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PRECLINICAL DATA SHOW CAMBRIDGE NEUROSCIENCE COMPOUND TO REDUCE BRAIN DAMAGE FOLLOWING STROKE

 PRECLINICAL DATA SHOW CAMBRIDGE NEUROSCIENCE COMPOUND
 TO REDUCE BRAIN DAMAGE FOLLOWING STROKE
 SAN DIEGO, Calif., May 6 /PRNewswire/ -- In vivo preclinical data presented today at the American Academy of Neurology meeting here by researchers, led by Dr. Marc Fisher, chief of Neurology at The Medical Center of Central Massachusetts, indicate that Cambridge NeuroScience's (NASDAQ: CNSI) neuroprotective compound, CNS 1102, has therapeutic potential for limiting the extent of brain damage in human beings following a stroke. Based on these encouraging data, the company has accelerated its preclinical development of this NMDA ion- channel blocker, and expects to begin human clinical trials by year- end.
 The researchers used an animal model of stroke that produced significant brain damage, and employed a technology that allowed for immediate and continuous viewing of changes in brain function during the stroke's progress. In the past, such ischemia-induced damage could be measured only post-mortem. Dr. Fisher and his colleagues have developed a technique for measuring such damage using a type of Magnetic Resonance Imaging (MRI) on the living animal, and his results correlate with the post-mortem examination. This technique offers an important clinical tool to immediately assess the potential of a given dose of CNS 1102 to prevent brain damage in stroke patients.
 "The results of this study are particularly encouraging because they provide additional evidence for CNS 1102's potential efficacy in stroke, as well as providing new techniques for assessing the agent as we go forward into human clinical trials," stated Fisher. "MRI holds the potential for detecting functional abnormalities in the brain within 30 minutes after the onset of stroke, which increases our understanding of the stroke process, as well as validating our assumptions about the efficacy of CNS 1102."
 It is known that nerve cell death following a stroke is triggered by excessive glutamate released from damaged nerve terminals. This excessive glutamate in turn stimulates the massive entry of calcium into nerve cells, resulting in cell death and brain damage. Cambridge NeuroScience is pursuing several approaches to limit the extent of such nerve cell death, including compounds which selectively block the NMDA ion-channel, thereby preventing the inward flow of calcium. CNS 1102 is the company's lead NMDA ion-channel blocker. The compound has demonstrated the capability of reducing brain damage in "in vivo" studies by independent investigators. NMDA blockers cross the blood- brain barrier, and therefore are likely to be administered without the need for special drug delivery systems.
 "There is currently no effective drug therapy available for the approximately 500,000 victims of stroke in the U.S. each year," said Dr. Elkan Gamzu, president and chief operating officer of Cambridge NeuroScience. "NMDA blockers are an exciting class of compounds which block the pathways or ion-channels that allow the entry of the lethal amounts of calcium ions into nerve cells. We are particularly pleased with the high degree of activity and selectivity that is being demonstrated by our proprietary compound, CNS 1102. The animal preclinical data are extremely encouraging."
 The Medical Center of Central Massachusetts is the fifth largest health care institution in Massachusetts, and one of the largest in New England. It is the regional center for seriously ill and small newborns and for women experiencing high risk pregnancies. It is the regional dialysis center and the New England regional hemophilia center. The Med Center has two main campuses, Hahnemann and Memorial in Worcester, and several satellite facilities.
 Cambridge Neuroscience is a leading neuroscience company engaged in the discovery and development of proprietary pharmaceuticals with a focus on nerve cell survival. The company is developing a number of products to treat stroke, traumatic brain injury, schizophrenia and chronic neurodegenerative disorders such as diabetic peripheral neuropathy and amyotrophic lateral sclerosis (Lou Gehrig's disease).
 -0- 5/6/92
 /CONTACT: John T. Smith of Cambridge Neuroscience, 617-225-0600 ext. 151, or Melinda Everett of The Medical Center of Central Massachusetts, 508-792-8589/
 (CNSI) CO: Cambridge Neuroscience ST: Massachusetts IN: MTC SU:


TM -- NE006 -- 7052 05/06/92 11:44 EDT
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Date:May 6, 1992
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