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DB2313 treatment leads to a profound decrease in the growth of PU.1 URE-/- acute myeloid leukemia (AML) cells (IC50 of 7.1 μM), while showing little effect on normal hematopoietic cells at similar concentrations. DB2313 treatment leads to a 3.5-fold increase in apoptotic cells in murine PU.1 URE-/- AML cells. DB2313 also leads to a significant decrease in clonogenicity in the second and third rounds of plating and a complete disruption of clonogenic capacity in the fourth and higher rounds of plating[1].In AML cells, DB2313 decreases PU.1 occupancy on E2f1, Junb, and Csf1r promoters[1].

DB2313 (17 mg/kg; i.p.; three times per week; for 3 weeks) treatment decreases leukemia progression and results in increased survival in mice[1].

[1]. Iléana Antony-Debré, et al. Pharmacological inhibition of the transcription factor PU.1 in leukemia. J Clin Invest. 2017 Dec 1;127(12):4297-4313.

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