Design and Structural Optimization of Methionine Adenosyltransferase 2A (MAT2A) Inhibitors with High In Vivo Potency and Oral Bioavailability-Reference-Cited by-同舟云学术

Design and Structural Optimization of Methionine Adenosyltransferase 2A (MAT2A) Inhibitors with High In Vivo Potency and Oral Bioavailability

Published:2023-03-24 Issue:7 Volume:66 Page:4849-4867
ISSN:0022-2623
Container-title:Journal of Medicinal Chemistry
language:en
Short-container-title:J. Med. Chem.

Author:

Zhang Silong¹²³^ORCID,Qing Luolong²,Wang Ziwei²,Zhang Yu²,Li Yuanyuan³⁴,Fang Huaxiang³,Liu Yi²⁴⁵^ORCID,He Huan¹²³

Affiliation:

1. School of Pharmaceutical Sciences, Guizhou University, Guiyang 550025, P. R. China

2. Key Laboratory of Coal Conversion and New Carbon Materials of Hubei Province, College of Chemistry and Chemical Engineering, Wuhan University of Science and Technology, Wuhan 430081, P. R. China

3. Wuhan Yuxiang Pharmaceutical Technology Company, Limited, Wuhan 430200, P. R. China

4. School of Life Science and Technology & School of Chemical and Environmental Engineering, Wuhan Polytechnic University, Wuhan 430023, P. R. China

5. Hubei Key Laboratory of Radiation Chemistry and Functional Materials, Hubei University of Science and Technology, Xianning 437100, P. R. China

Funder

Tianjin Municipal Science and Technology Bureau

National Natural Science Foundation of China

Wuhan Yuxiang Pharmaceutial Technology Co., Ltd.

Publisher

American Chemical Society (ACS)

Subject

Drug Discovery,Molecular Medicine

Link

https://pubs.acs.org/doi/pdf/10.1021/acs.jmedchem.2c02006

Reference30 articles.

1. The U6 snRNA m 6 A Methyltransferase METTL16 Regulates SAM Synthetase Intron Retention

2. Methionine is a metabolic dependency of tumor-initiating cells

3. Methionine adenosyltransferases in cancers: Mechanisms of dysregulation and implications for therapy

4. S-adenosylmethionine biosynthesis is a targetable metabolic vulnerability of cancer stem cells

5. MAT2A Inhibition Blocks the Growth of MTAP-Deleted Cancer Cells by Reducing PRMT5-Dependent mRNA Splicing and Inducing DNA Damage

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