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Journal articles on the topic 'Gilteritinib'

Author: Grafiati
Published: 28 June 2021
Last updated: 29 July 2025

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1

Perl, Alexander E., Richard A. Larson, Nikolai Alexandrovich Podoltsev, et al. "Follow-up of patients with FLT3-mutated R/R AML in the phase 3 ADMIRAL trial." Journal of Clinical Oncology 39, no. 15_suppl (2021): 7013. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.7013.

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7013 Background: The phase 3 ADMIRAL trial demonstrated the superiority of gilteritinib to salvage chemotherapy (SC) in patients (pts) with FLT3-mutated ( FLT3mut+) R/R AML. Aim/Objective: A follow-up of ADMIRAL assessed long-term survivors, transplant (HSCT) outcomes. and gilteritinib safety beyond 1 year. Methods: A data cut was performed on September 20, 2020—2 years after the primary analysis. Patients who were alive without relapse, pts who underwent HSCT, and adverse events of interest (AEIs) in Years 1 (≤12 months) and 2 ( > 12 months) of gilteritinib therapy were evaluated. Results:
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2

Lee, Jae-Seon, Min Ji Park, Ningning Sun, et al. "Plm-102, a Next Generation FLT3 Inhibitor, Shows Potent Anti-Leukemic Activity on Resistance to Gilteritinib in FLT3 Mutated Acute Myeloid Leukemia." Blood 142, Supplement 1 (2023): 2919. http://dx.doi.org/10.1182/blood-2023-180483.

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Introduction: Mutations in the FMS-like tyrosine kinase 3 (FLT3) gene occur in approximately 25 ~ 30% of all acute myeloid leukemia (AML) cases, with FLT3-ITD mutations having a poor prognosis. In 2022, the FDA granted approval to Gilteritinib, a 2nd generation FLT3 inhibitor, for the treatment of relapsed or refractory AML. Although Gilteritinib has demonstrated efficacy in R/R AML patients, its response duration is limited due to the development of secondary resistance. Herein, we report a next-generation drug candidate, PLM-102, which has shown promising pre-clinical results to overcome the
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3

Zavorka Thomas, Megan E., Jae Yoon Jeon, Zahra Talebi, et al. "Gilteritinib-induced upregulation of S100A9 is mediated through BCL6 in acute myeloid leukemia." Blood Advances 5, no. 23 (2021): 5041–46. http://dx.doi.org/10.1182/bloodadvances.2021005614.

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Abstract Drug resistance and relapse are common challenges in acute myeloid leukemia (AML), particularly in an aggressive subset bearing internal tandem duplications (ITDs) of the FLT3 receptor (FLT3-ITD+). The tyrosine kinase inhibitor gilteritinib is approved for the treatment of relapse/refractory AML with FLT3 mutations, yet resistance to gilteritinib remains a clinical concern, and the underlying mechanisms remain incompletely understood. Using transcriptomic analyses and functional validation studies, we identified the calcium-binding proteins S100A8 and S100A9 (S100A8/A9) as contributor
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4

Perl, Alexander E., Giovanni Martinelli, Andreas Neubauer, et al. "Long-term survivors and gilteritinib safety beyond one year in FLT3-mutated R/R AML: ADMIRAL trial follow-up." Journal of Clinical Oncology 38, no. 15_suppl (2020): 7514. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.7514.

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7514 Background: The phase 3 ADMIRAL trial showed that gilteritinib was superior to salvage chemotherapy (SC; median overall survival [OS]: 9.3 vs 5.6 mo, respectively) in FLT3mut+ R/R AML patients (pts; Perl, et al. N Engl J Med. 2019). This follow up (FU) of the ADMIRAL trial assessed long-term (LT) survivors and gilteritinib safety beyond 1 year. Methods: A data cut was performed 1 year after the primary analysis. Response outcomes in LT survivors (OS ≥18 mo) in the gilteritinib arm, and safety during and after 12 mo of gilteritinib therapy were assessed. Results: At 1 year after the primar
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5

Ueno, Yoko, Masamichi Mori, Yoshiteru Kamiyama, Naoki Kaneko, Eriko Isshiki, and Masahiro Takeuchi. "Gilteritinib (ASP2215), a Novel FLT3/AXL Inhibitor: Preclinical Evaluation in Combination with Azacitidine in Acute Myeloid Leukemia." Blood 128, no. 22 (2016): 2830. http://dx.doi.org/10.1182/blood.v128.22.2830.2830.

