Halsa Pharmaceuticals Announces ZAG Demonstrates Weight Loss, Rise in Temperature and Reduction of Diabetes Symptoms in Preclinical Studies at Obesity 2009 Annual Scientific Meeting

Suggests Increase in Energy Expenditure and Potential as Treatment for Obesity
and Type 2 Diabetes
HOUSTON--(Business Wire)--
Houston-based Halsa Pharmaceuticals, Inc., a biotechnology company developing
therapeutics for the treatment of obesity, diabetes, cachexia and other
metabolic diseases, today announced results from preclinical studies
demonstrating that recombinant human Zinc-α2-glycoprotein (ZAG) induced a
progressive loss of body weight in mice of 3.5g in five days, together with a
rise in temperature of 0.4°C, suggesting an increase in energy expenditure. In
addition, ZAG produced a normalization of the diabetic glucose tolerance curve
after three days of treatment, suggesting that ZAG may have a therapeutic
application in the treatment of obesity and Type 2 diabetes. The results from
this study were presented at Obesity 2009, the 27th Annual Scientific Meeting of
The Obesity Society, one of the largest scientific conferences in the field of
obesity, being held in Washington, D.C. October 24-28.

"ZAG acts normally in the body to regulate levels of fat, and these new results
tell us that ZAG regulates the metabolic hallmarks of Type 2 diabetes as well as
obesity," said Professor Michael J. Tisdale, Aston University, Birmingham, U.K.,
the inventor of ZAG as a therapeutic. "Certain disease states cause very high
over-expression of ZAG, and in those circumstances body fat is depleted, so we
know that humans possess a fat-depletion response to ZAG. In addition, there is
a low expectation of acute toxicity with ZAG because it occurs at medium
prevalence in the human body, and we were pleased that these preclinical studies
demonstrated this as well."

Summary Results:

* ZAG induced a progressive loss of body weight in mice of 3.5g in five days,
together with a rise in temperature of 0.4°C.
* Even before major changes in body mass, ZAG induced a decrease in blood
glucose and plasma insulin levels, while there was a four-fold increase in
pancreatic insulin, and normalization of the diabetic glucose tolerance curve.
* Weight loss was associated with an increase in weight of brown adipose tissue
and an increase in expression of uncoupling proteins-1 and -3, which would be
expected to channel metabolic substrates into heat as observed.
* ZAG-treated animals showed a significant decrease in plasma levels of
triglycerides and non-esterified fatty acids.
* ZAG administration also increased plasma glycerol, which is indicative of an
increased lipolysis and a decrease in carcass fat mass.
* ZAG administration increased glucose uptake into adipose tissue and skeletal
muscle both in the absence and presence of insulin, associated with an increased
expression of glucose transporter 4.
* Due to an increase in protein synthesis and a decrease in protein degradation
through the ubiquitin-proteasome pathway, there was an increase in skeletal
muscle mass.

"Halsa already has extensive animal proof-of-concept data on ZAG, along with an
understood and novel mechanism-of-action and robust patent rights, and we look
forward to bringing this compound into clinical testing," commented Halsa Chief
Executive Officer Phil Speros. "These new results demonstrate that the
anti-obesity action of ZAG is balanced with metabolic pathways to utilize and
dispose of fat breakdown products, pathways that also act to mitigate diabetes."

ZAG is a recombinant protein (biologic) being developed into a prescription
pharmaceutical product which will increase ZAG levels in obese patients to
normal levels and reduce body fat to normal levels. ZAG is a natural regulator
of fat in humans and other animals. Higher ZAG levels cause fat depletion, and
lower levels allow fat accumulation. ZAG utilizes a novel biochemical pathway
and acts directly on adipose - it does not impact food intake, water intake,
digestion or activity. There is strong scientific evidence that this compound
causes fat depletion in humans, as ZAG is an adipokine responsible for loss of
adipose tissue in cancer cachexia, and earlier preclinical studies have
demonstrated proof-of-concept data in animals. Halsa has exclusive intellectual
property rights to the therapeutic.

ABOUT HALSA PHARMACEUTICALS

Halsa Pharmaceuticals, Inc. is a biotechnology company that was founded in 2000
and is developing therapeutics for the treatment of obesity, diabetes, cachexia
and other metabolic diseases.

SAFE HARBOR STATEMENT

Under the Private Securities Litigation Reform Act of 1995, a "safe harbor" may
be provided to us for forward-looking statements. Words such as "outlook,"
"believes," "expects," "appears," "may," "will," "should," "anticipates" or the
negative thereof or comparable terminology, are intended to identify these
forward-looking statements. These forward-looking statements are estimates
reflecting the best judgment of our senior management and are based on our
current expectations and projections concerning future events, many of which are
outside of our control, and involve a number of risks and uncertainties that
could cause actual results to differ materially from those suggested by the
forward-looking statements.

Halsa Pharmaceuticals, Inc.
Phil Speros, 832-722-0513
psperos@halsapharma.com
or
PRonCall (media)
Kathryn Morris, 845-635-9828
kathryn@proncall.com

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