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SundayNew and Improved Copaxone?
New and Improved Copaxone?
Here is a story our friend Jayce sent to us about a company improving on Copaxone. Supposedly it will work more efficiently and only be needed to be injected subcutaneously once a week--eliminating the other six injections (yea!). Abstract from ECTRIMS 2006 below... Immunomodulation of experimental autoimmune encephalomyelitis by the novel copolymer PI-2301 B. Carrillo-Rivas, J.T. Kovalchin, J. Krieger, M. Augustyniak, I. Dufour, K. Johnson, H.M. Genova, K. Rafuse, A. Ward, S. Baldwin, R. Kolbeck, J-C. Gutierrez-Ramos, E. Zanelli (Cambridge, USA) Years of clinical experience have shown that daily subcutaneous administration of the peptide copolymer Copaxoneâ„¢ (Cop-1), a mixture of millions of peptides composed of the four amino acids YEAK in random order, is a safe and efficacious treatment for relapsing-remitting multiple sclerosis (RR-MS). Cop-1 was modeled to mimic myelin basic protein (MBP) and turned out to ameliorate experimental autoimmune encephalomyelitis (EAE) in mice, most likely by shifting the immune response away from an effector TH1 to an immunoregulatory TH2/TH3 immune response through presentation by MHC class II molecules. Recently, a series of new peptide copolymers have been synthesized with the goal to improve the in vivo efficacy of Cop-1. In the present study, we show that Copolymer PI-2301 produced by substituting E with F has improved beneficial effects in a relapsing-remitting murine model of EAE. Unlike Cop-1, PI-2301 shows long-term therapeutic efficacy when administered either daily or weekly at disease onset. In an adoptive EAE setting, efficacy of PI-2301 administered daily at the time of autoreactive lymph node cell transfer correlates with decreased serum level of Metalloproteinase-9 and increased level of Metalloproteinase Inhibitor-1. Antibody production against PI-2301 and T-cell recall proliferation assay using splenocytes from PI-2301-treated mice underscore the induction of a TH2/TH3 immunity. Evidences of the expansion of T-cells with regulatory properties expressing Forkhead box protein P3 (FoxP3) and producing Interleukin-10 following PI-2301 treatment are also apparent. We propose that PI-2301 is a potential novel immunomodulatory compound for the treatment of RR-MS. Clinical trials will soon be started to test this hypothesis. Also, here's a link to the company developing the drug. Interestingly though, it isn't Teva pharmaceuticals. |