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Abstract Background FMS-like tyrosine kinase 3 (FLT3) is one of the most frequently mutated genes in acute myeloid leukemia (AML). Activating mutations in FLT3 such as internal tandem duplications (ITD) at the juxtamembrane domain are present in approximately 25-30% of newly diagnosed AML cases. Patients with AML harboring the FLT3-ITD mutation have poorer prognosis following the current induction chemotherapy treatment of cytarabine (AraC) and an anthracycline (daunorubicin [DNR] or idarubicin [IDR]). Azacitidine (Aza) is a treatment option for AML patients who are not eligible for intensive
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6

Minden, Mark D., Jacob M. Rowe, Emmanuel Gyan, et al. "Abstract CT537: A phase 2, multicenter, randomized, double-blind trial of maintenance therapy with FLT3 inhibitor gilteritinib (ASP2215) in patients with FLT3/ITD AML (GOSSAMER study)." Cancer Research 82, no. 12_Supplement (2022): CT537. http://dx.doi.org/10.1158/1538-7445.am2022-ct537.

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Abstract Background: Patients with acute myeloid leukemia (AML) in remission are at high risk of relapse, warranting remission-prolonging therapy. Gilteritinib is the first FMS-like tyrosine kinase 3 (FLT3) inhibitor approved as monotherapy in FLT3-mutated relapsed/refractory AML. The aim of the study was to compare relapse-free survival (RFS) in patients with FLT3/internal tandem duplication AML in first complete remission who received gilteritinib or placebo. Method: In this phase 2, double-blind trial, patients were randomized 2:1 to gilteritinib (120 mg) or placebo once daily for up to 2 y
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7

Eid, Nibal, Jianlei Zhao, Jenna Thibodeau, et al. "Old Meets New: Hydroxyurea Synergistically Enhances the Antileukemic Activity of Gilteritinibagainst FLT3-ITD AML." Blood 144, Supplement 1 (2024): 5805. https://doi.org/10.1182/blood-2024-207855.

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About 25% of acute myeloid leukemia (AML) cases harbor FMS-like tyrosine kinase 3 (FLT3) internal tandem duplication (ITD) mutations which is associated with poor prognosis. Gilteritinib is a second generation FLT3 inhibitor approved for treating FLT3-mutated relapsed/refractory (R/R) AML patients. Monotherapy, while efficacious, shows short-lived responses, highlighting the need for combination therapies. Results from our preliminary studies show that ribonucleotide reductase (RNR), the rate-limiting enzyme in the biosynthesis of deoxynucleotides, is increased in a cytarabine (AraC)-resistant
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8

Zhang, Jian, Yang Xu, Shengli Xue, et al. "Efficacy and Safety of Gilteritinib-Based Therapy Combinated with Allo-HSCT in Relapsed or Refractory Acute Myeloid Leukemia Patients with Positive FLT3-ITD Mutation." Blood 144, Supplement 1 (2024): 6079. https://doi.org/10.1182/blood-2024-198895.

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Introduction In patients with relapsed or refractory acute myeloid leukemia (R/R AML), FMS-like tyrosine kinase 3 (FLT3) gene mutation portends a poorer prognosis and survival. Gilteritinib, as a novel type I inhibitor, is a kind of highly selective and potent FLT3 inhibitor. It has been recommended by NCCN and ESMO guidelines for the treatment of R/R AML patients with FLT3 gene mutation. The objective of this study is to evaluate the safety and efficacy of gilteritinib-based therapy combinated with allogeneic hematopoietic stem cell transplantation (allo-HSCT) for R/R AML patients with positi
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9

Garrison, Dominique A., Yan Jin, Zahra Talebi, et al. "Itraconazole-Induced Increases in Gilteritinib Exposure Are Mediated by CYP3A and OATP1B." Molecules 27, no. 20 (2022): 6815. http://dx.doi.org/10.3390/molecules27206815.

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Gilteritinib, an FDA-approved tyrosine kinase inhibitor approved for the treatment of relapsed/refractory FLT3-mutated acute myeloid leukemia, is primarily eliminated via CYP3A4-mediated metabolism, a pathway that is sensitive to the co-administration of known CYP3A4 inhibitors, such as itraconazole. However, the precise mechanism by which itraconazole and other CYP3A-modulating drugs affect the absorption and disposition of gilteritinib remains unclear. In the present investigation, we demonstrate that pretreatment with itraconazole is associated with a significant increase in the systemic ex
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10

Errasti, Gauthier, Thomas Delacroix, Kalpana Ghoshal, Robert Lee, Anisha Ghosh, and Raj Chakrabarti. "Novel potent and selective inhibitors targeting FLT3 for AML therapy." Journal of Clinical Oncology 43, no. 16_suppl (2025): 6542. https://doi.org/10.1200/jco.2025.43.16_suppl.6542.

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6542 Background: Acute Myeloid Leukemia (AML) is a malignancy frequently driven by mutations in the FMS-like tyrosine kinase 3 (FLT3) gene. The FLT3 internal tandem duplication (ITD) and tyrosine kinase domain (TKD) mutations, particularly D835 and F691, appear in approximately 30% of AML patients, often leading to poor prognosis and resistance to existing therapies. Gilteritinib and Quizartinib are two FDA-approved FLT3 inhibitors, with the former approved only for relapsed/refractory AML and the latter approved only for newly diagnosed AML. Quizartinib does not target TKD resistance mutation
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11

Cortes, Jorge E., Jessica Altman, Ellen K. Ritchie, et al. "A phase II/III, multicenter, open-label, 3-arm study of gilteritinib, gilteritinib plus azacitidine, or azacitidine alone in the treatment of newly diagnosed FLT3 mutation-positive acute myeloid leukemia (AML) patients ineligible for intensive induction chemotherapy." Journal of Clinical Oncology 35, no. 15_suppl (2017): TPS7068. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.tps7068.

