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ACCELERATE CLINICAL DEVELOPMENT, REDUCE COSTS, AND IMPROVE TRIAL OUTCOMES

RAS-RAF-SEQ Panel

Reliable, ultra-sensitive detection of genomic alterations in RAS-RAF and PI3K pathways

The RAS-RAF-SEQ panel is a clinical grade, ultra-sensitive liquid biopsy solution for the identification of gene mutations in KRAS, NRAS, BRAF, PIK3CA, and AKT1 to inform therapy selection by detecting established and emerging predictive markers, resistance mutations, and frequently occurring genetic alterations associated with various cancers.


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  • Therapeutic selection – Determine eligibility for anti-EGFR treatment (KRAS/NRAS wild-type), as well as inhibitors of BRAF, PI3K, AKT1, and KRAS. The RAS-RAF-SEQ Panel enables maximum identification of patients eligible for therapy. Less sensitive technologies can miss a significant subset of patients who may benefit from targeted therapy.
  • Determine therapeutic efficacy and monitor disease dynamics – Identify and monitor molecular alterations, including those that may evolve under the influence of treatment exposure. By accurately monitoring disease response and clonal dynamics, the RAS-RAF-SEQ Panel enables informed adaptation of therapeutic strategies.

Clinical Revelance

  • Identify clinically relevant mutations in RAS-RAF and PI3K pathways for targeted therapy in a variety of cancers
  • Identify and monitor molecular alterations, including those evolving during therapy
  • Accelerate development of novel therapeutics through ultra-sensitive detection of clinically relevant mutations


Panel features

RAS-RAF-SEQ exemplary targets mutations and regions

GENE EXON EXAMPLES FOR COVERED ALTERATIONS WITH KNOWN CLINICAL RELEVANCE
AKT1 2 E17K [c49G>A]
BRAF 6, 11, 15 V600X [c1799T>A/C/G, c. 1798_1799delinAA, c1798G>A/C/T
KRAS 2, 3, 4 G12X [c.35G>A/C/T, c.34G>A/C/T, c.34_35delinsTT and others]

G13X [c.38G>A/C/T, c.37G>A/C/T, c.38_39delinsAT and others]

G61X [c.183A>C/G/T, c.182A>C/G/T, c.181C>A/G and others]
NRAS 2, 3, 4 G12X [c.35G>A/C/T, c.34G>A/C/T, c.34_35delinsAA and others]

G13X [c.38G>A/C/T, c.37G>A/C/T, c.37_38delinsAA and others]

Q611X [c.183A>C/G/T, c.182A>C/G/T, c.181C>A/G and others]
PIK3CA 1, 2, 4, 5, 7, 8, 9, 13, 18, 20 C420R [c.1258T>C]
E545X [c.1635G>A/C/T, c.1634A>C/G/T, c.c.1683G>A/C]

M10431 [c.3129G>T], H1047X [c.3140A>G/T, c.3139G>T]
References
  1. U.S. Food and Drug Administration, Center for Drug Evaluation and Research. Erbitux BLA 125084/SUPPL-46 supplement. March 1, 2006. Accessed October 9, 2018. https://www.accessdata.fda.gov/drugsatfda_docs/appletter/2006/125084s046LTR.pdf
  2. FDA Approves Pembrolizumab for Head and Neck Cancer.  August 24, 2016. Accessed  October 9, 2018. https://www.cancer.gov/news-events/cancer-currents-blog/2016/fda-pembrolizumab-hnscc.
  3. FDA Approves Pembrolizumab for Head and Neck Cancer.  August 24, 2016. Accessed  October 9, 2018. https://www.cancer.gov/news-events/cancer-currents-blog/2016/fda-pembrolizumab-hnscc.
  4. Jiang X, Ye J, Dong Z, Hu S, Xiao M. Novel genetic alterations and their impact on target therapy response in head and neck squamous cell carcinoma. Cancer Manag Res. 2019;11:1321-1336. Published 2019 Feb 8. doi:10.2147/CMAR.S187780.