ReviewArchiv der Pharmazie2026
Medicinal Insights Into FLT3 Inhibitors as Anticancer Agents: Current Status and Future Direction.
Review in Archiv der Pharmazie, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FMS-like tyrosine kinase 3 (FLT3) is a receptor tyrosine kinase (RTK) important for hematopoietic stem cell proliferation, differentiation, and survival. Ligand-induced dimerization activates the downstream pathways such as RAS/MAPK, PI3K/AKT, and STAT5. Mutations such as internal tandem duplications (ITD) and tyrosine kinase domain (TKD) cause constitutive activation, poor prognosis, and driving leukemogenesis in acute myeloid leukemia (AML). Over the past 5 years, FLT3-targeted therapy has advanced significantly. Second-generation FLT3 inhibitors such as gilteritinib and quizartinib displayed improved selectivity and durable efficacy. Quizartinib was approved in 2023 for FLT3-ITD-positive AML alongside intensive chemotherapy. Clinical trials have explored some compounds such as crenolanib, momelotinib, and various novel molecules in combination regimens, which are enhancing remission rates. This review comprehensively compiles diverse chemical scaffolds investigated as FLT3 inhibitors such as pyrimidine, benzimidazole, imidazole, indole, isoxazole, quinazoline, and so on. Structure-activity relationship (SAR) analyses and molecular docking studies are briefly discussed along with highlighting potency against FLT3-ITD and resistant FLT3-TKD mutants. Despite therapeutic gains, resistance through secondary mutations or compensatory pathway activation remains a challenge. Future directions should focus on structure-guided design, rational combination therapies, and expanding applications to other FLT3-altered malignancies. This review integrates updated FLT3 biology, clinical outcomes, medicinal chemistry, and computational insights to support personalized FLT3-targeted treatment strategies.
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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.