Corporate Overview - The Global Investment Banking Firm · Corporate Overview Anat Cohen-Dayag ... Adapted from Cowen & Company March 2017 Research Report ... Martinet & Smyth, 2015

1

FROM CODE TO CURE

www.cgen.com

CorporateOverview

Anat Cohen-Dayag, PhD

President & CEO

TM

Jefferies 2017 Global Healthcare Conference

June 6, 2017

2

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.

2

3

Transforming patient lives by

developing first-in-class therapeutics

based on computational predictive

discovery of novel targets

Our Vision

FROM CODE TO CURE TM

4

COMPUGEN: FROM CODE TO CURE

4

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

5

TWO CENTERS OF EXCELLENCE

5

Therapeutic mAbResearch &

Development

Compugen USA, Inc.

South San Francisco, USA

Compugen Ltd. Headquarters

Holon, Israel

Predictive Discovery &

Target Validation

6

COMPUGEN: FOUR PROGRAM AREAS

6

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

7

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

7

Miriam Merad, MD PhD

8

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

8

9

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

9

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

10

11

STRATEGICPARTNERSHIPS

PIPELINEPROGRAM

PREDICTIVE DISCOVERY

PIPELINEPROGRAM

FROM GENOMIC CODE TO CLINICAL CUREAn Integrated Approach

12

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

12

13

PVRIG BLOCKADE IS DIFFERENT FROM AND SYNERGISTIC WITH TIGIT BLOCKADE

Martinet & Smyth, 2015 (modified)

+-

TUMOR/

APC

T CELL-

PVRIG

13

• Separate inhibitory pathways

• Different temporal and spatial

distribution of targets and ligands

14

MATCHING PREDICTION TO FUNCTION: PVRIG OVEREXPRESSION INHIBITS T CELL ACTIVATION

Cohen and Safyon, Bar Ilan Univ.1414

F4MART1/

14

15

PVRIG IS EXPRESSED ON CD8+ T CELLS AND NK CELLS IN THE TUMOR MICROENVIRONMENT

15

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

16

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

16

17

• 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

17

COM701: LEAD CHECKPOINT INHIBITORFrom computer prediction to functional activity in preclinical models

IND-ENABLING STUDIES

18

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

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Ct r l

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Ab

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1 0 0

2 0 0

3 0 0

4 0 0

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up

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0

5 0 0

1 0 0 0

1 5 0 0

IFN

(

pg

/m

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18

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

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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


Tu

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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

19

20

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

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me

(m

m3

)


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



Tu

mo

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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


Tu

mo

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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


Tu

mo

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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


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

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m3

* * *

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0 2 0 4 0 6 0 8 0 1 0 0

0

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*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

22

+-

-

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


COM701 / PVRIG

COM902 / TIGIT

CGEN-XXXX (Myeloid)


CGEN-15001T

CGEN-15022

Screening/ lead


IMMUNO-ONCOLOGY THERAPEUTIC PIPELINE: COM902 / TIGIT (CGEN-15137)

Lead selectionPartnered IO (Bayer)Internal IO

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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

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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

*

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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

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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 %

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29


COM701 / PVRIG

COM902 / TIGIT

CGEN-XXXX (Myeloid)


CGEN-15001T

CGEN-15022

Screening/ lead


IMMUNO-ONCOLOGY THERAPEUTIC PIPELINE: CGEN-XXXX (MYELOID)


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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


COM701 / PVRIG

COM902 / TIGIT

CGEN-XXXX (Myeloid)


CGEN-15001T

CGEN-15022

Screening/ lead


IMMUNO-ONCOLOGY THERAPEUTIC PIPELINE: BAYER PROGRAMS


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CGEN-15001T & CGEN-15022:TWO NOVEL IMMUNE CHECKPOINTS

BAYER CANCER IMMUNOTHERAPY PARTNERSHIPNew Targets for Anti-Tumor Immunity

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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

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$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

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COM701 / PVRIG

COM902 / TIGIT

CGEN-XXXX (Myeloid)


CGEN-15001T

CGEN-15022

CGEN-15001

Screening/ lead


Lead selectionPartnered IO (Bayer)Internal IO Autoimmune

COMPUGEN’S PIPELINE PROGRAM: CGEN-15001 AUTOIMMUNE FC-FUSION PROGRAM

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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

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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.

37

FROM CODE TO CURE

www.cgen.com

CorporateOverview

Anat Cohen-Dayag, PhD

President & CEO

TM

Jefferies 2017 Global Healthcare Conference

June 6, 2017

Documents

Corporate Overview - The Global Investment Banking Firm · Corporate Overview Anat Cohen-Dayag ... Adapted from Cowen & Company March 2017 Research Report ... Martinet & Smyth, 2015