©Copyright 2013 Galapagos NV

R&D update

Onno van de Stolpe, CEO Piet Wigerinck, CSO 27 March 2013

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Neither Galapagos nor any of its officers, employees, advisers, or agents makes any representation or warranty, express or implied, as to any matter or as to the truth, accuracy, or completeness of any statement made in this presentation, made in conjunction therewith or in any accompanying materials or made at any time, orally or otherwise, in connection with the matters referred to herein and all liability in respect of any such matter or statements is expressly excluded.

Disclaimer

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Executive team

Founded Galapagos in 1999 Previously MD Genomics at Crucell

Onno van de Stolpe CEO

Previously CFO of Wolters Kluwer Health Registered Accountant

Guillaume Jetten CFO

Previously VP Drug Discovery at Tibotec Brought 3 HIV drugs to market, including Prezista™

Piet Wigerinck CSO

Previously MD Corporate Development Europe at Invitrogen Architect of Abbott GLPG0634 deal and Galapagos’ alliances

Andre Hoekema Sr VP Corp Dev

Previously founder CSO and Board Director at Argenta > 50 publications and patents on the discovery of new drugs

Chris Newton Sr VP Services

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R&D Update

• Company strategy Onno van de Stolpe, CEO

• R&D portfolio Piet Wigerinck, CSO

• 2013 Outlook Onno van de Stolpe, CEO

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Galapagos: leading European biotech

• Two selective JAK1 molecules in Phase 2 in three indications

• Major risk sharing alliances with pharma

• Large pipeline: 4 clinical, 6 PCC, >30 discovery programs

• Leading fee-for-service provider with BioFocus & Argenta

• 800 staff, research sites in 5 countries, HQ in Belgium

• Ticker symbol

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How we built Galapagos

1999 2002 2005 2006 2009 2010

1st profitable

year

1st pharma alliance

Acquired BioFocus

IPO on Euronext

VC financing

Founded by Tibotec and Crucell

Acquired Argenta and GSK Zagreb

First novel target with clinical PoC

2011 2012

AbbVie deal

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Revenue generating business model

New mode-of-action medicine platform

Fee-for-service

Alliance business

Licensing

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Indication Partner Deal value Year

Inflammation $260 M + royalties 2006

Inflammation $1.3 B + royalties 2007

Osteoarthritis $390 M + US rights + royalties 2010

Oncology $340 M + US rights + royalties 2011

Autoimmune $1.35 B + double-digit royalties 2012

Pharma alliances

• Alliances have brought in >$440 M in cash since 2006 • Source of promising molecules and targets for GLPG

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Deal structure with AbbVie • Upfront payment $150 million

• Galapagos performs & funds Phase 2 in RA

• License fee $200 million after Phase 2b completion

• AbbVie performs & funds Phase 3, registration & commercialization

• GLPG to receive up to $1 billion in milestones + double digit royalties

• Tax benefits from Belgian Patent Income Deduction law

Phase 2

handover after

Phase 2b

Phase 3 Marketing and sales

Benelux

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Broad pipeline

Indications Company Target Lead program: stage

RA AbbVie JAK1 ‘634: Phase 2b

Lupus & Psoriasis GSK JAK1 ‘184: Phase 2

Metastasis IRA ‘187: Phase 1b

IBD GPR43 ‘974: Phase 2 start

MRSA DNA pol IIIα PCC

Inflammation JnJ novel 2 PCC’s

Osteoarthritis Servier/GLPG novel PCC

Inflammation GSK novel 2 PCC’s

Oncology Servier/GLPG novel Lead optimization

Cystic fibrosis novel Lead optimization

4 clinical programs, 6 PCC’s >30 discovery programs

Licensing

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Growth strategy

• Execute development of JAK1 program to Phase 2b results late 2014

• Build mature clinical portfolio – partnered and non-partnered

• Increase share of non-partnered programs

• Continue profitable and productive pharma alliances

• Sign new alliances and partnerships to leverage our technology

• Grow Service division revenues

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R&D Update

• Company strategy Onno van de Stolpe, CEO

• R&D portfolio Piet Wigerinck, CSO

• 2013 Outlook Onno van de Stolpe, CEO

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‘634 validates our approach 8 years from assay development to Phase 2 data

