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Biotech / Medical : Indications -- Psoriasis/Chronic Inflammation -- Ignore unavailable to you. Want to Upgrade?

To: Icebrg who wrote (350)	2/23/2003 11:41:12 AM
From: scaram(o)uche	Respond to of 631

Almost everyone else viewed targeting cytokines as a waste of time. "The thought was, if you just block one of them, then all the others will just keep on driving the biological processes," Feldmann remembers. That was my prediction, minus the "waste of time". I was adamant, insisting that efficacy of anti-TNF would be marginal. :-( And then the results started showing "for real". :-) That said, the article is good but overdoes it a bit on the "we were considered heretics" side. The work was rational, even if most believed that efficacy would not be pronounced. It's been a blast, being in immunology during this period. 99% of stuff is BS dogma that gets lost, but the foundation to immunology continues to firm. Aside........... I was involved, early, in anti-TNF. At Bayer (Cutter), we were considering the early evaluation of Chiron's anti-TNF. I left when it was in the formative stage (1986), before the antibody arrived. I believe that Mike Collins (Bayer-Cutter) was the first to show that anti-TNF could lead to systemic infection that would otherwise resolve. I may remember incorrectly, but I think that he used Listeria. This may be the reason that Bayer dropped the project, and didn't collaborate further with Chiron?? Regardless the reason, yet another wise decision by Bayer re. biotech. Not.

To: Icebrg who wrote (350)	2/23/2003 1:01:48 PM
From: scaram(o)uche	Read Replies (1) \| Respond to of 631

Erik: If I've understood you correctly............. You have implied that evidence exists indicating that anti-alpha4 integrin should not be more effective than anti-beta7 for at least some inflammatory diseases. For what it's worth............ I've looked hard, and can't find significant studies that would support that assumption. I still worry, however, that other adhesion molecules can substitute for alpha4 beta2 and alpha4 beta7, and that anti-alpha4 efficacy will be marginal. Sort of like I argued that other cytokines would mask the efficacy of anti-TNF. :-) Conversely, I have found substantial evidence that at least some anti-alpha4s can block both beta2- and beta7-mediated adhesion. So............ I'm not assuming that MLN02 is dead for UC, but............ I was confused by your response, a couple of months ago, in the VDXX thread. Could you please clarify and/or expand? Thanks! Rick