Corporate Overview - The Global Investment Banking Firm · Corporate Overview Anat Cohen-Dayag ......
Transcript of Corporate Overview - The Global Investment Banking Firm · Corporate Overview Anat Cohen-Dayag ......
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FROM CODE TO CURE
www.cgen.com
CorporateOverview
Anat Cohen-Dayag, PhD
President & CEO
TM
Jefferies 2017 Global Healthcare Conference
June 6, 2017
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SAFE HARBOR STATEMENT
This presentation contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of
1995. Forward-looking statements can be identified by the use of terminology such as “will,” “may,” “expects,” “anticipates,”
“believes,” “potential,” and “intends,” and describe opinions about possible future events. These forward-looking statements
involve known and unknown risks and uncertainties that may cause the actual results, performance or achievements of Compugen
to be materially different from any future results, performance or achievements expressed or implied by such forward-looking
statements. Among these risks: Compugen’s business model is substantially dependent on entering into collaboration agreements
with third parties, and Compugen may not be successful in generating adequate revenues, or commercializing aspects of its
business model. Moreover, the development and commercialization of therapeutic candidates involve many inherent risks,
including failure to progress to clinical trials or, if they progress to or enter clinical trials, failure to receive regulatory approval.
These and other factors are more fully discussed in the "Risk Factors" section of Compugen’s most recent Annual Report on Form
20-F as filed with the Securities and Exchange Commission as well as other documents that may be subsequently filed by
Compugen from time to time with the Securities and Exchange Commission. In addition, any forward-looking statements represent
Compugen’s views only as of the date of this presentation and should not be relied upon as representing its views as of any
subsequent date. Compugen does not assume any obligation to update any forward-looking statements unless required by law.
Certain studies and data presented herein have been conducted for us by other entities as indicated where relevant. All intellectual
property, including trade marks, trade names, slogan, logos, service marks, patents, copyrights or trade secret displayed in this
Presentation, including the name Compugen, are registered and unregistered intellectual property rights of Compugen.
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Transforming patient lives by
developing first-in-class therapeutics
based on computational predictive
discovery of novel targets
Our Vision
FROM CODE TO CURE TM
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COMPUGEN: FROM CODE TO CURE
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Pioneeringpredictive drug discovery
Focusingnext wave of immuno-oncology drug targets for cancer immunotherapy
Discoveringnovel drug targets
Collaboratingfirst-in-class biologics at various development stages under revenue sharing agreements
Buildingbroad early-stage
immuno-oncology pipeline
Developingfirst-in-class biologics first internal program in IND-enabling studies
TM
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TWO CENTERS OF EXCELLENCE
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Therapeutic mAbResearch &
Development
Compugen USA, Inc.
South San Francisco, USA
Compugen Ltd. Headquarters
Holon, Israel
Predictive Discovery &
Target Validation
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COMPUGEN: FOUR PROGRAM AREAS
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COM701Anti-PVRIG drug candidate for cancer immunotherapy
Myeloid Targets
COM902Anti-TIGIT drug candidate for
cancer immunotherapy
CGEN-15001Fc fusion protein drug candidate
for autoimmune diseases therapy
Complementary portfolio to T cell checkpoint programs for cancer immunotherapy
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Antoni Ribas, MD PhD
STRATEGIC ADVISORSSCIENTIFIC ADVISORY BOARD
Elliott Sigal, MD PhDFormer CSO, EVP and Director
Richard HaiduckFormer CBO and CEO Life science companies
Steven HoltzmanFormer CBO and CEO
Charles Drake, MD PhD
Howard Soule, PhD
Iain McInnes, MD PhD
Drew Pardoll, MD PhDChairman of the SAB
KEY STRATEGIC ADVISORSIndustry Veterans, Renowned Oncologists and Immunologists
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Miriam Merad, MD PhD
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THE IMMUNO-ONCOLOGY MARKET IS RAPIDLY GROWING
Adapted from Cowen & Company March 2017 Research Report
• Checkpoint inhibitor sales forecasted to exceed $35B by 2022
• Projected to be the biggest drug class in the industry
• Checkpoint inhibitors expected to be the backbone of all cancer treatments
$0
$5,000
$10,000
$15,000
$20,000
$25,000
$30,000
$35,000
2016 2017 2018 2019 2020 2021 2022
Sa
les
Es
tim
ate
s (
$M
M)
PD-1/PD-L1 Sales Estimates
Durvalumab Nivolumab Pembrolizumab
Atezolizumab Avelumab Total
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DESPITE BROAD RESPONSES ONLY A SUBSET OF PATIENTS RESPOND TO ANTI PD-1/L1 TREATMENT
Significant opportunity to treat non-responders to PD-1/L1 checkpoint inhibitors
0
10
20
30
40
50
60
70
80
90
100
Ove
rall
Res
po
nse
Rat
e %
~20% Average
Response Rate
Gap to Bridge
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10
CTLA-4CD28
B7.1 B7.2
LAG-3TIM3
GAL-9
PD-1
PD-L1
TIGIT
VISTA
?
