NEXT GENERATION IMMUNOTHERAPIES

NEOVACS

FEBRUARY 2015

BIO CEO INVESTOR CONFERENCE Miguel Sieler, CEO

2

Disclaimer

This presentation and the information contained herein does not constitute or form part of, and should not be construed as, an offer or invitation to sell or subscribe for, or a solicitation of any offer or invitation to acquire, dispose of or subscribe for, shares in NEOVACS ("the Company") in any country. The decision to buy or sell shares of the Company should be based solely on the documents which have been reviewed by the "Autorité des Marchés Financiers"(AMF). The AMF has a "Document de Référence" registered with the AMF under number R.14-074 on December 11, 2014 (available in French only). The publication of this presentation in certain countries may violate applicable regulations. With respect to the member states of the European Economic Area whichhave implemented the Directive 2003/71/EC of the European Parliament and the Council of November 4, 2003 (the “Prospectus Directive”), other than France, no action has been undertaken or will be undertaken to make an offer to the public of the securities referred to herein requiring a publication of a prospectus in any relevant member state (other than France). As a result, the securities may not and will not be offered in any relevant member state (other than France) except in accordance with the exemptions set forth in Article 3(2) of the Prospectus Directive, if they have been implemented in that relevant member state, or under any other circumstances which do not require the publication by NEOVACS of a prospectus pursuant to Article 3 of the Prospectus Directive and/or to applicable regulations of that relevant member state. The information contained therein does not constitute an offer for securities in the United States, Canada, Australia or Japan or in any other jurisdiction. This presentation should not be published, transmitted or distributed, directly or indirectly, in the United States, Canada, Australia or Japan. This presentation is not an offer for sale or a solicitation of offers to purchase NEOVACS securities in the United States. The securities of NEOVACS may not be offered or sold in the United States absent registration or an exemption from registration under the U.S. Securities Act of 1933, as amended. NEOVACS does not intend to register any portion of the offering in the United States or to conduct a public offering of securities in the United States. This presentation does not constitute an invitation or inducement to engage in investment activity under section 21 of the Financial Services and Markets Act 2000 and is for distribution only to persons who (A) are outside the United Kingdom, or (B) are qualified investors as described in section 86(7) of the Financial Services and Markets Act 2000 (being persons falling within Article 2.1(e)(i), (ii) or (iii) of Directive 2003/71/EC) and (i) have professional experience in matters relating to investments falling within the definition of "investment professionals" in Article 19(5) of the Financial Services and Markets Act 2000 (Financial Promotion) Order 2005 (the "Order"), or (ii) are persons falling within Article 49(2)(a) to (d) ("high net worth companies, unincorporated associations etc") of the Order, or (iii) to whom it may otherwise be lawfully communicated (all such persons together being referred to as "relevant persons"). This presentation is directed only at relevant persons and must not be acted on or relied on by persons who are not relevant persons. Any investment or investment activity to which this presentation relates is available only to relevant persons. This presentation contains forward-looking statements. No guarantee can be given as to any of the events anticipated by the forward-looking statements, which are subject to inherent risks, including those described in the Document de Référence registered with the Autorité des Marchés Financiers under number R.12-008 on March 30, 2012 and the Note d’Opération that was approved by the Autorité des Marchés Financiers on February 14, 2013, changes in economic conditions, the financial markets or the markets in which NEOVACS operates.

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Overview

1 2

3 4

CORPORATE HIGHLIGHTS CLINICAL AND PRECLINICAL PROGRAMS

APPENDIX FINANCIALS AND STOCK INFORMATION

4

Corporate Highlights

A CLINICAL-STAGE COMPANY DEVELOPING IMMUNOTHERAPIES FOR AUTO-IMMUNE AND CHRONIC DISEASES

Company University spin-off (Pierre and Marie Curie University) in 1993, Company formed in 2003. Seasoned leadership, 20-strong team including 6 Ph.D.s, headquartered in Paris.

