Systemic activation of NRF2 contributes to the therapeutic efficacy of clinically-approved KRAS-G12C anti-cancer drugs
8.0
来源：
Nature
发布时间：
2025-09-02 00:12
摘要：
The research demonstrates that clinically-approved KRAS-G12C inhibitors, Sotorasib and Adagrasib, not only inhibit oncogenic KRAS but also activate NRF2, enhancing anti-cancer immunity. This dual mechanism contributes significantly to their therapeutic efficacy, suggesting that NRF2 activation could be a critical factor in optimizing cancer treatment strategies. The findings have broad implications for the management of lung cancer and potentially other cancers with KRAS mutations.
原文：
查看原文
价值分投票
评分标准
新闻价值分采用0-10分制，综合考虑新闻的真实性、重要性、时效性、影响力等多个维度。
评分越高，表示该新闻的价值越大，越值得关注。
价值维度分析
domain_focus
1.0
business_impact
1.0
scientific_rigor
1.5
timeliness_innovation
1.5
investment_perspective
2.5
market_value_relevance
1.0
team_institution_background
0.5
technical_barrier_competition
0.5
关键证据
NRF2 activation by KRAS inhibitors contributes to anti-cancer immunity.
Study shows that Sotorasib and Adagrasib induce NRF2 independently of KRAS inhibition.
Activation of NRF2 enhances the efficacy of anti-cancer therapies.
真实性检查
否
AI评分总结
The research demonstrates that clinically-approved KRAS-G12C inhibitors, Sotorasib and Adagrasib, not only inhibit oncogenic KRAS but also activate NRF2, enhancing anti-cancer immunity. This dual mechanism contributes significantly to their therapeutic efficacy, suggesting that NRF2 activation could be a critical factor in optimizing cancer treatment strategies. The findings have broad implications for the management of lung cancer and potentially other cancers with KRAS mutations.