PVR
10
M
PII
PI
PI
PC
PC
PC
PII
PI
PI
PI
PI
PI
PC
PC
PI
PI
PC
PC
PC
PC
PC
PC
PI
PC
M
M
M
PI
PI
PI
PC
Tumor/APC
T cell
MH
CT
CR
M
M
PI
PI
PI
PIII
PC
PI
PI
PIII
PI
PI
PC
PC
PI
PC
PC
PC
TARGETING IMMUNE CHECKPOINTS TODAY:FIERCE COMPETITION AGAINST SAME TARGETS
PI
PI
PI
PI
PC
PC
PC
PVRL2
PVRIG
PC
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STRATEGICPARTNERSHIPS
PIPELINEPROGRAM
PREDICTIVE DISCOVERY
PIPELINEPROGRAM
FROM GENOMIC CODE TO CLINICAL CUREAn Integrated Approach
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Target discovery IND Filing
COM701 / PVRIG
COM902 / TIGIT
CGEN-XXXX (Myeloid)
Undisclosed Multiple programs
CGEN-15001T
CGEN-15022
CGEN-15001
Screening/ lead
selectionCell line developmntTarget validation mAb discovery CMC/IND enabling
COMPUGEN’S PIPELINE PROGRAMFrom Code to Cure
Lead selectionPartnered IO (Bayer)Internal IO Autoimmune
From computer prediction to preclinical POC
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PVRIG BLOCKADE IS DIFFERENT FROM AND SYNERGISTIC WITH TIGIT BLOCKADE
Martinet & Smyth, 2015 (modified)
+-
TUMOR/
APC
T CELL-
PVRIG
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• Separate inhibitory pathways
• Different temporal and spatial
distribution of targets and ligands
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MATCHING PREDICTION TO FUNCTION: PVRIG OVEREXPRESSION INHIBITS T CELL ACTIVATION
Cohen and Safyon, Bar Ilan Univ.1414
F4MART1/
14
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PVRIG IS EXPRESSED ON CD8+ T CELLS AND NK CELLS IN THE TUMOR MICROENVIRONMENT
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CD8+ T CD56+ NK
Lung Cancer
Lung CancerPVRIG expression in effector TILs
Co-expression with TIGIT and PD-1 on CD8+ TILs
PVRIG
TIG
IT
PVRIG
TIGIT
PD
1P
D1
- isotype - PVRIG
Renal Cancer
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PVRIG & ITS LIGAND PVRL2 ARE CO-EXPRESSED IN MULTIPLE TUMOR TYPES
PV
RIG
(C
D8+
TIL
s)
PVRL2 (Monocytes)
Bladder
Breast
Colorectal
Endometrial
Head & Neck
Kidney
Lung
Ovarian
Prostate
Relevance in multiple tumor types
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• COM701 is a high affinity monoclonal antibody targeting PVRIG
• PVRIG (CGEN-15029) identified as novel immune checkpoint by Compugen and plays a unique role in the validated TIGIT axis
• COM701 is synergistic with anti-TIGIT and anti-PD-1/L1 as a potential cancer immunotherapy treatment
• First-in-class opportunities as mono- and combination therapies
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COM701: LEAD CHECKPOINT INHIBITORFrom computer prediction to functional activity in preclinical models
