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

To: mistermj who wrote (6058)	3/30/2002 12:26:34 PM
From: Miljenko Zuanic	Read Replies (1) \| Respond to of 52153

mjfld, <<Miljenko ,would you be so kind as to come over to the Raging Bull ENMD board to elaborate on your thoughts and perhaps debate a few of these issues? My hopes are that it would be most instructive for all parties involved.>> Sorry, but I have nor time nor inclination to start debate (at yahoo or RB) on ES and ENMD. ES, AS,..are for me only as follow story at this point. Without in-depth view. I will probably ask ENMD for this year AACR/ASCO presentation reprints, and look in details what are results? Maybe few additional thoughts. Regards the ES, so far we still do not know its true rule in agiogenesis. Idea as inhibitors of the endothelial cells motility and proliferation (supported by in-vitro results) has to be confirmed by more rigorous experiments (in-vivo and in humans) and with confirmed mechanisms. Like JCI article on VEGF/Angio-2 rule and description of the each protein action in very early stage of the tumor-angiogenesis. Some will say that mechanism isn’t important as long as drug work. However, so far anti-agio candidates did show only limited success, alone or in combination. There is explanation for this, and only science can put results in right perspective. IMW, understanding mechanisms of the tumor-angiogenesis is crucial to solve problems and bring new and better cancer drug on market. Unfortunately, ES isn’t yet there, imo. What I would like is explanation about E level rise (from 10-15 ng/ml in normal to 100-1200 ng/ml in advance cancer pts), and is this response post-mortal (side reaction, or too little too late) or true attempt to reduce and/or control angiogenesis? At this point seams to me that E have rule in stabilization of the new blood vessels, probably preventing further uncontrolled re-vascularization. Supporting protein with control/break property, or keep status quo for mature blood vessels.. This may be in agreement with its endogenous nature. However, this will also translate into E utility as ADJUVANT to cancer therapy. Not for early stage, and not for advance stage cancer. As help for those who are into remission/ stable, to stay that way. Much different than cure. Also, this my speculation has to be confirmed in large comparable drug controlled, randomized PIII trial, not open label PII trial. Bottom line, risk of the E failure to make difference in cancer therapy is still very high. If this change I may change my opinion. Miljenko