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 : SIBIA Neurosciences (SIBI) -- Ignore unavailable to you. Want to Upgrade?

To: tommysdad who wrote (505)	8/4/1999 5:08:00 PM
From: scaram(o)uche	Respond to of 579

wake up, everyone. BVF filing today...... (excerpt) ITEM 3. SOURCE AND AMOUNT OF FUNDS OR OTHER CONSIDERATION. Since June 3, 1999, Partners, in its capacity as general partner of BVF, has purchased on behalf of such limited partnership an aggregate number of 151,200 shares of the Stock for an aggregate consideration of $1,270,013.58, utilizing funds provided by BVF from its working capital pursuant to the terms of its limited partnership agreement with Partners. In addition, Partners, in its capacity as investment manager with respect to certain managed accounts, has purchased on behalf of such managed accounts an aggregate number of 126,000 shares of the Stock for an aggregate consideration of $1,055,788.20, utilizing funds under management by Partners pursuant to investment management agreements between Partners and such managed accounts. Item 4 is hereby amended to read in its entirety as follows: ITEM 4. PURPOSE OF TRANSACTIONS. Partners believes the terms of the proposed acquisition of SIBIA by Merck & Co. do not adequately reflect the fair value of SIBIA's world-class drug discovery organization plus the extraordinary potential of SIBIA's royalties derived from preexisting, fully-funded, partnered programs. Accordingly, Partners may explore various alternatives for enhancing SIBIA's shareholder value. To this end, Partners has communicated with, and may communicate with in the future, SIBIA's management, Board and other shareholders, with Merck, and with other interested parties. There can be no assurance that Partners will develop any alternatives or that such alternatives, if developed, will be provided by SIBIA or that, if provided, will succeed. ************************************* some of us were wondering why the sucker was sometimes trading at 8 15/32.

To: tommysdad who wrote (505)	8/4/1999 5:17:00 PM
From: scaram(o)uche	Read Replies (1) \| Respond to of 579

I don't know if someone posted the actual abstract from Athena Neuro. This news broke while I was on vacation. So, here's the abstract, relevant to BMY/SIBI collaboration........ Nature 1999 Jul 8;400(6740):173-7 Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Schenk D, Barbour R, Dunn W, Gordon G, Grajeda H, Guido T, Hu K, Huang J, Johnson-Wood K, Khan K, Kholodenko D, Lee M, Liao Z, Lieberburg I, Motter R, Mutter L, Soriano F, Shopp G, Vasquez N, Vandevert C, Walker S, Wogulis M, Yednock T, Games D, Seubert P Elan Pharmaceuticals, South San Francisco, California 94080, USA. dschenk@elanpharma.com Amyloid-beta peptide (Abeta) seems to have a central role in the neuropathology of Alzheimer's disease (AD). Familial forms of the disease have been linked to mutations in the amyloid precursor protein (APP) and the presenilin genes. Disease-linked mutations in these genes result in increased production of the 42-amino-acid form of the peptide (Abeta42), which is the predominant form found in the amyloid plaques of Alzheimer's disease. The PDAPP transgenic mouse, which overexpresses mutant human APP (in which the amino acid at position 717 is phenylalanine instead of the normal valine), progressively develops many of the neuropathological hallmarks of Alzheimer's disease in an age- and brain-region-dependent manner. In the present study, transgenic animals were immunized with Abeta42, either before the onset of AD-type neuropathologies (at 6 weeks of age) or at an older age (11 months), when amyloid-beta deposition and several of the subsequent neuropathological changes were well established. We report that immunization of the young animals essentially prevented the development of beta-amyloid-plaque formation, neuritic dystrophy and astrogliosis. Treatment of the older animals also markedly reduced the extent and progression of these AD-like neuropathologies. Our results raise the possibility that immunization with amyloid-beta may be effective in preventing and treating Alzheimer's disease.