Soluble CD52 as a therapeutic for inflammatory disease

Soluble CD52 as a therapeutic for inflammatory disease

Partnering opportunity in inflammation:

Soluble CD52 as a therapeutic for inflammatory disease

 

Team

Professor Len Harrison, Dr Esther Bandala-Sanchez, Dr Maryam Rashidi

Background

Autoimmune disorders affect up to 4 per cent of the global population. Numerous pharmaceutical products are currently marketed to treat immuno-inflammatory conditions, however these therapies have limited efficacy, can be associated with serious side effects and may only offer symptomatic relief.

From a commercial perspective, many of the top selling immuno-modulatory drugs are off patent or facing patent expiry, and many products in the pipeline are based on existing therapies.

As such, there is a clinical and commercial need for a novel class of immuno-modulatory drugs.

The technology

Our scientists have found that CD52, a GPI-linked protein found on white blood cells, is highly expressed by human activated CD4+ regulatory T cells (CD52hi CD4+ T cells), and gives these cells a suppressive function. Following activation, CD52 is cleaved from CD52hi CD4+ T cells and binds to Siglec-10, a T cell inhibitory receptor.

Our researchers have shown that CD52hi T cells retard the development of diabetes in NOD models. Soluble CD52 is therefore a potential therapeutic agent for autoimmune disease. We have developed a recombinant CD52-Fc fusion protein that suppresses a range of T-cell responses including proliferation and cytokine release, both in vitro and in vivo, as well as suppression of immune-inflammatory disease in models of diabetes and sepsis.

Applications

This technology has potentially broad applications in immune-inflammatory diseases such as Type 1 diabetes, sepsis, rheumatoid arthritis and multiple sclerosis.

Intellectual property

The intellectual property is protected by multiple national phase patent applications (WO2014075125).

Opportunity for partnership

We are seeking a partner to invest in the ongoing development of synthetic CD52 as a therapeutic candidate.

The proposed plan is to develop a lead candidate and determine scope of efficacy and safety, which will position the technology for entry into pre-clinical toxicity program and IND filing.

Key publication

  • Bandala-Sanchez E. et al. T cell regulation mediated by interaction of soluble CD52 with the inhibitory receptor Siglec-10. Nat Immunol 2013 Jul;14(7):741-8. PMID: 23685786

Contact

Dr Lauren Giorgio, Business Development Associate

Phone: +61 3 9345 2779 Email: giorgio.l@wehi.edu.au

 

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