Computational Analysis of SAM Analogs as Methyltransferase Inhibitors of nsp16/nsp10 Complex from SARS-CoV-2

Int J Mol Sci. 2022 Nov 12;23(22):13972. doi: 10.3390/ijms232213972.

Abstract

Methyltransferases (MTases) enzymes, responsible for RNA capping into severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), are emerging important targets for the design of new anti-SARS-CoV-2 agents. Here, analogs of S-adenosylmethionine (SAM), obtained from the bioisosteric substitution of the sulfonium and amino acid groups, were evaluated by rigorous computational modeling techniques such as molecular dynamics (MD) simulations followed by relative binding free analysis against nsp16/nsp10 complex from SARS-CoV-2. The most potent inhibitor (2a) shows the lowest binding free energy (-58.75 Kcal/mol) and more potency than Sinefungin (SFG) (-39.8 Kcal/mol), a pan-MTase inhibitor, which agrees with experimental observations. Besides, our results suggest that the total binding free energy of each evaluated SAM analog is driven by van der Waals interactions which can explain their poor cell permeability, as observed in experimental essays. Overall, we provide a structural and energetic analysis for the inhibition of the nsp16/nsp10 complex involving the evaluated SAM analogs as potential inhibitors.

Keywords: MD simulations; SAM analog; SARS-CoV-2; binding free energy; inhibition mechanism; nsp16/nsp10.

MeSH terms

  • COVID-19 Drug Treatment*
  • Humans
  • Methyltransferases / metabolism
  • S-Adenosylmethionine* / metabolism
  • S-Adenosylmethionine* / pharmacology
  • SARS-CoV-2
  • Viral Nonstructural Proteins / metabolism

Substances

  • S-Adenosylmethionine
  • Viral Nonstructural Proteins
  • Methyltransferases