-- PBT2 potently inhibits synthetic Abeta forming toxic soluble oligomers
in vitro;
-- PBT2 reduces Abeta oligomer levels detected in secretions from the
brains of conscious, freely moving AD transgenic mice within 4 hrs of oral
administration. This observation was reproduced in two genetically
distinct mouse models;
-- PBT2 sharply improves cognitive performance in the Morris Water Maze
for two genetically distinct mouse models of AD within 5 to 7 days of
treatment; and
-- The brains of the mice with improved cognition showed a substantial
reduction in the biomarkers phosphorylated tau and Abeta, while
simultaneously raising the level of the neuronal marker protein
synaptophysin.
The amyloid plaques which are the main pathological feature of the brains
of Alzheimer's sufferers are composed of aggregates of the Abeta protein.
The Alzheimer's research community largely supports the hypothesis that
small, soluble, mobile aggregates (oligomers) of the Abeta protein are the
cause of neurotoxicity in AD. PBT2's ability to inhibit the generation
and toxicity of these oligomers, as well as preventing the
hyperphosphorylation of tau, while improving cognition, supports the
disease modifying potential of PBT2 and other drugs in the Prana
development pipeline.
Geoffrey Kempler, Chairman and Chief Executive Officer of Prana, commented:
"The results of these studies are encouraging and lend further support to
the theories driving development of PBT2. We continue to improve our
understanding of PBT2's functionality and potential for disease
modification as we move forward with formal clinical development. The
ongoing PBT2 Phase IIa trial in early Alzheimer's patients is on track to
complete dosing by the end of this year and report early in 2008."
The technique of in vivo brain microdialysis recently adopted as a research
tool by Prana scientists provides a unique insight into a dynamic metabolic
process, allowing researchers to sample secretions from the brains of
conscious, unrestrained test animals freely interacting with their
environment. Sampling from the brains of genetically engineered AD mouse
models which have received single or sequential oral doses of PBT2, it was
found that the drug exerts its inhibitory effects upon the target molecule,
Abeta, rapidly and reproducibly without causing "rebound" effects observed
with other drugs in development. Most particularly, a dramatic reduction
was observed in soluble oligomers of the size range identified in the
literature as the most toxic form of Abeta amyloid in AD.
The findings of these studies confirm and expand upon data presented by the
Company at the International Conference of Alzheimer's Disease in Madrid
last July, describing potent effects of PBT2 on memory acquisition and
retention in Alzheimer's mice.
About Prana Biotechnology Limited
Prana Biotechnology was established to commercialise research into
Alzheimer's disease and other major age-related neurodegenerative
disorders. The company was incorporated in 1997 and listed on the
Australian Stock Exchange in March 2000 and listed on NASDAQ in September
2002. Researchers at prominent international institutions including The
University of Melbourne, The Mental Health Research Institute (Melbourne)
and Massachusetts General Hospital, a teaching hospital of Harvard Medical
School, contributed to the discovery of Prana's technology.
For further information, please visit our web site at www.pranabio.com.
Forward Looking Statements
This press release contains "forward-looking statements" within the meaning
of section 27A of the Securities Act of 1933 and section 21E of the
Securities Exchange Act of 1934. The Company has tried to identify such
forward-looking statements by use of such words as "expects," "intends,"
"hopes," "anticipates," "believes," "could," "may," "evidences" and
"estimates," and other similar expressions, but these words are not the
exclusive means of identifying such statements. Such statements include,
but are not limited to any statements relating to the Company's drug
development program, including, but not limited to the initiation, progress
and outcomes of clinical trials of the Company's drug development program,
including, but not limited to, PBT2, and any other statements that are not
historical facts. Such statements involve risks and uncertainties,
including, but not limited to, those risks and uncertainties relating to
the difficulties or delays in financing, development, testing, regulatory
approval, production and marketing of the Company's drug components,
including, but not limited to, PBT2, the ability of the Company to procure
additional future sources of financing, unexpected adverse side effects or
inadequate therapeutic efficacy of the Company's drug compounds, including,
but not limited to, PBT2, that could slow or prevent products coming to
market, the uncertainty of patent protection for the Company's intellectual
property or trade secrets, including, but not limited to, the intellectual
property relating to PBT2, and other risks detailed from time to time in
the filings the Company makes with Securities and Exchange Commission
including its annual reports on Form 20-F and its reports on Form 6-K.
Such statements are based on management's current expectations, but actual
results may differ materially due to various factions including those risks
and uncertainties mentioned or referred to in this press release.
Accordingly, you should not rely on those forward-looking statements as a
prediction of actual future results.
Contact Information: Contacts: Investor Relations Mark Jones T: 646-284-9414 E: mjones@hfgcg.com Media Relations Ivette Almeida T: 646-284-9455 E: ialmeida@hfgcg.com