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TPS7068 Background: Gilteritinib, a highly selective, potent FLT3/AXL inhibitor, showed antileukemic activity with favorable tolerability in a Phase 1/2 trial of FLT3 mutation-positive (FLT3mut+) relapsed/refractory AML. In FLT3mut+ AML cell lines, gilteritinib plus azacitidine (AZA) inhibited growth, and induced apoptosis and differentiation. This ongoing Phase 2/3 trial will examine the efficacy, safety, and tolerability of gilteritinib alone, gilteritinib plus AZA or AZA alone in newly diagnosed FLT3mut+AML patients ineligible for intensive induction chemotherapy. Methods: This open-label,
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12

Tarver, Theodore C., Jason E. Hill, Leena Rahmat, et al. "Gilteritinib is a clinically active FLT3 inhibitor with broad activity against FLT3 kinase domain mutations." Blood Advances 4, no. 3 (2020): 514–24. http://dx.doi.org/10.1182/bloodadvances.2019000919.

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Abstract Gilteritinib is the first FMS-like tyrosine kinase 3 (FLT3) tyrosine kinase inhibitor (TKI) approved as monotherapy in acute myeloid leukemia with FLT3 internal tandem duplication and D835/I836 tyrosine kinase domain (TKD) mutations. Sequencing studies in patients have uncovered less common, noncanonical (NC) mutations in FLT3 and have implicated secondary TKD mutations in FLT3 TKI resistance. We report that gilteritinib is active against FLT3 NC and TKI resistance-causing mutations in vitro. A mutagenesis screen identified FLT3 F691L, Y693C/N, and G697S as mutations that confer moder
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13

Katta, Sreenivasa Rao, Immani Ramachandra Rao, P. Punitha, and Thota Siva prasad. "LC-MS/MS characterization of stress degradation products of Gilteritinib and establishment of HPLC method for analysis of process related impurities of Gilteritinib." Journal of Applied Pharmaceutical Research 12, no. 2 (2024): 109–23. http://dx.doi.org/10.18231/j.joapr.2024.12.2.109.123.

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Background: The current investigation entails the characterization of seven degradation products (DPs) formed in different stress conditions of gilteritinib employing liquid chromatography-tandem mass spectrometry (LC-MS/MS). Methodology: This study developed a stability-indicating reversed-phase high-performance liquid chromatographic (HPLC) method for precisely determining gilteritinib in the presence of its process-related impurities in bulk drug and formulation samples. To explore the stability profile of gilteritinib, it was exposed to forced degradation experiments conducted under variou
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14

Greco, Rosa, Silvia Imbergamo, Elisabetta Pierdomenico, et al. "Italian Real-World Experience of Gilteritinib Monotherapy in Patients with Relapsed/Refractory FLT3-Mutated Acute Myeloid Leukemia: Preliminary Results." Blood 144, Supplement 1 (2024): 5188. https://doi.org/10.1182/blood-2024-205427.

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Background The FMS-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD) mutation is associated with a poor prognosis in patients with acute myeloid leukemia (AML). Gilteritinib, an oral FLT3 inhibitor, is the first approved monotherapy for relapsed or refractory (R/R) FLT3-mutated AML, demonstrating a survival benefit. The ADMIRAL phase 3 trial showed that gilteritinib monotherapy was superior to standard treatments, including intensive or non-intensive chemotherapy and hypomethylating therapy with azacitidine. However, real-world data on the efficacy and safety of gilteritinib in cli
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15

Diller, Elizabeth, and Janelle E. Mann. "Gilteritinib (Xospata®)." Oncology Times 41, no. 4 (2019): 14. http://dx.doi.org/10.1097/01.cot.0000553980.60791.5c.

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16

Knight, Tristan, Xinan Qiao, Jun Ma, et al. "The Combination of CUDC-907 and Gilteritinib Shows Promising Antileukemic Activity in Vitro and In Vivo in Preclinical Models of FLT3-ITD AML." Blood 134, Supplement_1 (2019): 1262. http://dx.doi.org/10.1182/blood-2019-123793.

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Introduction FMS-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD) mutations are found in approximately one quarter of acute myeloid leukemia (AML) cases. Its presence results in constitutive activation of the FLT3 receptor tyrosine kinase and its downstream growth/pro-survival pathways including MAPK/ERK, PI3K/AKT, and JAK/STAT, and confers a poor prognosis. Gilteritinib is a selective inhibitor of FLT3 recently approved by the Food and Drug Administration for treatment of patients with relapsed/refractory AML and a FLT3 mutation. However, gilteritinib exposure induces upregulatio
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17

Niswander, Lisa M., Samantha McClellan, Diego Alberto Barcenas-Lopez, et al. "Gilteritinib Augments Preclinical FLT3 and CD19 CAR T Cell Immunotherapy in High-Risk Pediatric Leukemias." Blood 144, Supplement 1 (2024): 370. https://doi.org/10.1182/blood-2024-206467.

