Molecular Partners Announces Publication in Cancer Immunology Research of Preclinical Data Supporting MP0533’s Proposed Mechanism of Action

• Preclinical data of tetra-specific T cell engager MP0533 demonstrate preferential T cell mediated killing of AML cells, while sparing healthy cells
  
• Results highlight MP0533-mediated T-cell activation and tumor regression, as well as cytokine release in AML models without systemic adverse effects
  
• Published data build on results previously presented at ASH 2021 and 2022, and support the rationale for the clinical development of MP0533 as monotherapy and in combination with azacitidine/venetoclax
  
• Ongoing Phase 1/2a clinical study continues to progress well, currently dosing patients in cohort 7 
  

ZURICH-SCHLIEREN, Switzerland and CONCORD, Mass., April 29, 2024 (GLOBE NEWSWIRE) -- Molecular Partners AG (SIX: MOLN; NASDAQ: MOLN), a clinical-stage biotech company developing a new class of custom-built protein drugs known as DARPin therapeutics, today announced a comprehensive, peer-reviewed publication of preclinical data supporting MP0533’s proposed unique mechanism of action (MoA) for the treatment of acute myeloid leukemia (AML) in Cancer Immunology Research, a journal of the American Association for Cancer Research. The publication collates and discusses multiple studies undertaken to characterize MP0533’s preclinical profile and evaluate its therapeutic potential.

Developing safe and efficacious targeted therapies for patients with AML has proven challenging as AML cells share many of the relevant target antigens with healthy cells. Through its unique MoA, MP0533 was designed to simultaneously target the proteins CD33, CD123, and CD70, which are commonly co-expressed on AML cells and rarely on healthy cells. MP0533’s binding strength increases with the number of target proteins present, leading to increased engagement of T cells when at least two of the targets are present. This results in preferential killing of AML cells.

The data published by Bianchi et al in Cancer Immunology Research in collaboration with the University of Bern build on the results presented at the American Society of Hematology (ASH) Annual Meeting and Exposition in December 2021 and 2022, and support MP0533’s intended MoA. MP0533 induces selective T cell-mediated killing of AML cell lines, as well as patient bone marrow-derived AML blasts and leukemic stem cells (LSCs) expressing two or three of the target antigens, while sparing healthy hematopoietic stem cells, blood and endothelial cells. MP0533 also demonstrated reduced risk of T cell fratricide observed with other CD70-targeting agents related to CD70’s upregulation on activated T cells. MP0533 was equivalent to non-CD70 targeting therapies in terms of impact on T cell count and viability, further supporting its potentially favorable on-target, off-tumor profile.