"Effects of Toxic Iron Deposits"

----------------
BaroFold Inc. Initiates First Human Studies For Multiple Sclerosis
Drug Candidate, BaroFeron(tm)
Main Category: Multiple Sclerosis
Also Included In: Clinical Trials / Drug Trials
Article Date: 18 Jun 2008 - 6:00 PDT

BaroFold Inc. announced that it has initiated a two-stage Phase 1,
repeat dosing, single-center, double-blinded study in up to sixty
healthy volunteers to determine the safety, tolerability,
pharmacokinetics and pharmacodynamics of escalating doses of
BaroFeron(tm) (IFNβ-1b).

In published preclinical studies BaroFeron demonstrated enhanced
pharmacological properties, both pharmacokinetics and
pharmacodynamics, when compared to commercial interferon beta
products. BaroFeron has the potential to offer significant benefits to
multiple sclerosis patients as these properties have been demonstrated
to correlate with lesion formation by MRI measurements and clinical
exacerbations.

"BaroFeron is posed to set a new standard for biologics incorporating
our novel PreEMT(tm) technology that produces a product with
biopharmaceutical properties that may be superior to conventionally
produced proteins," stated Jeffrey L. Cleland, Ph.D., Vice President
of Therapeutic Development. "We believe that MS patients will
ultimately benefit from the unique properties of BaroFeron."

"This is the Company's first clinical milestone and demonstrates our
ability to advance product programs from concept to the clinic in less
than 18 months," stated Lyndal Hesterberg, President and CEO. "The
tremendous team at BaroFold, combined with the utilization of our
unique technology to improve existing biopharmaceutical products,
provides us with the ability to rapidly generate multiple product
candidates that address large markets. Our goal is to have BaroFeron
for multiple sclerosis in late-stage clinical trials and advance two
additional two pipeline products targeting allergic asthma and
rheumatoid arthritis in the clinic by the end of 2010."

About BaroFeron

BaroFeron is a proprietary recombinant human interferon beta being
developed for the treatment of multiple sclerosis. Interferon beta
products are considered the "gold" standard for first line treatment
options for managing the progression of multiple sclerosis. However,
clinical evidence and physician surveys indicate the need to improve
upon the efficacy and safety of currently available therapies.
BaroFeron is produced using BaroFold's proprietary PreEMT(tm) technology
to yield a formulation essentially free of protein aggregates.
BaroFeron could potentially be differentiated from other interferon-
beta products by improved safety and greater bioavailability enabled
by BaroFold's proprietary PreEMTTM technology.

About PreEMT

BaroFold's proprietary PreEMT technology incorporates hydrostatic
pressure to disaggregate and refold proteins into the
biopharmaceutical manufacturing process. The technology improves
product quality by producing essentially "aggregate-free" final
product that may have superior homogeneity and stability. PreEMT
enables the production of new biologics that are difficult to
manufacture with conventional methods as well as novel protein
structures can be generated by reactions performed with the
technology. PreEMT production systems are reliable and scalable using
commercially available equipment currently used in the food and
chemical industries.

About BaroFold

BaroFold is developing improved biopharmaceuticals for patients
suffering from chronic immunologic disorders. Utilizing proprietary
process technologies, BaroFold creates novel protein therapeutics
targeting validated disease pathways with blockbuster potential.
BaroFold's development candidates target chronic indications having
significant physician and patient demand for therapies that are more
tolerable and efficacious than those currently available. BaroFold has
leveraged its unique technology to form relationships with several
biopharmaceutical companies.

This press release contains forward-looking statements that involve
risks and uncertainties, including statements relating to initiation
and progress of the Company's clinical trial programs. Actual results
could differ materially from those projected and the Company cautions
investors not to place undue reliance on the forward-looking
statements contained in this release.

http://www.barofold.com

-----------------------------

From the University of Buffalo:

Study Proposes Interferon Beta-1A May Lessen Brain Atrophy in MS
Patients by
Minimizing Effects of Toxic Iron Deposits

Release date: Thursday, April 10, 2003
Contact: Lois Baker, ljba...@buffalo.edu
Phone: 716-645-5000 ext 1417
Fax: 716-645-3765

BUFFALO, N.Y. -- Specialists in neuroimaging at the University at
Buffalo have
proposed a mechanism by which interferon beta-1a may limit brain
atrophy in
multiple sclerosis (MS) patients.

