KRAS G12C mutation
Select a target

KRASG12C

KRAS is the most frequently mutated oncogene

KRAS, a member of the RAS family, is a key regulator of signaling pathways responsible for cell proliferation, differentiation, and survival.1,2 KRAS is the most frequently mutated oncogene in human cancer and mutations in KRAS can result in continuous cellular proliferation and cancer development.1,2

KRAS G12C is an oncogenic driver mutation

The KRAS G12C mutation occurs in about 13% of NSCLC patients, and 1%-3% of colorectal and other solid tumors. G12C is a single point mutation with a glycine-to-cysteine substitution at codon 12.1,3,4 This substitution favors the activated state of KRAS, amplifying signaling pathways that lead to oncogenesis.5


Learn more about modalities targeting KRASG12C:
small molecules.

MCL video

Watch this video to learn more about the mechanism of disease for KRASG12C mutated cancers

MCL video

Watch this video trailer for gamified medical education on KRAS G12C for healthcare professions. To access the Medical Educational Interactive, click here.

Search our clinical trials.

Visit our resources section for additional information on potential oncogenic targets.

Mutant KRASG12C supports cancer cell growth and survival1,5-8

Illustration of wild type KRAS in a normal cell

Drawings are not to scale and proteins are enlarged and separated for clarity.

CLICK to learn more about GTP/GDP cycling in wild-type KRAS
Illustration of mutant KRAS in a tumor cell

Drawings are not to scale and proteins are enlarged and separated for clarity.

CLICK to learn more about GTP/GDP cycling in mutant KRASG12C
Learn more about small molecules:
Clinical trials are underway in9:

Amgen is committed to helping patients with NSCLC and other solid tumors with KRAS G12C mutations

KRAS - A key Oncogenic Driver and Novel Investigational Target in NSCLC
Download an educational slide deck on KRAS and biomarker testing in NSCLC
KRAS - A key Oncogenic Driver and Novel Investigational Target in NSCLC
Download a fact sheet on KRAS G12C mutations and biomarker testing in NSCLC
Learn More at www.FindKRASG12C.com

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; mTOR: mammalian target of rapamycin; NF- κB: nuclear factor kappa-light chain enhancer of activated B cells; NSCLC: non-small cell lung cancer; PI3K: phosphatidylinositol 3-kinase; RAF: rapidly accelerated fibrosarcoma; RAL: ras-like; RAS: rat sarcoma; RTK: receptor tyrosine kinase.

References

1. Cox AD, Fesik SW, Kimmelman AC, Luo J, Der CJ. Nat Rev Drug Discov. 2014;13(11):828-851. 2. Downward J. Nat Rev Cancer. 2003;3(1):11-22. 3. Biernacka A, Tsongalis PD, Peterson JD, et al. Cancer Genet. 2016;209(5):195-198. 4. Neumann J, Zeindl-Eberhart E, Kirchner T, Jung A. Pathol Res Pract. 2009;205:858-862. 5. Ryan MB, Corcoran RB. Nat Rev Clin Oncol. 2018;15(11):709-720. 6. Simanshu DK, Nissley DV, McCormick F. Cell. 2017;170(1):17-33. 7. Neel NF, Martin TD, Stratford JK, Zand TP, Reiner DJ, Der CJ. Genes Cancer. 2011;2(3):275-287. 8. Ahmadzada T, Kao S, Reid G, Boyer M, Mahar A, Cooper WA. J Clin Med. 2018;7(6):E153. doi: 10.3390/jcm7060153. 9. Q2 2019 pipeline, Amgen. https://www.amgenpipeline.com/~/media/amgen/full/www-amgenpipeline-com/charts/amgen-pipeline-chart.ashx. Accessed October 15, 2019.