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

To: Bluegreen who wrote (16356)	10/18/2003 10:23:08 PM
From: aknahow	Respond to of 17367

Check the e-mail, the address is dedrick@xoma for this other abstract. Could be different people as one set of abstracts says RL and your post only R. 1: Expert Opin Biol Ther. 2003 Feb;3(1):85-95. Related Articles, Links Adhesion molecules as therapeutic targets for autoimmune diseases and transplant rejection. Dedrick RL, Bodary S, Garovoy MR. Xoma (US) LLC, 2910 Seventh Street, Berkeley, CA 94710, USA. dedrick@xoma.com Inflammatory disorders such as autoimmune diseases and graft rejection are mediated by activated leukocytes, particularly T lymphocytes, which penetrate the inflamed tissue and perpetuate or amplify the immune reaction. In an unstimulated state, leukocytes do not readily adhere to the vascular endothelium. However, inflammatory signals induce the expression of proteins on the endothelial cell surface that promote the adhesion and extravasation of activated immune cells from the circulation into the underlying tissues. Key among these molecules are P- and E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on the endothelial cells, and their respective counter receptors, P-selectin glycoprotein ligand-1 (PSGL-1), leukocyte function-associated antigen-1 (LFA-1) and very late antigen-4 (VLA-4), on the leukocytes. In vitro blockade of these molecules inhibits the adhesion of leukocytes. In many cases there is attenuation of leukocyte activation as well. Adhesion blockade in animal models prevents or ameliorates graft rejection and disease severity in autoimmune models. Clinical studies with humanised monoclonal antibodies which interfere with LFA-1/ICAM-1 or VLA-4/VCAM-1 interactions have shown significant efficacy and good safety profiles in autoimmune disease, including psoriasis, multiple sclerosis and inflammatory bowel disease. Thus, adhesion blockade is emerging as a useful therapeutic strategy in several inflammatory settings. PMID: 12718733 [PubMed - in process] .

To: Bluegreen who wrote (16356)	10/18/2003 10:27:35 PM
From: aknahow	Read Replies (1) \| Respond to of 17367

BPI may work bu so does other stuff. ODonoghue has been busy. 1: O'Donoghue GT, Pidgeon G, Harmey J, Dedrick R, Redmond PH, Bouchier-Hayes DJ. Related Articles, Links The anti-endotoxin agent, rBPI21, significantly attenuates surgically induced tumour growth in an experimental metatases murine model of breast cancer. J Surg Res. 2003 Oct;114(2):300. PMID: 14559642 [PubMed - in process] 2: O'Donoghue GT, Roche-Nagle G, Harmey JH, Bouchier-Hayes DJ. Related Articles, Links Cyclooxygenase-2 inhibition attenuates surgically induced residual tumour growth and metatases following cytoreductive surgery in a murine model of breast cancer. J Surg Res. 2003 Oct;114(2):277-8. PMID: 14559570 [PubMed - in process] 3: O'Donoghue GT, Roche-Nagle G, Connolly EM, Harmey J, Bouchier-Hayes DJ. Related Articles, Links Selective Cox-2 inhibition attenuates the perioperative increase of the tumour enhancing pro-angiogenic cytokine Vegf in human breast cancer patients. J Surg Res. 2003 Oct;114(2):243. PMID: 14559462 [PubMed - in process]

To: Bluegreen who wrote (16356)	10/19/2003 12:08:42 PM
From: Robert K.	Respond to of 17367

Ok , now a thoughtful post to my critically thinking friends. Dr C. I can already guess your response but you might surprise me. Question> In what ways (if any) is the newest bpi21 trial with heart surgery similiar (or dis-similiar) to the meningo trial. The more pointedly, is it possible in any way that the newest bpi21 trial could provide "additional data" which is complimentary to the meningo trial which may provide the mystery "additional data" the fda requests for a initial submission. Its a new FDA after all. Responces greatly appreciated....thanks.