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Protein degraders drug delivery in Multiple Myeloma

Abstract #309 Posted on28 March 202524 April 2025 24 April 2025 22h47

Abstract

Multiple Myeloma (MM) is the second most common hematological malignancy, with most patients eventually relapsing and developing resistance to existing therapies. Proteolysis-targeting chimeras (PROTACs) and molecular glues (MGs) represent emerging therapeutic strategies that selectively degrade disease-associated proteins. Among them, Cereblon E3 Ligase Modulating Drugs (CeLMODs) targeting GSPT1 have demonstrated high efficacy in MM but are limited by potential toxicity and restricted biodistribution.

To address these challenges, we developed a Polymer-CeLMOD conjugate targeting GSPT1. Using a Lenalidomide-based scaffold, we synthesized a library of novel CeLMODs. Through drug screening in cancer cell lines, we identified a hit compound based on its potent activity and its ability to induce targeted protein degradation in vitro. Proteomic analysis using mass spectrometry was performed to comprehensively characterize the compound’s selectivity, degradation efficiency, and downstream effects in MM cells.

Our findings demonstrate the successful development of a Polymer-CeLMOD conjugate with effective GSPT1 degradation, highlighting its therapeutic potential.

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To address these challenges, we developed a Polymer-CeLMOD conjugate targeting GSPT1. Using a Lenalidomide-based scaffold, we synthesized a library of novel CeLMODs. Through drug screening in cancer cell lines, we identified a hit compound based on its potent activity and its ability to induce targeted protein degradation in vitro. Proteomic analysis using mass spectrometry was performed to comprehensively characterize the compound’s selectivity, degradation efficiency, and downstream effects in MM cells.

Our findings demonstrate the successful development of a Polymer-CeLMOD conjugate with effective GSPT1 degradation, highlighting its therapeutic potential.

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