IND-ENABLING STUDIES
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gp100 pulsed CHO-HLA-
A2
MART-1/624-mel
624-mel or
peptide-
pulsed
CHO-HLA-A2
PVRIG PVRL2
gp100/MART-1
specific TILs
COM701 ENHANCES TIL ACTIVATION
I so
Ct r l
CO
M7
01
Ba
c ku
p m
Ab
0
1 0 0
2 0 0
3 0 0
4 0 0
IFN
(
pg
/m
L) + 2 8 % + 2 0 %
I so
Ct r
l
CO
M7
01
Ba
ck
up
mA
b
0
5 0 0
1 0 0 0
1 5 0 0
IFN
(
pg
/m
L) + 3 7 % + 4 0 %
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19
7 1 0 1 3 1 6 2 0 2 3 2 70
1 0 0 0
2 0 0 0
3 0 0 0
4 0 0 0
5 0 0 0
M C 3 8
0 2 9 K O r Ig G 2 b
D a y s p o s t- tu m o r im p la n ta t io n
Tu
mo
r v
olu
me
(m
m3)
D e a d
7 1 0 1 3 1 6 2 0 2 3 2 70
1 0 0 0
2 0 0 0
3 0 0 0
4 0 0 0
5 0 0 0
M C 3 8
W ild - ty p e r Ig G 2 b
D a y s p o s t- tu m o r im p la n ta t io n
Tu
mo
r v
olu
me
(m
m3)
D e a d
D e a d
WT PVRIG-/-
*
0 5 1 0 1 5 2 0 2 5 3 0
0
5 0 0
1 0 0 0
1 5 0 0
2 0 0 0
2 5 0 0
3 0 0 0
3 5 0 0
4 0 0 0
D a y s
vo
lum
e (
mm
3)
W ild - ty p e
P V R IG- / -
Tumor growth in PVRIG-/- mice
Ganguly and Pardoll, Johns Hopkins Univ. MC38 model
PVRIG KNOCKOUT REDUCES TUMOR GROWTH AND SUPPORTS MONOTHERAPY APPROACH
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PVRIG KNOCKOUT AND ANTI-PD-L1 COMBINES IN PRODUCING TUMOR GROWTH REDUCTION
Ganguly and Pardoll, Johns Hopkins Univ. MC38 model20
WT PVRIG KO
PVRIG KO + anti-PD-L1WT + anti-PD-L1
7 1 0 1 3 1 6 2 0 2 3 2 7
0
1 5 0 0
3 0 0 0
4 5 0 0
M C 3 8
W ild -ty p e v s 0 2 9 K O
D a y s p o s t - tu m o r im p la n ta t io n
Tu
mo
r v
olu
me
(m
m3
)
W ild - ty p e r Ig G 2 b
W ild - ty p e a n t i-P D L 1
0 2 9 K O r Ig G 2 b
0 2 9 K O a n t i-P D L 1
7 1 0 1 3 1 6 2 0 2 3 2 70
1 0 0 0
2 0 0 0
3 0 0 0
4 0 0 0
5 0 0 0
M C 3 8
W ild - ty p e r Ig G 2 b
D a y s p o s t- tu m o r im p la n ta t io n
Tu
mo
r v
olu
me
(m
m3)
D e a d
D e a d
7 1 0 1 3 1 6 2 0 2 3 2 70
1 0 0 0
2 0 0 0
3 0 0 0
4 0 0 0
5 0 0 0
M C 3 8
0 2 9 K O r Ig G 2 b
D a y s p o s t- tu m o r im p la n ta t io n
Tu
mo
r v
olu
me
(m
m3)
D e a d
7 1 0 1 3 1 6 2 0 2 3 2 70
1 0 0 0
2 0 0 0
3 0 0 0
4 0 0 0
5 0 0 0
M C 3 8
W ild - ty p e a n t i-P D L 1
D a y s p o s t- tu m o r im p la n ta t io n
Tu
mo
r v
olu
me
(m
m3)
7 1 0 1 3 1 6 2 0 2 3 2 70
1 0 0 0
2 0 0 0
3 0 0 0
4 0 0 0
5 0 0 0
M C 3 8
0 2 9 K O a n t i-P D L 1
D a y s p o s t- tu m o r im p la n ta t io n
Tu
mo
r v
olu
me
(m
m3)
D e a d
WT = wild typeKO = knockout
WT
WT + anti-PD-L1
PVRIG KO
PVRIG KO
+ anti-PD-L1
21
mIgG1+ rIgG2b
αPD-L1+rIgG2b
αPD-L1+AB 407
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
D a y s
Vo
