Article

Tumor-targeted PROTAC prodrug nanoplatform enables precise protein degradation and combination cancer therapy

Zhi-feng Zou1,2, Lei Yang2,3, Hui-jun Nie3, Jing Gao2, Shu-min Lei3, Yi Lai2, Fan Zhang4, Ernst Wagner5, Hai-jun Yu2,3, Xiao-hua Chen3,6, Zhi-ai Xu1
1 School of Chemistry and Molecular Engineering, East China Normal University, Shanghai 200241, China
2 State Key Laboratory of Chemistry Biology & Center of Pharmaceutics, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China
3 School of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing 210023, China
4 Department of Chemistry, Fudan University, Shanghai 20043, China
5 Department of Pharmacy, Ludwig-Maximilians-Universität, 81377 München, Germany
6 School of Pharmaceutical Science and Technology, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou 310024, China
Correspondence to: Jing Gao: jgao@simm.ac.cn, Hai-jun Yu: hjyu@simm.ac.cn, Xiao-hua Chen: xhchen@simm.ac.cn, Zhi-ai Xu: zaxu@chem.ecnu.edu.cn,
DOI: 10.1038/s41401-024-01266-z
Received: 23 December 2023
Accepted: 12 March 2024
Advance online: 12 April 2024

Abstract

Proteolysis targeting chimeras (PROTACs) have emerged as revolutionary anticancer therapeutics that degrade disease-causing proteins. However, the anticancer performance of PROTACs is often impaired by their insufficient bioavailability, unsatisfactory tumor specificity and ability to induce acquired drug resistance. Herein, we propose a polymer-conjugated PROTAC prodrug platform for the tumor-targeted delivery of the most prevalent von Hippel–Lindau (VHL)- and cereblon (CRBN)-based PROTACs, as well as for the precise codelivery of a degrader and conventional small-molecule drugs. The self-assembling PROTAC prodrug nanoparticles (NPs) can specifically target and be activated inside tumor cells to release the free PROTAC for precise protein degradation. The PROTAC prodrug NPs caused more efficient regression of MDA-MB-231 breast tumors in a mouse model by degrading bromodomain-containing protein 4 (BRD4) or cyclin-dependent kinase 9 (CDK9) with decreased systemic toxicity. In addition, we demonstrated that the PROTAC prodrug NPs can serve as a versatile platform for the codelivery of a PROTAC and chemotherapeutics for enhanced anticancer efficiency and combination benefits. This study paves the way for utilizing tumor-targeted protein degradation for precise anticancer therapy and the effective combination treatment of complex diseases.

Keywords: proteolysis-targeting chimeras; tumor-targeted delivery; precise protein degradation; combination therapy; triple- negative breast cancer

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