ON01210.Na (Ex-RAD®) mitigates radiation damage through activation of the AKT pathway

PLoS One. 2013;8(3):e58355. doi: 10.1371/journal.pone.0058355. Epub 2013 Mar 7.

Abstract

Development of radio-protective agents that are non-toxic is critical in light of ever increasing threats associated with proliferation of nuclear materials, terrorism and occupational risks associated with medical and space exploration. In this communication, we describe the discovery, characterization and mechanism of action of ON01210.Na, which effectively protects mouse and human bone marrow cells from radiation-induced damage both in vitro and in vivo. Our results show that treatment of normal fibroblasts with ON01210.Na before and after exposure to ionizing radiation provides dose dependent protection against radiation-induced damage. Treatment of mice with ON01210.Na prior to radiation exposure was found to result in a more rapid recovery of their hematopoietic system. The mechanistic studies described here show that ON01210.Na manifests its protective effects through the up-regulation of PI3-Kinase/AKT pathways in cells exposed to radiation. These results suggest that ON 01210.Na is a safe and effective radioprotectant and could be a novel agent for use in radiobiological disasters.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bone Marrow Cells / drug effects
  • Bone Marrow Cells / radiation effects
  • Cell Cycle / drug effects
  • Cell Proliferation / drug effects
  • Cell Survival
  • DNA Damage / drug effects*
  • DNA Damage / radiation effects*
  • Hematopoietic Stem Cells / drug effects
  • Hematopoietic Stem Cells / radiation effects
  • Humans
  • Mice
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Radiation-Protective Agents / pharmacology*
  • Signal Transduction / drug effects*
  • Signal Transduction / radiation effects*
  • Small Molecule Libraries
  • Sulfonamides / pharmacology*

Substances

  • (E)-4-carboxystyryl-4-chlorobenzylsulfone, sodium salt
  • Radiation-Protective Agents
  • Small Molecule Libraries
  • Sulfonamides
  • Proto-Oncogene Proteins c-akt

Grants and funding

This work was supported by Onconova Therapeutics Inc. The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript.