在一项具有里程碑意义的临床试验中，胰腺癌药物daraxonrasib将中位生存时间从6.7个月几乎翻倍至13.2个月。该药物通过抑制突变的KRAS蛋白发挥作用，这种蛋白充当了推动肿瘤生长的卡住的分子开关。

KRAS是RAS癌基因家族的一部分，RAS突变存在于所有癌症的20%中，全球每年约有340万例病例。这些蛋白质于1982年被发现，由于其具有挑战性的分子结构，在过去的四十年里一直被认为是“不可成药”的。

虽然daraxonrasib不是一种根治方法，但它改变肿瘤微环境的能力可能会使侵袭性癌症对免疫疗法和其他联合疗法更加敏感。此外，该药物及其未来的改进版本有可能治疗其他RAS驱动的疾病，例如肺癌和儿童神经母细胞瘤。

In a landmark clinical trial, the pancreatic cancer drug daraxonrasib nearly doubled median survival times from 6.7 months to 13.2 months. The drug works by inhibiting the mutated KRAS protein, which acts as a jammed molecular switch driving tumor growth.

KRAS is part of the RAS oncogene family, with RAS mutations present in 20% of all cancers, representing approximately 3.4 million cases globally each year. Discovered in 1982, these proteins were deemed "undruggable" for four decades due to their challenging molecular structures.

While daraxonrasib is not a cure, its ability to alter the tumor microenvironment may make aggressive cancers more susceptible to immunotherapy and other combined treatments. Furthermore, the drug and its future iterations could potentially treat other RAS-driven diseases, such as lung cancer and childhood neuroblastoma.

Source: A new drug targets one of cancer’s master switches

Subtitle: The pancreatic-cancer drug could be the first of an entirely new class of treatments

Dateline: 6月 18, 2026 03:38 上午