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免疫调节亚胺类药物基分子胶和蛋白水解靶向嵌合体的叶酸引导的蛋白降解。

Folate-Guided Protein Degradation by Immunomodulatory Imide Drug-Based Molecular Glues and Proteolysis Targeting Chimeras.

机构信息

Mount Sinai Center for Therapeutics Discovery, Departments of Pharmacological Sciences and Oncological Sciences, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029, United States.

Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, United States.

出版信息

J Med Chem. 2021 Aug 26;64(16):12273-12285. doi: 10.1021/acs.jmedchem.1c00901. Epub 2021 Aug 11.

Abstract

Molecular glues and proteolysis targeting chimeras (PROTACs) are promising new therapeutic modalities. However, the lack of specificity for molecular glue- or PROTAC-mediated proteolysis in cancer cells versus normal cells raises potential toxicity concerns that will likely limit their clinical applications. Here, we developed a general strategy to deliver immunomodulatory imide drug (IMiD)-based molecular glues and PROTACs to folate receptor α (FOLR1)-positive cancer cells. Specifically, we designed a folate-caged pomalidomide prodrug, FA-S2-POMA, by incorporating a folate group as a caging and guiding element and validated its degradation effect on its neo-substrates in FOLR1-positive cancer cells in a FOLR1-dependent manner. We also developed a folate-caged pomalidomide-based anaplastic lymphoma kinase (ALK) PROTAC, FA-S2-MS4048, which effectively degraded ALK fusion proteins in cancer cells, again in a FOLR1-dependent manner. This novel approach provides a generalizable platform for the targeted delivery of IMiD-based molecular glues and PROTACs to FOLR1-expressing cancer cells with the potential to ameliorate toxicity.

摘要

分子胶和蛋白水解靶向嵌合体(PROTACs)是很有前途的新型治疗模式。然而,在癌细胞与正常细胞中,分子胶或 PROTAC 介导的蛋白水解缺乏特异性,这引发了潜在的毒性问题,可能会限制它们的临床应用。在这里,我们开发了一种将免疫调节亚胺二酮类药物(IMiD)基分子胶和 PROTAC 递送至叶酸受体 α(FOLR1)阳性癌细胞的通用策略。具体而言,我们设计了一种叶酸封闭的泊马度胺前药 FA-S2-POMA,通过将叶酸基团作为封闭和导向基团进行掺入,并验证了其在 FOLR1 阳性癌细胞中对其新底物的降解作用,这种降解作用依赖于 FOLR1。我们还开发了一种叶酸封闭的泊马度胺基间变性淋巴瘤激酶(ALK)PROTAC,FA-S2-MS4048,它可以有效地降解癌细胞中的 ALK 融合蛋白,同样也是依赖于 FOLR1。这种新方法为将基于 IMiD 的分子胶和 PROTAC 靶向递送至表达 FOLR1 的癌细胞提供了一个通用的平台,具有减轻毒性的潜力。

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