Design, synthesis and biological activity of N5-substituted tetrahydropteroate analogs as non-classical antifolates against cobalamin-dependent methionine synthase and potential anticancer agents

  • Eur J Med Chem. 2020 Mar 15:190:112113. doi: 10.1016/j.ejmech.2020.112113.
Meng Wang  1 Chao Tian  2 Liangmin Xue  2 Hao Li  2 Jing Cong  2 Fang Fang  2 Jiajia Yang  2 Mengmeng Yuan  2 Ying Chen  2 Ying Guo  2 Xiaowei Wang  2 Junyi Liu  3 Zhili Zhang  4
Affiliations
  • 1. Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University, Beijing, 100191, China; College of Pharmacy, Beihua University, Jilin, 132013, China.
  • 2. Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University, Beijing, 100191, China.
  • 3. Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University, Beijing, 100191, China; State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing, 100191, China. Electronic address: [email protected].
  • 4. Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University, Beijing, 100191, China. Electronic address: [email protected].
Abstract

Cobalamin-dependent methionine synthase (MetH) is involved in the process of tumor cell growth and survival. In this study, a novel series of N5-electrophilic substituted tetrahydropteroate analogs without glutamate residue were designed as non-classical antifolates and evaluated for their inhibitory activities against MetH. In addition, the cytotoxicity of target compounds was evaluated in human tumor cell lines. With N5-chloracetyl as the optimum group, further structure research on the benzene substituent and on the 2,4-diamino group was also performed. Compound 6c, with IC50 value of 12.1 μM against MetH and 0.16-6.12 μM against five Cancer cells, acted as competitive inhibitor of MetH. Flow cytometry studies indicated that compound 6c arrested HL-60 cells in the G1-phase and then inducted late Apoptosis. The molecular docking further explained the structure-activity relationship.

Keywords
Anticancer; Antifolate; Inhibitor; Methionine synthase; Pyrido[3,2-d]pyrimidine.