Treatment with SP2509 (25 mg/kg) and/or PS (5 mg/kg) markedly increases the loss of viability in CD34⁺ primary AML cells induced by PS and enhances the survival of mice with AML xenografts and primagrafts^[2].

SP2509 (250, 500, 1000 nM) suppresses LSD1 activity, reduces colony growth, and triggers apoptosis and cell death in human acute myeloid leukemia (AML) cells in culture. It also elevates H3K4Me3 levels at the promoters of p57 Kip, KLF4, and p21, leading to increased mRNA levels of these genes in AML cells. Furthermore, SP2509 (250, 1000 nM) promotes morphological differentiation in both cultured and primary AML cells. Additionally, when used in conjunction with PS, SP2509 demonstrates synergistic lethal effects on both cultured and primary AML cells^[1].

SP2509 does not disrupt the CoREST-LSD1 interaction, nor does it significantly destabilize the CRC. At concentrations of 1 or 10 µM, SP2509 induces cell death without causing morphological changes at a lower concentration of 0.1 µM. Similarly, SP2509 impacts the viability of medulloblastoma cells^[2].