2003 2005 2006 2009 2010

PCC nomination

Hit Finding

JAK1 selected

Target Discovery

Assay Development

Start Phase 1 trial

Start PoC

2011

End PoC

2004

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R&D Portfolio

• GLPG0634

• GSK alliance

• GLPG0974

• GLPG0187

• Cystic Fibrosis

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‘634 in RA

• Selective JAK1 inhibitor in development for rheumatoid arthritis (RA)

• JAK1 selectivity could lead to better safety profile than current JAK

inhibitors

• ‘634 showed good efficacy & safety in POC trial in RA patients

• Good results confirmed in Phase 2a trial

• Phase 1 drug interaction study in the US ongoing

• Start Phase 2b program in June 2013

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JAKs in RA

Company RA drug JAK profile Phase

Pfizer Xeljanz® JAK3 >JAK1>JAK2 Approved in RA

Incyte/Lilly baricitinib JAK1=JAK2 Phase 3

Vertex VX-509 JAK3 Phase 2

GLPG/AbbVie ‘634 JAK1 Phase 2

Astellas/JnJ ASP015K JAK3/JAK1 Phase 2

Incyte INCB039110 JAK1/JAK2 Phase 2

‘634: opportunity to differentiate from other JAK inhibitors

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Design PoC vs Phase 2a Moderate to severe RA patients

PoC Phase 2a

# patients on stable MTX 36 91

doses Placebo vs 200 mg daily (100 mg BID, 200 mg QD)

Placebo vs 30, 75, 150, 300 mg QD

duration 28 days 28 days

study centers 1 19

countries Moldova Hungary, Moldova Russia, Ukraine

PoC: designed to give rapid evaluation Phase 2a: extended version of PoC

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Results PoC vs Phase 2a Moderate to severe RA patients

PoC Phase 2a

Efficacy

ACR √ √ DAS28 √ √ CRP √ √

HAQ-DI - √

Good efficacy & unique safety profile confirmed

Safety

Discontinuations none none

SAE none none

LDL cholesterol stable stable

Liver enzymes stable stable

Anemia absent absent

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‘634 Phase 2b program in RA Moderate to severe RA patients with inadequate MTX response

Add-on to MTX

Monotherapy

Long term extension

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Design RA Phase 2 studies

POC Add-on to MTX 12/24 w Monotherapy Long-term

Follow-up

‘634

36 + 91 pt, 4w Add-on to MTX Biologics naïve

Xeljanz® 264 pt, 6 w Monotherapy 509 pt 384 pt, 12/24 w

(vs adalimumab) Yes

Baricitinib 127 pt, 12/24 w Add-on to DMARDs 301 pt - Yes

VX-509 - 350 pt 164 pt, 12 w Yes

ASP015K - 375 pt, 12 w only 275 pt, 12 w Yes

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Add-on to MTX 7 equal cohorts

