Bivalent design enables avid binding to clustered receptors* for potent target cell killing
Avid binding imparts selectivity for target cells* while sparing differentiated myeloid cells
* CD33 actively signals on MDSC, and clusters in lipid rafts
Enhanced target cell selectivity and T cell activation profile from bivalent target engagement leads to a more manageable safety profile
AMV564 harnesses the patient’s own T-cells to both relieve immune suppression and restore anti-cancer T cell function systemically and in the tumor microenvironment. AMV564 induces T cell mediated killing of myeloid derived suppressor cells (MDSC) and AML leukemic blasts, while sparing differentiated myeloid cells (e.g., neutrophils and monocytes) and drives activation and
repolarization of T cells and improved T effector function.
To date, over 80 patients have received AMV564 across three Phase 1 clinical trials for solid tumors, acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS), and AMV564 has demonstrated monotherapy activity in solid tumor and hematologic cancer patients with an excellent safety profile as well as combinability with checkpoint inhibition. We are uniquely positioned to leverage the simultaneous relief of immune suppression and enhanced T cell effector function to restore anti-cancer immunity in patients.