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Biotech / Medical : Biotech Valuation -- Ignore unavailable to you. Want to Upgrade?

To: Biomaven who wrote (5351)	1/7/2002 9:35:24 AM
From: Biomaven	Respond to of 52153

Here's an abstract on P38 inhibitors in development. It's from October 2000; I believe there are currently a bunch more big pharma in this race than are mentioned in this article. prous.com (Subscription required for full-text). Drug News & Perspectives Vol. 13, No. 8, October 2000 -------------------------------------------------------------------------------- Preclinical pharmacology indicates strongly that p38 inhibitors are likely to be efficacious in the treatment of human rheumatoid arthritis. Ongoing clinical studies on at least two structurally different p38 inhibitors should reveal whether efficacy can be demonstrated at tolerated doses. Potential of p38 Inhibitors in the Treatment of Rheumatoid Arthritis by Martyn L. Foster, Frank Halley and John E. Souness -------------------------------------------------------------------------------- Summary Rheumatoid arthritis (RA) is a chronic debilitating disease estimated to afflict 13% of the world population. Although palliative treatments (nonsteroidal antiinflammatory drugs or NSAIDs) are widely prescribed, there are currently only a few treatments that can modify the insidious progression of the disease (disease-modifying antirheumatic drugs or DMARDs), which frequently leads to physical incapacitation and, on occasion, death. Proinflammatory cytokines such as tumor necrosis factor-a (TNF-a) and interleukin-1b (IL-1b) are implicated in the disease onset and in the progression of bone and joint destruction that characterizes chronic RA. p38 is an intracellular mitogen/stress-activated protein kinase (MAPK/SAPK) that regulates both the release and the actions of TNF-a and IL-1b. Inhibition of p38 kinase is thus an important potential target for novel DMARDs. Following the pioneering work conducted at SmithKline Beecham and elucidation of the roles of p38 with potent and selective inhibitors such as SB-203580, many pharmaceutical companies have embarked upon p38 synthetic programs, as indicated by the ever-increasing number of patents in this domain. At Aventis, a rapid parallel synthesis project led to the identification of RPR-200765A, a potent and selective p38 inhibitor of the lipopolysaccharide-induced release of TNF-a in vitro in mononuclear phagocytes and in vivo in the rat. It also reduces disease incidence and progression in the rat streptococcal cell wall arthritis model when administered orally in either a prophylactic or a therapeutic dosing regimen. Development of p38 inhibitors has been slow, probably because of toxicological problems, which might explain why only two oral p38 inhibitors, SB-242235 and VX-745, have advanced into clinical development. In the present article, the preclinical data exemplified in studies on RPR-200765A indicating why p38 inhibitors are attracting so much attention as potential novel anti-RA drugs are reviewed. Current information on the different structural classes of p38 inhibitors is presented and possible reasons for the delays in their development are critically discussed. © 2000 Prous Science. All rights reserved.

To: Biomaven who wrote (5351)	1/7/2002 9:52:50 AM
From: rkrw	Read Replies (2) \| Respond to of 52153

<<<the Actimmune Fast Track designation - although the latter news might not have been saved up for the conference).>>> Not sure you caught this which was tucked into the itmn announcement.... "In addition, the Company reported that in its ongoing Phase III trial for IPF, approximately 60% of the trial is complete in terms of patient treatment days. Furthermore, less than 5% of patients have withdrawn from the study prior to meeting the primary endpoint. This retention rate is well within the assumptions underlying the statistical power and sample size of the 330-patient trial. Dr. Harkonen also stated, ``We are very pleased with this high level of patient retention as of January and expect that patient retention going forward will continue to be strong. We would like to thank all participating investigators, coordinators and patients for their tremendous commitment and dedication to this trial.''