Small molecules for Kirsten rat sarcoma viral oncogene homolog mutant cancers: Past, present, and future.

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Tác giả: Peiliang Dong, Hua Han, Jiating Ni, Mingtao Wang, Meng Yang, Xinyue Zheng

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: Netherlands : European journal of pharmacology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 740484

Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations have been identified in more than 20% of human cancers as one of the most common oncogenes, especially in non-small cell lung, colorectal, and pancreatic cancers. KRAS regulates the activation of multiple proteins involved in cell growth and proliferation, such as extracellular regulated protein kinases and mammalian target of rapamycin, as a hub between the epidermal growth factor receptor (EGFR) and downstream MAPK and AKT pathways. However, due to the lack of a binding pocket, KRAS has long been considered an undruggable target in recent decades until the discovery of Sotorasib (AMG510). With the approval of Glecirasib (JAB-21822), there are three approved small molecule inhibitors of KRAS, all of which are KRAS G12C inhibitors. At the same time, the limited clinical benefits and rapid emergence of drug resistance to the approved inhibitors have also promoted the emergence of more therapeutics, such as tri-complexes and proteolysis-targeting chimeras (PROTAC). In this paper, we summarize the development of KRAS inhibitors (KRAS
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