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Background: Despite impressive remission induction rates achieved with CD19 CAR T cells (CD19CART) in pediatric patients with relapsed/refractory B-ALL, long-term CD19-positive and CD19-negative relapse risk remains approximately 50%. We recently established potent preclinical efficacy of FLT3-directed CAR T cells (FLT3CART) against FLT3-mutant AML and KMT2A-rearranged (KMT2A-R) ALL, two high-risk pediatric leukemias characterized by activated intracellular FLT3 kinase signaling and/or high FLT3 cell surface expression (Niswander Haematologica 2023). We tested a dual FLT3 targeting strategy co
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18

Peretz, Cheryl A. C., Elaine Tran, Bogdan Popescu, et al. "Threshold Attenuation of Perk Signaling Is Sufficient to Overcome RAS-Mediated FLT3 Inhibitor Resistance." Blood 142, Supplement 1 (2023): 4171. http://dx.doi.org/10.1182/blood-2023-182426.

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Introduction Acute myeloid leukemia (AML) with activation of FMS-related receptor tyrosine kinase 3 ( FLT3) confers a poor prognosis, principally due to disease relapse. The FLT3 inhibitor (FLT3i) gilteritinib is standard of care in relapsed/refractory FLT3-mutant AML, however its efficacy is limited by drug resistance, primarily due to RAS mutations. This suggests that RAS signaling is the critical mediator of downstream FLT3 signaling, but there is no standardized treatment for patients who relapse on FLT3i due to RAS pathway activation. Efforts to overcome resistance have been limited both
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19

Buzzatti, Elisa, Francesco Marchesi, Federica Lessi, et al. "Real-Life Study on Gilteritinib Related Infections (GilteRInf): An Italian Seifem Study." Blood 144, Supplement 1 (2024): 5970. https://doi.org/10.1182/blood-2024-198445.

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Background. Refractory/relapsed (R/R) acute myeloid leukemia (AML) patients (pts) have a poor prognosis with standard chemotherapy, even worsened by the occurrence of infections due to persistent neutropenia. In patients with R/R FLT3-mutated AML, ADMIRAL trial demonstrated Gilteritinib's superiority over chemotherapy in terms of overall survival (OS), with a good safety profile. Given the recent approval, real-life experiences in the management and outcome of infectious complications are lacking, especially regarding invasive fungal diseases (IFD), since azoles are known for their interaction
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Zhu, Ruiqi, Li Li, Bao Nguyen, Amy S. Duffield, and Donald Small. "Gilteritinib and Venetoclax Synergize to Eliminate FLT3/ITD+ Leukemia Cells through BIM." Blood 134, Supplement_1 (2019): 2564. http://dx.doi.org/10.1182/blood-2019-131635.

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Gilteritinib and Venetoclax synergize to eliminate FLT3/ITD+ leukemia cells through BIM Abstract Acute myeloid leukemia (AML) is characterized by a clonal proliferation of immature myeloid cells in the bone marrow or other tissues. The most commonly mutated gene in AML is FMS-like tyrosine kinase (FLT3). FLT3 downstream signaling pathways include PI3K/AKT, STAT5 and MAPK, which affect apoptosis, differentiation and cell proliferation. An internal tandem duplication mutation in FLT3 (FLT3/ITD) is identified in approximately 25% of patients with AML, and this mutation is associated with a partic
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21

Izumi, Shintaro, Yosuke Minami, Shinichi Masuda, Yoshikazu Utsu, Emiko Sakaida, and Nobuyuki Aotsuka. "Emergence of Natural Killer Cell Large Granular Lymphocytes during Gilteritinib Treatment in Acute Myeloid Leukemia with FLT3-ITD Mutation." Reports—Medical Cases, Images, and Videos 3, no. 3 (2020): 25. http://dx.doi.org/10.3390/reports3030025.

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As the potent, selective Fms-Like Tyrosine Kinase 3 (FLT3) inhibitor gilteritinib has only been approved for use for a few years, its efficacy and complications remain incompletely understood. We herein report an elderly patient with FLT3 internal tandem duplications (FLT3-ITD) mutated acute myeloid leukemia (AML) who developed natural killer cell large granular lymphocytes (NK-LGL) in the bone marrow and peripheral blood during gilteritinib treatment. Case: A 79-year-old Japanese female had been diagnosed with FLT3-ITD-mutated AML. The patient received hydroxycarbamide 2000 mg daily for induc
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22

Molica, Matteo, Salvatore Perrone, and Marco Rossi. "Gilteritinib: The Story of a Proceeding Success into Hard-to-Treat FLT3-Mutated AML Patients." Journal of Clinical Medicine 12, no. 11 (2023): 3647. http://dx.doi.org/10.3390/jcm12113647.

