{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["42(4)"],"submitter":["Yu M"],"pubmed_abstract":["The kinase FLT3 internal tandem duplication (FLT3-ITD) is related to poor clinical outcomes of acute myeloid leukemia (AML). FLT3 inhibitors have provided novel strategies for the treatment of FLT3-ITD-positive AML. But they are limited by rapid development of acquired resistance and refractory in monotherapy. Recent evidence shows that inducing the degradation of FLT3-mutated protein is an attractive strategy for the treatment of FLT3-ITD-positive AML, especially those with FLT3 inhibitor resistance. In this study we identified Wu-5 as a novel USP10 inhibitor inducing the degradation of FLT3-mutated protein. We showed that Wu-5 selectively inhibited the viability of FLT3 inhibitor-sensitive (MV4-11, Molm13) and -resistant (MV4-11R) FLT3-ITD-positive AML cells with IC<sub>50</sub> of 3.794"],"journal":["Acta pharmacologica Sinica"],"pagination":["604-612"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8115260"],"repository":["biostudies-literature"],"pubmed_title":["Wu-5, a novel USP10 inhibitor, enhances crenolanib-induced FLT3-ITD-positive AML cell death via inhibiting FLT3 and AMPK pathways."],"pmcid":["PMC8115260"],"pubmed_authors":["Yu M","Liu M","Lei H","Bu ZL","Xiao XH","Wu YL","Liu W","Zhang ZL","Zhang Y","Cao Y","Xu HZ","Wang WW","Zhang XM","Wang YY","Wu YZ","Fang ZX"],"additional_accession":[]},"is_claimable":false,"name":"Wu-5, a novel USP10 inhibitor, enhances crenolanib-induced FLT3-ITD-positive AML cell death via inhibiting FLT3 and AMPK pathways.","description":"The kinase FLT3 internal tandem duplication (FLT3-ITD) is related to poor clinical outcomes of acute myeloid leukemia (AML). FLT3 inhibitors have provided novel strategies for the treatment of FLT3-ITD-positive AML. But they are limited by rapid development of acquired resistance and refractory in monotherapy. Recent evidence shows that inducing the degradation of FLT3-mutated protein is an attractive strategy for the treatment of FLT3-ITD-positive AML, especially those with FLT3 inhibitor resistance. In this study we identified Wu-5 as a novel USP10 inhibitor inducing the degradation of FLT3-mutated protein. We showed that Wu-5 selectively inhibited the viability of FLT3 inhibitor-sensitive (MV4-11, Molm13) and -resistant (MV4-11R) FLT3-ITD-positive AML cells with IC<sub>50</sub> of 3.794","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Apr","modification":"2025-04-29T11:33:24.847Z","creation":"2025-04-06T19:54:40.473Z"},"accession":"S-EPMC8115260","cross_references":{"pubmed":["32694757"],"doi":["10.1038/s41401-020-0455-x"]}}