ArticleBlood2013
Crenolanib is active against models of drug-resistant FLT3-ITD-positive acute myeloid leukemia.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed.
- Clinical resistance to crenolanib in acute myeloid leukemia due to diverse molecular mechanisms.Nature communications · 2019Trial
- FLT3 mutational status is an independent risk factor for adverse outcomes after allogeneic transplantation in AML.Bone marrow transplantation · 2016Trial
- Clinical utilities of platelet-derived growth factor signaling in breast cancer.Pharmacological research · 2026Review
- New selective and allosteric FLT3 inhibitors show efficacy against resistant acute myeloid leukemia cells.iScience · 2026Article
- TIP-20, a novel feline McDonough sarcoma-like tyrosine kinase 3 inhibitor with potent antileukemia activity.The Journal of international medical research · 2026Article
- 3H-pyrazolo[4,3-f]quinoline hinge binder, a tunable scaffold for development of novel kinase inhibitors against FLT3-driven leukemia.European journal of medicinal chemistry · 2026Article
- Targeting p16Leukemia · 2025Article
- Current Therapeutic Strategies for FLT3-Mutated Acute Myeloid Leukemia: A Narrative Review.Cureus · 2025Review
- Article
- Decursin induces FLT3-ITD acute myeloid leukemia cell apoptosis by increasing the expression of the ubiquitin-conjugase UBE2L6.Cell communication and signaling : CCS · 2025Article
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- Article
- Classification of FLT3 inhibitors and SAR analysis by machine learning methods.Molecular diversity · 2024Article
- Ningetinib, a novel FLT3 inhibitor, overcomes secondary drug resistance in acute myeloid leukemia.Cell communication and signaling : CCS · 2024Article
- Perspectives and challenges of small molecule inhibitor therapy for FLT3-mutated acute myeloid leukemia.Annals of hematology · 2024Review
- Developments of Fms-like Tyrosine Kinase 3 Inhibitors as Anticancer Agents for AML Treatment.Current medicinal chemistry · 2024Review
- Indole-based FLT3 inhibitors and related scaffolds as potential therapeutic agents for acute myeloid leukemia.BMC chemistry · 2023Review
- Design, synthesis, and biological evaluation with molecular dynamics study of novel pyrazolo[3,4-RSC advances · 2023Article
- Choosing the Right Cell Line for Acute Myeloid Leukemia (AML) Research.International journal of molecular sciences · 2023Review
- Sitravatinib as a potent FLT3 inhibitor can overcome gilteritinib resistance in acute myeloid leukemia.Biomarker research · 2023Article
48 more citing papers are in PubMed but not listed here.
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11 authors.
Funding
Abstract
FLT3 kinase internal tandem duplication (ITD) mutations are common in acute myeloid leukemia (AML) and are associated with poor clinical outcomes. Although initial responses to FLT3 tyrosine kinase inhibitors (TKIs) are observed in FLT3-ITD-positive patients, subsequent relapse often occurs upon acquisition of secondary FLT3 kinase domain (KD) mutations, primarily at residues D835 and F691. Using biochemical assays, we determined that crenolanib, a novel TKI, demonstrates type I properties and is active against FLT3 containing ITD and/or D835- or F691-activating mutations. Potent activity was observed in FLT3-ITD-positive AML cell lines. Crenolanib delayed the outgrowth of MV4-11 cells in a xenograft mouse model, whereas in combination with the type II TKI sorafenib, a significant decrease in leukemic burden (P < .001) and prolonged survival (P < .01) was observed compared with either type I or II TKI alone. Crenolanib was active against Ba/F3 cells harboring FLT3-ITD and secondary KD mutations and sorafenib-resistant MOLM-13 cells containing FLT3-ITD/D835Y both in vitro and in vivo. In addition, crenolanib inhibited drug-resistant AML primary blasts with FLT3-ITD and D835H/Y mutations. These preclinical data demonstrate that crenolanib is effective against FLT3-ITD containing secondary KD mutations, suggesting that crenolanib may be a useful therapeutic agent for TKI-naive and drug-resistant FLT3-ITD-positive AML.
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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.