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


To: Miljenko Zuanic who wrote (1104)10/19/2006 6:18:02 AM
From: nigel bates  Respond to of 3557
 
>>Anything new...angiogenesis<<

This looks interesting -

Message 22923211



To: Miljenko Zuanic who wrote (1104)10/19/2006 9:07:23 AM
From: scaram(o)uche  Respond to of 3557
 
(duplicate post)



To: Miljenko Zuanic who wrote (1104)10/19/2006 9:07:57 AM
From: scaram(o)uche  Respond to of 3557
 
No, stayed home to trade. So I know nada re. preclinical or the quality of antigen interaction. Just know what CEO spit out. BTW, he walked away wearing the microphone, and could be heard making his way to the breakout during the ACAD presentation...... if I had shares now, I might be selling them after that "disclosure".

Ugh.

New? Antisoma's vascular disrupting agent?

biz.yahoo.com

Not following new stuff.

Hope life is good!

Rick



To: Miljenko Zuanic who wrote (1104)10/24/2006 11:48:39 AM
From: scaram(o)uche  Read Replies (1) | Respond to of 3557
 
Nature Reviews Cancer 6, 833 (November 2006)

Angiogenesis: Blunting the spikes
Ezzie Hutchinson

The role of circulating endothelial progenitors (CEPs; bone-marrow derived endothelial progenitor cells that enter the circulation and migrate to sites of angiogenesis) in tumours has been controversial. Their contribution to tumour endothelium has been estimated to be as low as 5% or less in many studies of tumours from untreated hosts. However, Robert Kerbel and colleagues have now shown that if CEPs are acutely mobilized in tumour-bearing mice using vascular disrupting agents (VDAs), treatment with anti-angiogenic agents disrupts this spike in CEP numbers, and thereby reduces tumour cell growth at the viable tumour periphery that remains after VDA treatments. The use of VDAs combined with anti-angiogenic agents might therefore be an efficacious combination to treat solid tumours.

VDAs cause the acute occlusion of existing blood vessels and rapid tumour necrosis — unlike anti-angiogenic agents that mainly inhibit new blood vessel formation. The authors proposed that the rapid mobilization of CEPs as a consequence of treatment with VDAs might contribute to the rapid regrowth that is seen at the tumour periphery after VDA treatment. First, the authors showed that the treatment of non-tumour-bearing mice with the VDA combretastine-A4 phosphate or its more potent derivative OXi-4503 did cause a CEP spike of about three times normal levels. If the anti-angiogenic agent DC101 was injected into tumour-bearing mice 24 hours before giving OXi-4503, the size of the viable tumour rim was reduced threefold compared with that seen in mice treated with OXi-4503 alone. In addition, the combination of the VDA and anti-angiogenic agent led to markedly decreased perfusion, increased hypoxia and necrosis of the tumours.

So, does the VDA-induced spike in CEPs lead to preferential homing of the cells to the viable tumour rim? To investigate this, Kerbel and colleagues used lethally irradiated mice transplanted with green fluorescent protein (GFP+) bone marrow cells before allowing syngeneic Lewis lung carcinomas to establish. Although untreated and DC101-treated mice showed only some modest homing of the bone marrow cells to the tumour rim, mice treated with OXi-4503 alone showed greater homing and incorporation of some of the GFP+ cells into the peripheral tumou vasculature. Mice treated with both drugs had a reduced number of GFP+ cells at the tumour periphery. If mice that are incapable of mobilizing CEPs (Idmut mice) are treated with OXi-4503 no CEP spike is seen. When these mice bear Lewis lung tumours and are treated with OXi-4503, the viable tumour rim and perfusion are reduced, confirming the significant role of therapy-induced mobilization and tumour-homing of CEPs in tumour regrowth.

The authors conclude that CEPs are a key contributor to the growth of the viable tumour rim after treatment with VDAs, and suggest that treatment with cytotoxic chemotherapy drugs at maximum tolerated doses might have the same effect. If so, the combination of an anti-angiogenic drug given with chemotherapy might be one way the anti-tumour efficacy of chemotherapy can be improved.

ORIGINAL RESEARCH PAPER
Shaked, Y. et al. Therapy-induced acute recruitment of circulating endothelial progenitor cells to tumors. Science 313, 1785–1787 (2006)

Bertolini, F., Shaked, Y., Mancuso, P. & Kerbel, R. S. The multifaceted circulating endothelial cell in cancer: towards marker and target identification. Nature Rev. Cancer 5 October 2006 (doi:10.1038/nrc1971)



To: Miljenko Zuanic who wrote (1104)2/12/2008 1:49:42 AM
From: scaram(o)uche  Read Replies (1) | Respond to of 3557
 
Dyax Corp. Enters Into Antibody Agreements with Sanofi-aventis for the Fully Human Monoclonal Antibody DX-2240 and Phage Display Technology
Tuesday February 12, 12:05 am ET
-Upfront Fees and Milestone Payments Total Up to $500 Million-
-Dyax Retains Co-development Rights and Profit Sharing for Certain Partner Programs-

CAMBRIDGE, Mass.--(BUSINESS WIRE)--Dyax Corp. (NASDAQ: DYAX - News) and sanofi-aventis (EURONEXT: SAN and NYSE: SNY) announced today that they have entered into agreements in which sanofi-aventis has been granted an exclusive worldwide license for the development and commercialization of the fully human monoclonal antibody DX-2240, as well as a nonexclusive license to Dyax’s proprietary antibody phage display technology.

Under the terms of the two agreements, Dyax is eligible to receive up to $500 million in license fees and milestone payments in the case of full commercial success of the first five antibody candidates, including DX-2240. Dyax will receive $25 million in 2008. In addition, Dyax is eligible to receive royalties based on commercial sales of DX-2240 and other antibodies developed by sanofi-aventis.