Approach Active immunotherapy: using a patient’s own immune system to regulate inappropriate immune responses

Products Kinoids, new anti-cytokine therapeutic vaccines

Pipeline

3 products in immunology and inflammatory diseases and immuno-oncology:

1 clinical-phase product in Lupus

2 pre-clinical phase products in 3 indications (Age-related Macular Degeneration, solid tumors, allergy)

Markets Inflammatory and autoimmune diseases, allergies and cancers: billion dollar markets

Financials Public Listing on NYSE Alternext Paris since April 2010 (ALNEV, ISIN: FR0004032746)

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– VEGF-mediated diseases

– AMD: 1.4 million patients in the US, nearly 3 million in Europe(2)

– IFNα-mediated diseases

– Lupus: 1.5 million cases in the US alone(1), 1.2 million in China(2)

Lupus

Clinical Focus: Auto-Immune and Chronic Diseases

Notes: (1) Lupus Foundation of America (2) estimates for the seven major markets (USA, Japan, Germany, France, UK, Italy and Spain) and China, Datamonitor 2011

Current treatments: Corticosteroids, immunosuppressive drugs, biologics (monoclonal antibodies …)

IFNα-Kinoid

VEGF-Kinoid

BROAD TECHNOLOGY PLATFORM WITH APPLICATIONS IN SEVERAL INDICATIONS

Age-related Macular Degeneration & Solid tumors

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Treatment Resistance Creates Major Unmet Need

CDAI 70 (Week 30)

Accent I

MAJOR NEED FOR NEW TREATMENTS WHICH ARE NOT SUSCEPTIBLE TO REJECTION OR RESISTANCE

CDAI 70 (Week 26)

Charm

CDAI 100 and HBI* (Week 26)

Precise 2 – 3

Note: * CZP given open label after 6 months and HBI used

49% 57%

48% 59%

37% 53% 59%

Infliximab

Placebo

Adalimumab

Placebo

Certolizumab pegol

Placebo

100%

0%

100%

0%

100%

0% 6 12 18 6 12 6 12

Months Months Months

Loss of response to 3 monoclonal antibodies in Crohn’s Disease – Study by Professor M. Allez, M.D., Ph.D., Hôpital Saint-Louis, Paris

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Biologic Penetration Limited by High Prices

A MARKET WITH CONTINUED HIGH GROWTH POTENTIAL, ESPECIALLY FOR LESS COSTLY THERAPEUTICS, ESPECIALLY IN LUPUS

Note: (1) source: Datamonitor, August 2011

/ yr USA France/Europe

Enbrel (Amgen/Pfizer) 14 300 $ 14 861 €

Humira (Abbvie) 17 700 $ 15 118 €

Remicade (J&J/Merck) 20 390 $ 11 567 €

Benlysta (HGS/GSK) 30 540 $ 19 067 €

Drug (molecule) Pharma Sales (M$) Growth

Humira (adalimumab) ABBVIE 10,659 15,0%

Remicade (infliximab) J&J / MERCK 8,944 8,90%

Enbrel (etanercept) PFIZER/AMGEN 8,325 4,50%

Benlysta (HGS/GSK) GSK 229 130%

48%

18%

30%

22%

33%

25%

20%

USA Japan France Germany Italy Spain U.K.

Proportion of diagnosed patients receiving a biologic in 2010

Cost of treatment of selected biologics

2013 sales of top 3 anti-TNF biologics

Source: Corporate data, 2011 and Datamonitor Report on Benlysta

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Kinoid Technology: Vaccine-Like Approach to Treating Chronic Diseases

– Target multiple epitopes

– Blocking of overproduced cytokine, and its pro inflammatory effects

– Specific to cytokine: no cross-neutralization with other cytokines

– No blocking anti-antibodies (ADA)

– Broad and sustained efficacy

– T cell tolerance is NOT broken: no uncontrolled autoimmunity

The Kinoid is an immunogenic compound made of: T Cells generated by the carrier protein (KLH) bypass B cell tolerance to induce self polyclonal anti-cytokine antibodies:

