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Biotech / Medical : SCIO Scios Inc. -- Ignore unavailable to you. Want to Upgrade?

To: quidditch who wrote (1429)	4/20/2002 1:06:58 PM
From: scaram(o)uche	Read Replies (1) \| Respond to of 1477

>> the CSO or VP Medicine indicated that other molecules targeting p38 were in pre-clinical testing backing up S-469 lead candidate. << blushing..... oh. Never mind. :-) The company has been around for 21 years. To understand how bad the confrontations between management and shareholders became, read these....... sec.gov sec.gov sec.gov I hated them. I wasn't a shareholder, but I believe that there was one point where deception was active. I resented what they had done to biotech. It's been sensational to watch the transition. I'm a fan, now.

To: quidditch who wrote (1429)	7/12/2002 12:23:38 PM
From: scaram(o)uche	Read Replies (2) \| Respond to of 1477

wandered across this while looking for other stuff, thought that it might be of interest to some here....... Eur J Pharmacol 2002 Jun 28;447(1):37-42 The selective p38 inhibitor SB-239063 protects primary neurons from mild to moderate excitotoxic injury. Legos JJ, McLaughlin B, Skaper SD, Strijbos PJ, Parsons AA, Aizenman E, Herin GA, Barone FC, Erhardt JA. High Throughput Biology, Discovery Research, GlaxoSmithKline, PO Box 1539, Mail Code UW 2523, 709 Swedeland Road, 19406, King of Prussia, PA, USA Inhibition of the p38 mitogen-activated protein kinase (MAP Kinase) pathway reduces acute ischemic injury in vivo, suggesting a direct role for this signaling pathway in a number of neurodegenerative processes. The present study was designed to evaluate further the role of p38 MAP Kinase in acute excitotoxic neuronal injury using the selective p38 inhibitor SB-239063 (trans-1-(4hydroxycyclohexyl)-4-(fluorophenyl)-5-(2-methoxy-pyrimidin-4-yl) imidazole). Unlike the widely used p38 inhibitor, SB-203580 (4-(4-Fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole), this second generation p38 inhibitor more selectively inhibits p38 MAP Kinase without affecting the activity of other MAP Kinase signaling pathways and provides a more accurate means to selectively assess the role of p38 in excitotoxicity that has not been previously possible. SB-239063 provided substantial protection against cell death induced by either oxygen glucose deprivation (OGD) or magnesium deprivation in cultured neurons. The ability of this compound to block excitotoxicity was not due to direct inhibition of N-methyl-D-aspartate (NMDA) receptor-mediated currents as SB-239063 did not alter NMDA electrophysiological responses. SB-239063 did not protect against a severe excitotoxic insult induced by 60-min exposure to NMDA. However, when tested against a less severe, brief (5 min) NMDA exposure, p38 inhibition provided substantial protection. These data demonstrate that inhibition of p38 MAP Kinase can confer neuroprotection in vitro against mild but not severe excitotoxic exposure, and suggests that other additional pathways/mechanism(s) may be involved in severe excitotoxic cell death.