25 mg BID

50 mg BID

100 mg BID

Placebo

Week 0

200 mg QD

100 mg QD

50 mg QD

25 mg BID

50 mg BID

100 mg BID

Placebo

200 mg QD

100 mg QD

50 mg QD

Week 24 Study end

Week 12 Primary endpoint

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Add-on to MTX

25 mg BID

50 mg BID

100 mg BID

Placebo

Week 0 Week 24 Study end

Week 12 Primary endpoint

* if 20% improvement in SJC and TJC not achieved

R randomization

200 mg QD

100 mg QD

50 mg QD

25 mg BID

50 mg BID

100 mg BID

Placebo

200 mg QD

100 mg QD

50 mg QD

R

*

*

*

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50 mg QD

Placebo

50 mg QD

Week 0 Week 24 Study end

Week 12 Primary endpoint

100 mg QD

200 mg QD

100 mg QD

200 mg QD

Monotherapy 4 equal cohorts

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50 mg QD

Placebo

50 mg QD

Week 0

* 100 mg QD

200 mg QD

100 mg QD

200 mg QD

Monotherapy

* if 20% improvement in SJC and TJC not achieved

Week 24 Study end

Week 12 Primary endpoint

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ʃʃ

Darwin 2 Monotherapy QD

Darwin 3 100 mg BID

Week 0 …Week 260 Week 24 = BL for Long Term Follow Up

Darwin 1 MTX add-on BID

Darwin 1 MTX add-on QD

Darwin 3 200 mg QD

Long term extension

Option

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Design RA Phase 2 studies

POC Add-on to MTX 12/24 w Monotherapy Long-term

Follow-up

‘634

36 + 91 pt, 4w Add-on to MTX Biologics naïve

Yes

Xeljanz® 264 pt, 6 w Monotherapy 509 pt 384 pt, 12/24 w

(vs adalimumab) Yes

Baricitinib 127 pt, 12/24 w Add-on to DMARDs 301 pt - Yes

VX-509 - 350 pt 164 pt, 12 w Yes

ASP015K - 375 pt, 12 w only 275 pt, 12 w Yes

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‘634 Phase 2b program Geography

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Timelines ‘634 in RA

2013 2014

1st patient in

Trial application submissions

Last patient at 12 wk analysis

Topline 12 wk Darwin 1 & 2

Last Patient in

Presentations at major conferences

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R&D Portfolio

• GLPG0634

• GSK alliance

• GLPG0974

• GLPG0187

• Cystic Fibrosis

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GSK alliance History

2006 2009 2012 2013

GLPG platform quickly generates Phase 2 molecules

1st candidate

Start alliance

5th candidate

2 compounds inlicensed

(GLPG0778/0555) GSK Progresses GSK 2586184

(GLPG0778) into Phase 2

First program in the clinic

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GSK alliance Clinical studies with GSK2586184 (previously ‘778)

• GSK2586184 is an investigational selective JAK1 inhibitor in Phase 2

• GLPG performed innovative Phase 1 study

1. safety, PK study

2. inhibition inflammation pathway

• Results: dose-dependent, statistically-significant suppression of an induced inflammatory response specific inhibition of target in vivo

• Upon these results, GSK inlicensed GSK2586184 and its back-up GLPG0555 and progresses the compound into Phase 2

eligible to receive $45 M future milestones

up to double-digit royalties on global commercial sales

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Phase 2 studies with GSK2586184 GSK led studies

• Systemic lupus erythematosus

dose range 50 to 400 mg, oral BID vs placebo for up to 12 weeks

approx 150-250 patients in 66 centers in Europe, South America, Asia

primary Outcome Measures include: SELENA SEDAI score, interferon biomarkers

estimated study completion June 2014

• Chronic plaque psoriasis

oral BID for up to 12 weeks in UK and Germany

cohort A: dose range 100, 200, 400 mg vs placebo, estimated 56 patients

cohort B: open-label skin biopsy gene expression study, estimated 8 patients

estimated study completion December 2013

Source: ClinicalTrials.gov

Galapagos milestone payment upon successful POC

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R&D Portfolio

• GLPG0634

• GSK alliance

• GLPG0974

• GLPG0187

• Cystic Fibrosis

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‘974 Inhibits novel target for inflammatory diseases

• GPR43 (FFA2) is a GPCR

ligand: Short Chain Fatty Acids (SCFA)

SCFAs induce human neutrophil chemotaxis GPR43 plays key role in neutrophil biology

mainly expressed on immune cells, GI epithelium, and adipocytes

• GPR43 is upregulated in gut tissue of IBD patients

• GLPG0974 is a potent & selective antagonist of human GPR43

reduces migration of neutrophils

first inhibitor of GPR43 to be evaluated clinically

no animal models available

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‘974 mode of action SCFA induced neutrophil migration

• Inflammation

• Loose interactions between endothelial cells & neutrophils

• Neutrophil rolling

• Interaction CD11b with ICAM1

• Neutrophil adherence

• Neutrophil migration to site of inflammation by interaction with chemokines

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‘974 Results multiple ascending dose (MAD) study

Pharmacokinetics (Day 13) Pharmacodynamics (Day 13) Acetate-induced CD11b up regulation

Dose-proportional increase in exposure, 24 h inhibition at 200 mg BID

32 healthy volunteers, 4 cohorts, per cohort 6 active & 2 placebo

1

10

100

1000

10000

0 4 8 12 16 20 24

GLP

G09

74 (

ng/m

L)

