AMX-883 a selective and orally active BRD9 molecular glue degrader that drives differentiation in acute myeloid leukaemia. AMX-883 shows selectivity over all other bromodomain containing proteins and proteome wide. AMX-883 does not employ the commonly used E3 ligases ( cereblon, VHL) but instead drives degradation via DCAF16 as a targeted glue. AMX-883 can be used for the study of acute myeloid leukaemia (AML) [1].
In Vivo, AMX-883 (14 days) induced dose-dependent degradation of BRD9 in a luciferase-labeled MV4-11 dissemination model, accompanied by time-dependent induction of CD11b and CD86. Measurements of total disease burden in animals showed a significant reduction in tumor burden in the AMX-883-treated groups compared to the vector control group[1].
In Vitro, Combination of AMX-883 with Venetoclax resulted in synergistic efficacy in MV4-11 and MOLM-13 cell lines[1].
References:
[1]. Martin O'Rourke, et al. Amx-883, a potent and selective degrader of BRD9 drives differentiation in acute myeloid leukaemia and shows synergistic efficacy in combination with venetoclax In Vivo and prevents the emergence of resistance to venetoclax in vitro. Blood (2025) 146 (Supplement 1): 1489.
In Vivo, AMX-883 (14 days) induced dose-dependent degradation of BRD9 in a luciferase-labeled MV4-11 dissemination model, accompanied by time-dependent induction of CD11b and CD86. Measurements of total disease burden in animals showed a significant reduction in tumor burden in the AMX-883-treated groups compared to the vector control group[1].
In Vitro, Combination of AMX-883 with Venetoclax resulted in synergistic efficacy in MV4-11 and MOLM-13 cell lines[1].
References:
[1]. Martin O'Rourke, et al. Amx-883, a potent and selective degrader of BRD9 drives differentiation in acute myeloid leukaemia and shows synergistic efficacy in combination with venetoclax In Vivo and prevents the emergence of resistance to venetoclax in vitro. Blood (2025) 146 (Supplement 1): 1489.