This article may be too technical for most readers to understand.(August 2014) |
Names | |
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Preferred IUPAC name
N-{1-[(2,4-Dichlorophenoxy)acetyl]piperidin-4-yl}-4-sulfanylbutanamide | |
Identifiers | |
3D model (
JSmol)
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ChemSpider | |
PubChem
CID
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UNII | |
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Properties | |
C17H22Cl2N2O3S | |
Molar mass | 405.33 g·mol−1 |
Except where otherwise noted, data are given for materials in their
standard state (at 25 °C [77 °F], 100 kPa).
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K-Ras(G12C) inhibitor 6 is an irreversible inhibitor of oncogenic K-Ras(G12C), [1] subverting the native nucleotide preference to favour GDP over GTP. Its family of inhibitors allosterically control GTP affinity and effector interactions by fitting inside a "pocket", or binding site, of mutant K-Ras. It is the most frequently mutated oncogene. [2]
Investigators and pathologists previously thought that K-Ras is undruggable. [3] However, Kevan M. Shokat and his colleagues, in the Howard Hughes Medical Institute (HHMI) at the University of California, recently reported a novel discovery of "Achilles heel" on K-RAs, and believed that it has real translational implications for patients with K-RAs mutation.[ citation needed]
In recent years, significant research efforts have focused on finding effective inhibitors for the Kras-G12C mutation. For instance, sotorasib (Lumakras) became the first FDA-approved targeted therapy for the treatment of patients with NSCLC harboring the Kras-G12C mutation in 2021. [4] Adagrasib (MRTX849) is another inhibitor that has shown promising results in clinical trials. [5]