Conjugation and

inactivation

Kinoid

Polyclonal antibodies to targeted cytokine

Targeted cytokine

Carrier protein

Components of active immunotherapy Immunization Stimulation of the body’s immune system

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Polyclonal antibodies

Kinoid Technology: Superiority of the Polyclonal Approach

INDUCING A SAFE AND EFFECTIVE POLYCLONAL RESPONSE FROM THE BODY’S OWN IMMUNE SYSTEM

Monoclonal antibodies:

– Injection of non-self Abs

– Abs bind to one specific epitope of the cytokine

– Risk of MAb rejection and loss of efficacy (Anti-drug Abs)

Current treatments

Monoclonal antibodies

Polyclonal antibodies:

– Self Abs generated by the patient’s immune system

– Abs bind to multiple epitopes of the targeted cytokine

– Better and sustained antibody efficacy

– Excellent tolerance

Neovacs treatment

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Kinoid Technology: Competitive Positioning vs. Monoclonal Antibodies

KINOIDS: A MAJOR BREAKTHROUGH WITH THE POTENTIAL TO SUPERSEDE MONOCLONAL ANTIBODIES

Fully human response: no risk of rejection

3 to 5 injections per year vs. once every 2 – 4 weeks

~ 1mg of protein/year vs. > 1g /year with mAbs

Binding to multiple epitopes vs. single epitopes

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Scientific Advisory Board New York, NY 12-13 February 2015

Pr. JACQUES BANCHEREAU, PhD

Président du SAB

• Director of immunological sciences The Jackson Laboratory for Genomics Medicine, At the UConn Health Center

• Baylor Institute for Immunology Research, Dallas, Texas, USA

Dr. VIRGINIA PASCUAL

• Director, Center for Inflammation and Autoimmune Diseases

• Director, Center for Personalized Medicine

• Adjunct Professor of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas

• Adjunct Professor of Pediatrics, Mount Sinai School of Medicine, New York, New York

• Adjunct Associate Professor of Biomedical Studies, Baylor University

Pr. MIRIAM MERAD, MD, PhD

• Professor Oncological Sciences and Medicine, Tisch Cancer Institute, New York

Pr. STEVE A GREENBERG, MD • Department of Neurology, Brigham and Women's

Hospital and Children's Hospital Informatics Program, • Harvard Medical School and Harvard-MIT Division of

Health Sciences and Technology, Boston, Massachusetts

Pr. BETTY DIAMOND, MD • Investigator & Head, Center for Autoimmune and

Musculoskeletal Diseases, The Feinstein Institute for Medical Research

• Professor of Molecular Medicine and Medicine, Hofstra North Shore-LIJ School of Medicine, Manhasset, NY

Pr. NAPOLEONE FERRARA, MD • Professor of Ophthalmology and Pathology Senior

Deputy • Director for Basic Sciences, UC San Diego Health System

- La Jolla, CA

Pr. LAURENCE ZITVOGEL, MD • Research Director at INSERM U1015, Gustave

Roussy Cancer Campus • Center of Clinical Investigations in Biotherapies of

Cancer (CICBT) 507, Villejuif, France

Pr. BERNARD LAUWERYS, MD, PhD

• Service de Rhumatologie, SSS/IREC/RUMA, Cliniques Universitaires Saint Luc & Université Catholique de Louvain

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Overview

1 2

3 4

CORPORATE HIGHLIGHTS CLINICAL AND PRECLINICAL PROGRAMS

APPENDIX FINANCIALS AND STOCK INFORMATION

13

Pipeline

TWO CLINICAL STUDIES TO BEGIN IN COMING MONTHS, OTHER TRIALS UNDER EVALUATION FOR NEAR-TERM LAUNCH

Preclinical Phase I Phase II Phase III

IFNα-Kinoid in SLE – Europe, Latin America, Asia

VEGF-Kinoid in AMD

VEGF-Kinoid in solid tumors

IL-4 Kinoid in allergies

Study design under evaluation

Phase I/II study results Q4 2011 Phase IIb launch mid 2015

IFNα-Kinoid in SLE– USA Phase I/IIa launch early 2016

TNF-Kinoid in RA and Crohn’s Disease

Most advanced program to launch in 2015/2016

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Systemic Lupus Erythematosus (SLE) or Lupus

