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Animal studies show CA4P suppresses development and induces regression of ocular neovascularization.





July 31, 2003.

Press Release.
Contact: Scott Solomon,
ssolomon@investorrelations.com
617-542-5300
Sharon Merrill Associates, Inc.




Watertown, Mass.


OXiGENE, Inc. (NASDAQ: OXGN, XSSE: OXGN) today announced the results of independent animal studies demonstrating the potential role of the Company's lead compound, Combretastatin A4 Prodrug (CA4P), in preventing and treating certain retinal degenerative diseases. Findings of the study are published in the current issue of the peer-reviewed journal Investigative Ophthalmology and Visual Science (IOVS).


The studies were conducted at The Johns Hopkins University School of Medicine by a team of researchers including Peter A. Campochiaro, M.D., a professor of ophthalmology at the school's renowned Wilmer Eye Institute. Dr. Campochiaro and Assistant Professor of Ophthalmology Quan Dong Nguyen, M.D. are leading the current Phase I/II clinical trial of CA4P in patients with wet age-related macular degeneration, known as wet AMD. Between 2 million and 3 million people in the United States have significant vision loss caused by wet AMD.


"The pre-clinical research produced by Dr. Campochiaro and his colleagues, as well as several other pre-clinical ophthalmic models using CA4P, provided the impetus for OXiGENE to move CA4P into human trials at Johns Hopkins," said Fred Driscoll, OXiGENE's president and CEO. "We are very pleased that Dr. Campochiaro considered the data from this study compelling enough to take CA4P into trials at one of the world's leading research institutions."


The study was designed to gauge CA4P's ability to suppress the development of choroidal neovascularization (CNV), a condition in which aberrant blood vessels beneath the retina leak blood and fluid into the retina. CNV is the primary cause of severe vision loss in patients with retinal degenerative diseases such as wet AMD. Researchers conducted experiments using transgenic mice with CNV caused by an over expression of vascular endothelial growth factor in the retina (rho/VEGF mice) and mice with laser-induced rupture of Bruch's membrane.


In both groups of mice, daily intraperitoneal injections of CA4P resulted in a "significant reduction" in CNV. Dr. Campochiaro and his colleagues concluded, "In this study, we have demonstrated that a tubulin-binding agent, CA-4-P, suppresses the development of subretinal neovascularization in rhodopsin/VEGF transgenic mice and suppresses the development of CNV at Bruch's membrane rupture sites. This suggests that when administered before onset of an angiogenic stimulus, CA-4-P can prevent these two forms of ocular neovascularization. A recent study has shown that CA-4-P can also prevent ischemia-induced retinal neovascularization in mice. Therefore, CA-4-P joins a growing list of drugs that have potential as prophylactic agents for retinal and/or choroidal neovascularization. However, CA-4-P also caused partial regression of established CNV, a finding that sets it apart from other drugs. To our knowledge, intraocular gene transfer of pigment epithelium-derived factor (PEDF) is the only other gene-therapy-based or drug treatment that has been shown conclusively to cause partial regression of CNV, and therefore CA-4-P is in select company. Therefore, similar to PEDF gene transfer, treatment with CA-4-P has potential for treatment of established CNV."


The Johns Hopkins trial is the first human study of OXiGENE's lead compound in a non-life-threatening indication. CA4P also is being studied in four late-stage cancer trials in five indications including anaplastic thyroid cancer, ovarian cancer and malignancies of the lung, head & neck and prostate.






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