Malolactone strikes: K-Ras-G12D's Achilles' heel

Trends Pharmacol Sci. 2024 Jun;45(6):472-474. doi: 10.1016/j.tips.2024.04.001. Epub 2024 Apr 22.

Abstract

In a recent study in Nature Chemical Biology, Zheng et al. exploiting strain release by malolactone-based electrophiles designed a first-in-class covalent inhibitor that targets the elusive aspartate of the Kirsten rat sarcoma viral oncogene homolog (K-Ras)-G12D variant, which is highly prevalent in pancreatic cancer. The compound drastically inhibited oncogenic signaling and tumor growth in preclinical K-Ras-G12D-mutant pancreatic cancer models, expanding treatment potential beyond K-Ras-G12C-targeted therapies.

Keywords: K-Ras-G12D; alkylation; covalent inhibitor; malolactone; strain release.

MeSH terms

  • Animals
  • Antineoplastic Agents / chemistry
  • Antineoplastic Agents / pharmacology
  • Humans
  • Mutation
  • Pancreatic Neoplasms* / drug therapy
  • Pancreatic Neoplasms* / pathology
  • Proto-Oncogene Proteins p21(ras)* / antagonists & inhibitors
  • Proto-Oncogene Proteins p21(ras)* / genetics
  • Proto-Oncogene Proteins p21(ras)* / metabolism
  • Signal Transduction / drug effects

Substances

  • Proto-Oncogene Proteins p21(ras)
  • Antineoplastic Agents
  • KRAS protein, human