Available Technology
Novel peptide therapeutic for multiple sclerosis
Technology:
Peptide therapy
Markets Addressed
The main commercial application for this technology is as a pharmaceutical drug for the treatment of multiple sclerosis. The market is quite large; there are approximately 350,000 in the US and 2.5 million worldwide that suffer from MS.
Innovations and Advantages
In multiple sclerosis, the host's immune system (lead by T-cells) attacks and destroys myelin basic protein, the principle component necessary for nerve transmission. Part and parcel of this immune response pathway are the so-called Major Histocompatibility Complex (MHC) molecules. MHC molecules interact with myelin basic protein and bring it to the cell surface for interaction with T-cells, which in turn proliferate and dispose lethal inflammatory cytokines to the cell. This trimeric interaction between T-cells, myelin basic protein, and MHC molecules forms the foundation of Multiple Schlerosis' autoimmune response. Consequently, there is a need to develop agents that can target and inhibit this critical focal point of the disease.
This invention is a peptide therapy for the treatment of multiple sclerosis. The peptides mimic myelin basic protein and inhibit proliferation of T-cells. The amino acid sequences of the peptide are made with modifications to their structure so as to enhance binding to MHC and the T-cell receptor. This enhanced binding between the peptides, MHC, and T cell receptor inhibits downstream effectors of the MS autoimmune response and induces immunological tolerance.
The myelin basic protein peptides have a greater affinity for binding to the MHC class II HLA-DR2 protein groove than an immunodominant epitope from myelin basic protein and an epitope comprising MBP residues 85-99. These agents have also been tested and proven efficacious in an animal model of MS.
Additional Information
Intellectual Property Status: U.S. Patent 6,930,168; other patents pending
Publication:
-Fridkis-Hareli, M., Santambrogio, L., Stern, J.N., Fugger, L., Brosnan, C., and Strominger, J.L. Novel synthetic amino acid copolymers that inhibit autoantigen-specific T cell responses and suppress experimental autoimmune encephalomyelitis. J. Clin. Invest. 109: 1635-1643 (2002).
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Inventor(s):
Fridkis-Hareli, Masha
Strominger, Jack L.
Categories:
For further information, please contact:
Debra Peattie, Director of Business Development
(617) 495-3067
Reference Harvard Case #1846