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KRAS G12D is an important driver mutation in solid tumors such as pancreatic, colorectal, and lung cancers. The emergence of molecules such as MRTX1133 has demonstrated that KRAS G12D can be directly targeted pharmacologically, whereas targeted protein degradation technologies such as PROTACs ...
KRAS G12D是胰腺癌、结直肠癌和肺癌等实体瘤中的重要驱动突变。MRTX1133等分子的出现证明了KRAS G12D可以被直接药理干预，而PROTAC等靶向蛋白降解技术进一步将作用模式从“占据并抑制KRAS”推进到“募集E3连接酶并清除KRAS蛋白”。
RAS mutations drive many tumors, including pancreatic cancer, colorectal cancer, and lung cancer. However, RAS was long considered difficult to drug because of its shallow structural pockets and tight GTP binding. The emergence of RAS(ON) inhibitors, molecular glues, and PROTACs has shifted RAS ...
RAS突变驱动胰腺癌、结直肠癌和肺癌等多种肿瘤，但因结构口袋浅、GTP结合紧密，长期难以成药。RAS(ON)抑制剂、分子胶和PROTAC的出现，使RAS干预从阻断信号走向清除致癌蛋白。
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