1

FROM CODE TO CURE

www.cgen.com

CorporateOverview

November 2017

Anat Cohen-Dayag, PhD

President & CEO

TM

2

SAFE HARBOR STATEMENTThis 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,” “plan,” “goal,” “estimate,” “likely,” “should,” 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. Compugen also may not meet expected milestones in its

development pipeline. 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, including the ability to finance the Company, 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 (“SEC”) 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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MARKET OPPORTUNITY: 70-80% OF PATIENTS NON-RESPONSIVE TO APPROVED IMMUNOTHERAPIES

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10

20

30

40

50

60

70

80

90

100

Ove

rall

Res

po

nse

Rat

e %

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TARGETING NEW IMMUNE CHECKPOINT PATHWAYS MAY ADDRESS NON-RESPONSIVE PATIENT POPULATION

~20% Average Response Rate

Gap to Bridge

Approved indications

In clinical testing

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KEY HIGHLIGHTS

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Transitioning to a clinical stage company with lead asset PVRIG mAb (COM701)▪ IND expected towards end of Q1 2018, Phase 1 open-label study to begin in 2018▪ Synergy with both TIGIT and PD-1/L1 blockers

Broadly applicable predictive discovery capabilities▪ Continuous discovery of novel targets for internal development or collaborations▪ Immune tolerance mechanism may represent next generation treatment for

autoimmune diseases

Diversified pipeline of novel targets and therapeutic candidates▪ Novel immune checkpoint targets including PVRIG, TIGIT and myeloid candidates▪ Potential for PD-L1 non-responsive patients and/or for combination with existing therapies

World class scientific advisory team and collaboration partners▪ Long term research collaborations with Johns Hopkins and Mount Sinai▪ Development collaboration and license agreement with Bayer

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Target discovery IND Filing

IMMUNO-ONCOLOGY

COM701 / PVRIG

CGEN-15001T

COM902 / TIGIT

CGENXXXX / Myeloid

Other programs

AUTOIMMUNE

CGEN-15001

Target validation mAb discoveryScreening/lead

selection

Cell line

developmntCMC/IND enabling

COMPUGEN’S PIPELINE PROGRAMFrom Code to Cure™

4 Programs, from computer prediction to preclinical POC

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end of Q1 2018

in 2019

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BUILDING THE COMPUGEN IO PIPELINE: ADDING MULTIPLE MECHANISMS TO BROADLY ADDRESS CANCER TREATMENT

+Tumor/ APC

-

-

PVRIG

DNAM

TIGIT

PVRL2

PVR

-PD-1 PD-L1

Tumor/APC

T Cell

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ADDRESS VARIOUS IMMUNE SUPRESSIVE COMPONENT IN THE TME

COM701

COM902

CGEN-XXXX

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APPLYING OUR PREDICTIVE APPROACH TO IMMUNE CHECKPOINT DISCOVERY

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CGEN novel targets

A DISCOVERY ENGINE TO REPLENISH PIPELINE WITH NEW DRUG PROGRAMS

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• PVRIG high T cell activation

• PVRIG is expressed in tumor microenvironment (CD8/TILs)

• Co-expressed in multiple tumor types with other checkpoints (TIGIT/PD-1)

• PVRIG ligand expressed in PD-L1 positive and negative tumors

• PVRIG-/- knockout mice have reduced tumor growth

• Potential monotherapy, dual and triple combination therapy with PD-1 and/or TIGIT blockers

PVRIG BLOCKADE IS DIFFERENT FROM AND SYNERGISTIC WITH TIGIT BLOCKADE

Martinet & Smyth, 2015 (modified)9

• Separate inhibitory pathways

• Different temporal and spatial distribution of targets

and ligands

KEY FINDINGS

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• COM701 is a high affinity humanized IgG4 mAb targeting PVRIG

• PVRIG identified as a novel immune checkpoint by Compugen and plays a unique role in the validated TIGIT axis

• COM701 is synergistic with anti-TIGIT and PD-1 pathway blockers as a potential cancer immunotherapy treatment

• First-in-class opportunities as monotherapy and dual/triple combination therapies

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COM701: PVRIG CHECKPOINT INHIBITORFrom Computer Prediction to Functional Activity in Preclinical Models

IND FILING EXPECTED TOWARDS THE END OF Q1 2018

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ENHANCED T CELL ACTIVATION BY COM701 ALONE AND IN COMBINATION WITH ANTI-PD-1 +/- ANTI-TIGIT

