One of the most prevalent biomarkers in non-small cell lung cancer (NSCLC)1

Targeting driver alterations enables personalized medicine.

KRAS mutations, including KRAS G12C, are common oncogenic drivers in NSCLC and do not typically overlap with other driver mutations such as EGFR, ALK and ROS1.1,2KRAS mutations are truncal, meaning they occur early and are generally stable throughout the course of the disease, as opposed to other mutations, like EGFR T790M, that may develop over time.3,4

Prevalence of oncogenic drivers in non-squamous NSCLC1

KRAS Chart

KRAS G12C is a prevalent actionable biomarker in NSCLC1

KRAS G12C People Diagram

~1/8 patients (13%)

with non-squamous NSCLC has an actionable KRAS G12C mutation1

Guidelines support testing for KRAS mutations5-7

Identification of driver alterations through biomarker testing is a key component to creating personalized approaches to managing a patient's treatment options. Upfront testing for KRAS mutations may be helpful in patients with advanced NSCLC.5,6,†

KRAS Testing at Diagnosis5,7
✔ CAP / IASLC / AMP Expanded panel recommended
✔ ASCO Expanded panel recommended

† Upfront testing for KRAS mutations may identify patients who are unlikely to benefit from further molecular testing because of the low probability of overlapping targetable alterations.2,5

Biomarker testing reveals activated KRAS

KRAS is a membrane-associated GTPase that regulates cell proliferation and differentiation.8,9 KRAS G12C is a point mutation in codon 12 causing a glycine-to-cysteine substitution near a narrow pocket in the KRAS protein.10,11 Advances in understanding the protein structure have led to the investigation of inhibitors that target the pocket, potentially locking the KRAS G12C mutant protein in the inactive state.12

KRAS G12C mutation drives oncogenic signaling8,9,13


Cell membrane image
The KRAS G12C mutation favors the active form of KRAS mutant protein.8,13

How to test for the KRAS G12C mutation in tissue and plasma

*KRAS educational content provided by Amgen Inc. for use by NeoGenomics.

Biomarker Assist™ KRAS Single Gene Testing (SGT) Program

The Biomarker Assist™ KRAS SGT Program is an Amgen sponsored testing program through NeoGenomics Laboratories to provide a single gene biomarker test, KRAS G12C mutation analysis at no cost to patients living with metastatic (stage IV) non-small cell lung cancer. Eligible patients will receive access to one (1) KRAS Mutation Analysis by Sanger Sequencing. Please note the program does not cover any other costs, including, but not limited to, office visit fees and biopsy fees.

To enroll your patients in the KRAS SGT Program, please follow 3 simple steps:


Order the test and collect sample for a single gene biomarker test to detect KRAS G12C in metastatic (stage IV) non-small cell lung cancer (NSCLC) patients


Send the completed KRAS SGT request form and the sample to NeoGenomics Laboratories (if sample is not sent, ensure Specimen Retrieval is completed on the form and fax to 1-239-690-4237)


Results will be delivered within 7 days of receipt of form and specimen that meets all requirements

If you have questions, please call NeoGenomics Client Services at 1(866)776-5907 option 3.

Download the form and see full terms and conditions.

For more information on Amgen's Biomarker Assist™ KRAS Single Gene Testing Program or Next Generation Sequencing (NGS) Affordability Program, please visit or call Amgen Assist 360™ at 1-888-4ASSIST (1-888-427-7478) for details.

Biomarker Assist™ is a registered trademark of Amgen Inc.


  1. Data on file, Amgen; [Analysis of AACR Genie v8].
  2. Aggarwal S, et al. Presented at: The European Society for Medical Oncology; September 2020; Virtual Congress. Poster 1339P.
  3. McGranahan N, et al. Sci Transl Med. 2015;7:283ra54.
  4. Lindeman NI, et al. Arch Pathol Lab Med. 2018:142;321-346.
  5. Lindeman NI, et al. J Thorac Oncol. 2019;13:323-358.
  6. Pennell NA, et al. Am Soc Clin Oncol Educ Book. 2019;39:531-542.
  7. Kalemkerian GP, et al. J Clin Oncol. 2018;36:911-919.
  8. Ryan MB, et al. Nat Rev Clin Oncol. 2018;36:911-919.
  9. Ferrer I, et al. Lung Cancer. 2018;124:53-64.
  10. Kim D, et al. Cell. 2020. doi:10.1016/j.cell.2020.09.044.
  11. Ihle NT, et al. J Natl Cancer Inst. 2012;104:228-239.
  12. Canon J, et al. Nature. 2018;575:217-223.
  13. Neel NF, et al. Genes Cancer. 2011;2:275-287.