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The traditionally dismal outcome of acute myeloid leukemia (AML) patients carrying the FMS-related tyrosine kinase 3 (FLT3) mutations has been mitigated by the recent introduction of tyrosine kinase inhibitors (TKI) into clinics, such as midostaurin and gilteritinib. The present work summarizes the clinical data that led to the use of gilteritinib in clinical practice. Gilteritinib is a second-generation TKI with deeper single-agent activity than first-generation drugs against both FLT3FLT3–ITD and TKD mutations in human studies. Moreover, the phase I/II dose-escalation, dose-expansion Chrysal
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23

Smith, Catherine C., Mark J. Levis, Alexander E. Perl, Jason E. Hill, Matt Rosales, and Erkut Bahceci. "Molecular profile of FLT3-mutated relapsed/refractory patients with AML in the phase 3 ADMIRAL study of gilteritinib." Blood Advances 6, no. 7 (2022): 2144–55. http://dx.doi.org/10.1182/bloodadvances.2021006489.

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Abstract The phase 3 Study of ASP2215 Versus Salvage Chemotherapy in Patients With Relapsed or Refractory Acute Myeloid Leukemia (AML) With FMS-like Tyrosine Kinase (FLT3) Mutation (ADMIRAL) trial demonstrated the superiority of the FLT3 inhibitor, gilteritinib, to salvage chemotherapy (SC) in patients with FLT3-mutated relapsed or refractory (R/R) AML. Baseline comutations, FLT3-internal tandem duplication (ITD) allelic ratio and length, and treatment-emergent mutations were analyzed in patients in the ADMIRAL trial. Baseline comutations were grouped according to gene subgroups (DNA methylati
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24

Knight, Tristan, Xinan Qiao, Holly Edwards, Hai Lin, Jeffrey W. Taub, and Yubin Ge. "Novel Therapy for FLT3-ITD Acute Myeloid Leukemia Utilizing the Combination of CUDC-907 and Gilteritinib." Blood 132, Supplement 1 (2018): 1427. http://dx.doi.org/10.1182/blood-2018-99-111177.

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Abstract Introduction: FMS-like tyrosine kinase 3 (FLT3) is a receptor tyrosine kinase, and is mutated in approximately one third of acute myeloid leukemia (AML) patients; this mutation confers a poor prognosis. Two FLT3 mutations are commonly seen in AML: internal tandem duplications (ITD) in the juxtamembrane domain (~25% of AML), and point mutations in the receptor tyrosine kinase at codon 835 (D835) (~7% of AML). Both mutations result in constitutive FLT3 activation, causing downstream activation of multiple pathways, in particular, those involved in cell survival including the RAS-RAF-MEK
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25

Joshi, Sunil K., Janét Pittsenbarger, Xiaolin Luo, et al. "Abstract B019: ASO-mediated NRAS knockdown overcomes gilteritinib late resistance in FLT3-AML." Molecular Cancer Research 21, no. 5_Supplement (2023): B019. http://dx.doi.org/10.1158/1557-3125.ras23-b019.

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Abstract The internal tandem duplication of the FLT3 receptor (FLT3-ITD) leads to constitutive receptor activation and is one of the most common mutations (~30%) in acute myeloid leukemia (AML), resulting in poor prognosis. Multiple FLT3 inhibitors (FLT3i) have been developed, including the potent FDA-approved FLT3i, gilteritinib. However, AML patients only respond to gilteritinib for approximately 6 months due to the emergence of drug resistance. Through an approach that integrated genomic, metabolomic, proteomic, and phosphoproteomic analyses with complementary genetic and pharmacologic scre
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26

Wang, Jianxiang, Bin Jiang, Jian Li, et al. "Gilteritinib Versus Salvage Chemotherapy for Relapsed/Refractory FLT3-Mutated Acute Myeloid Leukemia: A Phase 3, Randomized, Multicenter, Open-Label Trial in Asia." Blood 138, Supplement 1 (2021): 695. http://dx.doi.org/10.1182/blood-2021-145436.

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Abstract Background: Due to poor prognosis, treatment options for patients with FLT3-mutated (FLT3mut+) acute myeloid leukemia (AML) who are refractory to therapy or have relapsed (R/R) are needed globally. Gilteritinib is approved in multiple countries, including Japan, and has recently received conditional approval in China for the treatment of R/R FLT3mut+ AML; in the phase 3 ADMIRAL trial, superior survival benefit and a favorable safety profile were shown for patients receiving gilteritinib compared to those receiving salvage chemotherapy (SC) (HR 0.64 [95% CI: 0.49, 0.83]; P<0.001
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27

Huang, R. J., Z. Y. Jiang, and K. Lin. "A study of the synthetic route and resistance of gilteritinib." Theoretical and Natural Science 15, no. 1 (2023): 255–62. http://dx.doi.org/10.54254/2753-8818/15/20240495.