A chronic auto-immune disease:

– Auto-antibodies

– Fluctuating disease course: relapses-remissions

– Can affect all organs (skin, kidneys, liver, heart)

– Accumulations of manifestations over time

– Increased mortality

Population:

– Young women: 15-40 Y, F:M ratio: 6-10:1

– Blacks>Asians/Hispanics>Caucasians

No curative therapy

– Largely undiagnosed

Prevalence:

– 0.05% of the general population

– USA: 500,000 (CDC) to 1.5 million (Lupus Foundation of America)

– Europe: 500,000

Source: adapted from Houssiau F 2008

Arthritis 84%

Serositis 36%

Nephritis 39%

Immune thrombocytopenia 5%

CNS inflammation 10%

Malar rash 58 % Photosensitivity 45%

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IFNα-Kinoid And The Market For SLE

MARKET THAT HAS LITTLE COMPETITION AND SIZEABLE GROWTH PROSPECTS

Source: 1 FDA / 2 Datamonitor Report on Benlysta 2014

Million dollars

Significant market

– US$ 3.5 billion estimate (2019)

– 18% CAGR potential by 2019

– GSK $3.6 bn takeover of HGS (Benlysta)

An unmet medical need

– Benlysta, first new drug in 50 years

– FDA: “marginal efficacy”1

– cost: 30 540 US$ per patient per year2

Market for lupus therapies 2010 vs. 2019

0

500

1 000

1 500

2 000

2 500

3 000

3 500

2010 2019

Generic & Offlabel Novel

Source: Datamonitor 2011

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Clinical Advisory Board November 2014 Boston, MA

Pr. BERNARD LAUWERYS, MD, PhD

• Service de Rhumatologie, SSS/IREC/RUMA, Cliniques Universitaires Saint Luc & Université Catholique de Louvain, Brussels

Pr. FRÉDÉRIC HOUSSIAU, MD

• Chief of Rheumatology Unit, SSS/IREC/RUMA, Cliniques Universitaires Saint Luc & Université Catholique de Louvain, Brussels

Pr. ERIC HACHULLA, MD

• Professor and clinical expert Centre Hospitalier

Universitaire de Lille; Centre de Référence des

Maladies Auto-immunes et Systémiques rares,

France

Pr. KIRYAKOS KIROU, MD, DSc, FACP

• Mary Kirkland Center for Lupus Research, New-York

• Director, Lupus Nephritis Program, Hospital for Special Surgery, New-York

Pr. JOAN MERRILL, MD

• , Professor of Medicine, Adjunct Professor, Oklahoma Medical Research Foundation; School of Pharmacy University of Oklahoma Health Sciences Center

• Medical Director of the Lupus Foundation of America, and member of the Systemic Lupus International Collaborating Clinics

Pr. VIBEKE STRAND, MD, FACP, FACR

• Clinical Professor, Adjunct, Division of Immunology

and Rheumatology of the clinical faculty at Stanford

University,

• Consultant in clinical research and regulatory affairs

Pr. RONALD VAN VOLLENHOVEN, MD

• Chief of the Unit for Clinical Therapy Research,

Inflammatory Diseases (ClinTRID) at the Karolinska

Institute, and of the Clinical Trials Unit Rheumatology

at the Karolinska University Hospital, Stockholm

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IFNα-Kinoid: Development Strategy

Preclinical studies of IFNα-Kinoid in lupus

Establish POC in mouse model

Toxicology in rabbits & monkeys up to 400mcg x5: no safety issue

No T cell response to IFNα

No cross-reactivity to IFNβ,γ, ω: preserved anti viral defences

2005 – 2009

Phase I/II study of IFNα-Kinoid in lupus: established POC in SLE patients

N = 28 SLE patients

Completed

2010 – 2011

Phase IIb study of IFNα-Kinoid in lupus in (Europe, Latin-America and Asia)

