Corporate Presentation

Corporate Presentation
February 2014
Overview and background
• History
• Addex was founded in 2002 in Geneva, Switzerland
• ADXN is traded on the SIX Swiss Stock Exchange since 2007
• Focus: pioneering oral small molecule allosteric modulation-based drug discovery
•
•
and development
Invested more than CHF300m in building allosteric modulator platform and pipeline
Due to a recent shortfall in funding, Addex was forced to put the majority of its
programs on hold and scale down operations
• Going forward, focus on:
• Maintaining mGlu2PAM collaboration with Janssen Pharmaceuticals Inc.
• Seek partners for clinical and preclinical programs – dipraglurant, ADX71441, etc
• Maintain and continue to establish risk sharing partnerships with industry and
academia:
• to advance early discovery programs; and
• leverage allosteric modulator platform
2
Status of rebuild
•
Restructuring completed
•
•
•
•
•
•
IP portfolio and allosteric modulator technology platform secured
Cash burn significantly reduced - runway through end 2014
Current headcount – 6FTE
Infrastructure reduced to 500m2 of lab & office space
Majority of liabilities and commitments extinguished
Rebuild plan in process of being executed
• Bridge financing of CHF3.2m raised in August 2013
• Restart team in place – know how protected
• Academic / patient group relationships and collaborations established to
advance research at low cost
• Relationships with outsourced R&D suppliers established
• Partnering outreach launched
3
Value drivers and competitive advantage
Leading allosteric
z
drug discovery
• Proprietary 85,000 knowledge-based HTS library
• Proprietary HTS high-fidelity pharmacology systems
• Deep allosteric know-how & expertise
Validated therapeutic
z
class
• Proven mechanism, that has led to marketed products
• Significant investment from all major pharma
• Growing pipeline of allosteric modulators in the clinic
Robust pipeline with
z
orphan drug potential
• 3 Phase 2 programs
• 1 Phase 1 ready program
• Multiple preclinical & discovery programs
z
Partnership with
leading pharma
• Janssen Pharmaceuticals Inc. (JPI) for mGlu2 PAM
z
Extensive IP portfolio
• 12 issued patents
• 43 pending patents
Financials
• CHF4.5M (US$4.9M/ €3.7M) in cash as of June 30, 2013
• Capital increase 9 Aug 2013 of CHF3.2M
• No debt & Cash through to end of 2014
z
4
Addex clinical pipeline, preclinical
& discovery programs
5
Clinical stage pipeline
Target
R&D stage
Indication
Additional Information
ADX71149
mGlu2PAM
Phase IIa PoC in
schizophrenia
Completed.
Signal in negative
symptoms in
schizophrenia
Partnered with Janssen Pharmaceuticals Inc.
Phase IIa POC in
anxious depression
- Completed
Primary endpoint
not met; however
signal seen in
some anxiety
scores and all
depression scores
Dipraglurant
mGlu5NAM
Phase IIa PoC in
PD-LID achieved
Back-up series in
LO
L-DOPA induced
dyskinesia
DYT1 Dystonia
(orphan indication)
Potential in
treatment resistant
depression
Clinical PoC of mGlu5 NAMs in PD-LID*, migraine*, GERD*,
generalised anxiety disorders and FXS
Preclinical PoC in PD-LID*, anxiety*, depression*, obsessive
compulsive disorders*, PD*, PD-LID*, dystonia*, HD, addiction,
and pain.
Other mGlu5NAMs are undergoing clinical tested in FXS,
OCD, TRD
ADX71441
GABABPAM
Phase I ready
1 follow-up series in
LO
CMT1A (orphan
indication)
Addiction (nicotine
and alcohol)
OAB
Clinical PoC in several indication with baclofen
Preclinical PoC in CMT1A*, anxiety*, alcohol and nicotine
addiction*, OA pain*, visceral pain*, overactive bladder*.
Potential in FXS, autism and spasticity in MS or cerebral palsy
Collaboration with NIDA to generate data in preclinical models
of addiction
Following the lack of signal in the primary outcome measure in
the anxious depression trial, Janssen has halted development
in anxious depression and is reviewing future development of
the program in other indications
* Data generated with compound
6
Pre-clinical stage pipeline
Target
R&D stage
Indication
Additional Information
mGlu4 PAM
1 main series in LO
2 back-up series
L-DOPA sparing in PD
Anxiety
Multiple Sclerosis
Preclinical PoC in PD*, MS (EAE mice and early
immune response*), anxiety*and OCD*.
