Silicon Investor (SI) -- The First Internet Community

STOCKTALK

We've detected that you're using an ad content blocking browser plug-in or feature. Ads provide a critical source of revenue to the continued operation of Silicon Investor. We ask that you disable ad blocking while on Silicon Investor in the best interests of our community. If you are not using an ad blocker but are still receiving this message, make sure your browser's tracking protection is set to the 'standard' level.

Biotech / Medical : Indications -- Asthma/Allergy -- Ignore unavailable to you. Want to Upgrade?

To: nigel bates who wrote (29)	5/1/2002 3:35:49 PM
From: keokalani'nui	Respond to of 86

Tanox, Inc. Announces Positive Preliminary Results in Peanut Trial HOUSTON, May 1 /PRNewswire-FirstCall/ -- Tanox, Inc. (Nasdaq: TNOX - news) today announced positive preliminary results in its Phase 2 peanut allergy clinical trial involving TNX-901. The trial involved 84 patients in 4 dose groups, (0, 150, 300, and 450mg). TNX-901 is an anti-IgE antibody being developed by Tanox to provide protection against reactions to accidental peanut ingestion by individuals with peanut allergy. The primary endpoint, based on an increase in symptom threshold to peanuts by oral food challenge, was met with statistical significance. Further studies are being planned. "Peanut allergy is a growing problem, and we are excited that we may have a method of protecting people from the life-threatening risks of accidental peanut exposure," said Nancy Chang, CEO of Tanox. The detailed results of the study will be published in a medical journal or presented at a medical conference later this year.

To: nigel bates who wrote (29)	5/16/2002 12:47:15 AM
From: scaram(o)uche	Respond to of 86

Here's the abstract. I know Andy Saxon, which means that he's been around UCLA forever....... Nat Med 2002 May;8(5):518-21 A novel human immunoglobulin Fcgamma Fcvarepsilon bifunctional fusion protein inhibits FcvarepsilonRI-mediated degranulation. Zhu D, Kepley CL, Zhang M, Zhang K, Saxon A. [1] The Hart and Louise Lyon Laboratory, Division of Clinical Immunology/Allergy, Department of Medicine, University of California Los Angeles School of Medicine, Los Angeles, California, USA [2] D.Z. and C.L.K. contributed equally to this study. Human mast cells and basophils that express the high-affinity immunoglobulin E (IgE) receptor, Fcvarepsilon receptor 1 (FcvarepsilonRI), have key roles in allergic diseases. FcvarepsilonRI cross-linking stimulates the release of allergic mediators. Mast cells and basophils co-express FcgammaRIIb, a low affinity receptor containing an immunoreceptor tyrosine-based inhibitory motif and whose co-aggregation with FcvarepsilonRI can block FcvarepsilonRI-mediated reactivity. Here we designed, expressed and tested the human basophil and mast-cell inhibitory function of a novel chimeric fusion protein, whose structure is gammaHinge-CHgamma2-CHgamma3-15aa linker-CHvarepsilon2-CHvarepsilon3-CHvarepsilon4. This Fcgamma Fcvarepsilon fusion protein was expressed as the predicted 140-kappaD dimer that reacted with anti-human varepsilon- and gamma-chain specific antibodies. Fcgamma Fcvarepsilon bound to both human FcvarepsilonRI and FcgammaRII. It also showed dose- and time-dependent inhibition of antigen-driven IgE-mediated histamine release from fresh human basophils sensitized with IgE directed against NIP (4-hydroxy-3-iodo-5-nitrophenylacetyl). This was associated with altered Syk signaling. The fusion protein also showed increased inhibition of human anti-NP (4-hydroxy-3-nitrophenylacetyl) and anti-dansyl IgE-mediated passive cutaneous anaphylaxis in transgenic mice expressing human FcvarepsilonRIalpha. Our results show that this chimeric protein is able to form complexes with both FcvarepsilonRI and FcgammaRII, and inhibit mast-cell and basophil function. This approach, using a Fcgamma Fcvarepsilon fusion protein to co-aggregate FcvarepsilonRI with a receptor containing an immunoreceptor tyrosine-based inhibition motif, has therapeutic potential in IgE- and FcvarepsilonRI-mediated diseases.