Fully Human Antibody Eradicates Established Tumors as Monotherapy
FREMONT, Calif., March 15, 1999 -- Abgenix, Inc. (Nasdaq: ABGX) reported today in Cancer Research (Volume 59, Issue no. 6), encouraging results of preclinical studies with its proprietary fully human monoclonal antibody, ABX-EGF. Developed using the company's XenoMouseTM technology, ABX-EGF targets the receptor for human epidermal growth factor (EGFr) which is overexpressed on many major human tumor types including renal, prostate, colorectal, head and neck, and breast. As reported in a paper titled, "Eradication of Established Tumors by a Fully Human Monoclonal Antibody to the Epidermal Growth Factor Receptor without Concomitant Chemotherapy," Abgenix scientists demonstrated that ABX-EGF alone, in mouse models, can both block the growth of human tumors, is potent at comparatively low doses and, more importantly, eradicates established tumors. Another member of the EGFr family, Her-2, is the target for a monoclonal antibody currently being marketed by Genentech, Inc. for treatment of breast cancer.
With cancer cells, expression of EGFr is significantly increased, which increases growth stimuli and causes cells to divide abnormally. Consequently, many cancer cells require EGFr for their survival. ABX-EGF binds with high affinity to the EGFr and selectively targets these cancer cells by blocking the binding of important tumor growth factors to the receptor. A key finding of the Abgenix studies was that relatively low doses of ABX-EGF, without concomitant chemotherapy, could eradicate human tumors with a size of up to 1.2cm3 in mice. Although the treatment period was relatively short, no recurrence of tumors was seen in these mice out to 250 days after the last dose of antibody. Abgenix plans to begin clinical trials with ABX-EGF around midyear.
"We believe that these results indicate the potential of ABX-EGF as a
monotherapy for the treatment of multiple EGF-depend
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Contact: Amy Flood
a.flood@noonanrusso.com
415-677-4455 x211
Noonan/Russo Communications
15-Mar-1999