Aposense Pipeline: From Platform to Products

Aposense
Presentation at the UBS Global Life Sciences Conference
Yoram Ashery, CEO
September, 2012

FORWARD LOOKING STATEMENTS
The following slides contain forward-looking statements that include, but are not limited to, projections about our
business and our future revenues, expenses and profitability. Forward-looking statements involve known and
unknown risks, uncertainties and other factors which may cause the actual events, results, performance,
circumstances or achievements of the Company to be materially different from those expressed or implied by such
forward-looking statements due to factors that include, but are not limited to: (1) our ability to develop and bring to
market new products, (2) our ability to successfully complete any necessary or required pre-clinical and clinical
studies with our products, (3) our ability to receive regulatory clearance or approval to market our products or
changes in regulatory environment, (4) our success in implementing our sales, marketing and manufacturing plans,
(5) the level of adoption of our products by medical practitioners, (6) the emergence of other products that may make
our products obsolete, (7) protection and validity of patents and other intellectual property rights, (8) the effect of
competition by other companies and technologies, and (9) our ability to obtain reimbursement for our products from
government and commercial payers. You are cautioned not to place undue reliance on these forward-looking
statements, which speak only as of the date of this slides. The Company undertakes no obligation to update any
forward-looking statements, to report events or to report the occurrence of unanticipated events that may lead to the
actual events, results, performance, circumstances or achievements of the Company being different than as
envisaged by such forward looking statements.
2

Apoptosis, a biological process involved in most diseases…
Cell Apoptosis
Programmed Cell Death
3

A new paper every 25 minutes
22,000
No. of New Publication relating to Apoptosis, p per Year
20,000
18,000
16,000
14,000
12,000
10,000
8,000
6,000
4,000
2,000
-
1988
1990
1992
1994
1996
1998
2000
2002
2004
2006
2008
2010
* Based on Medline search

MISSION
Translate Apoptosis to Patient Care
Diagnosis, Treatment
5

Mechanism of Action
Membrane alterations trigger
conformational and electric changes
in switch moiety
• A set of membrane alterations specific to the apoptotic cells identified
• A molecular switch designed to respond to the apoptotic membrane
changes
Enables membrane anchoring and
subsequent intra-cellular accumulation
Aposense (fluorescent labeled)
Preservation of
membrane
integrity
Interfacial
NanoSwitch
Activation of the
Phospholipid
Scrambling System
(PLS)
Permanent
depolarization of
plasma
membrane
potential
Acidification of
external
membrane leaflet
Irreversible
loss of
cellular pH
control
Annexin V

Molecular Imaging
First sight of disease
US Market
PET Radiopharmaceuticals
2009 $358 million
2017E
$3,430 million
Source: Bio-Tech Systems report 2010

Molecular Imaging of Apoptosis:
Multiple Opportunities
Oncology
Treatment Monitoring
Neurology
Cardio-vascular
Acute MI
Responder
Non-Responder
CT
PET [ 18 F]-ML-10
Vulnerable
Plaque
• Radiation
• Chemo-Radiation
• Chemotherapy
• Targeted / Biologics
• Stroke
• Neuro-muscular disorders
• Traumatic Brain Injury (TBI)
• Multiple Sclerosis
• Atherosclerosis (vulnerable plaque)
• Acute MI
• Heart Failure
• Transplant rejection
9

Molecular Imaging of Apoptosis:
Clinical Development Program
Phase 1
Phase 2a Phase 2b Phase 3
Healthy volunteers
Stroke
Brain metastases
R 2 = 0.84 between
EarliTest and MRI 6-8
weeks after treatment
Brain metastases
Lung (NSCLC)
Head & Neck
Clinical Centers
U.S. 11
Israel 3
France 2
10

Molecular Imaging of Apoptosis:
Phase 2: Design and Status
CA004
Brain
metastases
∆
∆
SRS
24h
8 weeks
Diagnosis &
Eligibility
Baseline
Anatomical
Imaging
Baseline
ML-10
Imaging
Treatment
Follow-up
ML-10
Imaging
Follow-up
Anatomical
Imaging
1w
Combined Chemo-Radiation
7 weeks
8 weeks
CA007
H&N and
NSCLC
∆
∆
Timeline
CA004 Brain metastases treated with SRS
Recruitment
Completed
CA007 H&N treated with chemo-radiation October 2012
CA007 Lung treated with chemo-radiation Postponed, image
analysis
Results
November 2012
February 2013
Safety status:
212 procedures
106 patients
No related
adverse event
Forward-Looking Information Notice: The Company’s assessments and estimates regarding the above timeline depend,
among other factors, on continuation of present patient recruitment rate, sufficient clinical data and successful clinical trials
results analysis, and other risk factors which apply to the Company’s activity, as described on Company’s annual reports

Commercialization Partner
World’s widest PET radio-pharmacy network
Labeling & Distribution
• IBA to distribute radio-labeled ML-10 ready to inject
• Global coverage with specific timelines
12

Aposense ®
Targeted
Therapy
(ATT)

N
Targeting apoptosis
Extending pharmaco-kinetics
Selective activation on target
Overcoming cancer cell resistance
Oral administration
Aposense ®
Active Drug
New Drug
14

ATT-11T
Irinotecan, SN-38
Topoisomerase
Conjugate
Approved
indications
SN-38, the active metabolite of irinotecan
(Camptosar®, Pfizer)
• metastatic colon cancer (US, EU)
• small cell lung cancer (Japan)
Also shown activity in ovarian and other
gastrointestinal cancers
Commercial
Status
Patent expired 2008/9
Pre-expiration sales >$1.0B
Mechanism
Inhibits Topoisomerase I
Topoisomerase I inhibition
Limitations
Toxicity
Short half-life
IV administered

ATT-11T: Prolonging SN-38 Half-life
SN-38 half-life when released from ATT-11T is >5X longer
Active moiety (SN-38) in ATT-11T compared to Irinotecan (dog study)
Concentration, ng/mL (log scale)
10.0
1.0
0.1
0.0
* Not detectable
Slow
Clearance
ATT-11T
irinotecan
* *
0 4 8 12 16 20 24 28 32 36 40 44 48
t 1/2 (hr)
14
12
10
8
6
4
2
0
SN-38 derived from ATT-11T vs. Irinotecan X5.2
12.1
2.3
irinotecan
ATT-11T
Results reproduced in additional studies
16

ATT-11T is >13X More Selective to Tumor
Bio-distribution studies in A375 bearing mice; concentration of SN38 (active metabolite) in Tumor and Muscle
ng/gr*hr
(AUC)
4000
3000
3855
Tumor
Tumor/Muscle Selectivity Ratio
2000
1000
0
ATT-11T
1153
Irinotecan
200
160
120
200
ng/gr*hr
(AUC)
80
Muscle
80
40
14.8
60
40
78
0
ATT-11T
Irinotecan
20
0
19.2
ATT-11T
Irinotecan

ATT-11T showed superior efficacy
Melanoma
Model A375
Ovarian Carcinoma
Model OVCAR
Tumor size (mm 3 )
4000
Human
3500 melanoma
implanted in
3000 mice
Non-Treated
(Control group)
Irinotecan
(75 X 3 mg)
Tumor size (mm 3 )
Control-vehicle
1000
CPT-11 3x18mg/kg
900
ATT-11T 3x20mg/kg
800
Non-Treated
(Control group)
Irinotecan
(3 X 18 mg)
2500
2000
700
600
500
1500
400
1000
500
0
10 15 20 25 30 35 40 45 50 55 60
ATT-11T
(5 X 9 mg)
300
200
100
0
ATT-11T
(3 X 20 mg)
1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 31 33 35 37 39 41
Tx End
Tx End

ATT-11T Preliminary Safety
MTD studies: daily administration in rats (n=3 per group); no toxicity observed
Weight
(% from
baseline)
110
105
100
ATT-11T, 200 mg/Kg, PO
95
90
85
80
Irinotecan, 90 mg/Kg, IP
75
70
1 2 3 4 5
Days
Irinotecan
ATT-11T
Weight at day 5(%) 77-96 99-102
Diarrhea 2 / 3 None

TEVA agreement
• TEVA collaboration: generic cytotoxics conjugated to Aposense® molecule (2005)
• TEVA to invest up to $11M
• $2M in equity, up to $9M in development (after Aposense invests $2M)
• Economics
After Teva’s full investment, Aposense to choose between:
• 7% royalty
• 32% share in proceeds and participate in 25% of costs; and
• 50% share in proceeds and costs
• IND 2013 (updated)
Forward-Looking Information Notice: The Company’s assessments and estimates
regarding the above timeline depend, among other factors, on continuation of present patient
recruitment rate, sufficient clinical data and successful clinical trials results analysis, and other
risk factors which apply to the Company’s activity, as described on Company’s annual reports

ATT-GEM
Conjugate
Approved
Indications
(solid
tumors)
Commercial
Status
Mechanism
Limitations
Gemcitabine (Gemzar®, Eli Lilly)
Pancreas
Bladder
Lung (NSCLC)
Breast
Ovarian
Patent expired 2010-2013
Peak sales $1.72B (2008)
Blocking DNA synthesis
Tumor resistance (cellular uptake
is depends on hENT-1)
Short half-life (32-94 minutes)
Toxicity (neutropenia)
IV administration
Resistant
Source: Spratlin et al. Clin Can Res (2004)
Responsive

