1

FROM CODE TO CURE

CorporateOverview

www.cgen.com

January 2018

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 SEC. 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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3

Transforming patient lives by

developing first-in-class therapeutics

based on Compugen’s foundational

predictive target discovery

and functional validation

Our Vision

FROM CODE TO CURE TM

4

KEY HIGHLIGHTS

4

Diverse therapeutic pipeline based on original targets ▪ Immuno-oncology checkpoint programs: PVRIG, TIGIT, and myeloid candidates▪ Next-generation immune tolerance induction autoimmune program

Becoming a clinical stage company in 2018

▪ IND filing for COM701 (anti-PVRIG mAb) towards the end of Q1▪ Phase 1b study in COM701, monotherapy and combination therapy

Proven target discovery capabilities and mAb development expertise

▪ 4 programs, from computational discovery to preclinical POC▪ Continuously generating original targets for earlier stage pipeline and

collaborations

World-class scientific advisory team and collaboration partners

▪ Immuno-oncology collaboration with Bayer ▪ Multi-year strategic collaborations with Johns Hopkins and Mount Sinai

5

Target Discovery &

ValidationPhase I

IMMUNO-ONCOLOGY

COM701 / PVRIG

CGEN-15001T

COM902 / TIGIT

AUTOIMMUNE

CGEN-15001

IMMUNO-ONCOLOGY

EARLY STAGE PIPELINE

CGENXXXX / Myeloid

Other programs

mAb Discovery Preclinical Development

COMPUGEN’S PIPELINEFrom Code to Cure™

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IND in Q1 2018

IND-enabling studies in 2018; IND in 2019

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MARKET OPPORTUNITY: 70-80% OF PATIENTS NON-RESPONSIVE TO APPROVED CANCER IMMUNOTHERAPIES

6

TARGETING NEW PATHWAYS MAY ADDRESS NON-RESPONSIVE PATIENT POPULATIONS

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

Approved indications

In clinical testing

7

ADDING MULTIPLE MECHANISMS TO BROADLY ADDRESS CANCER TREATMENT

+Tumor/ APC

PVRIG

DNAM

TIGIT

PVRL2

PVR

PD-1 PD-L1

T Cell

7

ADDRESSING MULTIPLE IMMUNE SUPRESSIVE COMPONENTS IN THE TME

15001T

Tumor/ APC

CGEN-XXXXCOM902

COM701

15001T mAb

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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

Anat Cohen-Dayag, PhD President and CEO

Ari KrashinChief Financial & Operating Officer

Kirk ChristoffersenSVP, 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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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

10CONFIDENTIAL 10

COM701: PVRIG CHECKPOINT INHIBITOR

11

• COM701 is a high-affinity humanized IgG4 mAb targeting PVRIG─ PVRIG was computationally identified and validated by Compugen as an immune checkpoint

target

─ Shown to play a unique role in a PVRIG/TIGIT axis

• First-in-class opportunities for monotherapy and combination therapy in multiple solid tumor indications

─ Strong clinical rationale for dual and triple combination with TIGIT and PD-1 pathway blockers

• Clinical opportunities in endometrial, ovarian, breast, lung, kidney, colorectal, and head & neck cancers

─ Based on expression of the TIGIT and PVRIG and their ligands

• Shown to be safe at high doses in GLP toxicity study

11

COM701: FIRST-IN-CLASS PVRIG CHECKPOINT INHIBITOR

IND FILING EXPECTED TOWARDS THE END OF Q1 2018

12

COMPUGEN DISCOVERED AND VALIDATED PVRIG TARGET

12

PVRIG BLOCKADE IS DIFFERENT FROM AND

SYNERGISTIC WITH TIGIT BLOCKADE

Martinet & Smyth, 2015 (modified)

13

+Tumor/

APC

-

-

PVRIG

DNAM

TIGIT

PVRL2

PVR

-PD-1 PD-L1

Tumor/

APC

T Cell

MOLECULAR INTERATIONS OF PD-1 AND TIGIT/PVRIG PATHWAYS SUPPORT DRUG COMBINATION APPROACH

13

BIOLOGIC RATIONALE FOR COM701 CLINICAL COMBINATIONS

14

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

14

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-PD-1 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

