Aphton Collaborators Receive Blue Ribbon Poster of Distinction Award for One of Four Studies Presented At the Annual AGA Meeting.

Business Editors/Health & Medical Writers

SAN FRANCISCO--(BW HealthWire)--May 23, 2002

Aphton Corporation (Nasdaq:APHT) - At the annual meeting of the American Gastroenterological Association (AGA) being held in San Francisco, CA, Aphton collaborators received a Blue Ribbon Award Poster of Distinction for one of the four scientific posters relating to Aphton's anti-gastrin immunogen (G17DT), the gastrin family of growth factors and their receptors, the inhibition of these growth factors and receptors, their role in tumor growth, new blood vasculature (angiogenesis) and apoptosis, or cell suicide.

The Blue Ribbon Award was given for the studies showing that both gastrin 17 (G-17) and the precursor gly-G-17 are able to induce specific growth responses that lead to the branching and tubular networks characteristic of angiogenesis, in a human endothelial cell system (cells responsible for the development of new blood vasculature). Most importantly, their work showed that the angiogenic stimulus in this cell system "...is equal in magnitude to that caused by VEGF..." (VEGF has received much attention in the scientific and drug development literature), and that "...neutralization of G-17 and gly-G-17, by Aphton's anti-G17-DT caused a strong and significant reversal of (angiogenic) effects confirming their specificity of action...." They also demonstrated in these angiogenic cells, at both the molecular and protein level, that gastrin/CCK-2 receptor was expressed, and "...of note, gastrin/CCK-2R" in these blood vessel forming cells was of the type that had 3 times increased affinity for gly-gastrin than for G-17 (amidated) gastrin, which is characteristic of the receptors found in metastatic tumors. They concluded that these studies presented evidence for an angiogenic role for gastrin, in addition to its widely acknowledged role as a growth factor for GI-cancer cells and its spread.

A second study reported upon at the meeting investigated the mechanism of action by which an Aphton monoclonal antibody (Mab) targeted against the receptor to which G-17 binds, called the CCKB/Gastrin receptor, is taken up by a liver tumor cell, enters the cell nucleus and results in cell death. Five liver cancer (hepatoma) cell lines, both human and animal, were studied. The results were that in all five cell lines, uptake of the (Aphton) labeled anti-CCK-BR antibody was correlated with apoptosis. The investigators concluded: "Here, we demonstrate a direct relationship between the uptake of the antibody and cell death by apoptosis. This observation has important implications in the treatment of CCK-BR positive tumors including hepatomas where there are limited therapeutic options."

A third study presented findings on the varying structure of the receptors for gastrin 17 and gly-gastrin 17 during the progression of malignancy; and a fourth study investigated the effect of Aphton's anti-gastrin immunogen (G17DT) on human pancreatic cancer cells, concluding that "gastrin inhibition increases the potency of the cytotoxic agent Gemcitabine in pancreatic cancer."

Aphton is conducting one Phase III and three Phase II clinical trials. Aphton's anti-gastrin targeted therapy induces antibodies in patients that bind to both gastrin 17 and gly-gastrin and removes them from circulation before they can bind to the cancer cell and initiate cell growth. (Aphton believes this is the optimum method for achieving "growth factor inhibition.") Gastrin 17 and gly-gastrin are believed to be central growth factors, or the initiating signals, for cell growth, cell proliferation and metastasis (spread) in gastric, i.e. stomach, pancreatic, esophageal, colorectal and other gastrointestinal (GI) system cancers. This signaling program is accomplished by gastrin binding to the large numbers of gastrin receptors which appear, de novo, in the great majority of cases, on tumor cell surfaces throughout the gastrointestinal system. Interrupting this process by immunizing the patient with Aphton's anti-gastrin immunogen is a precisely "targeted" immunotherapy. This specificity of targeting only cancer cells occurs because gastrin is not normally secreted and gastrin receptors are not normally found on "healthy" cells in the GI system, unless they are malignant, or on the path to malignancy (except for cells involved with normal acid secretion). Recent findings have shown that inhibiting gastrin not only inhibits cell growth, proliferation and metastasis directly, but also "unblocks" a central pathway leading to apoptosis. This tilts the balance, from cell growth, to cell suicide. This effect is amplified synergistically when Aphton's drug is given together with a chemotherapeutic. Gastrin also stimulates the secretion and expression of other important growth factors and receptors within and on the surfaces of the cancer cells involved in tumor growth. Hence, inhibiting gastrin inhibits all of the foregoing factors contributing to tumor growth and spread, while simultaneously opening a central pathway to cell suicide. Aphton's anti-gastrin targeted therapy adds a biological dimension to the treatment of gastrointestinal cancers.

Aphton Corporation is a biopharmaceutical company developing products using its innovative targeted immunotherapy technology for neutralizing hormones that participate in gastrointestinal system and reproductive system cancer and non-cancer diseases; and the prevention of pregnancy. Aphton has strategic alliances with Aventis Pasteur (NYSE:AVE) for treating gastrointestinal system and other cancers with G17DT; GlaxoSmithKline (NYSE:GSK) for reproductive system cancer and non-cancer diseases; and others.

Except for the historical information herein, the matters discussed herein are forward-looking statements that involve a number of risks and uncertainties and are not a guarantee of future performance. Future results may vary significantly based on a number of factors including, but not limited to, intellectual property risks, risks in regulatory and market acceptance of new products and continuing demand for same, the impact of competitive products and pricing, changing economic conditions and other risk factors that are inherent in the drug development process and the company's business including those set forth in Aphton's most recent 10-K and other filings with the Securities and Exchange Commission. It is not possible to predict or identify all such risk factors that could cause actual results to differ from expected or historical results. The company's actual results could differ from these forward-looking statements and the company undertakes no obligation to update publicly any forward-looking statement.