ATT-GEM potent in resistant cells
hENT-1 inhibited K562 cells
Growing cells (% of control)
100
80
60
40
20
0
100
80
60
40
20
0
Resistant
cells
0 0.2 0.4 0.6 0.8 1
Resistant
cells
0 0.2 0.4 0.6 0.8 1
DP (Dipyridamole), 10μM for 30min
Incubation time with the drug: 72h
GEM
GEM+DP
TBE-es ATT-GEM2
TBE-es+DP
ATT-GEM2+DP
GEM
GEM+DP
Tes ATT-GEM1
Tes+DP ATT-GEM1+DP
90
80
70
60
50
40
30
20
10
0
Resistant index =
0.8
4.7
IC50 (*) Resistant
IC50 Normal
ATT-GEM1 ATT-GEM2 Gemcitabine
* IC50 = concentration
required to kill 50% of cells
83
CONFIDENTIAL

ATT-GEM
Initial in-vivo performance data in responding (sensitive) tumor
(HCT116 colon carcinoma)
Similar efficacy in responsive tumors, with safety benefit
Weight (% of control)
Tumor growth inhibition
115
2000
Control
110
105
100
1800
1600
1400
1200
Gemcitabine 50mg
Gemcitabine 100mg
ATT-GEM1 120mg
ATT-GEM2 120mg
95
1000
800
90
600
85
400
80
0 5 10 15 20 25 30
200
0
0 5 10 15 20 25 30

ATT-LD
Long-acting levodopa for treatment of Parkinson’s disease
Parkinson’s
disease
Progressive neuro-degenerative disorder, caused
by depletion of the neuro-transmitter dopamine
Prevalence 1.4 million (US, 5 EU and JP)
Levodopa (L-Dopa) mainstay treatment of
moderate-advanced PD
Mechanism
Precursor of dopamine
Key Limitations
Short half-life (45-90 minutes)
Absorbed mainly in the duodenum, only 5-10%
reaches the brain

The short half-life problem

ATT-LD Significantly Extends Levodopa Formation
Rat model; concentration levels under effective range (should be increased)
500
450
5 hrs steady levodopa formation
PO 45mg/kg 7M
PO 180mg/kg 8M
400
350
Levodopa, ng/ml
300
250
200
150
100
50
0
0 60 120 180 240 300 360 420 480
Time, min
* Levodopa T ½ in rat 42-48 minutes

Pipeline
Molecular Imaging
Discovery Pre-Clinical Phase 1 Phase 2 Phase 3
ML-10
Apoptosis Imaging
Therapeutic
Oncology
ATT-11
ATT-GEM
CRC, Esophageal, SCLC
Pancreatic cancer
Neurology
ATT-LD
Parkinson’s Disease

New Product Initiation Process
Identify unmet
clinical needs
Select active
therapeutic
Apply Aposense®
technology to create
a new drug that
addresses the need
R&D

Discovery
In Vivo
In Vitro
• Medicinal chemistry
• Rational drug design
• Molecular modeling
• Synthesis via network of contractors
• Fully equipped biochemistry lab
• Licensed radioactive suite for β
emitters
• Cancer cell lines bank
• Established apoptosis models
• Cytotoxic drug handling
• Cell culture
unit
• Animal house,
wild type species
and immune
deficient mice
• An array of established
xenograft mice models
• In-house histology unit for sectioning
and various staining techniques with
top tier histopathologists consultancy
• Expertise in IV and oral formulations,
including poorly soluble drugs
• CRO network for formal pre-clinical
development, PK/PD, oralbioavailability,
ADME and
toxicology studies
• In-house management of
CMC via contractors
Final
Drug Product

Financial Information
Shareholder Base
Cash position:
$25.3 million
(June 30, 2012)
11%
31%
Cash used for operations:
FY2010
FY2011
Jun 30, 2012
$5.5 million
$6.7 million
$3.8 million
21%
4%
14%
20%
Private Investment Firms
Public Listing:
TASE: APOS
Venture Capital
Financial Institutions (≥5%)
Big Pharma
Directors, Officer & Employees
Public, Institutions (

Summary
• Core Core Capabilities
Capabilities
– Novel platform technologies
– Full drug development capabilities
– New Product Generation Process
• Pipeline
Pipeline
– Lead clinical program: Apoptosis Imaging (ML-10) near completion of phase 2
– Growing & maturing pre-clinical portfolio: 3 new drugs, major unmet needs
– New compounds continuously added by application of platform
• Corporate Infrastructure
– Experienced board and management team
– Strong financial position

Thank you.