UK-based biotechnology company Oxford BioDynamics (OBD) has collaborated with an undisclosed biopharmaceutical company in the US to advance the discovery and development of new treatments for patients with abnormal wound healing response, leading to fibrosis.

Fibrosis can affect nearly every tissue in the body and if left to progress, the process eventually leads to organ malfunction and may ultimately lead to death.

If the multifaceted and complex healing process is not controlled it can lead to considerable tissue remodelling, which in turn may result in the replacement of functional tissue with permanent fibrous scar tissue.

Oxford BioDynamics CEO Christian Hoyer Millar said: “We are pleased to be collaborating with a major global biopharma company to support the development of potential novel drug candidates, and the identification of patients suitable for a new fibrosis treatment.

“This new collaboration is further evidence of broad adoption of our validated proprietary technology EpiSwitch for practical use in highly challenging therapeutic development programmes.”

“This new collaboration is further evidence of broad adoption of our validated proprietary technology EpiSwitch for practical use in highly challenging therapeutic development programmes.”

Under the agreement, the US company will gain access to OBD’s EpiSwitch technology to be used in the analysis of structure-function of genome architecture and new insights into fibrotic mechanisms.

With this, new therapeutic candidates and next-generation companion diagnostics can be developed, enabling patient population stratification for clinical trials in the area of fibrosis.

Oxford BioDynamics’ technology platform EpiSwitch aims to accelerate the drug discovery and development process and improve the success rate of therapeutic product development.

It is capable of reducing time to market, failure rates and the costs at every stage of drug discovery and provides insights into disease mechanisms for drug discovery and product re‐positioning programmes.