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CuraGen and Abgenix Scientists Develop Fully Human Monoclonal Antibodies to PDGF D

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Title:

CuraGen and Abgenix Scientists Develop Fully Human Monoclonal Antibodies to PDGF D

Entities:

Abgenix, Inc.; CuraGen Corp.

Date:

2002

Size:

Preview shows 2KB of 7KB total

Price:

$34

ID:

#288540

► Miscellany ► News ► Press Releases ► 2002 Press Releases
► Biotech & Drugs ► Commercial Physical & Biological Research
► Biotech & Drugs ► Biological Products

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[CURAGEN CORPORATION LOGO]



Contact:

--------



Mark R. Vincent

CuraGen Corporation

Director of Corporate and Investor Relations

1-888-GENOMICS

www.curagen.com



FOR IMMEDIATE RELEASE

---------------------



          CuraGen and Abgenix Scientists Develop Fully Human Monoclonal

                              Antibodies to PDGF D



New Haven, CT -- May 2, 2002 -- CuraGen Corporation (NASDAQ: CRGN), an

integrated, genomics-based pharmaceutical company, announced today that CuraGen

and Abgenix scientists have successfully developed highly-specific, fully human

monoclonal antibodies (mAbs) that precisely bind to PDGF D, a member of the

Platelet-Derived Growth Factor (PDGF) family. Importantly, these antibodies are

specific to PDGF D and do not bind to other members of the PDGF family. PDGF D

is a newly discovered growth factor that has proliferative activity on a wide

variety of cells that express PDGF receptors. Recently, CuraGen demonstrated

that PDGF D is associated with a number of diseases in the areas of Oncology and

Inflammation. Thus, antagonism of PDGF D through the use of fully human mAbs is

a potentially important method for treating unmet diseases in Oncology and

Inflammation.



These antibodies, as well as the role of PDGF D in Oncology, are revealed in the

May 1, 2002 issue of Cancer Research, a publication of the American Association

for Cancer Research. An online abstract of the paper is accessible on the

Internet at http://cancerres.aacrjournals.org/cgi/content/abstract/62/9/2468.

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PDGF D was shown to be dysregulated in cancers and cause tumor formation when

inappropriately expressed in an in vivo disease model. The publication also

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