11

hIg

G4

CO

M701

TIG

IT

CO

M701 +

TIG

IT

PD

-1

0

1 0 0

2 0 0

3 0 0

4 0 0

T a rg e t C e ll: P a n c .0 5 .0 4 T u m o r c e lls

T c e ll: C M V p p 6 5 s p e c if ic C D 8 T c e lls

IFN

(p

g/m

L)

+ 4 0 %

+ 9 8 %

+ 2 4 5 %

+ 2 9 %

hIg

G4

CO

M701

TIG

IT

CO

M701 +

TIG

IT

PD

-1

0

5 0

1 0 0

1 5 0

T a rg e t c e ll : C o lo 2 0 5 T u m o r c e lls

T c e ll: C M V p p 6 5 s p e c if ic C D 8 T c e lls

IFN

(p

g/m

L)

+ 6 %

+ 4 9 %

+ 7 7 %

+ 8 %

Anti-TIGIT combination Anti-PD1 combination

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 %

Triple combination

COM701 IN VITRO EFFECTS MATCH PD-1 INHIBITOR

12

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 %

TUMOR GROWTH REDUCTION AND INCREASED SURVIVAL WITH PVRIG AND PD-1 PATHWAY BLOCKADE

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 %

12

12

αPDL-1+rlgG2b αPDL-1+α-mPVRIG

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

*m Ig G 1 + rIg G 2 b

P D L -1 + rIg G 2 b

P D L -1 + -m P V R IG

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

D a y s

mm

3

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

D a y s

mm

3

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TUMOR GROWTH REDUCTION IN PVRIG KNOCK OUTENHANCED IN COMBINATION WITH PD-1 PATHWAY BLOCKERS

Ganguly and Pardoll, Johns Hopkins Univ. MC38 model13

WT PVRIG KO

PVRIG KO + anti-PD-L1WT + anti-PD-L1

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

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

WT = wild typeKO = knockout

WT

WT + anti-PD-L1

PVRIG KO

PVRIG KO

+ anti-PD-L1

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SYNERGISTIC REDUCTION IN TUMOR GROWTH TIGIT KNOCKOUT PLUS PVRIG BLOCKADE

Tumor growth; B16 model

B16-Db-

gp100

model

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TGI compared to WT + mIgG1 Day 11 Day 14 Day 18

WT+ α-mPVRIG 17% 13% 8%

TIGIT-KO + mIgG1 17% 17% 13%

TIGIT-KO + α-mPVRIG 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

mm

3

W T + -m P V R IG

T IG IT K O + m Ig G 1 T IG IT K O + -m P V R IG

W T + m Ig G 1

*

14

WT + mIgG1

TIGIT KO + mIgG1 TIGIT KO + α-mPVRIG

WT + α-mPVRIG

0 3 6 9 1 2 1 5 1 8

0

1 0 0 0

2 0 0 0

3 0 0 0

D a y s

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

D a y s

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

D a y s

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

D a y s

mm

3

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BIOLOGIC RATIONALE DRIVES COM701 CLINICAL DEVELOPMENT STRATEGY

+Tumor/

APC

-

-

PVRIG

DNAM

TIGIT

PVRL2

PVR

-PD-1 PD-L1

Tumor/

APC

T Cell

INTERACTIONS OF THE PD-1 AND TIGIT/PVRIG PATHWAYS SUPPORT DRUG COMBINATION APPROACH

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COM701 CLINICAL DEVELOPMENT STRATEGY

• Goal is to significantly expand the number of patients responsive to PD-1 blockade• Targeting refractory and relapsing patient populations

• Potential to treat multiple patient populations based on expression• Opportunities in lung, ovary, breast, endometrial, kidney, head & neck

• First-in-class opportunities as monotherapy and in combinations

• Biomarker strategy: enrich for patients most likely to respond• Select patients with tumors where PVRIG, TIGIT pathways may be dominant

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Naïve Patients

PD-L1low/neg Non-Responsive Tumors(MSS CRC)

COM701 ± COM902

Refractory & Relapsing Patients

PD-L1high Responsive Tumors(NSCLC, RCC)

COM701 + PD-1 ± COM902

Naïve & Refractory & Relapsing Patients

PD-L1low/neg Poorly Responsive Tumors(Ovarian, TNBC, HNSCC)

COM701 ± COM902

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STA

GE

1A

COM701 PHASE 1 CLINICAL STUDY

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COM701Phase 1

• First-in-man• 3-stage design• Oncology

• Single agent, Simon 3x3 dose escalation• Safety, tolerability, PK/PD, clinical activity• All-comers trial; no pre-selection• Progressed on SOC• Maximum Tolerated Dose (MTD)

