Presentation at 4th Annual Nicotine Research Conference
            Bryan Center, Duke University, Durham, North Carolina

    LA JOLLA, Calif., Nov. 4 /PRNewswire/ -- In a presentation at Duke
University, scientists from SIBIA Neurosciences, Inc. (Nasdaq: SIBI) reported
that preclinical studies of SIB-1508Y, one of the Company's proprietary
neuronal nicotinic acetylcholine receptor (nAChR) agonists, and currently in
Phase 2 clinical trials, has shown the ability to substantially protect
neurons from degenerative changes in a rodent model of Parkinson's disease.
    Previous studies in rat and primate models of Parkinson's disease
suggested that SIB-1508Y could offer a new approach to treatment with distinct
advantages over existing Parkinson's disease therapies because of its ability
to improve both cognitive and motor deficits.  It is now recognized that
cognitive impairment is a serious and frequent symptom in many Parkinson's
patients, but no available product addresses this aspect of the disease.  The
animal data on neuroprotection suggests the potential for this compound to
treat not only the cognitive and motor symptoms of Parkinson's disease, but to
retard the degeneration of neurons, which is a hallmark of the disease
process.
    Human Parkinson's disease is characterized by loss of the neurotransmitter
dopamine in the nigrostriatal pathway, resulting in marked impairment of
movement and often accompanied by deficits in affect and cognition.  In the
studies reported by Tadimeti Rao, Ph.D., Associate Research Director at SIBIA,
SIB-1508Y offered protection against the decrease in dopamine levels in the
striatum and substantia nigra in rat models of Parkinson's disease following
injection of a neurotoxin, 6-OHDA, into the rat striatum.  This type of lesion
damages dopamine neuron terminals in the striatum and leads to a progressive
degeneration of the dopamine cell bodies in the substantia nigra.  The best
protection was seen when SIB-1508Y was given prior to the 6-OHDA injection and
followed by continued administration over a period of four weeks.  In this
paradigm, SIB-1508Y was able to completely protect against toxin-induced loss
of dopamine in the substantia nigra and protect up to 75% of the dopamine loss
in the striatum.  In addition, the repeated administration of SIB-1508Y
increased levels of choline acetyltransferase, a critical enzyme involved in
the synthesis of acetylcholine, an important neurotransmitter for cognition.
    SIBIA Neurosciences, Inc. is engaged in the discovery and development of
novel small molecule therapeutics for the treatment of neurodegenerative,
neuropsychiatric and neurological disorders, many of which have large patient
populations and represent critical unmet medical needs.  SIBIA is a leader in
the development of proprietary drug discovery platforms that combine key tools
necessary for modern drug discovery, including genomics, high throughput
screening, advanced combinatorial chemistry techniques and pharmacology.  The
Company's proprietary molecular targets and drug candidates, together with its
drug discovery technologies and research expertise, have enabled the Company
to establish several corporate collaborations, which currently include
Bristol-Myers Squibb Company and Meiji Seika Kaisha, Ltd., and multiple
technology licensing arrangements.

    This press release contains forward-looking statements that involve risks
and uncertainties.  As a result, actual results could differ materially from
those discussed herein.  These risks and uncertainties include SIBIA's
reliance on corporate partnerships and ability to enter into new corporate
partnerships, whether SIBIA will be successful in demonstrating the safety and
efficacy of SIB-1508Y in humans, whether SIBIA will be able to meet its
development goals with respect to its drug candidates and proprietary targets,
SIBIA's early stage of development, uncertainties regarding regulatory
matters, and other research, development and market risks.  These and other
risks and uncertainties are more fully set forth in SIBIA's most recently
filed Forms 10-Q and 10-K.

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