Presentations on the Mechanism of Action of VEGFb(TM), the World's Only "Angiogenesis...

Presentations on the Mechanism of Action of VEGFb(TM), the World's Only "Angiogenesis Modulator," Support VEGFb's Role as an Epical Treatment for Solid Cancers, Macular Degeneration, and Other Diseases

SUMMIT, N.J.--(Business Wire)--
Increasingly, VEGFb is becoming recognized as a drug that will
begin a new era in cancer treatment, due to its revolutionary
mechanism of action. VEGFb is the world's only "angiogenesis
modulator;" a drug that regresses pathological blood vessels (such as
those in solid tumors, wet macular degeneration, and other disorders),
promotes the formation of normal blood vessels, while also acting as
an essential survival factor for endothelial cells, neurons, and other
cells and tissues.

The European Congress on Microcirculation, held in Budapest,
Hungary, featured a symposium focused on VEGFb on Aug 26(th) 2OO8. The
results presented at this symposium, showcased the
breakthrough aspects of VEGFb's activities and its promise as a more
effective and safer anti-angiogenic drug. Presenting, were Professor
David Bates and Dr. Jeanette Woolard from the University of Bristol,
Dr. Kurt Ballmer Hofer from the Paul Scherer Institute, Zurich, and
Dr. Andrea Cupp from the University of Nebraska.

Professor Bates reviewed recent data showing that VEGFb prevents
the formation of new blood vessels in response to injury in the retina
(a model of choroidal neovascularization, that relates to the clinical
problem in wet age related macular degeneration). Dr. Bates also
presented a preclinical study demonstrating that VEGFb is remarkably
effective in preventing the formation and growth of metastases,
following surgical removal of primary human melanoma tumors in mice.

If caught early, a number of cancers can be treated by surgically
removing the tumor. As we know from the deaths of friends and family,
cancer often reoccurs and spreads to sites distant from the original
tumor (metastases). Metastases are usually the cause of death from
solid tumors. For instance, in early stage colon cancer, after
surgical removal of the primary colon tumor, metastases form and grow
in various organs within a year in half the patients. Patients with
widespread colon cancer metastases are often untreatable, as is the
case of metastases in a number of cancer types.

VEGFb has been shown to be a non-toxic and effective drug in
preclinical models, and promises to play a critical role in preventing
the postsurgical reoccurrence of cancer, that is metastatic colon,
melanoma, renal, and breast cancer. VEGFb appears to be so safe, that
it could be used to treat all colon cancer patients undergoing surgery
to prevent metastatic reoccurrence, unlike other cancer drugs, which
are too toxic to be ethically used in the prevention of metastases.
Preclinical models have also demonstrated that VEGFb, as a sole agent,
causes the regression of a variety of primary tumors, hence, VEGFb
also promises to be a safer and more effective first-line treatment
for a variety of solid tumors.

At the meeting in Budapest, specific efficacy and mechanism data
was presented from a variety of labs. Dr. Woolard presented recent
work from his lab, which advances our understanding of how VEGFb
expression is regulated by growth factors and splice factors. Dr. Cupp
showed that VEGFb is involved in the development of reproductive
organs in mice, inhibiting endogenous VEGFb resulted in increased
angiogenesis in the testis, and increased maturity of antral follicles
in the developing ovary. Dr. Ballmer Hofer showed that VEGFb acts by
partially activating the VEGFR2 resulting in signaling that prevents
angiogenesis, and he provided evidence that this partial activation is
due to VEGFb's inability to bind neuropilin. The mechanisms of VEGFb's
receptor binding was elucidated, explaining the mechanism for the
anti-angiogenic effect of VEGFb.

Further work at the conference presented from Dr. Leach's
laboratory at Nottingham University showed that VEGFb is down
regulated in diabetic placenta, and could be switched off by
excess insulin perfusion.

This meeting, with presentations from a number of independent
laboratories, further elucidates and validates the scientific
community's understanding of the mechanism of VEGFb's actions and is
expected to expedite the process of obtaining regulatory approval for
this breakthrough drug.

About VEGFb

PhiloGene's most advanced program is VEGFb (Vascular Endothelial
Growth Factor "b"). VEGFb is a naturally occurring anti-angiogenic
(angiogenesis- growth of new blood vessels) factor. VEGFb causes
regression of pathological blood vessels, such as those that are
essential for the growth and survival of tumors. VEGFb also regresses
(eliminates) abnormal new blood vessels generated in eye diseases,
such as wet macular degeneration and diabetic retinopathy. Extensive
efficacy animal data indicate that VEGFb is safe, potent, and a
specific anti-angiogenic factor that inhibits tumor growth, causes
tumor regression (renal, colon, and other), and regresses pathological
vascularization in the eye. VEGFb is also a survival factor that is
essential for many tissue types in the body such as endothelial cells
(cells that line the inside of blood vessels), kidney tissue, neurons
in the eye and other cell types. VEGFb promotes normal
vascularization, while reversing pathological vascularization.
Preclinical data indicates that VEGFb's survival effects will prevent
most of the side effects seen with the current generation of
anti-angiogenic drugs.

The discovery of VEGFb, the native anti-angiogenic form of VEGF,
and the elucidation of the mechanisms that control the ratio between
the pro- and anti-angiogenic forms of VEGF is a paradigm shift from
current therapeutic approaches. Current therapeutic approaches are
non-specific and remove both, the pro- and anti-angiogenic forms of
VEGF. PhiloGene's completely novel approach is more selective and
specific. To treat cancer, VEGFb is administered to patients to create
a therapeutic ratio of the pro- and anti-angiogenic forms of VEGF. As
a result, the tumor's blood vessels and the tumor fed by these blood
vessels both regress. The elegance of PhiloGene's approach is that it
utilizes the body's endogenous, natural, homeostatic system, which
controls the creation and/or regression of blood vessels. In animal
models of human cancer, the administration of VEGFb has led to the
complete disappearance of a variety of established human tumors.

About PhiloGene

PhiloGene Inc. is a biopharmaceutical company focused on
developing and commercializing novel protein therapeutics for unmet
medical and patient needs. PhiloGene exploits the therapeutic
potential of native growth and differentiation factors. The first drug
in PhiloGene's pipeline is VEGFb, which is a triple action drug to
treat cancer and other diseases with pathological angiogenesis.
Because the anti-angiogenesis pathway is one of the most validated and
explored in medicine, the development path of VEGFb will be
accelerated. VEGFb is not only "first in class," but also in a class
by itself, the only triple action, "angiogenesis modulator" in
development in the pharmaceutical industry. PhiloGene has a worldwide,
exclusive, license for the anti-angiogenic family of VEGFb proteins
from Bristol University, UK.

PhiloGene Inc.
Press and Investors:
President
Dr. Mendi Ze'evi, 908-998-2402
mendi.zeevi@philogene-inc.com
or
Bus. Dev.
Stephen Rowe, 617-794-2220
steve.rowe@philogene-inc.com
http://www.philogene-inc.com
or
The University of Bristol:
Dr. Sandie Cree, +44 (0)117 9546968
www.mvrl.org

Copyright Business Wire 2008