ASCO, June 2017, Ophir, et al., poster presentation

15

TUMOR GROWTH REDUCTION IN PVRIG KNOCKOUT MICEENHANCED IN COMBINATION WITH PD-1 PATHWAY BLOCKERS

Ganguly and Pardoll, Johns Hopkins Univ. MC38 model15

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

STIC, November 2016, Hunter, et al., oral presentation

16

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 Survival

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 %

16

16

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

CT26 syngeneic model

STIC, November 2016, Hunter, et al., oral presentation

PVRIG/PVRL2 PATHWAY BIOLOGY IN MICE UNDERESTIMATED COMPARED TOHUMANS, ANTICIPATING GREATER THERAPEUTIC EFFECT IN HUMANS

17

SYNERGISTIC REDUCTION IN TUMOR GROWTH FROM TIGIT KNOCKOUT PLUS PVRIG BLOCKADE

Tumor growth; B16 model

B16-Db-

gp100

model

17

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

*

17

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

ASCO, June 2017, Ophir, et al., poster presentation

18

BIOLOGIC RATIONALE DRIVES COM701 CLINICAL DEVELOPMENT STRATEGY

+Tumor/

APC

-

-

PVRIG

DNAM

TIGIT

PVRL2

PVR

-PD-1 PD-L1

Tumor/

APC

T Cell

RECEPTOR/LIGAND EXPRESSION IN THE TME INFORMING PATIENT SELECTION BIOMARKER STRATEGY

18

19

COM701: BIOMARKER STRATEGY AND INITIAL DATA

• Goal is to select for patients most likely to respond to COM701, either

alone or in combination

─ Select patients with tumors in which PVRIG pathway may be dominant based on expression patterns

• Expression profiles of various axis components provide indication for a

dominant role of the PVRIG/TIGIT axis multiple cancers

─ PVRL2 is commonly upregulated in multiple tumor types─ Frequently expressed in PD-L1 negative tumors

─ Expressed in PVR negative tumor and immune cell subpopulations in the TME

─ PVRIG expressed on TILs and NK cells in the TME of multiple tumor types─ Majority of exhausted TILs in the tumor are PD-1, TIGIT and PVRIG positive

19

20

RELATIVE EXPRESSION OF PVRL2 VS PVR VARIES BY TUMOR TYPE

20

TCGA RNA Analysis

Higher PVRL2Higher PVR

HIGH PVRL2 EXPRESSION SUGGESTS PVRIG DOMINANCE; TUMOR CELLS FROM BREAST, OVARIAN, AND ENDOMETRIAL TUMORS ARE FREQUENTLY PDL1NEG

20Keystone, January 2018, Ofir, et al., poster presentation

21

PVRL2 IS INDUCED IN THE TME AND EXPRESSED IN PD-L1NEG

TUMORS

21

PVRL2 expression in PD-L1- tumors

Lung

Adenocarcinoma

Endometrioid

Cancer

SITC, November 2017, Whelan, et al., poster presentation

22

COM701 CLINICAL DEVELOPMENT STRATEGY

• Goal is to target PD-1 pathway inhibitor refractory and relapsing patient populations

• Biomarker strategy to allow selection of tumors based on expression of pathway components

• Data support potential to treat multiple patient populations as monotherapy or

combination therapy

• Opportunities in lung, ovary, breast, endometrial, kidney, and head & neck cancers

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Refractory & Relapsing Patients

Anti-PD1 failures in approved indications

(e.g. NSCLC, RCC)

(COM701 + PD-1) ± COM902

Naïve & Refractory & Relapsing Patients

PD1 refractory indications(e.g. Ovarian, TNBC, MSS CRC)

(COM701) ± COM902

23

STA

GE

1A

COM701 PHASE 1B CLINICAL STUDY – TO BE INITIATED IN 2018

23

• 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

24

ADDITIONAL IMMUNO-ONCOLOGY DEVELOPMENT PROGRAMS

25

IND-ENABLING ACTIVITIES IN 2018; IND EXPECTED IN 2019

COM902 – ANTI-TIGIT MONOCLONAL ANTIBODY

• COM902 is a high-affinity (femtomolar) mAb targeting TIGIT─ TIGIT identified as a putative immune checkpoint by Compugen’s predictive

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

─ Potential Best-in-Class ─ In vitro activity comparable to or better than the top clinical TIGIT antibodies

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

• Combination of COM701 and COM902 provides potential unique clinical differentiation

25

26 26

COM701 + COM902 POTENTLY ENHANCES TIL ACTIVATION

Kidney CD3 TIL+ Endometrium CD3 TIL+ Ovarian CD3 TIL+

T c

el l

s a

l on

e

hI g

G4

CO

M

70

1

CO

M

90

2

Pe

m

bro

l iz

um

ab

CO

M

70

1 +

CO

M

90

2

0

5 0 0

1 0 0 0

1 5 0 0

L u n g C D 3+

T I L

IF

N

(

pg

/m

L)

1 4 % 1 2 %2 1 %

4 3 %

T c

el l

s a

l on

e

hI g

G4

CO

M

70

1

CO

M

90

2

Pe

m

bro

l iz

um

ab

CO

M

70

1+

CO

M

90

2

0

5 0 0

1 0 0 0

1 5 0 0

2 0 0 0

2 5 0 0

K i d n e y C D 3+

T I L

IF

N

(

pg

/m

L)

4 3 %

6 8 %5 0 %

8 3 %

T c

el l

s a

l on

e

hI g

G4

CO

M

70

1

CO

M

90

2

Pe

m

bro

l iz

um

ab

CO

M

70

1 +

CO

M

90

2 H

4

0

4 0

8 0

1 2 0

E n d o m e t r i u m C D 3+

T I L

IF

N

(

pg

/m

L)

