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Biotech / Medical : Imclone systems (IMCL)
IMCL 0.1590.0%Oct 5 5:00 PM EST

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To: 5,17,37,5,101,... who wrote (57)11/14/1997 6:38:00 AM
From: CPAMarty  Read Replies (2) of 2515
 
NEW YORK--(BW HealthWire)--Nov. 11, 1997--ImClone Systems
Incorporated (Nasdaq:IMCL) announced today that the Company has
received from the National Cancer Institute (NCI) a Phase I Small
Business Innovation Research (SBIR) grant of $100,000 to support
preclinical research on the validation of vascular-specific cadherin
(VE-cadherin) as a novel potential drug target to inhibit
cancer-associated angiogenesis.

VE-cadherin is believed to play an important role in angiogenesis
by enabling the assembly of endothelial cells into vascular tubes.
Cancer growth is dependent on the formation of a capillary blood
vessel network in the tumor, and VE-cadherin antagonists may thus
have utility as anti-cancer agents. ImClone will test monoclonal
antibodies against VE-cadherin as potential angiogenesis inhibitors
and use its high-throughput assays for the identification of small
molecule VE-cadherin inhibitors. ImClone announced last week that
the Company has acquired exclusive rights to the newly discovered
protein VE-cadherin-2.

"The SBIR grant from the NCI affirms ImClone's dual commitments
to early discovery research and to broadening its cancer-related
angiogenesis program," commented Daniel J. Hicklin, Ph.D.,
Principal Investigator and Director of Immunology at ImClone Systems.
"We appreciate the NCI's eagerness to support such novel work as the
VE-cadherin program, which complements our ongoing anti-angiogenesis
studies and represents a potentially important method of inhibiting
tumor vascularization."

ImClone Systems' lead anti-angiogenesis compound is a monoclonal
antibody that inhibits the tyrosine kinase receptor known as
KDR/FLK-1, located on tumor-associated capillary blood vessels. The
KDR/FLK-1 receptor, when stimulated by tumor-derived vascular growth
factor, VEGF, mediates the tumor-associated formation of new blood
vessels. ImClone scientists are conducting preclinical research to
determine potential clinical utility of the Company's
monoclonal-antibody antagonist of KDR/FLK-1 and to obtain regulatory
approval for clinical studies.

ImClone Systems has two oncology products in late-stage clinical
development and is advancing earlier drug candidates to the clinical
stage. The Company is currently evaluating C225, an epidermal growth
factor receptor (EGFr) antagonist, in head and neck cancer patients
in three Phase Ib/IIa dose-escalation trials in combination with
other anti-cancer therapies. ImClone expects to initiate Phase
II/III studies to evaluate the potential of C225 in various tumor
types. In addition, ImClone intends to initiate a Phase III
multinational trial in small cell lung cancer patients with the
Company's anti-cancer vaccine BEC2.

ImClone Systems Incorporated, headquartered in New York, is a
biopharmaceutical company developing novel therapeutic products
including interventional therapeutics, cancer vaccines and blood cell
growth factors for the treatment of cancer and cancer-related
disorders.
-0-
Except for the historical information contained herein, the
matters discussed in this news release may include forward-looking
statements. Actual results may differ materially from those
predicted in such forward-looking statements due to the risks and
uncertainties inherent in the Company's business, including, without
limitation, risks and uncertainties in obtaining and maintaining
regulatory approval, market acceptance of and continuing demand for
the Company's products, the impact of competitive products and
pricing, and the Company's ability to obtain additional financing to
support its operations. The Company undertakes no obligation to
revise or update this press release to reflect events or
circumstances after the date hereof.

CONTACT:

ImClone Systems Incorporated, New York

Andrea F. Rabney, 212/645-1405

or

Burns McClellan, Inc., New York

Reagan Codner (Investors)

Justin Jackson (Media)

212/213-0006

KEYWORD: NEW YORK

BW1167 NOV 11,1997
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