Hours post dose

-60

-40

-20

0

20

40

60

80

100

0 4 8 12 16 20 24%

inhi

biti

on v

s pr

edos

e D

1 Time after last dosing (h)

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‘974 MAD study Conclusion

• Well tolerated and safe

no relevant treatment-emergent AEs

no relevant effects on lab safety parameters, ECGs and vital signs

• Excellent pharmacokinetics

good and dose-proportional exposure

terminal half life of 5.5 h

• Good pharmacodynamics

dose-dependent response

inhibition during 24 h, sustained over 14 days

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About ulcerative colitis

• Disease of the colon characterized by ulcers

• Intermittent disease with periods of exacerbated

symptoms, and relatively symptom-free periods

• Main symptom of active disease is constant diarrhea mixed with blood

• Peak incidence between 15 and 25 years

• Prevalence 200-250 per 100.000 individuals per year

• Total market value by 2021¹: $3.7 B

1 Source: Decision Resources

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‘974 PoC in ulcerative colitis

• 45 patients with mild to moderate ulcerative colitis

• 4 week dosing, 200 mg BID vs placebo

• Four countries: Belgium, Slovakia, Czech Republic, Latvia

• Evaluate safety & tolerability, characterize PK

• Explore efficacy & effects on selected biomarkers

mayo score, Partial Mayo score & histopathological Geboes index

faecal calprotectin, serum CRP, MPO in biopsies

Phase 2 PoC results expected Q1 2014

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R&D Portfolio

• GLPG0634

• GSK alliance

• GLPG0974

• GLPG0187

• Cystic Fibrosis

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‘187 vs Cilengitide

GLPG0187 Cilengitide

Small molecule Peptide

Highly potent in vitro cell assays Moderately potent in vitro cell assays Improvement in survival in animal model No effect on survival in animal model

Clinical i.v. dosing (continuous infusion) Clinical i.v. dosing (1h infusion 2x/wk)

Good clinical safety profile Good clinical safety profile

Comparative integrin receptor inhibition spectrum

Integrin binding affinity IC50 (nM) <10nM; 10-100nM; >100nM

αvβ1 αvβ3 αvβ5 αvβ6 αvβ8 α5β1

Cilengitide 11 6 5 122 436 30.5

GLPG0187 1 4 2 1 1 8

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‘187 status • Cilengitide (Merck-Serono)

missed primary endpoint Phase 3 study in GBM study

most advanced compound in class of RGD-integrin antagonists

GBM patients, MGMT-positive patients, on top of SOC

further analysis pending

• GLPG0187

enrollment completed for Phase 1b safety study

end-stage solid tumor patients

no treatment related adverse events

additional patients included following request of investigators

confirm early sign of clinical response in GBM patients

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R&D Portfolio

• GLPG0634

• GSK alliance

• GLPG0974

• GLPG0187

• Cystic Fibrosis

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About Cystic Fibrosis

• Fatal inherited disease of the lungs & digestive

system

• Debilitating disease, impairs quality of life

• Life expectancy: 37 years

• 70,000 patients worldwide, 30,000 in the US

• Patients carry a defective gene/protein (CFTR)

CFTR channel transports chloride across cell membrane

5 different classes of mutations

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Surface liquid allows cilia to efficiently clear mucus, particles and pathogens to maintain airway health

1. Dehydration of airway surface liquid

2. Mucus builds up on cilia, particles and pathogens become trapped

3. Lung infection

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Most CF patients are Class II (ΔF508) We target the main mutation

Representative genotype

W1282X ΔF508 G551D R117H D1152H

3849+10kb C→T

Allele frequency ~6% ~70% ~3% <2% <1%

Drugs in development PTC124 VX809+Kalydeco®

VX661+Kalydeco® Kalydeco® N/A N/A

Potentiator Potentiator + corrector

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Bring superior treatment to the patient

• Objective: superior combination of potentiator & corrector

• Testing cascade in place with state-of-the-art & gold standard technologies

• Learning from Vertex: Ussing chamber predicts clinical outcome

• 3 programs in hit-to-lead, new potentiator in lead optimization

• Programs proprietary to GLPG

CF programs on track to deliver PCC in 2013

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Galapagos CF potentiators Ussing chamber data

ΔF508-CFTR homozygous primary cells were grown for 21 days and corrected with 3 µM VX-809 for 48h Kalydeco®

GLPG 1 1 GLPG 2

Compound EC50 (nM)

