Biomarker platforms

Our approach to companion diagnostic biomarker discovery

Cancer therapy is dictated by risk benefit ratios. For every new therapeutic approved by regulatory agencies, every time a drug is assessed for reimbursement and every time a drug is prescribed in the clinic the Pros (Drug efficacy) are weighed against the Cons (Drug toxicity and cost) as the risk benefit ratio.

The Food and Drug Administration (FDA) and European Medicines Agency (EMA) ideally require a companion diagnostic test for each new cancer drug in the market.

Oxford Cancer Biomarkers (OCB) has developed two biomarker discovery platforms to address both sides of the treatment risk benefit ratio for new therapeutics giving the greatest chance of successful companion diagnostic development.

CancerNav® – anti-cancer drug efficacy biomarkers

  • Genome-wide functional screen patented in EU, US and Japan (Patents EP2005162, 2009-531051 & 2009-0311244).
  • Identifies genes that influence the sensitivity of tumour cells to cancer drugs.
  • Approach validated with a range of cancer drugs and published in peer review journals 1,2.

platform 1

ToxNavTM – drug toxicity biomarkers

Toxgnostic studies rebalance the risk benefit ratios for new therapeutics by:

  • Implementation of unbiased systematic genome-wide discovery of variants that predict severe drug toxicity (CTC Grade 3+).
  • Improved likelihood of approval by regulatory agencies, reimbursement by payers and adoption by clinicians.

Toxgnostic markers can be used alone or in conjunction with companion diagnostic efficacy markers to enhance the selection of patients that would benefit from drug treatment.

OCB is at the forefront of toxgnostic biomarkers 3 and works with some of the world’s best Genome Wide Association Study (GWAS) experts and oncologists.

Using DNA samples and toxicity profiles from Phase III studies, OCB can supply a toxgnostic signature to be used to increase the likelihood of approval with regulatory agencies.

platform 2

  1. Fotheringham S, et al (2008). Genome-wide loss-of-function screen reveals an important role for the proteasome in HDAC inhibitor-induced apoptosis. Cancer Cell. 6;15(1):57-66. doi: 10.1016/j.ccr.2008.12.001. PMID: 19111881.
  2. Khan O, et al (2010). HR23B is a biomarker for tumor sensitivity to HDAC inhibitor-based therapy. Proc Natl Acad Sci U S A. 6;107(14):6532-7. doi: 10.1073/pnas.0913912107. PMID: 20308564
  3. Church D, et al (2014). “‘Toxgnostics’: an unmet need in cancer medicine”. Nat Rev Cancer (6):440-5.