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gilteritinib (Xospata)

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中国药物化学杂志 2019年第6期29卷 496-496页

作者：徐伯轩(编译) 宫平(审校) 沈阳药科大学

gilteritinib由安斯泰来(Astellas)公司开发,分别于2017年在美国、2018年在欧盟和日本被授予指定孤儿药地位。2018年11月28日其富马酸盐片剂经美国FDA批准上市,用于治疗FMS-样酪氨酸激酶3(FLT3)突变阳性的复发性或难治性急性髓细胞白血... 详细信息

gilteritinib由安斯泰来(Astellas)公司开发,分别于2017年在美国、2018年在欧盟和日本被授予指定孤儿药地位。2018年11月28日其富马酸盐片剂经美国FDA批准上市,用于治疗FMS-样酪氨酸激酶3(FLT3)突变阳性的复发性或难治性急性髓细胞白血病(AML)[1]。

关键词：急性髓细胞白血病酪氨酸激酶 FMS AML gilteritinib Xospata

治疗急性髓系白血病新药:FLT3抑制剂 gilteritinib

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中国新药与临床杂志 2019年第6期38卷 336-339页

作者：杨君义接贵涛临沂市中心医院药学部山东临沂276400 临沂市中心医院血液科山东临沂276400

FMS样酪氨酸激酶3 (FLT3)的基因在造血干细胞增殖、分化及存活方面发挥重要作用。FLT3内部串联重复突变(FLT3-ITD)在急性髓系白血病(AML)中常见,且与迅速复发及生存率低密切相关。gilteritinib (Gil)为新型FLT3抑制剂,由Astellas制药公... 详细信息

FMS样酪氨酸激酶3 (FLT3)的基因在造血干细胞增殖、分化及存活方面发挥重要作用。FLT3内部串联重复突变(FLT3-ITD)在急性髓系白血病(AML)中常见,且与迅速复发及生存率低密切相关。gilteritinib (Gil)为新型FLT3抑制剂,由Astellas制药公司生产,于2018年11月经美国食品和药物管理局批准用于FLT3突变型复发难治性AML的治疗。临床试验表明对其他FLT3抑制剂耐药的AML患者,采用Gil治疗仍可取得较好疗效,其最常见的不良反应包括肌肉痛、关节痛、转氨酶升高、疲劳、发热等。

关键词：白血病,髓样,急性 fms样酪氨酸激酶3 gilteritinib 内部串联重复突变

FDA批准抗肿瘤药gilteritinib上市

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中国合理用药探索 2019年第1期 43-43页

美国FDA于2018年11月28日批准安斯泰来(Astellas)公司的gilteritinib(商品名:Xospata)片剂上市,用于FMS样酪氨酸激酶3(FLT3)突变阳性的复发性或难治性急性髓系白血病(AML)。gilteritinib是一种可抑制多种酪氨酸激酶受体(包括FLT3)的小... 详细信息

美国FDA于2018年11月28日批准安斯泰来(Astellas)公司的gilteritinib(商品名:Xospata)片剂上市,用于FMS样酪氨酸激酶3(FLT3)突变阳性的复发性或难治性急性髓系白血病(AML)。gilteritinib是一种可抑制多种酪氨酸激酶受体(包括FLT3)的小分子。gilteritinib可抑制FLT3受体信号和外源性表达FLT3(包括FLT3-

关键词： FDA FLT gilteritinib ITD

Inhibition of FLT3:A Prototype for Molecular Targeted Therapy in Acute Myeloid Leukemia

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Engineering 2021年第10期7卷 1354-1368页

作者： Meira Yisraeli Salman Jacob M.Rowe Nir Weigert Department of Hematology Shaare Zedek Medical CenterJerusalem 9103102Israel Department of Hematology and Bone Marrow Transplantation Rambam Medical CenterHaifa 3109601Israel Technion—Israel Institute of Technology Haifa 3200003Israel