STA

GE

1B

STA

GE

1C

• COM701 in combination with anti-PD-1• Safety, tolerability, PK/PD, clinical activity• Rolling delayed start, 1 level highest safe

1A dose • Combined w/ fixed dose of anti-PD-1• Current PK data suggest every 3 week dosing

• Select expansion cohorts in specific indications• 20-30 patients per cohort• COM701 in combination with anti-PD-1• Monotherapy indications (pending 1a response)• Safety, tolerability, PK/PD, clinical activity

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COM902 CMC ACTIVITIES ONGOING; IND EXPECTED IN 2019

COM902 COMBINATION WITH COM701• TIGIT identified as a putative immune checkpoint by Compugen’s

predictive discovery platform in 2009 (N. Stanietsky et al PNAS 2009)

• Potential best-in-class anti-TIGIT antibody, COM902, has high (femtomolar) binding affinity

• Combination of COM701 and COM902 antibodies provides potential unique clinical differentiation

• In vitro effects of TIGIT/PVRIG blockade equal or exceed those seen with PD-1 combinations

• Process development and manufacturing agreement with Bayer to produce COM902

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TAPPING INTO THE WORLD OF MYELOID TARGETSThe Next Wave of Cancer Immunotherapies

+Tumor/ APC

-

-

PVRIG

DNAM

TIGIT

PVRL2

PVR

-PD-1 PD-L1

Tumor/APC

T Cell

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TARGETING MYELOID BIOLOGY OFFER COMPLEMENTARY THERAPEUTIC APPROACHES TO CHECKPOINT INHIBITORS

COM701

COM902

CGEN-XXXX

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MYELOID TARGETS: MULTIPLE MOAs FOR EFFICACY AND ANTI-TUMOR IMMUNE RESPONSE

• Myeloid biology blockade offers potential for efficacy in

• Patients with strong immuno-suppressive tumor micro-environment (“cold tumors”)

• Patients refractory to available checkpoint inhibitors

• A limited number of programs in development for known targets

• CD47, SIRPα, CD40, CSF1R

Antibody MoA –

Cell Depletion

NK

Myeloid

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**

43% TGI WT+ PD-L1 vs.

KO+ PD-L1

46% TGI KO vs. WT

49% TGI rIgG2b vs. PDL-1

**

MYELOID TARGET EXAMPLE #1: CGEN-15032 KNOCKOUT REDUCES TUMOR GROWTH AND SUGGESTS MONOTHERAPY APROACH

** P<0.01* P<0.05

21Ganguly and Pardoll, Johns Hopkins Univ. MC38 model

CGEN-15032 CGEN-15032

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MYELOID TARGET EXAMPLE #2: INHIBITS T CELL ACTIVATION SIMILAR TO PD-L1

aCD3 (OKT3)

Target #2

T cells

Counterpart

+

-

TCRCHO-S

n=8 donors; p<0.05 for CD4 & CD8 proliferation, IFN, TNFa and IL10

Do

no

r 1

Do

no

r 2

Target 2

Target 2

22

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MYELOID TARGET EXAMPLE #2: OPPORTUNITY TO TREAT PD-1 INHIBITOR RESISTANT PATIENT POPULATION

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Target 2 +

Target 2 +

Target 2 -

Target 2 -

% Samples

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CANCER IMMUNOTHERAPY COLLABORATION WITH BAYERCollaboration and License Agreement, signed August 2013

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CGEN-15001T - NOVEL IMMUNE CHECKPOINT From computer prediction to functional activity in preclinical models

• Preclinical development on track

• Pivotal (GLP) toxicity studies ongoing

• GMP clinical trial material production ongoing

$10M*upfront payment

$15MPreclinical milestone payments to date

Over $250M in potential milestone payments Royalties on global net sales: mid-to-high single digit

* Received for CGEN15001T and CGEN-15022

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CGEN-15001: FIRST-IN-CLASS THERAPEUTICS INDUCING TOLERANCE IN AUTOIMMUNE DISEASES

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Fc fusion

CTLA4-lg(Orencia®)

Fc fusionCGEN-15001

CGEN-15001T mAb

Compugen retained all rights to develop Fc-fusions for autoimmune indications

counterpart

IMMUNE TOLERANCE MECHANISM REPRESENTS NEXT GENERATION TREATMENT FOR AUTOIMMUNE DISEASES

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CGEN-15001 DIFFERENTIATION AND VALUE PROPOSITION

Addressing widely anticipated ‘next step’ therapeutic revolution in autoimmunity

▪ Tolerance induction and restoration of immunologic homeostasis in immune diseases

