KRAS G12C Inhibition in Non-Small Cell Lung Cancer
Understanding the role of

The KRAS G12C mutation drives cancer cell growth and survival1

KRAS G12C is a point mutation at codon 12 that causes a glycine to cysteine amino acid substitution.2

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See below for a deeper look into the role of KRAS G12C in cancer3

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KRAS G12C oncogenic signaling

  • In normal cells, KRAS cycles between an active and inactive state to regulate downstream signaling pathways, leading to cellular proliferation, differentiation, and survival4
  • In tumor cells, the active GTP-bound form of KRASG12C is favored, resulting in oncogenic signaling and tumorigenesis1

Watch the video below for a deeper look into the role of KRAS G12C in cancer

Understanding KRASG12C represents an important approach that warrants further investigation

AKT, protein kinase B; EGFR, epidermal growth factor receptor; ERK, extracellular signal-regulated kinase; GDP, guanosine diphosphate; GTP, guanosine triphosphate; KRAS, Kirsten rat sarcoma; MEK, mitogen-activated protein kinase kinase; mTOR, mammalian target of rapamycin; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; NSCLC, non-small cell lung cancer; PI3K, phosphoinositide 3-kinase; RAF, rapidly accelerated fibrosarcoma; RAL, Ras-like; RTK, receptor tyrosine kinase.

References: 1. Ryan MB, et al. Nat Rev Clin Oncol. 2018;15:709-720. 2. Ihle NT, et al. J Natl Cancer Inst. 2012;104:228-239. 3. Neel NF, et al. Genes Cancer. 2011;2:275-287. 4. Ferrer I, et al. Lung Cancer. 2018;124:53-64.