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Orchestra Therapeutics Announces New Phase II Clinical Data on,NeuroVax Demonstrating Marked Expansion of Regulatory T Cell,Populations in Patients With Multiple Sclerosis

- New Data from Open-Label Study Presented at Federation of Clinical Immunology Societies (FOCIS) Annual Meeting -

CARLSBAD, Calif., June 11, 2007 /PRNewswire-FirstCall/ -- Orchestra Therapeutics, Inc. (Bulletin Board: OCHT) announced today positive new data from its completed Phase II open-label study of NeuroVax(TM), an investigational T Cell Receptor (TCR) peptide vaccine for the treatment of relapsing-remitting multiple sclerosis (MS). The new data, presented last week at the Federation of Clinical Immunology Societies (FOCIS) annual meeting, showed that monthly vaccinations over one year with NeuroVax(TM) markedly expanded the capacity of regulatory T cells (Tregs) to recognize TCRs expressed by potentially pathogenic T cells. New data were also presented that showed NeuroVax(TM) produced a significant increase in TCR-specific T cells in patients with MS, including increases in interleukin-10-secreting T cells (IL-10) and Foxp3+ Tregs.

"These new findings provide evidence to support the network hypothesis, in which internal cell-cell recognition of antigen receptors can be greatly expanded in regulatory T cells by activating the system with NeuroVax(TM). These vaccine induced responses may help control the autoimmune processes that are thought to be the main cause of the inflammatory phase of MS" said Arthur A. Vandenbark, M.D., Ph.D., Senior Research Career Scientist at the VA Medical Center, and Professor of Neurology and Molecular Microbiology and Immunology at Oregon Health & Science University in Portland, OR., and lead author on the study. "Increases in both IL-10-secreting T cells and the Foxp3+ Tregs suggest that NeuroVax(TM) can stimulate native thymus-derived Foxp3+ Tregs as well as induce peripheral Foxp3+ Tregs from CD4+CD25- T cells through an IL-10 controlled mechanism."

"These new data suggest that induction of an expanding population of TCR-reactive, Foxp3+ Tregs by NeuroV
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