KRAS G12C–Mutant Non–Small Cell Lung Cancer
Open accessAbstract
Mutation in the gene that encodes Kirsten rat sarcoma viral oncogene homolog ( KRAS ) is the most common oncogenic driver in advanced non–small cell lung cancer, occurring in approximately 30% of lung adenocarcinomas. Over 80% of oncogenic KRAS mutations occur at codon 12, where the glycine residue is substituted by different amino acids, leading to genomic heterogeneity of KRas-mutant tumors. The KRAS glycine-to-cysteine mutation (G12C) composes approximately 44% of KRAS mutations in non–small cell lung cancer, with mutant KRas G12C present in approximately 13% of all patients with lung adenocarcinoma. Mutant KRas has been an oncogenic target for decades, but no viable therapeutic agents were developed until recently. However, advances in KRas molecular modeling have led to the development and clinical testing of agents that directly inhibit mutant KRas G12C . These agents include sotorasib (AMG-510), adagrasib (MRTX-849), and JNJ-74699157. In addition to testing for known actionable oncogenic driver alterations in EGFR , ALK , ROS1 , BRAF , MET exon 14 skipping, RET , and NTRK and for the expression of programmed cell-death protein ligand 1, pathologists, medical oncologists, and community practitioners will need to incorporate routine testing for emerging biomarkers such as MET amplification, ERBB2 (alias HER2 ), and KRAS mutations, particularly KRAS G12C, considering the promising development of direct inhibitors of KRas G12C protein.
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JNJ-74699157 blocks downstream signaling of KRASG12C by covalently binding to the KRASG12C complex near S-II P of the KRAS mutant protein.
“It blocks downstream signaling of KRASG12C by covalently binding to the KRASG12C complex near S-II P of the KRAS mutant protein.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [65]
JNJ-74699157 is a new generation, oral, selective, covalent inhibitor of the KRASG12C subtype developed by Wellspring.
“JNJ-74699157 (4), also called ARS-3248, is a new generation, oral, selective, covalent inhibitor of the KRASG12C subtype developed by this company.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [65]
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- Authors
- Veluswamy, R., Mack, P. C., Houldsworth, J., Elkhouly, E., & Hirsch, F. R.
- Affiliations
- Mount Sinai Hospital (US)
- Amgen (United States) (US)
- Corresponding author
- Hirsch, Fred R.
- Venue
- The Journal of Molecular Diagnostics
- Publisher
- Elsevier BV
- Published
- 2021-05
- Volume
- 23
- Issue
- 5
- Pages
- 507-520
- ISSN
- 1525-1578 (ISSN-L)
- OpenAlex
- W3131881635
- Cited by
- 96
- References
- 87
- Citations by year
- 2026: 11 · 2025: 24 · 2024: 18 · 2023: 25 · 2022: 9 · 2021: 9
- FWCI
- 2.51
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Molecular Diagnostics (publishedVersion, other-oa)
- PubMed (publishedVersion)
- Funders
- AbbVie
- Amgen
- Merck
- Novartis
- Bristol-Myers Squibb
- AstraZeneca
- Genentech
- Lung Cancer Research Foundation
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- KRAS G12C mutation, non-small cell lung cancer, lung adenocarcinoma, KRAS inhibitors, sotorasib, adagrasib, driver mutations, actionable biomarkers, MET amplification, HER2, KRAS mutation testing
- MeSH terms
- Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Humans, Lung Neoplasms, Mutation, Proto-Oncogene Proteins p21(ras), Diagnostic Techniques and Procedures, Molecular Targeted Therapy
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