Virtual screening using covalent docking to find activators for G245S mutant p53

PLoS One. 2018 Sep 7;13(9):e0200769. doi: 10.1371/journal.pone.0200769. eCollection 2018.

Abstract

TP53 is the most mutated gene in all cancers. The mutant protein also accumulates in cells. The high frequency of p53 mutations makes the protein a promising target for anti-cancer therapy. Only a few molecules have been found, using in vitro screening, to reactivate the mutant protein. APR-246 is currently the most successful mutant p53 activator, which reactivates the transcriptional activity of p53 by covalently binding to C124 of the protein. We have recently created in silico models of G245S-mp53 in its apo and DNA-bound forms. In this paper we further report on our in silico screening for potential activators of G245S-mp53. We filtered the ZINC15 database (13 million compounds) to only include drug-like molecules with moderate to standard reactivity. Our filtered database of 130,000 compounds was screened using the DOCKTITE protocol in the Molecular Operating Environment software. We performed covalent docking at C124 of G245S-mp53 to identify potential activators of the mutant protein. The docked compounds were ranked using a consensus scoring approach. We also used ADMET Predictor™ to predict pharmacokinetics and the possible toxicities of the compounds. Our screening procedure has identified compounds, mostly thiosemicarbazones and halo-carbonyls, with the best potential as G245S-mp53 activators, which are described in this work. Based on its binding scores and ADMET risk score, compound 2 is likely to have the best potential as a G245S-mp53 activator compared to the other top hits.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Computer Simulation
  • Humans
  • Models, Genetic*
  • Mutation*
  • Neoplasms / genetics
  • Tumor Suppressor Protein p53 / genetics*

Substances

  • TP53 protein, human
  • Tumor Suppressor Protein p53

Grants and funding

JAT acknowledges funding from the Natural Sciences and Engineering Research Council of Canada and the Allard Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.