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Gilteritinib is used to treat acute myeloid leukemia (AML) carrying FMS-like tyrosine kinase 3 (FLT3) mutations. As it is a new drug, there are still many aspects that need improvement. This article will be written according to the following three points: Analysis of its mechanism of action with the receptor; Analysis of the three main synthetic routes of gilteritinib and reasonable suggestions are given; Causes and solutions to the emergence of drug resistance. The following 4 points have been found that:(1) FLT3-internal tandem duplication (ITD) mutation and FLT3-tyrosine kinase domain (TKD)
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28

Martin, Leenus, Roopal Patel, Jingchuan Zhang, et al. "Abstract 3345: ERAS-601, a potent inhibitor of SHP2, synergistically enhances the activity of a FLT3 inhibitor, gilteritinib, in FLT3-mutated AML tumor models." Cancer Research 82, no. 12_Supplement (2022): 3345. http://dx.doi.org/10.1158/1538-7445.am2022-3345.

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Abstract ERAS-601 is a potent, small molecule allosteric inhibitor of wildtype SHP2, a non-receptor protein tyrosine phosphatase (PTP) encoded by the PTPN11 gene. ERAS-601 inhibits wildtype SHP2 biochemically with an IC50 of 4.6 nM and demonstrates selectivity across panels of 300 kinases and 12 phosphatases. SHP2 mediates upstream receptor tyrosine kinase (RTK) signaling via its phosphatase-mediated regulation of guanine nucleotide exchange factors (GEFs). ERAS-601 inhibits the SHP2 dependent cycling of KRAS from the inactive GDP-bound state to the active GTP-bound state and demonstrates anti
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29

McMahon, Christine M., Jonathan Canaani, Bryan Rea, et al. "Gilteritinib induces differentiation in relapsed and refractory FLT3-mutated acute myeloid leukemia." Blood Advances 3, no. 10 (2019): 1581–85. http://dx.doi.org/10.1182/bloodadvances.2018029496.

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Key Points Gilteritinib induces 2 distinct marrow responses in FLT3-mutated AML: responses with and without differentiation. Ongoing clonal hematopoiesis is ubiquitous during gilteritinib therapy and may promote genetic evolution and drug resistance.
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30

Zeidan, Amer M., Adrienne M. Gilligan, Santosh Gautam, et al. "Streamline - Retrospective Cohort Study of Relapsed or Refractory (R/R) FLT3-Mutated Acute Myeloid Leukemia (AML): Real-World Treatment, Testing Patterns, and Outcomes." Blood 136, Supplement 1 (2020): 30–31. http://dx.doi.org/10.1182/blood-2020-136366.

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Introduction: The past decade in AML research has led to increased emphasis on disease-related mutations and associated targeted therapies. FMS-like tyrosine kinase 3 (FLT3) mutations (FLT3+) are found in about 30% of AML patients and confer a poorer prognosis. Also, the availability of targeted therapies increases the value of testing for FLT3+ AML. A paucity of data exists regarding the real-world FLT3 testing rates in AML patients in both the newly diagnosed and R/R settings. As the treatment landscape for patients with R/R FLT3+ AML expands, it is important to understand how utilization of
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31

Grinblatt, David L., Wei Han, David Nimke, Qi Feng, Loretta Sullivan, and Bhavik J. Pandya. "Real-World Use of FLT3 Tyrosine Kinase Inhibitors in Patients with Relapsed/Refractory FLT3 mutation-Positive Acute Myeloid Leukemia in the United States." Blood 138, Supplement 1 (2021): 5033. http://dx.doi.org/10.1182/blood-2021-145387.

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Abstract Background: FLT3 tyrosine kinase inhibitors (TKIs) have improved outcomes in clinical trials for patients with FLT3 mutation-positive acute myeloid leukemia (FLT3mut+ AML). Gilteritinib is the first FDA-approved (11/28/2018) targeted therapy for relapsed/refractory (R/R) FLT3mut+ AML in adults, although two other multikinase inhibitors, midostaurin and sorafenib, are used off-label in this population. This analysis characterized treatment duration for these three drugs in R/R FLT3mut+ AML, as little is known about the treatment of patients receiving a FLT3 inhibitor in the real world.
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Murray, Graeme, Ian Michael Bouligny, Tilak Patel, et al. "Gilteritinib or venetoclax in relapsed or refractory FLT3mut acute myeloid leukemia." Journal of Clinical Oncology 41, no. 16_suppl (2023): e19046-e19046. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.e19046.

