氨酸激酶3抑制剂吉瑞替尼治疗复发性/难治性FLT3突变阳...
与单纯化疗相比,抑制FLT3激酶活性的药物 (单用或与化疗联合使用) 明显提高了AML患者的生存率和缓解率。随机化的3期ADMIRAL试验对比了Gilteritinib和挽救化疗在FLT3突变阳性(+)的复发性或难治性AML患者中的疗效。在该试验中,受试患者被随机(2:1)分至Gilteritinib组(120 mg/天)或挽救化疗组。ADMIRAL的初步分析...
Researchers believe that AML is driven by somatic alterations in a “2 hit” process: a proliferative mutation in a class I gene such as FLT3 and an aberration in a class II gene that prevents cells from maturing.1 FLT3 mutations are among the epigenetic drivers of AML in normal karyotypes...