Kalydeco® 133

GLPG 1 81

GLPG 2 129

ΔF508 patient cells G551D assay

Superior opening CFTR confirmed with GLPG series in Ussing chamber

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CF strategy

• Successful collaboration with CF Foundation

• First disease in which Galapagos will discover, develop and launch its own

medicines

• Bring best in class potentiator to G551D population

• Progress correctors in discovery to address the ∆F508 population

• Galapagos in strong position with own potentiator

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Our scientific achievements in 2012 Pre-clinical programs (1)

• Alliance with GSK: delivered fifth PCC

• Alliance with J&J: delivered second PCC

• Alliance with Servier:

delivered first PCC in osteoarthritis (OA) alliance

achieved milestones in OA & oncology alliance

• Alliance with MorphoSys: on track to deliver PCC in 2013

• Cystic Fibrosis: on track to deliver PCC in 2013

• Anti-infectives:

delivered first candidate antibiotic against MRSA strains

on track to enter the clinic in 2014

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Our scientific achievements in 2012 Clinical programs (2)

• GLPG0634 selective JAK1 inhibitor

Phase 2a data in RA patients

• GLPG0974: novel GPR43 antagonist

excellent results second Phase I trial

• GLPG0187: Integrin Receptor Antagonist for cancer metastasis

study extended to confirm early sign of activity

• GLPG0778/GSK2586184:

start Phase 2 studies in SLE and Psoriasis

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Therapeutic scope

Target finding Discovery Early development Phase 2

Lupus

Inflammation

Osteoarthritis

Infectious disease

Oncology

Inflammatory bowel disease

RA Psoriasis

Cystic fibrosis

Metabolic

Fibrosis

GLPG0187

= Clinical development by partner

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Achieving excellence in R&D • Our strengths

novel modes of action discovered in relevant human primary cells

expertise in inflammation, orphan, metabolic, anti-infectives

synergies with service division

speed of execution

• Our challenges

aim for therapeutic value

select the right diseases

progress the best targets

kill projects early

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First into humans in next 18 months

Project Partner 2013 2014 (preliminary)

GLPG1179 GSK

GLPG1205 Janssen

GLPG1332 Servier - OA

CAM-1 (GLPG1492) unpartnered

GLPG1577 GSK

GLPG1690 Janssen

Healthy volunteers Preclinical

Undisclosed

Undisclosed

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Clinical progress in 2013

Disease area Phase 1 Phase 2a

Rheumatoid arthritis

Inflammation

Metastasis

SLE

Psoriasis

GLPG0974

= Expected progress in 2013

GSK2586184*

= Inlicensed at Phase 1 by GSK

* GLPG code = GLPG0778

GSK2586184*

Phase 2b

GLPG0187

PoC GLPG0974

GLPG0634

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News flow 2013

• Start 2 Phase 2 studies

‘634 in RA

‘974 in ulcerative colitis

• Start 2 Phase 1 First-in-Human with new modes-of-action

• Delivery of PCC with potentiator in cystic fibrosis

• Delivery of more PCCs in the alliances and internal programs

• Presence at scientific conferences

‘634: EULAR, ACR

‘974: ASPET meeting

Three Phase 2 and multiple Phase 1 programs by end 2013

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R&D Update

• Company strategy Onno van de Stolpe, CEO

• R&D portfolio Piet Wigerinck, CSO

• 2013 Outlook Onno van de Stolpe, CEO

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Bright outlook for Galapagos

• Leadership in JAK1 space: two compounds in Phase 2 in three indications

• AbbVie deal & inlicensing by GSK highlight success of our approach

• Broad pipeline provides further opportunities for clinical success

both in internal and alliance programs

• Business model supports investment in promising proprietary programs

Galapagos in excellent position to build on its R&D strengths

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2015 and beyond

• Expected licensing of ‘634 by AbbVie brings in $200 M

• Multiple clinical programs being progressed by our partners

• Maturing proprietary pipeline with multiple clinical programs

• Shift model from early out-licensing to late stage internal development

Galapagos on track to be successful beyond GLPG0634

©Copyright 2013 Galapagos NV

R&D update Q&A

Onno van de Stolpe, CEO Piet Wigerinck, CSO 27 March 2013