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Biotech / Medical : XOMA. Bull or Bear? -- Ignore unavailable to you. Want to Upgrade?

To: Robert S. who wrote (7768)	11/19/1998 7:35:00 AM
From: Robert K.	Read Replies (1) \| Respond to of 17367

Lets see. Bpi doesnt address the other mediators of sepsis you say. You better check your facts their dude. Major error IMO. Regarding your thought on Wall street recognizing profits and not proof of concept.>Total BS in my opinion. Consider Yahoo or Amazon. Lets see Yahoo>market cap 18.8 billion (vs xoma 180mil). Amazon>market cap 8.5 billion, last year losses 28million on 128million in sales. This year estimates are losses of 70mil on 500 mil sales. Are these proof of concept situations? Are these turning a profit? Do these have potential? Are these in any way similar or not? All IMO all disclaimers. .

To: Robert S. who wrote (7768)	11/19/1998 10:14:00 AM
From: Robert K.	Respond to of 17367

Hematologic and cytokine manifestations "may" be altered>>>>>>> >> J Clin Immunol 1994 Mar;14(2):120-33 The role of bactericidal/permeability-increasing protein in the treatment of primate bacteremia and septic shock. Rogy MA, Oldenburg HS, Calvano SE, Montegut WJ, Stackpole SA, Van Zee KJ, Marra MN, Scott RW, Seilhammer JJ, Moldawer LL, et al Department of Surgery, Cornell University Medical College, New York, New York 10021. Human neutrophil azurophilic granules contain an approximately 55-kDa protein, known as bactericidal/permeability-increasing protein (BPI), which possesses a high-affinity binding domain for the lipid A component of lipopolysaccharide (LPS). The in vivo LPS neutralizing activity of exogenous BPI was studied in a model of lethal Escherichia coli bacteremia. Five baboons were treated with BPI (5 mg/kg bolus injection followed by a 95 micrograms/kg/min BPI infusion over 4 hr), while four additional animals received a genetically engineered variant of BPI (NCY103). Five animals received a placebo treatment and served as controls. Both wild-type rhBPI and NCY103 significantly (P < 0.05) decreased blood levels of LPS throughout an 8-hr evaluation period following live bacterial challenge. Two hours following E. coli administration, LPS levels peaked in the controls, at 6.86 +/- 3.22 ng/ml, whereas LPS levels were 3.39 +/- 2.1 ng/ml in the BPI group and 2.04 +/- 1.18 ng/ml in the NCY103 group. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 levels likewise were attenuated in the treatment groups, whereas circulating sTNFR I was significantly (P < 0.05) reduced only in the BPI group. Leukocytopenia and granulocytopenia were significantly (P < 0.02) lessened in the BPI group, by an average of 59% leukocytopenia and 65% granulocytopenia, respectively. This study supports the concept of E. coli LPS neutralization by BPI in vivo and demonstrates that a moderate (70%) reduction in peak LPS-LAL activity is sufficient to alter some hematologic and cytokine manifestations of bacteremia.

To: Robert S. who wrote (7768)	11/20/1998 8:12:00 AM
From: Robert K.	Read Replies (3) \| Respond to of 17367

Robert S> your previous view......................................................... >..... >George, multifactorial diseases such as sepsis are very complex and the ability to intervene at one point with a cure is extremely problematic. It is all well and good that BPI binds to and neutralizes endotoxins, but this does not address the other mediators involved.

To: Robert S. who wrote (7768)	11/25/1998 8:43:00 AM
From: Robert K.	Respond to of 17367

Robert S> Your quote>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>> >>>"George, multifactorial diseases such as sepsis are very complex and the ability to intervene at one point with a cure is extremely problematic. It is all well and good that BPI binds to and neutralizes endotoxins, but this does not address the other mediators involved."End quote. 1. Do you think that bpi intervenes at only one point in sepsis? 2. At what point"s" do you agree bpi "may" intervene? 3. What do you think of bpi's prospects in sepsis in light of your answers to the above. RobertK