The KRAS-G12C inhibitor: activity and resistance

Cancer Gene Ther. 2022 Jul;29(7):875-878. doi: 10.1038/s41417-021-00383-9. Epub 2021 Sep 1.

Abstract

Although it has long been deemed "undruggable", with the development of drugs specifically binding the KRAS-G12C mutant protein, clinical trials that directly inhibit oncogenic RAS have recently made promising improvements. In particular, the covalent KRAS-G12C inhibitors sotorasib and adagrasib are used to treat patients with advanced non-small cell lung cancer (NSCLC) carrying KRAS-G12C mutations. Unfortunately, the vast majority of patients do not respond to KRAS-G12C inhibitor therapy, mainly due to intrinsic or acquired resistance caused by cellular, molecular, and genetic mechanisms. Improving the understanding of drug response in the tumor microenvironment may continue to promote the design, testing, and clinical application of KRAS-G12C inhibitors.

Publication types

  • Editorial

MeSH terms

  • Acetonitriles
  • Carcinoma, Non-Small-Cell Lung* / drug therapy
  • Carcinoma, Non-Small-Cell Lung* / genetics
  • Humans
  • Lung Neoplasms* / drug therapy
  • Lung Neoplasms* / genetics
  • Mutation
  • Piperazines
  • Proto-Oncogene Proteins p21(ras)* / antagonists & inhibitors
  • Proto-Oncogene Proteins p21(ras)* / genetics
  • Pyrimidines
  • Tumor Microenvironment / genetics

Substances

  • Acetonitriles
  • KRAS protein, human
  • Piperazines
  • Pyrimidines
  • adagrasib
  • Proto-Oncogene Proteins p21(ras)