Molecular Partners Presents Updated Data from Ongoing Phase 1/2a Trial of MP0533 in AML at ASH Annual Meeting

ZURICH-SCHLIEREN, Switzerland and CONCORD, Mass., Dec. 07, 2025 (GLOBE NEWSWIRE) — Ad hoc announcement pursuant to Art. 53 LR 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 (“Molecular Partners” or the “Company”), has today announced it will present updated data from a Phase 1/2a trial of the multispecific T-cell engager MP0533 in patients with acute myeloid leukemia (AML) in a poster at the 67th American Society of Hematology (ASH) Annual Meeting and Exposition, taking place December 6-9, 2025, in Orlando, Florida.

The poster outlines the latest results of this multicenter, open-label study evaluating MP0533 for the treatment of patients with relapsed/refractory (R/R) AML and myelodysplastic syndrome (MDS)/AML (ClinicalTrials.gov: NCT05673057). Data from cohorts 8 and 9 show that densified MP0533 dosing appears tolerable and leads to markedly improved serum exposure in treatment cycle 1, with encouraging preliminary antitumor activity.

“The results in patients with higher frequency dosing regimens of MP0533 are very encouraging. I am happy to see the clinical benefit of MP0533 in a mutation-agnostic manner in R/R AML patients, in particular those with lower disease burden. The data indicate that MP0533 has the potential to significantly improve treatment options for patients with AML and I support investigating MP0533 in a Phase 2 setting to confirm its safety and activity in earlier lines as consolidation addition to existing backbones,” said Prof. Courtney DiNardo, M.D., Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, and co-chair of the MP0533 dose escalation review committee (DERC).

As of the data cut-off of September 1, 2025, 54 patients had been treated with MP0533. Eight of 48 evaluable patients achieved a response, with five reaching composite complete responses (3 complete responses, CR, and 2 CR with partial hemotologic recovery) and three reaching morphologic leukemia-free state (MLFS). Six of the 8 responders, and 11 of 14 patients who achieved a reduction in bone marrow blasts of more than 50%, presented with less than 20% bone marrow blast at baseline, indicating that patients with low disease burden are most likely to benefit from MP0533. One patient in cohort 8 has been in complete remission for over a year, and one patient in cohort 9 is on the trial since 4 months. Cohort 10, which aims at reaching the same target dose as cohort 8 while exposing patients to more drug over time, is ongoing with data expected in 2026.

“The Phase 1/2a trial with MP0533 is making good progress, with the densified dosing regimen showing to be feasible, with an acceptable safety profile, and resulting in clinical benefit. The results warrant further exploration of MP0533’s potential, both in the R/R and front-line AML settings in combination with standard of care, and several consortia have approached us expressing interest in conducting such studies. We are actively engaging with potential partners and continue our dialogue with key opinion leaders and regulators to shape the next phase of development of our innovative T-cell engager for patients,” said Philippe Legenne, M.D., CMO of Molecular Partners.

MP0533 is a novel tetra-specific T cell-engaging DARPin designed for selective and broad killing of AML cells in a mutation-agnostic manner. MP0533 simultaneously targets three tumor-associated antigens CD33, CD123, and CD70 on AML cells as well as the immune activator CD3 on T cells. AML cells commonly co-express at least two of the three target antigens, whereas most healthy cells only express one or none. MP0533 binds with increasing avidity as the number of its target antigens present increases, thereby preferentially binding to AML cells over healthy cells. This unique mode of action is designed to enable T cell-mediated killing of AML cells while preserving a therapeutic window that minimizes damage to healthy cells.