Molecular Partners AG presented positive initial clinical data from its ongoing Phase 1/2a trial of MP0533, a novel tetra-specific T cell engager, in a poster at the 65thAmerican Society of Hematology (ASH) Annual Meeting and Exposition. These data, which highlight encouraging initial safety and antitumor activity, expand upon those previously disclosed in the conference abstract. As of the data cut-off (October 24, 2023), 11 patients had been enrolled in the first four dosing regimens (DR) of the ongoing Phase 1/2a trial of MP0533 monotherapy in patients with relapsed/refractory acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS/AML).

The trial enrollment remains on track with patients currently being treated in the fifth of seven dose-escalation cohorts planned. MP0533 continues to demonstrate an acceptable safety profile across all four DRs studied. No dose-limiting toxicities (DLTs) were observed as of data cut-off, and all patients were able to receive their full dose of MP0533.

The most frequently reported MP0533-related adverse events were infusion-related reactions and cytokine release syndrome (all Grade 1-2). Two responders have been observed to date, including a patient achieving complete response (CR) in DR 4 and another patient with morphological leukemia-free state (MFS) in DR 3 (initially identified as CRi at the time of abstract submission, data cutoff July 2023). These responses are particularly notable for having occurred at dose levels below those predicted for therapeutically relevant activity.

About MP0533: MP0533 is a novel, avidity-driven, tetra-specific T cell-engaging, half-life extended, DARPin, which simultaneously targets the tumor-associated antigens CD33, CD123 and CD70 as well as the immune activator CD3 on T cells. MP0533?s affinity to each tumor-associated antigen is tuned to preferentially kill AML cells which commonly co-express at least two of these three target antigens whereas most healthy blood cells only express one or none. MP0533?s unique avidity-driven mode of action therefore enables targeted T cell-mediated killing of AML cells while preserving a therapeutic window that minimizes damage to healthy cells.