(RTTNews) - Evotec SE (EVTCY.PK, EVOTF.PK), a German drug discovery and development company, announced a partnership agreement with the University of Oxford regarding access to biospecimens from the biobank Quality in Organ Donation or QUOD. The company did not disclose any financial terms of the agreement.
QUOD is an initiative of The Nuffield Department of Surgical Sciences or NDS at the University of Oxford in close collaboration with the National Health Service Blood and Transplant or NHSBT organisation in the UK.
The QUOD biobank, a joint programme by a consortium of UK academic transplant centres and NHSBT, is funded by NHSBT and the Medical Research Council. It provides blood, urine and tissue samples from heart, lung, liver and kidney from consented organ donors for researchers with anonymised integrated medical records.
Under the terms of the partnership, Evotec will investigate at first samples from 1,000 donors of the QUOD biobank using a comprehensive multi-omics analysis (genomics, transcriptomics, proteomics, metabolomics). This data will complement Evotec's existing patient database, generating a greater understanding of disease mechanisms across indications, i.e. cardio-vascular, kidney, and liver diseases.
Investigation of diseased versus healthy human biomaterial using a multi-omics approach combined with clinical data will provide extensive knowledge, indispensable for advancement of organ transplantation, drug discovery as well as clinical and biomarker research.
QUOD biobank's samples have been collected over several years with QUOD's primary goal to identify biomarkers, explain mechanisms of injury and repair, and improve organ utilisation and transplantation.
Cord Dohrmann, Chief Scientific Officer of Evotec, said, "We are proud to enter this collaboration with the QUOD programme, which expands our strategic partnership with the University of Oxford beyond LAB282, our first-of-its-kind academic BRIDGE partnership. Comprehensive molecular profiling of patient samples will re-define health and disease according to dysregulated molecular disease mechanisms. This will open new doors for intervention and corresponding patient stratification."
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