Modern therapy of acute myeloid leukemia(AML)began in 1973 with the first report of the successful combination of daunorubicin and cytarabine,which led to complete remission in approximately 45%of *** AML diagnosis was dependent on morphology,aided initially only by *** acute lymphoblastic leukemia(ALL),immunophenotyping offered little in the diagnosis of AML,at least during the 1970s and *** advent of reliable cytogenetics changed the entire prognostic outlook of *** karyotypic analysis,different groups of AML could be classified and stratified for various *** mutational profiling was a major advance in further categorizing AML patients,aided by the immunophenotypic identification of antigenic markers on the *** these advances were occurring as the understanding of the importance of the tumor burden—known as minimal residual disease(MRD)—became crucial for the management of AML *** efficacy of MRD has rapidly progressed in the past decade,from a specificity of 103 with immunophenotyping to 104 with polymerase chain reaction(PCR),which is only appropriate for some patients with AML,and finally to 105 or even 106 cells with the extraordinary sensitivity of next-generation sequencing(NGS).All of these advances have promoted the concept of personalized medicine,which has led to the advent of targeted agents that can accurately be used for specific diagnostic *** can be predicted and measured *** targeted agents have now become a cornerstone in the management of AML,increasing effi-cacy and dramatically reducing *** focus of this review is on one of the most well-studied targeted agents in AML:the FMS-like tyrosine kinase 3(FLT3)inhibitors,which have impacted the prognostication and therapeutics of *** review selectively discusses the FLT3 inhibitors in detail,as a model for the other burgeoning targeted agents that have already been approved,as well as tho

关键词： AML Targeted therapy FLT3 inhibitors Midostaurin gilteritinib Quizartinib Sorafenib

How acute myeloid leukemia(AML)escapes from FMS-related tyrosine kinase 3(FLT3)inhibitors?Still an overrated complication?

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Cancer Drug Resistance 2023年第2期6卷 223-238页

作者： Salvatore Perrone Tiziana Ottone Nadezda Zhdanovskaya Matteo Molica Hematology Polo Universitario PontinoS.M.Goretti HospitalLatina 04100Italy Department of Biomedicine and Prevention the University of Rome“Tor Vergata”Rome 00100 Italy Neuro-Oncohematology Santa Lucia FoundationI.R.C.C.S.Rome 00100Italy Hematology Department of Translational and Precision MedicineSapienza UniversityRome 00161Italy Hematology Unit S.Eugenio HospitalASL Roma 2Rome 00144Italy.

FMS-related tyrosine kinase 3(FLT3)mutations,present in about 25%-30%of acute myeloid leukemia(AML)patients,constitute one of the most frequently detected mutations in these *** binding of FLT3L to FLT3 activates the phosphatidylinositol 3-kinase(PI3K)and RAS pathways,producing increased cell proliferation and the inhibition of *** types of FLT3 mutations exist:FLT3-ITD and FLT3-TKD(point mutations in D835 and I836 or deletion of codon I836).A class of drugs,tyrosine-kinase inhibitors(TKI),targeting mutated FLT3,is already available with 1st and 2nd generation molecules,but only midostaurin and gilteritinib are currently ***,the emergence of resistance or the selection of clones not responding to FLT3 inhibitors has become an important clinical dilemma,as the duration of clinical responses is generally limited to a few *** review analyzes the insights into mechanisms of resistance to TKI and poses a particular view on the clinical relevance of this *** resistance been overlooked?Indeed,FLT3 inhibitors have significantly contributed to reducing the negative impact of FLT3 mutations on the prognosis of AML patients who are no longer considered at high risk by the European LeukemiaNet(ELN)***,several ongoing efforts to overcome resistance to FLT3-inhibitors will be presented:new generation FLT3 inhibitors in monotherapy or combined with standard chemotherapy,hypomethylating drugs,or IDH1/2 inhibitors,Bcl2 inhibitors;novel anti-human FLT3 monoclonal antibodies(e.g.,FLT3/CD3 bispecific antibodies);FLT3-CAR T-cells;CDK4/6 kinase inhibitor(e.g.,palbociclib).

关键词： Acute myeloid Leukemia FLT3 gilteritinib midostaurin TKI-inhibitor resistance quizartinib sorafenib crenolanib