2 1 % 8 %

2 3 %

1 0 8 %

T c

el l

s a

l on

e

hI g

G4

CO

M7

01

CO

M9

02

Pe

mb

r ol i

zu

ma

b

CO

M7

01

+ C

OM

90

2

0

4 0

8 0

1 2 0

E n d o m e t r i u m C D 3+

T I L

IFN

(

pg

/mL

)

2 1 % 8 %

2 3 %

1 0 8 %

T c

ells a

lon

e

Iso

typ

e C

on

tro

l

CO

M701

CO

M902

Pem

bro

lizu

mab

CO

M701 +

CO

M902

0

5 0

1 0 0

1 5 0

O v a r ia n C D 3+ T IL

IFN

(p

g/m

L)

+ 2 7 %

+ 7 4 %

+ 3 6 %

+ 3 4 1 %

SITC November 2017, Whelan, et al., poster presentation; andKeystone, January 2017, Ofir, et al., poster presentation

27 27

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

Antibody MoA –

Cell Depletion

NK

Myeloid

• Myeloid biology blockade offers potential for efficacy in

• Patients with strong immuno-suppressive tumor micro-environment, or cold tumors

• Patients refractory to available checkpoint inhibitors

• Programs in development by various industry players

• CD47, SIRPα, CD40, CSF1R

28 28

MYELOID TARGET EXAMPLE #1: CGEN-15032 KNOCKOUT REDUCES TUMOR GROWTH INDICATING ROLE IN TUMOR GROWTH REGULATION

Ganguly and Pardoll, Johns Hopkins Univ. MC38 model CRI, September 2017, Levy, et al., poster presentation

7 1 0 1 4 1 7 2 0 2 3 2 70

1 0 0 0

2 0 0 0

3 0 0 0

4 0 0 0

W ild - ty p e

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 4 1 7 2 0 2 3 2 70

1 0 0 0

2 0 0 0

3 0 0 0

4 0 0 0

C G E N - 1 5 0 3 2 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)

46% TGI (p<0.01)

43% TGI (p<0.01)

MC38 Wild-Type vs CGEN-15032 KOCGEN-15032 KO

CGEN-15032 KO

29

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

Similar data obtained by measuring T cell proliferation inhibition

Do

no

r 1

Do

no

r 2

aCD3 (OKT3)

Target #2

T cells

Counterpart

+

-

TCRCHO-S

n=8 donors; p<0.05 for IFN, TNFa

29

30

MYELOID TARGET EXAMPLE #2: OPPORTUNITY TO TREATPD-1 INHIBITOR RESISTANT PATIENT POPULATIONS

30

31

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

31

CGEN-15001T – NOVEL IMMUNE CHECKPOINT

• 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

32CONFIDENTIAL 32

AUTOIMMUNE PROGRAM

33

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

IMMUNE TOLERANCE MECHANISM REPRESENTS NEXT GENERATION TREATMENT FOR AUTOIMMUNE DISEASES

Fc fusion

CTLA4-lg(Orencia®)

Fc fusionCGEN-15001

CGEN-15001T mAb

Compugen retained all rights to develop Fc fusions for autoimmune indications

counterpart

32

34

CGEN-15001 DIFFERENTIATION AND VALUE PROPOSITION

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

Addressing widely anticipated ‘next step’ therapeutic revolution in autoimmunity

▪ Tolerance induction and restoration of immunologic homeostasis

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

▪ Robust efficacy in multiple animal models, presenting clinical and commercial opportunities in multiple autoimmune diseases

▪ Short term treatment leads to durable effect

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

34

35CONFIDENTIAL 35

PREDICTIVE TARGET DISCOVERY & FUNCTIONAL VALIDATION CAPABILITIES

36

APPLYING OUR PREDICTIVE APPROACH TO TARGET DISCOVERY AND FUNCTIONAL VALIDATION

36

A DISCOVERY ENGINE TO REPLENISH PIPELINE WITH NEW DRUG PROGRAMS

Therapeutic Development

Computational Discovery

Research reagents preparation

Functional in vitro analysis

Expression profiles

Functional in vivo analysis(KO/surrogate mAb)

Target Validation

Genome & ProteomeAnalysis

Biological knowledge

Experimental & Disease Data

ModelTest

Refine

37

FINANCIAL POSITION

37

Gross Cash Expenditures*

Market Capitalization

$38.5 million

(September 30, 2017)

No Debt

~$150 million (January 2018)

NASDAQ (CGEN)

TASE (CGEN.TA)

SME-150, 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

38

Becoming a clinical stage company in 2018

• COM701 (anti-PVRIG mAb) - IND filing anticipated towards the end of Q1 2018

• Phase 1b study – monotherapy and combination with PD-1 pathway blockade

• CGEN-15001T mAb (Bayer) - currently in IND-enabling studies

CURRENT AND UPCOMING ANTICIPATED MILESTONES

38

Advancing preclinical pipeline

• COM902 (anti-TIGIT mAb) - IND-enabling studies in 2018; IND expected in 2019

• Various myeloid programs progressing towards preclinical development

• Multiple programs progressing through validation

39

FROM CODE TO CURE

Thank you

www.cgen.com

January 2018

Anat Cohen-Dayag, PhD

President & CEO

TM