lum
e m
m3
* * *
* * *p = 0 .0 0 0 5 ; T G I= 5 6 %
0 2 0 4 0 6 0 8 0 1 0 0
0
5 0
1 0 0
T im e
Pe
rc
en
t s
urv
iva
l
*
*p = 0 .0 4 4 ; T F = 4 /1 0
BLOCKING PVRIG IN COMBINATION WITH ANTI-PDL-1 REDUCES TUMOR GROWTH AND INCREASES OF SURVIVAL
Tumor growth SurvivalCT26 syngeneic model
0 2 0 4 0 6 0 8 0 1 0 0
0
5 0
1 0 0
T im e
Pe
rc
en
t s
urv
iva
l
*
*p = 0 .0 4 4 ; T F = 4 /1 0
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
D a y s
Vo
lum
e m
m3
* * *
* * *p = 0 .0 0 0 5 ; T G I= 5 6 %
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 6
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 6
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
30 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 6
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 6
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
21
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 6
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 6
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
0 2 0 4 0 6 0 8 0 1 0 0
0
5 0
1 0 0
T im e
Pe
rc
en
t s
urv
iva
l
*
*p = 0 .0 4 4 ; T F = 4 /1 0
21
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 6
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
PD-L1+rlgG2b
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 6
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
0 5 1 0 1 5 2 0 2 5
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + r Ig G 2 b
D a y s
mm
3
0 1 0 2 0
0
2 5 0
5 0 0
7 5 0
1 0 0 0
1 2 5 0
1 5 0 0
1 7 5 0
2 0 0 0
2 2 5 0
P D L -1 + A b 4 0 7
D a y s
mm
3
PD-L1+Ab 407
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+-
-
TIGITBlockade
PVRIGPVRL2
DNAM
PVR TIGIT
+-
-PVRIGBlockade
+-
-Dual PVRIG/TIGITBlockade
Increased anti-tumor T cell reactivity
DUAL INHIBITION OF TIGIT AND PVRIG REMOVES BOTH BRAKES IN THE DNAM-1 CO-STIMULATORY PATHWAY
22 22
23
COMBINING PVRIG AND TIGIT BLOCKADE INCREASES TIL ACTIVATION
23
624 Mel orpeptide-pulsed
CHO-HLA-A2
PVRIG/TIGIT PVRL2 /PVR
MART-1 or gp100 specific
TILs
gp100 pulsed CHO-HLA-A2 MART-1/624-mel
23
I s o C t r l
C OM
7 0 1
a n t i - T I GI T
C o mb i n a t i o n
0
1 0 0
2 0 0
3 0 0
4 0 0
IFN
(
pg
/m
L)
+ 5 3 %
I so
Ct r l
CO
M7 0 1
a nt i -
TI G
I T
Co
mb
i na t i o
n
0
5 0 0
1 0 0 0
1 5 0 0
IFN
(p
g/m
l)
3 7 %
8 6 %
5 6 %
23
24
Target discovery IND Filing
COM701 / PVRIG
COM902 / TIGIT
CGEN-XXXX (Myeloid)
Undisclosed Multiple programs
CGEN-15001T
CGEN-15022
Screening/ lead
selectionCell line developmntTarget validation mAb discovery CMC/IND enabling
IMMUNO-ONCOLOGY THERAPEUTIC PIPELINE: COM902 / TIGIT (CGEN-15137)
