Ervaxx and Cardiff University enter collaboration to develop novel 
T-cell and T-cell receptor-based immunotherapeutics targeting 
Dark Antigens®

Ervaxx and Cardiff University enter collaboration to develop novel 
T-cell and T-cell receptor-based immunotherapeutics targeting 
Dark Antigens®

Press release.

London, UK – 24 January 2020. Ervaxx™, a biotechnology company pioneering the use of Dark Antigens™ to develop T-cell receptor (TCR)-based immunotherapies and off-the-shelf cancer vaccines, has entered a licensing and research collaboration with a leading T-cell immunology group at Cardiff University (Cardiff, UK).

The new collaboration will support a multi-year research program with Prof. Andrew Sewell’s T-cell modulation group at Cardiff University focusing on the discovery and characterization of T-cells and TCRs reactive to cancer-specific antigens and ligands, including Ervaxx’ proprietary Dark Antigens™. Ervaxx will fund the program.

The collaboration will also advance exciting new research published earlier this week by the Cardiff University team in Nature Immunology1, where they identified a T cell clone that recognized and killed multiple different types of human cancer, while remaining inert to non-cancerous cells. The T cell clone targets MR1, an MHC class 1-related protein, via an unidentified cancer-specific ligand. These exciting findings, validated in a preclinical model, open the prospect of immunotherapies with broad utility across patients with diverse cancers. This approach into previously unexplored cell surface epitopes complements and extends Ervaxx’s exploration of novel cancer-specific antigens.

Under the agreement, Ervaxx gains an exclusive license to relevant Cardiff University patents claiming T cells and TCRs reactive to cancer-specific antigens. The Company has the right to advance resulting candidate T-cell/TCR-based immunotherapeutics and cancer vaccines through development and commercialization. Cardiff University is eligible to receive milestone payments on any candidates that advance from the discovery collaboration into clinical development and royalty payments on sales of any products that reach the market.

Ervaxx’s Dark Antigens, which are derived from the 98% of the genome that does not encode known proteins, constitute a promising and yet untapped source of targets for immunotherapies. This collaboration will use our world-class expertise in T-cell biology to identify T cells and TCRs reactive to those targets and pave the way for a new wave of treatments in cancer, and potentially other areas. This includes our most recent discovery, published in Nature Immunology, of a T-cell clone that targets MR1 to recognize and kill cancer cells, irrespective of cancer or human leukocyte antigen (HLA) type, offering opportunities for pan-cancer, pan-population cancer immunotherapies.

Prof. Andrew Sewell, Head of the T-cell modulation group, Cardiff University

We are excited to announce this collaboration with Prof. Sewell’s world-class research group. We have great hope that through the combination of this expertise with our Dark Antigens™ and application of our EDAPT™ platform, we will be able to identify further targets to expand our portfolio of TCR-based therapies and cancer vaccines. We are also thrilled to contribute to the development of the group’s exciting new MR1 research, which shows early but enormous potential for the treatment of cancers. This partnership, which follows those with the University of Oxford, University of Cambridge and Johns Hopkins University School of Medicine, reinforces our ambition to collaborate with leading academic institutions and be at the cutting edge of the T-cell immunology field to drive the development of novel off-the-shelf cancer therapies .

Kevin Pojasek, CEO of Ervaxx

Prof. Andrew Sewell is a member of Ervaxx’ Scientific Advisory Board.

1 Crowther, M.D., Dolton, G., Legut, M. et al. Genome-wide CRISPR–Cas9 screening reveals ubiquitous T cell cancer targeting via the monomorphic MHC class I-related protein MR1. Nat Immunol (2020) doi:10.1038/s41590-019-0578-8

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