Molecular Partners Outlines Clinical Expansion Plans and Strengthens Radiopharma Strategic Focus for 2025 at 43rd Annual J.P. Morgan Healthcare Conference

Company Updates - Molecular Partners provided updates on its programs, development plans, and key milestones for 2025, to be presented at the 43rd Annual J P Morgan Healthcare Conference [1] - The company strengthened its partnership with Orano Med for co-development of up to ten 212Pb-based Radio-DARPins, with MP0712 being the most advanced program targeting DLL3 [2][3] - MP0712, a 212Pb Radio-DARPin candidate targeting DLL3, is preparing for an IND application submission in H1 2025, with the first-in-human study to follow regulatory clearance [6] - The second Radio-DARPin program targets Mesothelin (MSLN), with further details to be unveiled at the AACR Annual Meeting in Q2 2025 [3][9] - MP0533, a multispecific T cell engager, showed improved response rates and depth in cohort 8 of its Phase 1/2a trial for relapsed/refractory AML, with additional dose densification planned for cohort 9 [4][11][12] - The Switch-DARPin platform demonstrated preclinical proof-of-concept for conditional T cell activation in solid tumors, with further data expected in Q2 2025 [14][15] - MP0317, a localized CD40 agonist, completed Phase 1 trials in solid tumors, with potential combination trials planned for 2025 [16][17] Financial and Operational Highlights - As of December 31, 2024, Molecular Partners reported cash and cash equivalents of CHF 149 million (unaudited), with full-year financial results to be released on March 6, 2025 [5] - The company continues to progress its Radio-DARPin Therapy (RDT) portfolio in partnership with Novartis and is evaluating additional targets for RDT programs [10] Scientific and Clinical Progress - MP0712 demonstrated high affinity and specificity for DLL3 in preclinical studies, with homogeneous expression in small cell lung cancer tumors and low expression in healthy tissues [7] - MP0533 is a tetraspecific T cell engager targeting CD33, CD123, CD70, and CD3, designed to preferentially kill AML cells expressing at least two of the three tumor-associated antigens [13] - The CD3 Switch-DARPin molecule showed potent tumor regression in vivo with reduced cytokine release in healthy tissues, potentially reducing the risk of cytokine release syndrome (CRS) [15] - MP0317 activates immune cells within the tumor microenvironment by anchoring to fibroblast activation protein (FAP), offering potential for greater efficacy with fewer side effects compared to systemic therapies [16]