Potential to address multiple aspect of MS including
anti-inflammatory, disease modification and
neuroprotection
Collaboration with NIDA to generate data in preclinical
models of addiction
mGlu2 NAM
1 main series in LO
3 back-up series
Depression (treatment
resistant)
Cognitive deficits, AD
Preclinical PoC in cognition* and depression*.
mGlu2NAMs ongoing clinical trials include TRD
mGlu2 PAM
1 chemical series in
LO (outside of
Janssen agreement)
1 lead identified
New indications currently
explored
Preclinical PoC in anxiety*, schizophrenia*, addiction.
Clinical PoC in negative symptoms in schizophrenia
mGlu7 NAM
2 chemical series in
LO
1 lead identified
Psychosomatic disorders
Preclinical PoC in anxiety*. Other proposed
indications: pain, neuroprotection, schizophrenia,
ADHD, GI tract disorders and retino-protection
FSH NAM
1 main series in LO
5 sub-series
Women’s health:
endometriosis, uterine
fibrosis, polycystic ovarian
disease.
Hormone dependent
cancer (add-on therapy):
breast, ovarian, prostate
cancer
Preclinical PoC of in vivo modulation of FSH induced
estradiol production* . Opportunity to develop an orally
bioavailable non competitive FSHR antagonists
7
* Data generated with compound
Discovery programs
Target
R&D stage
Indication
Additional Information
mGlu3
PAM
HTS performed
screening HITs
neuroprotection in PD
Neuroprotection achieved through modulation of
growth factors
mGlu8
PAM
HTS performed
screening HITs
Exploratory target
mGlu8 activation has been linked to
anxiety/GAD, neuroprotection/anticonvulsive
activity, fear acquisition, PD, cognition, pain,
addiction, ADHD and MS
M4 PAM
HTS performed
screening HITs
Hit confirmation
Schizophrenia
cognitive deficits in AD
GLP1 PAM
1 main series in LO
2 additional chemical
series
Type II Diabetes
Clinically validated for type II diabetes
Alternative to peptidic GLP1 agonists
GLP1 PAM PoC in OGTT (achieved with
Addex lead)*
TNFR1
NAM
HTS performed
screening HITs
RA, psoriasis, osteoarthritis
Huntington’s disease and sickle
cell disease (rare disease)
Small molecule and broadly applicable antiinflammatory approach
A2a PAM
HTS performed
screening HITs
RA, psoriasis, osteoarthritis,
Huntington’s disease and sickle
cell disease (rare disease)
PAM vs. agonist are expected to provide antiinflammatory effects, devoid of cardiovascular
side-effects
TrkB PAM
HTS and hit validation
performed
3 chemical series
validated
Disease-modification,
neuroprotection in AD
Potential in PD, AD and
Huntington’s disease
Modulation of BDNF signalling pathways
8
* Data generated with compound
Pipeline program:
Dipraglurant in PD-LID and Dystonia
(subject to securing resources)
9
Dipraglurant (ADX48621) overview
• Dipraglurant is a highly selective oral brain penetrant small molecule
metabotropic glutamate receptor 5 (mGlu5) inhibitor (negative
allosteric modulator-NAM) discovered at Addex
• mGlu5 inhibition has been validated in multiple indications
Clinical validation for mGlu5 NAM
Parkinson’s disease levodopa-induced dyskinesia (PD-LID)
Generalized anxiety disorder (GAD)
Gastroesophageal reflux disease (GERD)
Fragile X Syndrome / Autism
Acute migraine pain
Preclinical validation for mGlu5 NAM
Dystonia
Tardive dyskinesia
Huntington’s Disease
Treatment-Resistant Depression
Lewy body dementia
Addiction
10
Dipraglurant - a compelling market opportunity
• Dipraglurant is a novel and highly differentiated drug candidate within
the movement disorders market
• Rare disease opportunities in dystonia could accelerate NDA filing
• Market potential of dipraglurant is significant
– Potential to be first in class after the decision of Novartis to pull out of PD–
–
LID
Datamonitor estimates dipraglurant sales over $1 billion/year for PD-LID
and dystonia indications
Label expansion to additional Parkinson’s and non-Parkinson’s indications
could more than double sales opportunity
• Pursing partner with vision and capabilities to broadly develop
dipraglurant in PD-LID and other indications.
