- About the technology
CTLA-4 is an immune regulator that controls response levels in antigen-specific activated effector T cell responses. Previously, it was thought such effects were mediated solely by cell surface CTLA-4, however it has since been shown by Aberdeen researchers that effector responses are also powerfully regulated by a secreted form of CTLA-4 called sCTLA-4 (Ward et al, Eur J Immunology, 2013 43:1274 - 1285). Therapeutic targeting of this effector suppression could release the handbrake on antigen driven immune responses and lead to powerful new treatments for cancer, infectious diseases and autoimmune conditions.
Cancer immunotherapy, encompassing anti-CTLA-4 antibodies, was recently hailed by Science journal as the most important scientific breakthrough of 2013. Dramatic results have been demonstrated by anti-CTLA-4 therapy in the treatment of metastatic melanoma and a range of other cancers, but treatment responses are not universal and side effects are numerous. Other CTLA-4 antibodies do not discriminate between various forms of CTLA-4 (membrane or soluble). The Aberdeen team believe their refined target approach offers a solution as it does not inhibit the membrane bound form.
Ward et al demonstrates blockade of sCTLA-4 can reduce spread of metastatic melanoma in a murine model
In vitro efficacy demonstrated through a 2 way mixed lymphocyte reaction where anti sCTLA4 mAb removes the suppressive effect of sCTLA4. Detailed data can be made available on request subject to appropriate confidentiality arrangements.
- Applications and benefits
- First monoclonal antibodies selective for human natural sCTLA-4
- Enhances antigen-specific immune responses
- In vitro and in vivo data
- Chimeric and humanized mAb variants produced
- Recombinant antigen production system
- Targeted anti-tumour responses
- Cancer vaccine
- Infectious diseases
- Autoimmune diseases
A patent application has been filed and is granted in the USA and national phase in EU, Canada, India, China, Japan and Australia
For further information, contact
Dr James Duncan, Research & Innovation
Email: James Duncan
Tel: 01224 272918