Relevant bibliographies by topics / Gilteritinib

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  1. Journal articles
  2. Dissertations / Theses
  3. Conference papers

Academic literature on the topic 'Gilteritinib'

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

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Journal articles on the topic "Gilteritinib"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Gilteritinib"

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Novotná, Kateřina. "Interakce gilteritinibu s transportéry OCT1 a OCT2; vztah ke konvenční terapii akutní myeloidní leukémie." Master's thesis, 2021. http://www.nusl.cz/ntk/nusl-446641.

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Univerzita Karlova Farmaceutická fakulta v Hradci Králové Katedra Farmakologie a toxikologie Student: Kateřina Novotná Supervisor: doc. PharmDr. Martina Čečková, Ph.D. Title of diploma thesis: Interaction of gilteritinib with OCT1 and OCT2 transporters; relation to conventional therapy of acute myeloid leukemia. Gilteritinib is one of the recently approved drugs which is primarily used in the treatment of relapsed/refractory acute myeloid leukemia (AML) with mutated FMS-like tyrosine kinase 3 (FLT3) receptor. In this project, gilteritinib was investigated in terms of its ability to interact wi
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Conference papers on the topic "Gilteritinib"

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Joshi, Sunil K., Tamilla Nechiporuk, Daniel Bottomly, et al. "Abstract LT022: The AML microenvironment catalyzes a step-wise evolution to gilteritinib resistance." In Abstracts: AACR Virtual Special Conference: The Evolving Tumor Microenvironment in Cancer Progression: Mechanisms and Emerging Therapeutic Opportunities; in association with the Tumor Microenvironment (TME) Working Group; January 11-12, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.tme21-lt022.

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van den Heuvel, Robert. "MRD-positive patients with FLT3-ITD AML may benefit from post-transplant gilteritinib." In EHA2023 Hybrid Congress, edited by Gert Ossenkoppele. Medicom Medical Publishers, 2023. http://dx.doi.org/10.55788/04292040.

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Stromatt, Jack C., Daelynn R. Buelow, Shelly J. Orwick, et al. "Characterization of microenvironmental-mediated gilteritinib resistance in Acute Myeloid Leukemia using a Bmx knockout mouse model." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.208400.

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Chen, Xiaoyue, Sean Caenepeel, Brian Belmontes, et al. "Abstract 1050: Efficacy of AMG 176 in combination with gilteritinib in preclinical models of acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1050.

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Joshi, Sunil K., Stephen Christy, Renata Scopim Ribeiro, et al. "Abstract 926: Extrinsic and intrinsic activation of RAS/MAPK signaling enables resistance to FLT3 inhibitor, gilteritinib, in acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-926.

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Joshi, Sunil K., Stephen Christy, Renata Scopim Ribeiro, et al. "Abstract 926: Extrinsic and intrinsic activation of RAS/MAPK signaling enables resistance to FLT3 inhibitor, gilteritinib, in acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-926.

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Viswanadha, Srikant, Satyanarayana Eleswarapu, Kumar V. Penmetsa, and Swaroop Vakkalanka. "Abstract C044: RP7214, a small molecule inhibitor of dihydroorotate dehydrogenase (DHODH), potentiates activity of Gilteritinib and Cytarabine in preclinical models of AML." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-c044.

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Li, Na, Vivek Mahajan, Lindsay Butler, et al. "Abstract 2933: Inhibition of FLT3 and AXL by gilteritinib controls systemic tumor growth in luciferase-transduced MV-4-11 acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2933.

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Viswanadha, Srikant, Satyanarayana Eleswarapu, Kumar V. Penmetsa, and Swaroop Vakkalanka. "Abstract C045: RP4010, a small molecule inhibitor of Store-Operated Calcium Entry (SOCE), potentiates activity of Gilteritinib and Cytarabine in preclinical models of AML." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-c045.

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Perl, Alexander E., Giovanni Martinelli, Jorge E. Cortes, et al. "Abstract CT184: Gilteritinib significantly prolongs overall survival in patients withFLT3-mutated (FLT3mut+) relapsed/refractory (R/R) acute myeloid leukemia (AML): Results from the Phase III ADMIRAL trial." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-ct184.

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