Out-licensing

Targeted Therapy for Specific Autoimmune Disease: Stimulation of sCTLA-4 that Targets Pathogenic T-cells Alone

Introduction/Background

Each year the incidence of autoimmune disease is increasing. The third largest category of illness in the industrialized world behind heart disease and cancer is autoimmune disease. Over sixty disease types are currently identified and the demand for therapies is increasing. Over the coming years new therapeutic approaches will drive the market for autoimmune disorder treatments to grow at a rate of over 15%. A recent market report on rheumatoid arthritis predicted that in 2009, segment distribution within the market will be COX-2 inhibitors at 19% and biological response modifiers at 76%, with other drugs accounting for 5% of revenue.

Autoimmune disease is caused by pathogenic T-cells attacking and destroying the body's own tissues. Specific proteins in the tissue are recognised erroneously by the immune system as a threat and targeted for destruction by T-cells. Studies have shown that all T-cells have a natural mechanism that switches the activated attacking T-cell into a resting non-attacking state. Current therapies in clinical trial utilize a recombinant fusion protein comprising immunoglobulin and cytotoxic T-lymphocyte antigen-4 (CTLA-4). CTLA-4 acts as a natural repressor and exerts immunosuppressive effects on pathogenic T cells.

Aims/Hypothesis

There is a need for the development of targeted therapy for specific autoimmune diseases.

Research

Aberdeen University researchers have discovered a peptide-based approach that stimulates production of a natural soluble form of CTLA-4 (sCTLA-4) that targets pathogenic T-cells alone. The resulting effect is a focused immune suppression of the disease-causing T cells, while retaining a normal functional immune system.

sCTLA-4 acts as a novel biological response modifier making this technology highly significant in the inflammatory response treatment market. Other autoimmune diseases to which the novel technology is applicable include autoimmune haemolytic anaemia and systemic lupus erythematosus where incidence rates are reported to be in the order of 40-50 per 100,000 persons (USA) and 200 per 100,000 woman aged from 18 to 65 years (UK). This technology is in contrast to current global immunosuppressive treatments, and offers targeted therapy specific to the disease-causing T-cells.

Conclusion

A peptide is described that selectively inactivates pathogenic T-cells responsible for autoimmune disease. Potential applications of this therapy include for example rheumatoid arthritis, psoriasis, multiple sclerosis and autoimmune haemolytic anaemia

Relevance/Opportunity

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Preclinical