Emerging landscape of KRAS inhibitors in cancer treatment

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Authors: Jakob M. Riedl, Hiroyuki Matsubara, Reid McNeil, Parasvi S. Patel, Ferran Fece de la Cruz, Doga C. Gulhan, Ryan B. Corcoran
Cited by: 28
References: 133

Abstract

Alterations in KRAS , NRAS , and HRAS occur in roughly 20% of patients with cancer, making RAS one of the most intensively studied oncogenic targets. The discovery of mutant-selective KRAS G12C inhibitors has provided a proof-of-concept for RAS-directed therapies, heralding a new era in the treatment of RAS-driven cancers. Yet, the efficacy of first-generation KRAS G12C inhibitors is limited by the rapid emergence of resistance. Novel classes of (K)RAS inhibitors with distinct mechanisms of action and broader target coverage hold promise to overcome resistance and extend the benefits of RAS-targeted therapies to a wider patient population. In this review, we summarize clinical evidence for KRAS G12C inhibitors across tumor types and delineate key mechanisms of resistance. We further discuss the rapidly evolving landscape of next-generation (K)RAS inhibitors, with particular emphasis on their target selectivity, mechanisms of action, preliminary clinical efficacy, and the therapeutic opportunities and challenges inherent to each class. RAS mutations drive ∼20% of human cancers. This review summarizes clinical outcomes and resistance mechanisms of KRAS G12C inhibitors and highlights emerging classes of next-generation (K)RAS inhibitors, focusing on their mechanisms of action, selectivity, early efficacy, and potential to overcome resistance in RAS-driven tumors.

Fields of Study & Subjects

Protein Kinase Regulation and GTPase Signaling PI3K/AKT/mTOR signaling in cancer Receptor Mechanisms and Signaling

Publication details

Journal / source
Cancer Cell
Publisher
Elsevier BV
Volume
44
Issue
3
Pages
471–497
Publication date
29 January 2026
Language
EN