ArticleMolecular cancer therapeutics2022
The Irreversible FLT3 Inhibitor FF-10101 Is Active Against a Diversity of FLT3 Inhibitor Resistance Mechanisms.
Article in Molecular cancer therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Review
- The new era of AML therapy: current standards and emerging targets.International journal of clinical oncology · 2026Review
- Medicinal Insights Into FLT3 Inhibitors as Anticancer Agents: Current Status and Future Direction.Archiv der Pharmazie · 2026Review
- New selective and allosteric FLT3 inhibitors show efficacy against resistant acute myeloid leukemia cells.iScience · 2026Article
- Resistance to Targeted Therapy in AML: Current Challenges and Emerging Treatment Strategies.Journal of clinical medicine · 2026Review
- Current Status of Molecularly Targeted Therapeutics in Blood Cancers.International journal of molecular sciences · 2025Review
- Current Therapeutic Strategies for FLT3-Mutated Acute Myeloid Leukemia: A Narrative Review.Cureus · 2025Review
- Counter-Therapeutic Strategies for Resistance of FLT3 Inhibitors in Acute Myeloid Leukemia.Cells · 2025Review
- Resistance to FLT3 inhibitors involves different molecular mechanisms and reduces new DNA synthesis.Biochemistry and biophysics reports · 2025Article
- Potential Off-Target Effect of Gilteritinib With Venetoclax Decreases Tumor Burden for Patients With Relapsed/Refractory Wild-TypeCase reports in hematology · 2025Article
- A phase 1 study of the irreversible FLT3 inhibitor FF-10101 in relapsed or refractory acute myeloid leukemia.Blood advances · 2024Article
- Current knowledge about FLT3 gene mutations, exploring the isoforms, and protein importance in AML.Molecular biology reports · 2024Review
- Recent advances in the treatment of non-small cell lung cancer with MET inhibitors.Frontiers in chemistry · 2024Review
- Developments of Fms-like Tyrosine Kinase 3 Inhibitors as Anticancer Agents for AML Treatment.Current medicinal chemistry · 2024Review
- The FLT3American journal of hematology · 2023Article
- Allosteric SHP2 inhibition increases apoptotic dependency on BCL2 and synergizes with venetoclax in FLT3- and KIT-mutant AML.Cell reports. Medicine · 2023Article
- Gilteritinib: The Story of a Proceeding Success into Hard-to-TreatJournal of clinical medicine · 2023Review
- The clinical impact of the molecular landscape of acute myeloid leukemia.Haematologica · 2023Review
- FMS-Like Tyrosine Kinase 3 Inhibitors in the Treatment of Acute Myeloid Leukemia: An Update on the Emerging Evidence and Safety Profile.OncoTargets and therapy · 2023Review
- Proliferation and Self-Renewal Are Differentially Sensitive to NRASG12V Oncogene Levels in an Acute Myeloid Leukemia Cell Line.Molecular cancer research : MCR · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Small-molecule FLT3 inhibitors have recently improved clinical outcomes for patients with FLT3-mutant acute myeloid leukemia (AML) after many years of development, but resistance remains an important clinical problem. FF-10101 is the first irreversible, covalent inhibitor of FLT3 which has previously shown activity against FLT3 tyrosine kinase inhibitor resistance-causing FLT3 F691L and D835 mutations. We report that FF-10101 is also active against an expanded panel of clinically identified FLT3 mutations associated with resistance to other FLT3 inhibitors. We also demonstrate that FF-10101 can potentially address resistance mechanisms associated with growth factors present in the bone marrow microenvironment but is vulnerable to mutation at C695, the amino acid required for covalent FLT3 binding. These data suggest that FF-10101 possesses a favorable resistance profile that may contribute to improved single-agent efficacy when used in patients with FLT3-mutant AML.
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Registered trials
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.