First-in-class therapeutic agent of a novel inhibitory checkpoint pathway

▪ Clinical and commercial opportunities in multiple autoimmune diseases

Paradigm shift from standard of care

▪ Tolerance induction offers safety advantages vs. immune-suppression

▪ Potentially efficacious in patients with inadequate response to standard of care

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27

Nu

mb

er

of

Do

no

r T

reg

s (

x10

6)

Rx

Rx

3.5

CGEN-15001: ROBUST EFFICACY IN MULTIPLE ANIMAL MODELS Short Term Treatment Consistently Leads to Durable Effect

CIA: Rheumatoid Arthritis NOD: Type 1 Diabetes

HY Mismatch: Bone Marrow Transplantation

EAE: Multiple Sclerosis

Number of Regulatory T cells in Spleen

Miller and Podojil, Northwestern Univ. Williams and McNamee, Univ. of Oxford, UK Miller and Podojil, Northwestern Univ.

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INTENTION TO PARTNER CGEN-15001, TO FOCUS RESOURCES ON DEVELOPING IMMUNO-ONCOLOGY PRODUCTS

Miller and Podojil, Northwestern Univ.

1 2 3 4 5 6 7 8 9 1 0

0

1

2

3

4

5

6

P B S

E n b re l

C G E N -1 5 0 0 1

A rth r it is D a y

Cli

nic

al

Sc

ore

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COMPUGEN: FOUR INTERNAL PROGRAM AREAS

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COM701Anti-PVRIG mAb drug candidate for

cancer immunotherapy• First-in-class advantage• Novel checkpoint in TIGIT pathway• Patent issued through

Cancer Moonshot program• Synergy with both -PD-1 and -TIGIT

Myeloid Targets Complementary portfolio to T cell checkpoint programs for cancer immunotherapy

• Enhanced anti-tumor response through inhibition of immunosuppressive myeloid activity

• Multiple programs in progress

COM902Anti-TIGIT mAb drug candidate for

cancer immunotherapy

• Potential “best-in-class” mAb with high (femtomolar) affinity

• Synergizes with COM701 and PD-1 pathways blockers

CGEN-15001Fc fusion protein drug candidate

for autoimmune diseases

• Unique immune tolerance mechanism• Broadly applicable in RA, MS, T1D• Durable response following short-term

treatment in preclinical models

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STRATEGIC ADVISORSSCIENTIFIC ADVISORY BOARD

Elliott Sigal, MD, PhDFormer CSO, EVP and Director

Richard HaiduckFormer CBO and CEO Life science companies

Charles Drake, MD, PhD

Howard Soule, PhD

Iain McInnes, MD, PhD

KEY STRATEGIC ADVISORSIndustry Veterans, Renowned Oncologists and Immunologists

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Miriam Merad, MD, PhD

Multi-year strategic collaboration

Steven HoltzmanPresident and CEO, Decibel TherapeuticsFormer CBO and CEO

Antoni Ribas, MD, PhDDrew Pardoll, MD, PhDChairman of the SAB

Multi-year strategic collaboration

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LEADERSHIP TEAM

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BOARD OF DIRECTORSMANAGEMENT TEAM

Paul SekhriChairman of the Board

Anat Cohen-Dayag, PhD President & CEO, Director

Yair Aharonowitz, PhDDirector

Ruth Arnon, PhDDirector

Martin S. GerstelDirector

Arie Ovadia, PhDDirector

Michal Preminger, PhD, MBADirector

Dov HershbergDirector

Joshua Shemer, MDDirector

Anat Cohen-Dayag, PhD President & CEO

Ari KrashinChief Financial & Operating Officer

Kirk A. ChristoffersenSenior VP - Corporate & Business

Development

Zurit Levine, PhDVP, Research & Discovery

John Hunter, PhDVP, Antibody R&D and Site Head

Compugen USA, Inc.

Yona Geffen, PhDVP, Research & Validation

Tsipi Keren-LehrerVP, Business Development

Dorit AmitayVP, Human Resources

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FINANCIAL POSITION

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Gross Cash Expenditures*

Market Capitalization

$38.5 million

(September 30, 2017)

No Debt

~$153 million (October 2017)

NASDAQ (CGEN)

NBI (Nasdaq Biotech Index)

TASE (CGEN.TA)

TA-90, TA-125, TA-Biomed, TA Global

BlueTech, TA Tech-Elite* Does not include cash receipts from any source

Cash Balance

~$8.5 million/quarter 2017 quarterly forecast

32

FROM CODE TO CURE

www.cgen.com

CorporateOverview

November 2017

Anat Cohen-Dayag, PhD

President & CEO

TM