The positive effect of interferon beta-1a, a standard treatment for
MS, on
brain atrophy is well known, but the process through which that occurs
remains
a mystery. UB scientists have shown that the treatment appears to
limit atrophy
by minimizing the toxic effect of pathologic iron deposits found in
gray-matter
structures of MS patients.

While the treatment did not diminish iron concentrations that had
already
accumulated, it appeared to interfere with the accumulation of iron-
induced
damage, said Robert A. Bermel, a fourth-year medical student in UB's
School of
Medicine and Biomedical Sciences and lead author on the study.

Bermel presented the research findings on April 3 at the annual
meeting of the
American Academy of Neurology in Hawaii. He also presented the study
in March
at the annual meeting of the American Society of Neuroimaging, which
selected
the work to receive the society's 2003 Oldendorf Award for the best
research
project first-authored by a trainee.

The MRI imaging work was conducted at the Buffalo Neuroimaging
Analysis Center
(BNAC) of the Jacobs Neurological Institute, affiliated with UB's
School of
Medicine and Biological Sciences and Kaleida Health. This group
reported
previously for the first time that in addition to the characteristic
white-matter lesions that are a traditional marker of the disease, MS
patients
show shrinkage, or atrophy, of certain structures in the brain's deep
gray
matter.

Their imaging studies have shown also that in MS patients these deep
gray-matter structures appear hypointense, or darker than normal,
signaling the
presence of iron concentrations. The researchers hypothesize that
brain atrophy
is linked to these iron deposits.

"We know that MS patients have defective blood-brain barriers, the
filter that
keeps chemicals, like iron, from leaking into the brain," said Bermel.
"Our
hypothesis is that this defect allows iron to accumulate in certain
parts of
the brain, which then can be directly neurotoxic to cells, causing
atrophy."

Knowing that interferon beta-1a treatment has a positive effect on
brain
atrophy, Bermel and colleagues set out to determine if the pathway of
action
was associated with iron concentration. They followed 159 patients who
were
enrolled in a randomized, double-blind treatment trial for the
relapsing form
of the disease for two years. Eighty-one patients received treatment;
78 who
received placebo served as controls.

Researchers took MRI scans of all patients to determine hypointensity
and brain
atrophy at baseline and at two years. Results showed that
hypointensity at
baseline was linked to brain atrophy over that time period in
controls, but not
in the treatment group. Hypointensity remained unchanged in the
treatment
group, but brain atrophy was significantly less.

"These findings suggest that interferon may disrupt the relationship
between
baseline T2H (hypointensity) and atrophy over time," Bermel said,
noting that
there may be several explanations for the finding.

"Interferon beta-1a is known to lower the levels of inflammatory
cytokines in
the blood of patients with MS. When the body is in a state without
inflammation, as it is normally, its cells, including neurons, can
better
regulate their contents and byproducts, including iron. In untreated
MS, which
is characterized by brain inflammation, iron may be allowed to build
up to
toxic levels in certain brain structures, causing toxic chemical
reactions and
death of nerve cells, leading to what we see as brain atrophy on MRI
scans.

"Also, interferon is known to help restore the body's natural blood-
brain
barrier, which would keep toxic iron from seeping into the cells,"
Bermel said.
"This study shows for the first time that interferon treatment may
result in
less brain atrophy in MS through a cascade of events that interferes
with the
pathologic iron deposition."

Additional authors on the study from Buffalo were: Srinivas R. Puli,
M.D.,
former research associate in the BNAC; Andrew J. Fabiano, third-year
medical
student doing research in the BNAC; Bianca Weinstock-Guttman, M.D.,
assistant
professor of neurology; Frederick E. Munschauer, M.D., professor and
chair of
the Department of Neurology, and Rohit Bakshi, M.D., associate
professor of
neurology and director of the BNAC.

Elizabeth Fisher, Ph.D., and Richard A. Rudick, M.D., from the
Cleveland
Clinic, performed measurements of whole brain atrophy. Jack H. Simon,
M.D.,
Ph.D., from the University of Colorado, performed additional
analysis.

The research was funded by a grant from Alpha Omega Alpha and a
scholarship
from the American Academy of Neurology to Bermel and by a grant to
Bakshi from
the National Institutes of Health.

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Tom

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