Use of a peptide enhancing the ability of radiation therapy to kill cancer cells: a patent evaluation of WO2012016918

Expert Opin Ther Pat. 2012 Dec;22(12):1485-7. doi: 10.1517/13543776.2012.711816. Epub 2012 Aug 8.

Abstract

Background: Faulty apoptosis is a known mechanism that leads to resistance to radiotherapy. The application (WO2012016918A1) deals with a peptide useful for disrupting this resistance mechanism and enhancing the efficiency of radiotherapy.

Methods: A peptide consisting essentially of the N2 sequence of the RasGAP protein is conjugated to the HIV-TAT(48-57) cell permeation sequence. The DNA sequence encoding the peptide (TAT-RasGAP(317-326)) is synthesized and introduced into the host cells.

Results: TAT-RasGAP(317-326) is demonstrated to potentiate the efficacy of γ-irradiation-mediated cell killing both in tumor cell lines and in mouse tumor models, disregarding the status of p53, but not in non-cancer cells.

Conclusion: TAT-RasGAP(317-326) peptide favors apoptosis of tumor cells, but not normal cells in response to radiotherapy. The invention provides a specific method that is probably to be used in cancers that are radio-resistant.

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / radiation effects
  • Drug Design*
  • GTPase-Activating Proteins / chemistry
  • GTPase-Activating Proteins / pharmacology*
  • Humans
  • Mice
  • Neoplasms / drug therapy
  • Neoplasms / pathology
  • Neoplasms / radiotherapy
  • Patents as Topic
  • Peptide Fragments / chemistry
  • Peptide Fragments / pharmacology*
  • Protein Conformation
  • Radiation Tolerance / drug effects
  • Radiation-Sensitizing Agents / chemistry
  • Radiation-Sensitizing Agents / pharmacology*
  • Structure-Activity Relationship
  • Xenograft Model Antitumor Assays

Substances

  • GTPase-Activating Proteins
  • Peptide Fragments
  • Radiation-Sensitizing Agents
  • TAT-RasGAP(317-326)