OXiGENE Announces Presentation of Encouraging OXi4503 Preclinical and Clinical Data in Acute Myelogenous Leukemia at American

OXiGENE Announces Presentation of Encouraging OXi4503 Preclinical and Clinical
Data in Acute Myelogenous Leukemia at American Society of Hematology Meeting

(Nasdaq:OXGN), a clinical-stage biopharmaceutical company developing novel
therapeutics to treat cancer, announced today that investigators at the
University of Florida presented encouraging clinical data using OXiGENE's
vascular disrupting agent (VDA), OXi4503, in patients with acute myelogenous
leukemia (AML) at the 2012 annual meeting of the American Society of
Hematology in Atlanta, Georgia. The data showed responses and a manageable
safety profile in this first-in-man trial of a VDA in AML.

The clinical data were presented as an online abstract from an
investigator-sponsored Phase 1 study of OXi4503, which is supported in part by
the Leukemia & Lymphoma Society, for the treatment of patients with AML or
myelodysplastic syndrome (MDS). The ongoing open-label, dose-escalating study
is evaluating the safety profile, maximum tolerated dose (MTD) and biologic
activity of OXi4503. Results were presented on 5 patients with refractory AML
enrolled between May, 2011 and August, 2012. The median number of prior
therapies was 4 (range, 1-7). Two subjects were assigned to the 2.5 mg/m^2
dosing cohort, 2 received 3.75 mg/m^2 and 1 received 5 mg/m^2. None of these
patients developed dose-limiting toxicities. Adverse events attributable to
OXi4503 infusion included bone pain, fever, anemia and thrombocytopenia.
Hypertension was manageable and plasma LDH and uric acid increased by at least
two-fold within hours after OXi4503 infusions, suggesting leukemia cell

Overall response was 2/5 (40%), with 1 patient achieving a marrow complete
remission (mCR) and 1 patient achieving a partial remission (PR). The median
number of cycles was 1 (range 1-6). Three of 5 subjects discontinued the study
due to AML progression and one due to pneumonia. One patient with AML treated
with 5 mg/m^2 OXi4503 has received 6 months of treatment and continues to
receive weekly infusions.

To further elucidate the mechanism of AML regression by combretastatins,
investigators at the University of Florida also presented preclinical data in
a poster presentation titled "Vascular Disrupting Combretastatins Impair Bone
Marrow Endothelial Cells by Depolymerizing the Microtubule Cytoskeleton." In
this study, bone marrow endothelial cells (BMECs) from both healthy subjects
and patients with AML were treated with various doses of the combretastatins
OXi4503 and ZYBRESTAT® for 24 and 48 hours.The results showed that both
combretastatins impaired BMECs migration and function compared to untreated
control. In addition, there was a distinct degradation of microtubule
cytoskeleton in BMECs treated with the two combretastatins. AML cells
co-cultured with BMECs treated with the two combretastatins showed a lower
survival rate than AML cells alone. Conclusions were that combretastatins
directly impair BMEC function and eliminate BMEC protection of AML cells, and
the dual targeting of combretastatins on BMECs and AML cells leads to enhanced
AML regression.

"We are excited to present these preclinical data as well as the preliminary
clinical data from the ongoing AML trial with OXi4503, and look forward to
further investigating the dual mechanism of activity of this novel vascular
disrupting agent," said Christopher Cogle, MD, of the University of Florida
and lead investigator of the clinical study."AML is a highly lethal cancer,
and there is an urgent need for therapeutic approaches based on new mechanisms
of action that can be used as monotherapy or that can potentially be combined
with current treatment regimens. These OXi4503 studies may demonstrate that
targeting both the leukemic cells and the endothelium is a promising and safe
way to treat AML in resistant populations."

"OXi4503 continues to be a valuable asset in our company's product portfolio
of vascular disrupting agents. We are collaborating with Dr. Cogle and his
team at the University of Florida to further explore its fundamental mechanism
of activity and therapeutic potential in AML and MDS," said Jai Balkissoon,
MD, FACS, and OXiGENE's Vice President of Clinical Development.

About OXi4503

OXi4503 (combretastatin A1 diphosphate / CA1P) is a dual-mechanism vascular
disrupting agent (VDA) that is being developed in clinical trials for the
treatment of leukemias. Like its structural analog, ZYBRESTAT (fosbretabulin /
CA4P), OXi4503 has been observed to block and destroy tumor vasculature,
resulting in extensive tumor cell death and necrosis. In addition, preclinical
data indicate that OXi4503 is metabolized by oxidative enzymes (e.g.,
tyrosinase and peroxidases), which are elevated in many solid tumors and tumor
white blood cell infiltrates, to an orthoquinone chemical species that has
direct cytotoxic effects on tumor cells. Preclinical studies have shown that
OXi4503 has (i) single-agent activity against a range of xenograft tumor
models; and (ii) synergistic or additive effects when incorporated in various
combination regimens with chemotherapy, molecularly-targeted therapies
(including tumor-angiogenesis inhibitors), and radiation therapy. OXi4503 has
been evaluated as a monotherapy in a Phase 1 dose-escalation trial in patients
with advanced solid tumors and in patients with cancers involving the liver.

The OXiGENE, Inc. logo is available at

Safe Harbor Statement

This news release contains "forward-looking statements" within the meaning of
the Private Securities Litigation Reform Act of 1995. Any or all of the
forward-looking statements in this press release, which include the timing of
advancement, outcomes, and regulatory guidance relative to our clinical
programs, achievement of our business and financing objectives may turn out to
be wrong. Forward-looking statements can be affected by inaccurate assumptions
OXiGENE might make or by known or unknown risks and uncertainties, including,
but not limited to, the inherent risks of drug development and regulatory
review, and the availability of additional financing to continue development
of our programs.

Additional information concerning factors that could cause actual results to
materially differ from those in the forward-looking statements is contained in
OXiGENE's reports to the Securities and Exchange Commission, including
OXiGENE's reports on Form 10-K, 10-Q and 8-K. However, OXiGENE undertakes no
obligation to publicly update forward-looking statements, whether because of
new information, future events or otherwise. Please refer to our Annual Report
on Form 10-K for the fiscal year ended December 31, 2011.

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