Lead selectionPartnered IO (Bayer)Internal IO
24
25
COM902 LEAD SELECTION COMPLETED Q1 2017;
PRECLINICAL DEVELOPMENT INITIATED
COM902 COMBINATION WITH COM701
• TIGIT identified as a putative immune checkpoint by Compugen’spredictive discovery platform in 2009 (N. Stanietsky et al PNAS 2009)
• Combination of COM701 and COM902 antibodies provide potential unique clinical differentiation
• In vitro effects of TIGIT/PVRIG blockade equal or exceed those seen with PD-1 combinations
25
26
TIGIT KNOCKOUT AND PVRIG BLOCKADE SYNERGIZE IN PRODUCING TUMOR GROWTH REDUCTION
Tumor growth; B16 model
B16-Db-
gp100
model
26
0 3 6 9 1 2 1 5 1 8
0
1 0 0 0
2 0 0 0
3 0 0 0
W T + m Ig G 1
D a y s
Vo
lum
e (
mm
3)
0 3 6 9 1 2 1 5 1 8
0
1 0 0 0
2 0 0 0
3 0 0 0
W T + a P V R IG
D a y s
Vo
lum
e (
mm
3)
0 3 6 9 1 2 1 5 1 8
0
1 0 0 0
2 0 0 0
3 0 0 0
T IG IT K O + m Ig G 1
D a y s
Vo
lum
e (
mm
3)
0 3 6 9 1 2 1 5 1 8
0
1 0 0 0
2 0 0 0
3 0 0 0
T IG IT K O + a P V R IG
D a y s
Vo
lum
e (
mm
3)
TGI compared to WT +
mIgG1
Day 11 Day 14 Day 18
WT+ aPVRIG 17% 13% 8%
TIGIT-KO + mIgG1 17% 17% 13%
TIGIT-KO + aPVRIG 63% 53% 49%
* p < 0.05 ANOVA
0 5 1 0 1 5 2 0
0
5 0 0
1 0 0 0
1 5 0 0
2 0 0 0
2 5 0 0
D a y s
Vo
lum
e (
mm
3)
W T + a -m P V R IG
T IG IT K O + m Ig G 1 T IG IT K O + a -m P V R IG
W T + m Ig G 1
*
26
27
INTERPLAY OF THE PD-1 AND TIGIT/PVRIG PATHWAYS SUPPORTING DUAL AND TRIPLE BLOCKADE
+Tumor/
APC
-
-
PVRIG
DNAM
TIGIT
PVRL2
PVR
-PD1 PDL1
Tumor/
APC
T Cell
PD-1 activation can result in DNAM-1 dephosphorylation
27
28
POTENCY OF ANTI-PVRIG AND ANTI-TIGIT COMBINATIONS EQUALS OR EXCEEDS PD-1 ANTIBODY COMBINATIONS
Colo205 (PDL1lo)Panc.05.04 (PDL1hi)
hIg
G4
CO
M7
01
+ T
IGIT
CO
M7
01
+P
D-1
TIG
IT +
PD
-1
CO
M7
01
+ T
IGIT
+ P
D-1
0
1 0 0
2 0 0
3 0 0
4 0 0
5 0 0
IFN
(p
g/m
L) + 2 4 5 %
+ 1 0 4 %
+ 2 1 4 %
+ 3 3 5 %
hIg
G4
CO
M7
01
+ T
IGIT
CO
M7
01
+P
D-1
TIG
IT +
PD
-1
CO
M7
01
+ T
IGIT
+ P
D-1
0
5 0
1 0 0
1 5 0
IFN
(p
g/m
L)
+ 7 7 %
+ 2 4 %
+ 6 3 %+ 7 2 %
28
29
Target discovery IND Filing
COM701 / PVRIG
COM902 / TIGIT
CGEN-XXXX (Myeloid)
Undisclosed Multiple programs
CGEN-15001T
CGEN-15022
Screening/ lead
selectionCell line developmntTarget validation mAb discovery CMC/IND enabling
IMMUNO-ONCOLOGY THERAPEUTIC PIPELINE: CGEN-XXXX (MYELOID)
Lead selectionPartnered IO (Bayer)Internal IO
29
30
BUILDING THE COMPUGEN IO PIPELINE: ADDING MULTIPLE MECHANISMS TO BROADLY ADDRESS CANCER TREATMENT
+Tumor/
APC
-
-
PVRIG
DNAM
TIGIT
PVRL2
PVR
-PD-1 PDL1
Tumor/
APC
T Cell
30
Discover and address various immune suppressive components in the TME
31
Target discovery IND Filing
COM701 / PVRIG
COM902 / TIGIT
