{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T16:03:10Z","timestamp":1792512190228,"version":"4.5.0"},"reference-count":29,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,5,29]],"date-time":"2025-05-29T00:00:00Z","timestamp":1748476800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Acute myeloid leukemia (AML), originating from myeloid hematopoietic stem\/progenitor cells, is a malignant hematological disorder. Resistance to current treatments, especially in FLT3-ITD AML cases, urgently demands the development of novel therapeutics. In this study, we pinpointed fostamatinib, an orally delivered small molecule SYK inhibitor for chronic immune thrombocytopenia (ITP), as a promising candidate for drug repurposing. It effectively inhibited FLT3-ITD+ AML cell proliferation and induced leukemic cell apoptosis. Network pharmacology analysis further deciphered the associated pharmacological mechanism related to the PI3K-AKT signaling pathway. Moreover, fostamatinib downregulated the expression of immune checkpoints such as PD-L1 and CD47. Overall, this study provided a conceptual foundation for evaluating the advantages of drug repurposing in AML drug development.<\/jats:p>","DOI":"10.3389\/fimmu.2025.1602189","type":"journal-article","created":{"date-parts":[[2025,5,29]],"date-time":"2025-05-29T05:26:19Z","timestamp":1748496379000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":7,"title":["Drug repurposing of fostamatinib against cancer via potential cytotoxicity and immune checkpoint 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