AMX-883 is an oral, highly selective BRD9-targeted molecular chaperone degrader. Unlike mainstream PROTAC-dependent CRBN/VHL systems, AMX-883 degrades BRD9 by recruiting the novel E3 ligase DCAF16. AMX-883 exhibits extremely high selectivity for BRD9 and has virtually no effect on other proteins containing a bromo domain. AMX-883 can be used in research on acute myeloid leukemia (AML).

AMX-883 specifically degrades BRD9 and exhibits no off-target effects on other bromodomain proteins. [1]
In acute myeloid leukemia (AML) cell lines with different mutational backgrounds (including TP53 mutations) and in normal peripheral blood mononuclear cells, AMX-883 time-dependently upregulates key proteins involved in myeloid differentiation in AML cells, inducing high expression of differentiation markers. [1]
AMX-883 broadly inhibits AML cell activity and exhibits no significant toxicity to normal cells.[1]

In the MV4-11 subcutaneous and disseminated AML xenograft models, as well as patient-derived xenograft (PDX) models of AML, daily oral administration of AMX-883 resulted in sustained, potent degradation of BRD9, significantly reduced the leukemic burden in bone marrow and blood, and prolonged the survival of the model mice.[1]