CGEN-XXXX (Myeloid)
Undisclosed Multiple programs
CGEN-15001T
CGEN-15022
Screening/ lead
selectionCell line developmntTarget validation mAb discovery CMC/IND enabling
IMMUNO-ONCOLOGY THERAPEUTIC PIPELINE: BAYER PROGRAMS
Lead selectionPartnered IO (Bayer)Internal IO
31
32
CGEN-15001T & CGEN-15022:TWO NOVEL IMMUNE CHECKPOINTS
BAYER CANCER IMMUNOTHERAPY PARTNERSHIPNew Targets for Anti-Tumor Immunity
32
CGEN-15001T antibody programFrom computer prediction to functional activity in preclinical models
• Transferred to full control of Bayer following achievement of 3 milestones
• Preclinical development on track
• Pivotal (GLP) toxicity studies ongoing
• GMP clinical trial material production ongoing
CGEN-15022 antibody program
• Joint preclinical research stage
• Novel mechanism of action
• Assessment of its role in anti-cancer immune responses
33
$10Mupfront payment
up to $30MPreclinical milestone payments
To date achieved all 3 preclinical milestones for
CGEN-15001T and first milestone for
CGEN-15022totaling
$15.4M Royalties on global net sales: Mid-to-high single digit
BAYER PARTNERSHIPStrategic Collaboration to Develop Cancer Immunotherapies
Over $500M in potential milestone payments
AUG 2013 Collaboration and license agreement
33
34
Target discovery IND Filing
COM701 / PVRIG
COM902 / TIGIT
CGEN-XXXX (Myeloid)
Undisclosed Multiple programs
CGEN-15001T
CGEN-15022
CGEN-15001
Screening/ lead
selectionCell line developmntTarget validation mAb discovery CMC/IND enabling
Lead selectionPartnered IO (Bayer)Internal IO Autoimmune
COMPUGEN’S PIPELINE PROGRAM: CGEN-15001 AUTOIMMUNE FC-FUSION PROGRAM
34
35
Product-oriented collaborations at various development stages
Four program areas; belief that at least one new industry partnership is achievable by the end of the year
Advancing internal programs to the clinic
COM701 in IND-enabling studies; expected to enter the clinic next year
COM902 in preclinical development, advancing toward the clinic
Multiple myeloid & immune checkpoint programs from research to preclinical stages
Continuing progress on Bayer collaboration
Progress in Bayer’s pipeline
Development milestones in collaborations – existing and future
KEY GROWTH DRIVERSFrom Genomic Code to Clinical Cure
35
36
Gross Cash
Expenditures*Market Capitalization
$54.5 million
(March 31, 2017)
No Debt
~$250 million (June 2017)
NASDAQ (CGEN);
NBI (Nasdaq Biotech Index)
TASE (CGEN.TA)
TA-75, TA-Biomed, TA BlueTech,
TA Tech-Elite
FINANCIAL POSITION
Cash Balance
36
~$8 million/quarter 2017 quarterly forecast
* Does not include cash receipts from any source.