ArticleBlood advances2020
Gilteritinib is a clinically active FLT3 inhibitor with broad activity against FLT3 kinase domain mutations.
Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 76 citations in OpenAlex.
- Azacitidine, Venetoclax, and Gilteritinib in Newly Diagnosed and Relapsed or RefractoryJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024Trial
- FDA Approval Summary: Gilteritinib for Relapsed or Refractory Acute Myeloid Leukemia with aClinical cancer research : an official journal of the American Association for Cancer Research · 2021Trial
- PHI-101: a novel FLT3 inhibitor with potent activity against the F691L gatekeeper resistance mutation.Leukemia · 2026Article
- Dynamic genetic and nongenetic RAS-pathway activation drives resistance to FLT3 and BCL2 inhibitor therapy.Blood · 2026Article
- The type I FLT3 inhibitor XL999 overrides secondary FLT3-ITD mutations that arise under gilteritinib and quizartinib treatment in acute myeloid leukemia.Molecular biomedicine · 2026Article
- A New Paradigm for Pediatric AML: Improving the Pipeline for Treatments Targeting Cytogenetic and Molecular Alterations.Cancers · 2026Review
- Targeting oncogenic FLT3 uncovers a ferroptosis vulnerability through selenocysteine recoding in acute myeloid leukaemia.Nature cell biology · 2026Article
- Review
- FLT3 as a germ line driver in AML: expanding the landscape of leukemia predisposition.Blood neoplasia · 2026Article
- Homoharringtonine and Gilteritinib Synergistically Induce Apoptosis and Suppress Viability in FLT3-ITD-Positive AML Cells.Biomedicines · 2026Article
- Acute Myeloid Leukemia With a Non-CanonicalJournal of medical cases · 2026Article
- The Novel Diketopiperazine Derivative, Compound 5-3, Selectively Inhibited the Proliferation of FLT3-ITD Mutant Acute Myeloid Leukemia (AML) Cells.Marine drugs · 2025Article
- Decursin induces FLT3-ITD acute myeloid leukemia cell apoptosis by increasing the expression of the ubiquitin-conjugase UBE2L6.Cell communication and signaling : CCS · 2025Article
- Anti-Tumor Effects of Gilteritinib onOncoTargets and therapy · 2025Article
- Article
- Efficacy and safety of second‑generation FLT3 inhibitors in acute myeloid leukemia: A systematic review and meta‑analysis of randomized controlled trials.Molecular and clinical oncology · 2024Article
- FLT3 targeting in the modern era: from clonal selection to combination therapies.International journal of hematology · 2024Review
- Structure-Based Optimization of Pyrazinamide-Containing Macrocyclic Derivatives as Fms-like Tyrosine Kinase 3 (FLT3) Inhibitors to Overcome Clinical Mutations.ACS pharmacology & translational science · 2024Article
- Foretinib Is Effective in Acute Myeloid Leukemia by Inhibiting FLT3 and Overcoming Secondary Mutations That Drive Resistance to Quizartinib and Gilteritinib.Cancer research · 2024Article
- Progress in the study of autophagy-related proteins affecting resistance to chemotherapeutic drugs in leukemia.Frontiers in cell and developmental biology · 2024Review
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
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 moderate resistance to gilteritinib in vitro. Analysis of patients treated with gilteritinib revealed that 2/9 patients with preexisting NC FLT3 mutations responded and that secondary TKD mutations are acquired in a minority (5/31) of patients treated with gilteritinib. Four of 5 patients developed F691L mutations (all treated at <200 mg). These studies suggest that gilteritinib has broad activity against FLT3 mutations and limited vulnerability to resistance-causing FLT3 TKD mutations, particularly when used at higher doses.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.