11
Summary of dipraglurant clinical development
• Initial Phase I program of dipraglurant successful
−
−
−
−
−
Three studies: single & multiple ascending doses, gender/food effects
132 subjects studied to date, including 30 older subjects
Dipraglurant – IR formulation developed and tested
Pharmacokinetics of IR is ideal for acute treatment of PD-LID
Safety & tolerability support further clinical study
• Dipraglurant-IR Phase IIa trial in 76 PD-LID patients achieved key
objectives
− Primary objectives: safety and tolerability in PD-LID patients
− Secondary objectives: clinical effect & dose characterization
• Top-line data showed statistically significant reduction in dyskinesia
− 50 min reduction in off-time in week 4
− 2.3 hours more of on-time without dyskinesia (i.e. good quality on-time)
− Concordance of mAIMS with the diary and the PGIC and CGIC data
• Michael J. Fox Foundation supported the trial with a $900,000 grant
12
ADX48621-201 trial design
EU and US Phase 2a dipraglurant trial for PD-LID
• Primary objective:
safety & tolerability
• Dipraglurant taken
with levodopa
• Randomized,
76
patients
• Dipraglurant titration
double-blind,
placebo-controlled,
multi-center trial
from 50mg q.d. to
100mg t.i.d over
4 weeks
• Moderate to severe
• Individual levodopa
LID patients
regimens remain
constant for duration
of study
(300 -1500mg/day)
• Secondary objective:
exploratory efficacy
• Objective evaluation in the clinic
on day 1 and 14 & 28
– Trained observer scores
LID severity using mAIMS –
modified Abnormal Involuntary
Movement Scale
• Patient diaries of on & off time
• Unified Parkinson’s Disease Rating
Scale (UPDRS)
• Patient and clinician global impression
of change (PGIC & CGIC)
• Evaluation of mood using Hospital
Anxiety & Depression Scale (HADS)
Positive Top-line results reported 1Q 2012
13
ADX48621-201 Phase 2a proof of concept study in
patients with PD-LID:
• Dipraglurant-IR Phase 2a trial in 76 PD-LID patients was successful
– Achieved significant reduction in dyskinesia severity
• Reduction in mAIMS (both at peak levodopa concentrations & area under the
curve over the three hours post-dose period)
• 50 min reduction in “off-time” in week 4
• 2.3 hours more “on-time” without dyskinesia in week 4
• Concordance of mAIMS with the patient-reported diary and the PGIC and
CGIC data
• Achieved key objectives:
– Primary objectives: safety and tolerability in PD-LID patients
– Secondary objectives: clinical effect & dose characterization
• Michael J. Fox Foundation for Parkinson’s disease supported the
trial with a $900,000 grant
14
Dipraglurant reduces LID severity
•
Dipraglurant reduced peak dose mAIMS (90 min after dosing)
dipra
placebo
*
35%
% reduction
30%
25%
‒ Day 1 (50mg):
*
19.9% vs 4.1% (p=0.042)
20%
‒ Day 14 (100mg): 32.3% vs 12.6% (p=0.034)
15%
‒ Day 28 (100mg): 31.4% vs 21.5%
10%
Placebo response likely due to trial design
5%
0%
Day 1
Day 14
Day 28
•
Dipraglurant reduced dyskinesia severity for the full 3 hour post-dosing
period - mAIMS area under the curve (AUC0-3)
•
A 30% reduction in mAIMS is clinically meaningful
‒ e.g. one patient was able to hold & read a newspaper for the first time in years
‒ e.g. another patient had improved speech and became more easily intelligible
NB: Dipraglurant was as effective in patients who had undergone deep brain
stimulation as in non DBS patients
15
Good correlations between Dipraglurant effect in reducing
PD-LID and plasma concentration: IC50 = 1317 ng/mL
0
Mean change in mAIMs from
baseline
mean plasma conc ( ng/mL)
1400
1200
1000
800
600
400
200
0
0
1
2
3
4
-1
-2
visit 3
-3
visit 4
-4
visit 5
-5
-6
0
time (h)
500
1000
1500
Mean dipraglurant plasma conc (ng/mL)
14
mean mAIMS
12
10
Visit 3 (Day 1)
50 mg
Visit 4 (Day 14)