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e19046 Background: FLT3 mutations in AML are associated with high relapse rates and shorter survival compared to FLT3 wild-type. After intensive chemotherapy (IC) failure, clinicians can choose between several salvage regimens; however, the optimal therapy sequence remains unclear. This study compares two salvage therapies: gilteritinib or venetoclax and a hypomethylating agent (HMA; decitabine or azacitidine). Methods: We retrospectively analyzed 129 patients with AML and mutated FLT3-ITD or FLT3-TKD. We identified those that failed first-line IC (CPX-351 or conventional 7+3 with or without m
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Leifheit, Malia E., Gunnar Johnson, Timothy M. Kuzel, et al. "Enhancing Therapeutic Efficacy of FLT3 Inhibitors with Combination Therapy for Treatment of Acute Myeloid Leukemia." International Journal of Molecular Sciences 25, no. 17 (2024): 9448. http://dx.doi.org/10.3390/ijms25179448.

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FMS-like tyrosine kinase 3 (FLT3) mutations are genetic changes found in approximately thirty percent of patients with acute myeloid leukemia (AML). FLT3 mutations in AML represent a challenging clinical scenario characterized by a high rate of relapse, even after allogeneic hematopoietic stem cell transplantation (allo-HSCT). The advent of FLT3 tyrosine kinase inhibitors (TKIs), such as midostaurin and gilteritinib, has shown promise in achieving complete remission. However, a substantial proportion of patients still experience relapse following TKI treatment, necessitating innovative therape
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Pandya, Bhavik J., Cynthia Z. Qi, Hongbo Yang, Andy Garnham, Manasee V. Shah, and Amer M. Zeidan. "Comparison of Gilteritinib and Salvage Chemotherapy in FLT3-Mutated Acute Myeloid Leukemia on the Number Needed to Treat for Various Clinical Outcomes: A Secondary Analysis of the Admiral Trial." Blood 136, Supplement 1 (2020): 7. http://dx.doi.org/10.1182/blood-2020-136184.

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Introduction/background: FMS-like receptor tyrosine kinase-3 (FLT3) mutations are common in acute myeloid leukemia (AML) and are associated with poor prognosis. Historically, patients with relapsed/refractory (R/R) FLT3 mutation-positive (FLT3mut+) AML experienced dismal survival outcomes. Gilteritinib, a highly potent and selective FLT3 inhibitor, was recently approved as the first targeted therapy for patients with R/R FLT3mut+ AML, and has the potential to bring significant clinical benefits to these patients. The randomized, phase 3 ADMIRAL trial (NCT02421939; Perl, et al. 2019) was the fi
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Carvajal, Luis A., Michael R. McKeown, Tressa Hood, Linlin Guo, Charles Y. Lin, and Jorge F. DiMartino. "The Combination of Lanraplenib, a Selective SYK Inhibitor, and Gilteritinib, a FLT3 Inhibitor, Targets Aberrant Proliferation and Differentiation Blockade in Acute Myeloid Leukemia." Blood 142, Supplement 1 (2023): 5951. http://dx.doi.org/10.1182/blood-2023-186605.

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Background: Acute myeloid leukemia (AML) is an aggressive disease characterized by uncontrolled clonal proliferation of poorly differentiated myeloid progenitor cells in the bone marrow and blood. Deregulated spleen tyrosine kinase (SYK) impairs myeloid differentiation and has been implicated in the pathogenesis of AML driven by FMS-like tyrosine kinase 3 (FLT3) internal tandem duplication (ITD) mutation (FLT3-ITD). While SYK is rarely mutated, it is highly activated in FLT3-ITD-mutated AML and directly phosphorylates FLT3-ITD, resulting in aberrant expression of multiple oncogenic pathways. L
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Buelow, Daelynn R., Bhavana Bhatnagar, Jae Yoon Jeon, et al. "High-Dimensional Analysis Identifies Mechanisms of Gilteritinib Resistance in FLT3-Mutated AML." Blood 138, Supplement 1 (2021): 207. http://dx.doi.org/10.1182/blood-2021-148569.

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Abstract While clinical benefit has been observed with gilteritinib in patients with FLT3 mutated relapsed/refractory acute myeloid leukemia (AML), most patients relapse through mechanisms that are incompletely understood. In this study, to investigate mechanisms of gilteritinib sensitivity and resistance, we performed targeted sequencing (21 patients) and scRNASeq analysis (8 patients) of FLT3-ITD-positive AML samples obtained before and during treatment. Before treatment, co-occurring mutations were observed in 33 genes among 21 patients. Mutations in RAS pathway genes (PTPN11, KRAS, NRAS, C
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37

Thawani, Rajat, Clare Keddy, Matteo Repetto, et al. "Abstract C148: Type II ROS1 inhibitors and their liability on ROS1 rearranged non-small cell lung cancer with L2086F mutation." Molecular Cancer Therapeutics 22, no. 12_Supplement (2023): C148. http://dx.doi.org/10.1158/1535-7163.targ-23-c148.

