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Quantitative Structure-Activity Relationship, Activity Prediction, and Molecular Dynamics of Non-nucleotide Reverse Transcriptase Inhibitors
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Pan-RAS Inhibitors: Expanding Therapeutic Potential and Evading Resistance.

Sindhu Ramesh1, Junwei Wang1, Chung-Hui Huang1

  • 1Department of Drug Discovery and Development, Harrison College of Pharmacy, Auburn University, Auburn, AL 36849, USA.

Cancers
|June 12, 2026
PubMed
Summary

Pan-RAS inhibitors offer a promising new approach to cancer treatment by targeting all RAS isozymes, potentially overcoming resistance seen with mutant-specific KRAS inhibitors. Emerging clinical data suggests these inhibitors may have a favorable safety profile.

Keywords:
RAScancerpan-KRASpan-RASresistancetherapeutic

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Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Development

Background:

  • Mutations in RAS genes (KRAS, HRAS, NRAS) drive approximately 30% of human cancers by activating RAS proteins and downstream signaling pathways.
  • Activated RAS, whether mutant or wild-type (WT), promotes cancer hallmarks like proliferation, metabolic reprogramming, immunosuppression, and metastasis.
  • Current therapies targeting specific RAS mutations, like KRAS G12C, show efficacy but have limitations due to rare mutation prevalence and adaptive resistance.

Purpose of the Study:

  • To review the evolution and current status of pan-RAS and pan-KRAS inhibitors in preclinical and clinical development.
  • To highlight the potential of pan-RAS inhibitors to overcome resistance mechanisms and offer broader efficacy.
  • To discuss emerging tumor models for advancing preclinical evaluation of these inhibitors.

Main Methods:

  • Review of existing preclinical and clinical research on pan-RAS and pan-KRAS inhibitors.
  • Analysis of therapeutic efficacy and resistance mechanisms associated with RAS-targeted therapies.
  • Evaluation of emerging human-relevant tumor models for drug development.

Main Results:

  • Mutant-specific KRAS G12C inhibitors (sotorasib, adagrasib) are FDA-approved but limited to a specific mutation.
  • Pan-RAS inhibitors, such as RMC-6236 (daraxonrasib), show potential for broader efficacy and overcoming resistance.
  • Early clinical data for RMC-6236 suggests a favorable safety profile, challenging previous predictions of severe toxicity.

Conclusions:

  • Pan-RAS inhibitors represent a promising therapeutic strategy for a wide range of RAS-driven cancers.
  • The development of pan-RAS inhibitors is crucial for addressing the unmet medical need in oncology.
  • Continued research and evaluation in advanced tumor models are essential for advancing pan-RAS inhibitors.