100 mg
Visit 5 (Day 28)
100 mg
8
Cmax (ng/mL)
793 ± 438
1683 ± 1107
1844 ± 1117
6
Tmax (hours)
1.14 ± 0.52
1.23 ± 0.66
1.08 ± 0.51
T1/2 (hours)
0.68 ± 0.81
0.75 ± 0.44
0.74 ± 0.44
4
2
16
0
0
1
2
time (h)
3
4
Receptor occupancy PET study in non human primates: dipraglurant
is brain penetrant and occupies the mGluR5 in a dose-dependent
manner: EC50 = 510 ng/mL
17
Patient-reported measurable clinical effects
“On” time with no dyskinesia - change from week -1
50 mg dose level
100mg dose level
18
Measurable clinical effects
Modified
AIMS
Dipraglurant
efficacy
Patient
Diary
CGIC &
PGIC
subjective observations (patient diaries & PGIC/CGIC) consistent with
objective measurements (mAIMS)
19
MGlu5 NAMs for the treatment of dystonia
•
Dystonias are movement disorders characterized by involuntary muscle
contractions that force the body into abnormal, sometimes painful,
movements and positions (postures)
•
Dystonia etiologies and symptoms are heterogeneous – can affect a single
part of the body (focal), multiple areas (segmental) or the whole body
(generalized). Further, dystonias are distinguished as either primary
(idiopathic, genetic) or secondary (drugs, toxins or metabolic disorders)
•
A number of types of dystonia are classified by NIH as “rare” (e.g., cervical
dystonia, DYT1 familial generalized dystonia or X-linked dystonia
parkinsonism)
•
An estimated 300,000 people in the United States have been diagnosed with
a dystonia of some type
•
Based on the literature and our own preclinical and clinical observations, the
scientific rationale for an mGlu5 negative allosteric modulator (NAM) as a
therapeutic agent in the treatment of dystonia is very strong.
20
Dipraglurant for the treatment of dystonia – a
compelling orphan drug opportunity
•
•
•
•
•
•
•
Dystonias are a set of heterogeneic diseases with a huge unmet medical
need and no viable treatment alternatives
Dipraglurant, a highly selective, oral mGlu5 NAM, has been shown to be
safe and effective in human clinical testing
Dipraglurant has shown positive anti-dystonia effect in multiple animal
models of dystonia as well as positive anti-dystonia effect in Parkinson’s
patients
Dipraglurant could be a first-in-class dystonia therapeutic with the potential
to significantly change the treatment paradigm for a variety of dystonias
Dipraglurant could establish a dominant position in the $500 MM+ dystonia
market
Dipraglurant could qualify for orphan drug designation in dystonia – fasted
path to market
Human POC clinical testing of dipraglurant in dystonia could benefit from
dystonia foundation funding
21
Preclinical and clinical efficacy of dipraglurant in dystonia
Phase 2a studies in PD-LID Patients
PD-LID MPTP monkey (drug induced dyskinesia
with features of dystonia)
DYT-1 mouse model (genetic dystonia)
Tottering mouse model (paroxysmal dystonia)
22
Preclinical and clinical efficacy of dipraglurant in dystonia
23
Dipraglurant - conclusions and perspectives
•
•
•
•
•
There is a strong rationale for developing mGlu5 NAMs for treatment in PDLID
(IR) dipraglurant has shown an optimal PK and PD profile for the indication
There are currently no other mGlu5 NAM in clinical development for this
indication, therefore dipraglurant could become a first in class
The recent decision of Novartis to terminate development of mavoglurant in
PD-LID seems to be related to the properties of the compound or to a
potential unappreciated mechanistic which results in different
pharmacological profile
(IR) dipraglurant can also be developed in a number of other major disease
areas where mGlu5 inhibition has been proven useful, and an acute and
short blockade of the receptor would be beneficial (acute treatment of
migraine, treatment resistant depression).
