Miletić Nebojša, Weckesser Janik, Mosler Thorsten, Rathore Rajeshwari, Hoffmann Marina E, Gehrtz Paul, Schlesiger Sarah, Hartung Ingo V, Berner Nicola, Wilhelm Stephanie, Müller Juliane, Adhikari Bikash, Němec Václav, Sivashanmugam Saran Aswathaman, Elson Lewis, Holzmann Hanna, Schwalm Martin P, Hoffmann Lasse, Abdul Azeez Kamal Rayees, Müller Susanne, Kuster Bernhard, Wolf Elmar, Đikić Ivan, Knapp Stefan
Institute of Pharmaceutical Chemistry, Goethe University, Max-von-Laue-Str. 9, 60438 Frankfurt am Main, Germany.
Structural Genomics Consortium (SGC), Buchmann Institute for Life Sciences, Max-von-Laue-Str. 15, 60438 Frankfurt am Main, Germany.
ACS Chem Biol. 2025 Feb 21;20(2):507-521. doi: 10.1021/acschembio.4c00812. Epub 2025 Feb 11.
Proteolysis targeting chimeras (PROTACs) have gained considerable attention as a new modality in drug discovery. The development of PROTACs has been mainly focused on using CRBN (Cereblon) and VHL (Von Hippel-Lindau ligase) E3 ligase ligands. However, the considerable size of the human E3 ligase family, newly developed E3 ligase ligands, and the favorable druggability of some E3 ligase families hold the promise that novel degraders with unique pharmacological properties will be designed in the future using this large E3 ligase space. Here, we developed a workflow aiming to improve and streamline the evaluation of E3 ligase ligand efficiency for PROTAC development and the assessment of the corresponding "degradable" target space using broad-spectrum kinase inhibitors and the well-established VHL ligand VH032 as a validation system. Our study revealed VH032 linker attachment points that are highly efficient for kinase degradation as well as some of the pitfalls when using protein degradation as a readout. For instance, cytotoxicity was identified as a major mechanism leading to PROTAC- and VHL-independent kinase degradation. The combination of E3 ligase ligand negative controls, competition by kinase parent compounds, and neddylation and proteasome inhibitors was essential to distinguish between VHL-dependent and -independent kinase degradation events. We share here the findings and limitations of our study and hope that this study will provide guidance for future evaluations of new E3 ligase ligand systems for degrader development.
靶向蛋白降解嵌合体(PROTACs)作为药物发现中的一种新方法已受到广泛关注。PROTACs的开发主要集中在使用CRBN(脑啡肽)和VHL(冯·希佩尔-林道连接酶)E3连接酶配体。然而,人类E3连接酶家族规模庞大,新开发的E3连接酶配体以及一些E3连接酶家族良好的成药潜力预示着,未来利用这个庞大的E3连接酶空间有望设计出具有独特药理特性的新型降解剂。在此,我们开发了一种工作流程,旨在改进和简化用于PROTAC开发的E3连接酶配体效率评估,以及使用广谱激酶抑制剂和成熟的VHL配体VH032作为验证系统来评估相应的“可降解”靶点空间。我们的研究揭示了VH032连接点对激酶降解具有高效性,同时也发现了以蛋白质降解作为读数时存在的一些陷阱。例如,细胞毒性被确定为导致PROTAC和VHL非依赖性激酶降解的主要机制。E3连接酶配体阴性对照、激酶母体化合物的竞争以及NEDDylation和蛋白酶体抑制剂的组合对于区分VHL依赖性和非依赖性激酶降解事件至关重要。我们在此分享研究结果和局限性,希望这项研究能为未来评估用于降解剂开发的新型E3连接酶配体系统提供指导。