Faculty, Staff and Student Publications

Language

English

Publication Date

2-13-2025

Journal

Journal of Medicinal Chemistry

DOI

10.1021/acs.jmedchem.4c02161

PMID

39905966

PMCID

PMC11932022

PubMedCentral® Posted Date

2-13-2026

PubMedCentral® Full Text Version

Author MSS

Abstract

DNA methyltransferase 1 (DNMT1), which catalyzes maintenance methylation of hemimethylated DNA during DNA replication, is overexpressed in cancer. Recently, the first-in-class DNMT1-selective noncovalent small-molecule inhibitors, GSK3484862 and GSK3685032, were discovered. These inhibitors were also reported to degrade DNMT1. However, structure–activity relationship (SAR) studies of these monovalent DNMT1 degraders are lacking. Here, we report our SAR studies of this scaffold on degrading DNMT1, which led to the discovery of multiple lead degraders, including compound 4 (MS9024). Compound 4 potently and selectively degraded DNMT1 in multiple cancer cell lines in a concentration-, time-, and proteasome-dependent manner without altering DNMT1 transcription. Further mechanism-of-action studies suggest that the DNMT1 degradation induced by 4 was not mediated by lysosome or cullin RING E3 ligases but could potentially be mediated by HECT E3 ligases and/or UHRF1. Collectively, these studies pave the way for further developing DNMT1 monovalent degraders as potential therapeutics and useful chemical tools.

Keywords

Humans, DNA (Cytosine-5-)-Methyltransferase 1, Structure-Activity Relationship, Cell Line, Tumor, Enzyme Inhibitors, Proteolysis, Antineoplastic Agents, Ubiquitin-Protein Ligases

Published Open-Access

yes

nihms-2058850-f0001.jpg (103 kB)
Graphical Abstract

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