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Abstract Introduction: Fusion oncoproteins involving the ROS1 receptor tyrosine kinase have been established as validated therapeutic targets in non-small cell lung cancer. FDA-approved ROS1 tyrosine kinase inhibitors (TKIs) such as crizotinib and entrectinib have shown substantial response rates in these patients, leading to improved outcomes. Historically, the solvent-front ROS1 kinase mutation, G2032R, was a recurrent resistance liability to first generation ROS1 TKI. Next-generation TKIs, including NVL-520, repotrectinib, and taletrectinib are active against the ROS1 G2032R and shown activ
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38

Niswander, Lisa M., Zachary Graff, Asen Bagashev, Lillie Leach, Terry J. Fry, and Sarah K. Tasian. "Multi-Modal Targeting of FLT3 with Chimeric Antigen Receptor T Cell Immunotherapy and Tyrosine Kinase Inhibition in High-Risk Pediatric Leukemias." Blood 138, Supplement 1 (2021): 404. http://dx.doi.org/10.1182/blood-2021-147321.

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Abstract Background: Clinical outcomes for children with FLT3-mutant AML and infants with KMT2A-rearranged (KMT2A-R) B-ALL remain dismal. These leukemias share a common feature of aberrant activation of FLT3 kinase signaling, which occurs by activating FLT3 mutations in AML and by overexpression of wild-type FLT3 in KMT2A-R ALL. Several FLT3 tyrosine kinase inhibitors (FLT3i) are approved for adults with FLT3-mutant AML, but potential efficacy against KMT2A-R ALL remains incompletely characterized and may differ from responses in AML. We previously developed and preclinically validated chimeri
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39

James, Sophie C., Samantha Atkinson, Richard Burt, Cristina Lo Celso, and Paolo Gallipoli. "Specific Bone Marrow Niche Components Determine Degree of Protection from Gilteritinib Induced Differentiation Response in FLT3-ITD AML." Blood 144, Supplement 1 (2024): 4152. https://doi.org/10.1182/blood-2024-205582.

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Background:the FLT3 tyrosine kinase inhibitor (TKI) gilteritinib relieves the differentiation blockade in around 50% of acute myeloid leukaemia (AML) patients carrying FLT3 internal tandem duplication (ITD) mutations. However, differentiation responses are often incomplete and are poorly understood. This limited understanding is partly due to the strong cytotoxic effects seen with gilteritinib in cellular in vitro models and suggests that the in vivo bone marrow microenvironment (BMM) plays roles in modulating the differentiation response. Recent evidence suggests that the BMM induces changes
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40

Perl, Alexander E., Qiaoyang Lu, Alan Fan, Nahla Hasabou, Erhan Berrak, and Ramon V. Tiu. "Clinical Outcomes Following Treatment with Gilteritinib or Quizartinib in Patients with Relapsed/Refractory FLT3-ITD+ Acute Myeloid Leukemia." Blood 136, Supplement 1 (2020): 42–43. http://dx.doi.org/10.1182/blood-2020-136118.

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Background: Gilteritinib is approved for patients (pts) with relapsed/refractory (R/R) FLT3-mutated acute myeloid leukemia (AML), based on findings from the phase 3 ADMIRAL trial (Perl AE, et al. N Engl J Med. 2019). A phase 3 trial, QuANTUM-R, demonstrated the benefit of quizartinib in pts with R/R AML with FLT3 internal tandem duplication (FLT3-ITD) mutations (Cortes JE, et al. Lancet Oncol. 2019). Although eligibility criteria across both studies were similar, QuANTUM-R was more stringent as to prior therapy intensity and remission duration, which potentially enriched for higher-risk pts. W
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41

Dhillon, Sohita. "Gilteritinib: First Global Approval." Drugs 79, no. 3 (2019): 331–39. http://dx.doi.org/10.1007/s40265-019-1062-3.

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42

"Gilteritinib." Reactions Weekly 1839, no. 1 (2021): 147. http://dx.doi.org/10.1007/s40278-021-89985-2.

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"Gilteritinib." Reactions Weekly 1878, no. 1 (2021): 253. http://dx.doi.org/10.1007/s40278-021-04223-4.

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"Gilteritinib." Reactions Weekly 1868, no. 1 (2021): 204. http://dx.doi.org/10.1007/s40278-021-00661-4.

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"Gilteritinib." Reactions Weekly 1897, no. 1 (2022): 184. http://dx.doi.org/10.1007/s40278-022-11421-0.

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"Gilteritinib." Reactions Weekly 1873, no. 1 (2021): 120. http://dx.doi.org/10.1007/s40278-021-02543-2.

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"Gilteritinib." Reactions Weekly 1896, no. 1 (2022): 220. http://dx.doi.org/10.1007/s40278-022-11011-9.

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"Gilteritinib." Reactions Weekly 1824, no. 1 (2020): 141. http://dx.doi.org/10.1007/s40278-020-84109-7.

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"Gilteritinib." Reactions Weekly 1768, no. 1 (2019): 168. http://dx.doi.org/10.1007/s40278-019-66852-3.

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"Gilteritinib." Reactions Weekly 1819, no. 1 (2020): 131. http://dx.doi.org/10.1007/s40278-020-82674-9.

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