24
pipeline program:
ADX71441 – GABABR positive
allosteric modulator
(subject to securing resources)
25
Oral GABAB receptor PAM (ADX71441)
•
•
ADX71441 is a novel, first-in-class, oral, small molecule activator of gammaaminobutyric acid subtype B (GABAB) receptor function through positive allosteric
modulation (PAM)
Activation of GABAB receptor is preclinically, clinically & commercially validated in a
number of indications
validation for GABABR activation
MS Spasticity
•
•
•
•
Visceral Pain
Osteoarthritis and other pain
Fragile X Syndrome / Autism
Overactive Bladder (OAB)
Anxiety
Alcohol and nicotine dependence
Epilepsy
Charcot-Marie-Tooth (CMT1a)
Addex GABAB receptor PAMs have shown efficacy in multiple preclinical models
including: OAB, pain, osteoarthritis pain, anxiety, alcohol and nicotine dependency and
CMT1a
IND enabling studies complete
CTA accepted for Phase 1 clinical testing in EU
Phase 1 data expected 9 months from start
26
ADX71441 pharmacology and tolerability
PoC in models of anxiety, pain, OAB and addiction
•
Efficacious in animal models:
•
•
•
•
•
•
Anxiety - mouse marble burying and rat elevated plus maze
Pain - mouse acetic-acid induced writhing test and rat MIA OA pain model
Overactive bladder - Mouse and Guinea pig overactive bladder model
Alcohol consumption – mouse
Nicotine withdrawal - rat
Genetic model of a rare neuropathy - CMT1A rat
•
CNS profile: Rat EEG (with LMA; body temperature); Rat Irwin; Mouse
rotarod; Mouse locomotor activity (acute and chronic administration);
Mouse body temperature
•
No sign of tolerance development on efficacy after repeated dosing while
CNS related clinical signs attenuate and disappear after repeated dosing
27
ADX71441: pharmacokinetics & non clinical safety package
Pharmacokinetics:
•
ADX71441 administered orally is slowly absorbed, has a good bioavailability and a
long half-life
•
ADX71441 administered IV shows: Low clearance, Large volume of distribution, Long
half life
•
ADX71441 is moderately protein bound
•
ADX71441 crosses the blood brain barrier
•
Very little ADX71441 is excreted unchanged in bile and urine (data not shown)
•
ADX71441 undergoes extensive metabolism (data not shown)
•
ADX71441 does not inhibit any of the major CYPs
Non Clinical Safety Package:
•
In vitro (GLP) – hERG, Ames and micronucleus tests
•
In vivo Safety Pharmacology (GLP) - CNS activity (Functional Observation Battery) in
rat, respiratory Function in rat, and Cardiovascular Function by Telemetry in nonrodent
•
General Toxicology Studies (GLP) - MTD & 4-week study in rat & non rodent
•
Reprotoxicology studies: Preliminary study for effects on Embryo-Fetal development
in rat and rabbit
28
ADX71441 has improved dosing regimen and PK/tolerability profile over
baclofen - simulation: profiles around efficacious plasma concentration and 3-times above
Steady state plasma profiles in humans
ADX71441: ADX71441:
simulation
of steady state plasma profile in humans
(simulated with: HL 30 h; Vss 2.2 L/kg; F 70%)
Plasma Conc. (ng/mL)
90 mg Q.D.
1000
30 mg Q.D.
separated profiles
500
Habituation following multiple
dosing improves tolerability in
monkeys and rodents
0
0
8
16
ADX71441 (human prediction)
- 1X daily oral (~30 mg)
- low peak-trough ratio
- flat plasma and CNS PK profile
- no Cmax driven side effects expected
24
Time (h)
ADX71441: predicted Improved PK and tolerability profile
Baclofen:
state
plasmain
profiles
in humans
Baclofen: steady
stateSteady
plasma
profile
humans
Plasma Conc. (ng/mL)
(simulated with: HL 2 h; Vss 0.9 L/kg; F 70%)
1000
overlapping profiles
75 mg T.I.D.
25 mg T.I.D.
Baclofen (max. dose ~25 mg t.i.d.)
-3X daily oral (or i.t. pump)
-high peak-trough ratio
-fluctuating PK profile
-Cmax driven side effects reported
500
0
0
8
16
24
Time (h)
Baclofen: Cmax driven side effects reported
29
Charcot-Marie-Tooth (CMT1a) disease
• Charcot-Marie-Tooth (CMT) disease was first recognized independently in
France and Great Britain (Charcot and Marie, 1886; Tooth, 1886).