As exclusive licensee, sanofi-aventis will be responsible for the ongoing development, commercialization and consolidation of sales of DX-2240. For certain other future antibody product candidates discovered by sanofi-aventis, Dyax will retain co-development and profit sharing rights, while sanofi-aventis will maintain the leadership in development and commercialization, and book sales worldwide.

“These strategic agreements validate Dyax’s capabilities to successfully discover novel antibody drug candidates utilizing our proprietary phage display technology and advance the resulting drug candidates into development,” commented Henry E. Blair, Chairman, President and Chief Executive Officer of Dyax. “Sanofi-aventis has industry-leading clinical and commercial development capabilities, particularly in oncology, and is ideally suited to maximize the potential of DX-2240. Furthermore, sanofi-aventis’ license to our phage display technology, combined with Dyax’s co-development rights, has significant potential to expand our pipeline of product candidates.”

DX-2240 is a fully human monoclonal antibody that targets the Tie-1 receptor on tumor blood vessels and has therapeutic potential in numerous oncology indications. In preclinical animal models, DX-2240 has demonstrated activity against a broad range of solid tumor types. The antibody works by altering tumor vascular morphology, thereby increasing hypoxia and necrosis. In addition, DX-2240 in vivo increases the anti-tumor activity of other cancer therapies such as VEGF pathway inhibitors and other chemotherapeutic agents when used in combination.

Moreover, Dyax’s state-of-the-art antibody, peptide, and protein proprietary phage display libraries will give sanofi-aventis the opportunity to identify novel, high quality antibody product candidates with the potential to be moved rapidly into development and ultimately commercialization.

About sanofi-aventis

Sanofi-aventis, a leading global pharmaceutical company, discovers, develops and distributes therapeutic solutions to improve the lives of everyone. Sanofi-aventis is listed in Paris (EURONEXT: SAN) and in New York (NYSE: SNY - News).

About Dyax

Dyax is focused on advancing novel biotherapeutics for unmet medical needs, with an emphasis on oncology and inflammatory indications. Dyax utilizes its proprietary drug discovery technology to identify antibody, small protein and peptide compounds for clinical development.

Dyax’s lead product candidate is DX-88, a recombinant small protein that is currently in clinical trials for its therapeutic potential in two separate indications. Dyax has completed three Phase 2 trials and a Phase 3 trial of DX-88 for the treatment of hereditary angioedema (HAE). A second Phase 3 trial, known as EDEMA4, is currently being conducted under a Special Protocol Assessment (SPA). DX-88 has orphan drug designation in the U.S. and E.U., as well as Fast Track designation in the U.S. for the treatment of acute attacks of HAE.

Additionally, Dyax has completed a Phase 1/2 trial of DX-88 for the prevention of blood loss during on-pump coronary artery bypass graft (CABG) procedures. A Phase 2 trial for further development of DX-88 in on-pump cardiothoracic surgery (CTS), including CABG and heart valve replacement or repair procedures, is ongoing.

Dyax identified DX-88 and other compounds in its pipeline using its patented phage display technology, which rapidly selects compounds that bind with high affinity and specificity to therapeutic targets. Dyax leverages this technology broadly with over 70 revenue generating licenses and collaborations for therapeutic discovery, as well as in non-core areas such as affinity separations, diagnostic imaging, and research reagents. Under a 2006 funding arrangement with Paul Royalty Fund II, Dyax received a $30 million upfront cash payment in exchange for granting Paul Royalty the right to receive a specified percentage of the net royalties, including all milestones fees and other payments, receivable by Dyax under the LFRP through 2017.

Dyax is headquartered in Cambridge, Massachusetts, and has antibody discovery facilities in Liege, Belgium. For online information about Dyax Corp., please visit www.dyax.com.

Dyax Disclaimer

This press release contains forward-looking statements, including statements regarding the expected benefits of Dyax’s collaboration agreement for DX-2240 and its library license agreement with sanofi-aventis. Statements that are not historical facts are based on Dyax’s current expectations, beliefs, assumptions, estimates, forecasts and projections about the industry and markets in which Dyax competes. The statements contained in this release are not guarantees of future performance and involve certain risks, uncertainties and assumptions, which are difficult to predict. Therefore, actual outcomes and results may differ materially from what is expressed in such forward-looking statements. Important factors which may affect the expected benefits of Dyax’s collaboration and license agreements with sanofi-aventis include the risks that: DX-2240 may not gain market acceptance; Dyax’s future benefits from sanofi-aventis’ license of Dyax’s phage display technology depend on the efforts and priorities of sanofi-aventis, which may be subject to changes in sanofi-aventis’ business direction or priorities; others may develop technologies or products superior to Dyax’s phage display technologies or sanofi-aventis’ product candidates developed through the use of Dyax’s technologies; Dyax may not be able to obtain and maintain intellectual property protection for its products and technologies; and other risk factors described or referred to in Dyax’s most recent Annual Report on Form 10-K and other periodic reports filed with the Securities and Exchange Commission. Dyax cautions investors not to place undue reliance on the forward-looking statements contained in this release. These statements speak only as of the date of this release, and Dyax undertakes no obligations to update or revise these statements, except as may be required by law. Dyax specifically disclaims responsibility for information describing sanofi-aventis and its business other than the license with Dyax.

Dyax, the Dyax logo and EDEMA4 are registered trademarks of Dyax Corp.

Contact:
Dyax Corp.
Ivana Magovcevic-Liebisch, 617-250-5759
General Counsel and Executive Vice President
of Administration
imagovcevic@dyax.com
or
Nicole Jones, 617-250-5744
Director, Investor Relations
njones@dyax.com