Trial reportBlood2014
Crenolanib is a potent inhibitor of FLT3 with activity against resistance-conferring point mutants.
Trial report in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
131 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- FLT3 inhibitors as maintenance therapy post allogeneic hematopoietic stem cell transplantation in acute myeloid leukemia patients with FLT3 mutations: A meta-analysis.Cancer medicine · 2023Pooled it
- FLT3 Tyrosine Kinase Inhibitors for the Treatment of Fit and Unfit Patients with FLT3-Mutated AML: A Systematic Review.International journal of molecular sciences · 2021Pooled it
- Midostaurin after allogeneic stem cell transplant in patients with FLT3-internal tandem duplication-positive acute myeloid leukemia.Bone marrow transplantation · 2021Trial
- Clinical resistance to crenolanib in acute myeloid leukemia due to diverse molecular mechanisms.Nature communications · 2019Trial
- A next-generation sequencing-based assay for minimal residual disease assessment in AML patients withBlood advances · 2018Trial
- Targeting FLT3 in Acute Myeloid Leukemia: Structural Insights and Key Challenges.ACS bio & med chem Au · 2026Review
- Pigmentary Changes Reported with Tyrosine Kinase Inhibitors: A Narrative Review of Mechanisms and Clinical Implications.Clinical drug investigation · 2026Review
- Review
- FLT3: A 35-Year Voyage from Discovery to the Next Generation of Targeted Therapy in AML.Cancers · 2025Review
- Current Therapeutic Strategies for FLT3-Mutated Acute Myeloid Leukemia: A Narrative Review.Cureus · 2025Review
- Accessing sulfonamides via formal SONature chemistry · 2025Article
- Tyrosine kinase inhibitor maintenance therapy after stem cell transplantation for FLT3-mutated acute myeloid leukemia.The Cochrane database of systematic reviews · 2025Article
- Article
- Insights into the cellular function and mechanism of action of quinone reductase 2 (NQO2).The Biochemical journal · 2025Review
- Recent Advancement in Drug Designing as Small Molecules in Targeted Cancer Therapy: Challenges and Future Directions.Current cancer drug targets · 2025Review
- OXPHOS mediators in acute myeloid leukemia patients: Prognostic biomarkers and therapeutic targets for personalized medicine.World journal of surgical oncology · 2024Article
- Gilteritinib Reduces FLT3 Expression in Acute Myeloid Leukemia Cells.Biomolecules & therapeutics · 2024Article
- Common Driver Mutations in AML: Biological Impact, Clinical Considerations, and Treatment Strategies.Cells · 2024Review
- Classification of FLT3 inhibitors and SAR analysis by machine learning methods.Molecular diversity · 2024Article
- Crenolanib and Intensive Chemotherapy in Adults With Newly Diagnosed FLT3-Mutated AML.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024Article
71 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Mutations of the type III receptor tyrosine kinase FLT3 occur in approximately 30% of acute myeloid leukemia patients and lead to constitutive activation. This has made FLT3-activating mutations an attractive drug target because they are probable driver mutations of this disease. As more potent FLT3 inhibitors are developed, a predictable development of resistance-conferring point mutations, commonly at residue D835, has been observed. Crenolanib is a highly selective and potent FLT3 tyrosine kinase inhibitor (TKI) with activity against the internal tandem duplication (FLT3/ITD) mutants and the FLT3/D835 point mutants. We tested crenolanib against a panel of D835 mutant cell lines and primary patient blasts and observed superior cytotoxic effects when compared with other available FLT3 TKIs such as quizartinib and sorafenib. Another potential advantage of crenolanib is its reduced inhibition of c-Kit compared with quizartinib. In progenitor cell assays, crenolanib was less disruptive of erythroid colony growth, which may result in relatively less myelosuppression than quizartinib. Finally, correlative data from an ongoing clinical trial demonstrate that acute myeloid leukemia patients can achieve sufficient levels of crenolanib to inhibit both FLT3/ITD and resistance-conferring FLT3/D835 mutants in vivo. Crenolanib is thus an important next-generation FLT3 TKI.
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What OpenQuestion holds
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.