AI-10-49 restores RUNX1 transcriptional activity, displays favorable pharmacokinetics, and delays leukemia progression in mice. Treatment of primary inv(16) AML patient with AI-10-49 triggers selective cell death. Direct inhibition of the oncogenic CBFβ-SMMHC fusion protein may be an effective therapeutic approach for inv(16) AML, and they provide support for transcription factor targeted therapy in other cancers
产品描述
AI-10-49 is a selective inhibitor of CBFβ –SMMHC and RUNX1 interaction with a FRET IC50 value of 260nM.