CancerVax Presents Preclinical Data Demonstrating Tumor Inhibition by D93, a Novel Anti-Angiogenic Monoclonal Antibody
Data Presented at AACR Annual Meeting
CARLSBAD, CA, Apr 04, 2006 (MARKET WIRE via COMTEX News Network) -- CancerVax Corporation (NASDAQ: CNVX) announced today that its wholly owned subsidiary, Cell-Matrix, Inc., presented preclinical data indicating that D93, the Company's leading anti-angiogenic and anti-tumorigenic, humanized, monoclonal antibody, inhibited human breast and pancreatic tumor growth in animal models. The presentation, which was made at the 97th Annual Meeting of the American Association for Cancer Research (AACR) in Washington, D.C., on April 2, 2006, also included the results of toxicological and pharmacokinetic studies with D93. On March 1, 2006, the Company announced that it had filed an Investigational New Drug application with the United States Food and Drug Administration for D93.
In a poster entitled "Anti-Denatured Collagen Antibody D93: An Extra-Cellular Matrix Approach to Treatment of Solid Tumors and Metastasis," Dr. Flavia Pernasetti and other CancerVax scientists highlighted results obtained in an orthotopic, staged human breast tumor model using human MDA-MB-435 cells implanted in mice. In this model, D93, which preferentially binds to cryptic sites on collagen that are exposed during tumor growth, was shown to inhibit tumor growth in a dose-dependent manner, with the maximum inhibition obtained at a dose of 10 mg/kg per week. When D93 was administered in combination with Taxol(R) (paclitaxel), inhibition of tumor growth was greater than with either single agent alone. The combination of D93 plus Taxol(R) inhibited tumor volume by 66% versus a control antibody, whereas the results for Taxol and D93 as single agents were 49% and 39%, respectively, versus the control antibody (p < 0.05). Data were also presented demonstrating that D93, but not the control antibody, preferentially targeted human breast tumor tissue when injected in vivo in the same model.
Additionally, data were presented showing that D93 inhibited tumor growth and metastasis to the lymph nodes and diaphragm in an orthotopic, human pancreatic tumor model in mice.
"The ability of the D93 antibody to target unique sites on collagen that are exposed in tumor tissues and that may be important in the growth and vascularization of tumors represents a novel therapeutic approach," said David F. Hale, President and CEO of CancerVax. "The results presented at AACR support earlier findings indicating that D93 may have the potential to treat a variety of solid tumors."
Summaries of the results of toxicology and pharmacokinetic studies of D93 in non-human primates were also presented, which indicated that no abnormalities or differences were observed between control and D93 groups, and no overt toxicity was seen with D93 when administered to non-human primates in weekly doses up to 50 mg/kg for 4 weeks.
The abstract is available on the AACR web site (www.aacr.org) and on CancerVax's home page (www.cancervax.com) in the "Focus" section.
About D93
D93 is a humanized, monoclonal antibody that inhibits tumor growth and angiogenesis, the formation of new blood vessels that feed rapidly growing tumors. Its mechanism of action differs from other angiogenesis inhibitors that are being evaluated in clinical trials or that have been approved by the FDA, such as Avastin(R) (bevacizumab). D93 selectively binds to targets in the extracellular matrix, a molecular network that provides structural support to tissues and regulates cellular processes such as adhesion, migration and cell growth. These targets are exposed during tumor formation, when the collagen comprising the extracellular matrix is denatured or remodeled by tumor cells.
In preclinical studies, D93 has been shown to preferentially bind to denatured collagen targets in melanoma and in colon, pancreas, lung and breast tumors. Administering D93 with Taxol(R) (paclitaxel) has been demonstrated to inhibit tumor growth in animal models of human breast cancer better than either treatment alone. D93 has also been shown to inhibit tumor growth in pancreatic and melanoma tumor models, and by fluorescent antibody techniques to bind preferentially to the extracellular matrix around blood vessels in tumor sections taken from patients with cancer, as compared to healthy tissues adjacent to the tumor.
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