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Biotech / Medical : Pharmos (PARS) -- Ignore unavailable to you. Want to Upgrade?

To: Dr. John M. de Castro who wrote (7)	10/30/1998 8:27:00 AM
From: Dr. John M. de Castro	Read Replies (1) \| Respond to of 1386

Another PARS Neuroscience Abstract Here is a copy of another abstract to be presented by PARS at the Society for the Neurosciences meeting in Los Angeles, Nov. 7-12. It demonstrates that HU-211 is an effective neuroprotectant against damage produced by nerve gas. This was a study done by the army. I have no idea what the market potential is here. But, given what the army is willing to pay for a wrench I have to imagine that the price they'd be willing to pay for a drug that can help protect soldiers who are exposed to chemical warfare agents is substantial. I also have no idea what is the approval process for military uses. Regardless, this is further substantiation of HU-211's effectiveness as a general purpose neuroprotectant that may be effective with a wide range of neuropathologies. This is a huge and open market with emense potential for future revenue generation. John de C NEUROPROTECTIVE EFFECTS OF HU-211 ON BRAIN DAMAGE RESULTING FROM SOMAN-INDUCED SEIZURES. M.G. Filbert, J. S. Forster, C. D. Smith, M. C. kovalenko, M.J. Jaworski, and G. P. H. Ballough. Neurotoxology Branch, Pharmacology Division, US Army Medical research Institute of Chemical Defenses, Aberdeen proving Ground, MD, USA 21010- 5245 and LaSalle University, Department of Biology, Philadelphia, PA 19141-1199. The present study was undertaken to examine the possible neuroprotective effects of HU- 211 on brain damage resulting from the soman-induced seizures. Male Sprague-Dawley rats were challenged with 180 ug/kg Soman (i.e., 1.6 LD50). They were subsequently given a single intraperitoneal injection of 25 mg/kg HU-211 at either 5 or 40 minutes post onset of seizures. HI- 6 (126mg/kg) and atropine methylnitrate (2 mg/kg) were administered to protect against the peripheral effects of soman. Electrocorticographic (EcoG) recordings were monitored via indwelling cortical electrodes. Rats were euthanized 27hr after soman administration. Alternate brain hemispheres were processed for microtubule-associated protein 2 (MAP2) and glial fibrillary acidic protein (GFAP) immunocytochemical staining or hematoxylin and eosin (H&E) histochemical staining. Morpohometric image analysis was used to assess the cross-sectional areas of temporal lobe necrosis (MAP2 negative) and reactive astrocytosis (GFAP positive) resulting from soman exposure. H&E stained sections were examined for classical histopathology. All rats that received soman showed EcoG evidence of sustained seizures and status epilepticus for several hours. Treatment with HU-211 had no apparent effect on the strength or duration of these seizures. Interestingly, HU-211 administration 5-minutes post onset of seizures significantly reduced (by 75.8%) the mean cross-sectional areas of temporal lobe necrosis. These findings were corroborated by H&E histopathological assessments which showed a significant reduction in piriform cortical damage in the HU-211 5 minute group ("mild damage", i.e., 11-25% neuronal loss) compared to soman controls ("severe damage", i.e., greater than 45% neuronal loss). It is concluded that HU-211 provides considerable neuroprotection against brain damage resulting from soman-induced seizures, despite having no apparent effect on the seizures themselves.