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Addex Presents ADX10059 PD-LID Data at GPCR Drug Discovery Conference

ADX10059 inhibited both chorea and dystonia induced by levodopa while
maintaining the anti-parkinsonian effect of levodopa on PD symptoms

Geneva, Switzerland, 3 November 2009 - Addex Pharmaceuticals
(SWX:ADXN), the allosteric modulation company, presented results
today from studies of its lead clinical candidate, ADX10059, in
animal models of Parkinson's disease levodopa induced dyskinesia
(PD-LID) at the Discovery on Target GPCR-based Drug Discovery
conference in Boston. Addex disclosed for the first time that in a
non-human primate model of PD-LID, ADX10059 had a statistically
significant impact on dystonia, a neurological movement disorder seen
in Parkinson's disease and other conditions, including generalized
dystonia, tardive dyskinesia, levodopa non responsive PD syndrome and
multiple system atrophy. There is no approved treatment available for

ADX10059 is the first-in-class negative allosteric modulator (NAM) of
metabotropic glutamate receptor 5 (mGluR5), a mechanism that is being
tested in multiple indications by Addex and competitors. ADX10059 is
currently being evaluated in Phase IIb clinical trials for the
treatment of gastroesophageal reflux disease (GERD) and to prevent
migraine. Separate announcements of data from the two ongoing GERD
trials are expected before year-end and early in 2010. The migraine
study will report data early in the second quarter of 2010.

Addex disclosed earlier this year that ADX10059 demonstrated
significant efficacy in well-established preclinical models of PD and
PD-LID. Importantly, these effects in PD and PD-LID were seen at
doses and plasma concentrations that have shown efficacy in both
clinical and preclinical studies with the compound in other
indications. The effects on dystonia announced today differentiate
the Addex mGluR5 inhibitor within the PD indication but also present
potential development opportunities for treatment of other types of

The oral slide presentation today will show that in the non-human
primate MPTP model of PD-LID, all doses of ADX10059 abolished LID
during the first hour following L-DOPA administration and a dose
response was observed during the second hour, reaching statistical
significance for the two higher doses tested. Statistically
significant reductions were seen for both chorea and dystonia in a
dose dependent fashion. Similar effects on dystonia have not
previously been reported in this model with drug-like molecules
either in development or on the market.

When tested in the rat model, oral administration of ADX10059
dose-dependently reversed the catalepsy induced by haloperidol in
three independent experiments.

Dystonia is a neurologic movement disorder characterized by sustained
muscle contractions that frequently cause twisting or repetitive
movements and abnormal, sometimes painful, postures or positions.
Dystonia may affect any part of the body including the arms, legs,
trunk, neck, head, or face.

PD-LID develops in most PD patients after receiving levodopa for
several years. It is a complication caused by dopamine replacement
therapy (i.e. levodopa). The two main components of LID are chorea
and dystonia. Chorea is manifest as abnormal involuntary movements.
Currently there are an estimated 1.2 million patients with PD-LID in
the U.S.

PD is a degenerative disease of the brain that often impairs motor
skills, speech, and other functions. It is estimated that 60,000 new
cases are diagnosed each year in the U.S., where more than 1.5
million people currently have PD. While the condition usually
develops after the age of 65, 15% of those diagnosed are under 50. PD
affects both men and women in almost equal numbers.

mGluR5 inhibition reduces signaling activity of the neurotransmitter
glutamate. Marketed blockbuster drugs treat multiple indications by
targeting other types of neurotransmitter signaling, including
selective serotonin reuptake inhibitors (SSRIs) used to treat
depression and dopamine receptor inhibitors used to treat
schizophrenia. The rationale for using mGluR5 inhibition in PD is
that the loss of dopamine producing cells leads to excess
glutamatergic stimulation in the brain's "striatopallidal pathway".
mGluR5 are found abundantly in the striatum and are implicated in the
excess glutamate activity in Parkinson's Disease. Research shows that
inhibition of glutamate stimulation in this pathway has generated
anti-Parkinsonian effects in animal models of PD and PD-LID, and in
humans with PD-LID.

Addex Pharmaceuticals (www.addexpharma.com) discovers and develops
allosteric modulators for human health. Allosteric modulators are a
different kind of orally available small molecule therapeutic agent,
which we believe will offer a competitive advantage over classical
drugs. Our lead allosteric modulator product, ADX10059, has achieved
clinical proof of concept and is in Phase IIb testing for the
treatment of GERD and, separately, migraine headache. ADX10059 is a
first-in-class mGluR5 inhibitor, a therapeutic strategy that also is
being pursued in multiple indications by large pharma competitors.
Our products and technology already have proven their value through
our relationships with four of the top 10 pharmaceutical companies in
the world. Specifically, under an agreement with Ortho-McNeil-Janssen
Inc., a Johnson & Johnson company, ADX71149, a positive allosteric
modulator (PAM) of mGluR2, is undergoing Phase I clinical testing and
has potential for treatment of schizophrenia and anxiety. Under two
separate agreements with Merck & Co., Inc., we are developing PAMs of
mGluR4 and mGluR5 as drugs to treat Parkinson's disease and
schizophrenia, respectively. In addition, GlaxoSmithKline and Roche
have made equity investments in Addex.

Chris Maggos
Investor Relations & Communications
Addex Pharmaceuticals
+41 22 884 15 11

Disclaimer: The foregoing release contains forward-looking statements
that can be identified by terminology such as "not approvable",
"continue", "believes", "believe", "will", "remained open to
exploring", "would", "could", or similar expressions, or by express
or implied discussions regarding Addex Pharmaceuticals Ltd, its
business, the potential approval of its products by regulatory
authorities, or regarding potential future revenues from such
products. Such forward-looking statements reflect the current views
of Addex Pharmaceuticals Ltd regarding future events, and involve
known and unknown risks, uncertainties and other factors that may
cause actual results with allosteric modulators of mGluR4, mGluR2,
mGluR5 or other therapeutic targets to be materially different from
any future results, performance or achievements expressed or implied
by such statements. There can be no guarantee that allosteric
modulators of mGluR4, mGluR2 or mGluR5 will be approved for sale in
any market or by any regulatory authority. Nor can there be any
guarantee that allosteric modulators of mGluR4, mGluR2, mGluR5 or
other therapeutic targets will achieve any particular levels of
revenue (if any) in the future. In particular, management's
expectations regarding allosteric modulators of mGluR4, mGluR2,
mGluR5 or other therapeutic targets could be affected by, among other
things, unexpected actions by our partners, unexpected regulatory
actions or delays or government regulation generally; unexpected
clinical trial results, including unexpected new clinical data and
unexpected additional analysis of existing clinical data; competition
in general; government, industry and general public pricing
pressures; the company's ability to obtain or maintain patent or
other proprietary intellectual property protection. Should one or
more of these risks or uncertainties materialize, or should
underlying assumptions prove incorrect, actual results may vary
materially from those anticipated, believed, estimated or expected.
Addex Pharmaceuticals is providing the information in this press
release as of this date and does not undertake any obligation to
update any forward-looking statements contained in this press release
as a result of new information, future events or otherwise.

This announcement was originally distributed by Hugin. The issuer is
solely responsible for the content of this announcement.
Copyright © Hugin AS 2009. All rights reserved.

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