• Orphan genetic peripheral polyneuropathies
‒ More recent nomenclature designated Charcot-Marie-Tooth disease as a hereditary
motor and sensory neuropathy (HMSN) or CMT1a
• Prevalence of CMT1a: 3 in 10,000
‒ Upper limit of orphan classification
‒ Most common inherited neurological disease
‒ CMT1a involves duplication of the PMP22 gene
• Disease characterized by:
‒ Severe and uniformly reduced nerve conduction velocities and primary hypertrophic
myelin
‒ CMT1a disease slowly gets worse with some parts of the body becoming numb, and
pain can range from mild to severe. The disease is highly debilitating and
accompanied by severe cases of neurological pain and muscular disability
‒ There is no known cure for this incapacitating disease
• ADX71441 demonstrated POC in validated transgenic CMT rats
‒ Down regulated PMP22 mRNA, reduced the amount of hypo-myelinated axons and
increased compound muscle action potentials in peripheral nerves in transgenic CMT
30
rats. It also prevented grip strength loss in CMT rats compared to wild type rats
GABAB R Activation Therapy with ADX71441 in CMT Rats
Key results: Treatment • CMT rats showed an overexpression of PMP22 mRNA,
axonal loss and reduced grip strength reflecting typical
of CMT rats with
CMT1A features
ADX71441 ameliorates
• In a comparative study with baclofen in CMT1A rats,
axonal survival which
ADX71441 significantly reduced Pmp22 mRNA at 3mg/kg
should be the primary
and 6 mg/kg p.o. (0.98-fold±0.49 and 0.93–fold±0.35,
respectively). Baclofen reduced PMP22 mRNA expression
aim of any CMT1A
at 3mg/kg BID (0.91-fold±0.25)
therapy
Hypomyelinated axons
• ADX71441 therapy (9 weeks) in CMT rats down regulated
•
•
•
PMP22 mRNA, reduced the amount of hypomyelinated
axons and increased compound muscle action potentials in
peripheral nerves
ADX71441 therapy (9 weeks) in wild-type rats did not affect
PMP22 mRNA expression, axonal number and electrophysiological parameters, however caused a reduction in
rat grip strength
Since there is not a comparable loss of grip strength
between CMT treated and untreated rats, the data
suggests some benefit by ADX71441 on underlying
pathophysiology
ADX71441 could lower toxic PMP22 overexpression and
potentially delay the progression of the disease and
therefore offer a unique therapeutic opportunity for CMT1A
patients
31
Janssen partnership
ADX71149: mGlu2 PAM
• significant potential in treating of CNS
disorders
32
Overview of Janssen partnership (ADX71149)
• ADX71149 is a highly selective oral brain penetrant small molecule
metabotropic glutamate receptor 2 (mGlu2) positive allosteric
modulator (PAM) discovered in collaboration with Janssen
Pharmaceuticals Inc.
• mGlu2 PAM is validated in multiple indications: schizophrenia and
anxiety
• Phase 1 complete (more than 8 studies conducted)
• Phase 2 study of ADX71149 in schizophrenia as adjunctive therapy:
− Reported positive data in November 2012
• Phase 2 study of ADX71149 as adjunctive therapy for anxiety seen in
major depressive disorder patients reported in Q1 2014
‒ Top-line results missed the primary end point but signals were seen on
some anxiety measures (HDRS17 anxiety somatization factor, IDS-C30
anxiety subscale) and on all depression measures (HDRS17, HAM-D6 and
IDS-C30)
• Janssen reviewing future development in other indications
33
ADX71149 Janssen partnership economics
•
•
•
•
To date, Addex has received €10.2 million in upfront, research funding and
milestones
Eligible to receive €109 million in additional pre-launch milestones for 2
indications
Eligible to receive low double-digit royalties on net sales
Janssen funds all development, launch and commercialization activities
34
Financial review & Summary
35
Financials and stock
• Cash runway through Q4 2014
− CHF4.5M (US$4.9M / €3.7M) million in cash as of June 30, 2013
− Capital increase of 9 August 2013 increased cash reserves by CHF3.2M
• Traded on SIX Swiss Exchange: ADXN (ISIN:CH0029850754)
• 10,173,576 shares outstanding (11 million fully diluted)
− Biotechnology Value Fund holds 27%
− Visium holds 4.8%
• Analysts coverage:
− Ladenburg Thalmann: Juan Sanchez (New York)
− Wedbush: Chris Marai & Greg Wade (San Francisco)
36
Summary
• Key strategic objectives
− Secure resources to advance clinical pipeline
− Collaborate with Industry / academia / patient groups to advance
clinical/preclinical/discovery programs
• Starting 2014 with sufficient financial resources & team to execute key
strategy objectives
• Dipraglurant - first in class mGlu5NAM for PD-LID with robust Phase 2a
data
• ADX71441 - first in class GABA B PAM ready for Phase 1, with potential
in several major indications as well as orphan indication
• Extensive IP portfolio on allosteric modulator preclinical and discovery
programs
37
allosteric modulators for human health
www.addextherapeutics.com