MIAMI BEACH, FL, Oct. 25, 1999 -- Researchers from the Harvard Medical School and Alexion Pharmaceuticals, Inc. (Nasdaq: ALXN) today reported that the transplantation of immunoprotected pig neurons into non-human primate models of Parkinson's disease resulted in successful engraftment and function of the transplanted cells. Presented here at the 29th Meeting of the Society for Neuroscience, the study shows that the acceptance of the engrafted cells was enhanced through the use of Alexion's proprietary C5 Complement Inhibitor. 5G1.1, an anti-inflammatory C5 Inhibitor drug, is currently being tested in Phase II clinical trials for the treatment of various chronic inflammatory disorders.
Entitled "Xenotransplantation of Transgenic Fetal Pig Dopamine Neurons Into Monkey with Complement Inhibition," the report comes from the laboratories of Dr. Ole Isacson of the Neuroregeneration Laboratories, Harvard Medical School, McLean Hospital, in Belmont, MA, working in collaboration with scientists from Alexion Pharmaceuticals, Inc., New Haven, CT.
Parkinson's disease is a progressive disorder of the central nervous system affecting over one million people in the United States. Clinically, the disease is characterized by a decrease in spontaneous movements, rigidity and tremor. Parkinson's disease is caused by the degeneration of the dopamine-producing neurons in the substantia nigra of the brain, resulting in decreased dopamine availability.
In the study, these scientists demonstrated that transplantation of neurons from Alexion's transgenic pigs restored dopamine production locally and selectively in the affected part of the brain in primates with Parkinson's-like disease. Additionally, the results show that the activity of Alexion's pharmaceutical C5 Inhibitor further improved the survival of the immunoprotected neurons.
"The combined use of Alexion's dual immunoprotective technologies now offers
hope for a significant improvement in the survival of
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Contact: Tom Baker
t.baker@noonanrusso.com
212-696-4455 ext 205
Noonan/Russo Communications
24-Oct-1999