Preparation ongoing

Study expected to launch mid 2015

2015 – 2016

2016 – 2017 Phase IIb study of IFNα-Kinoid in lupus (USA)

Preparation ongoing

Study expected to launch early 2016

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IFNα-Kinoid Phase I/II Study Systemic Lupus Erythematosus (Lupus)

4 doses tested: Kinoid 30/60/120/240 mcg by intramuscular injection

3 injections, days 0-7-28

4th dose at week 12 for 50% of patients

Multicenter, Double blind, placebo controlled clinical trial, randomized 3:1

28 patients with moderate disease

Safety and tolerability

Immunogenicity

Evolution of biomarkers

Clinical Response

Evaluation criteria

The IFNα-Kinoid induces an immune response against IFNα in 100% of patients, with strong dose impact

Dose related and potent neutralisation of IFNα gene signature

Excellent safety profile

Results presented in November 2011 at the Conference of the American College for Rheumatology and published in Arthritis & Rheumatism 2013

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IFNα-Kinoid in Systemic Lupus Erythematosus (Lupus)

IFN-Kinoid Induction of high

levels of anti-IFNα

antibodies: dose dependent

AND Neutralizing Antibodies

Anti-IFNα antibodies

Neutralizing antibodies

An

ti-I

FN

an

tib

od

y G

MT

100

1000

10000

100000

0 50 100 150 200 250 300 350

35000 Dil-1

1000

10000

NC

50

(ge

om

etr

ic m

ean

)

60 mcg IFN-K 120 mcg IFN-K 240 mcg IFN-K Placebo

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IFNα-Kinoid in Systemic Lupus Erythematosus (Lupus)

THE POLYCLONAL ANTIBODY RESPONSE STRONGLY

NEUTRALISES ALL IFNα SUBTYPES

Neutralizing polyclonal anti-IFNα antibodies

IFNα

IFNα

IFNα

NEUTRALISATION STRONG

NEUTRALISATION WEAK

NO NEUTRALISATION

IFNα subtypes (10 U/mL)

Polyclonal antibodies from IFN-K vaccinated lupus patient (Dilution)

Monoclonal antibody anti-IFNa (concentration ng/mL)

A 2a 1/22475 <7.8

B2 1/8936 98

C 1/8857 >1000

D 1/9648 >1000

F 1/2493 329

G 1/10693 78

H2 1/9147 57

I 1/13354 >1000

J1 1/5270 >1000

K 1/16878 >1000

4b 1/10154 >1000

WA 1/10148 945

A 2b 1/22326 <7.8

Neutralized subtypes 13/13

+++

2/13: +++

5/13: +/-

21 Décembre 2014

IFNα-Kinoid in Systemic Lupus Erythematosus (Lupus)

106

105

104

103

102

101

Day 112 Day 168

P=0.003 P=0.015

P=0.004 P=0.081

P=0.014

Low IFNα signature= less severe disease

High IFNα signature = severe disease

• THE POLYCLONAL ANTIBODY RESPONSE IS STRONGER IN PATIENTS

WITH MORE SEVERE DISEASE

• HIGHER IS THE ANTIBODY RESPONSE,

STRONGER IS THE NEUTRALIZING

RESPONSE AND BETTER IN THE IMPROVEMENT

OF BIOMARKERS OF LUPUS ( SIGNATURE IFN,

C3)

Variable

IFNα Signature– High

IFNα Signature– Low

Patients n (%) 18 (66.7) 9 (33.3)

IFN gene Score

Median Range

12.2 4.69–23.9

1.2 0.5–1.97

SLEDAI 2000

Median IQ range

8 6–9.5

8 4–8

Serum dsDNA Ab (U/mL)

Mean ± SEM

153a ± 60 43 ± 31

Serum C3 (U/mL)

Mean ± SEM

832a ± 59 1199 ± 114

Serum C4 (U/mL)

Mean ± SEM

124a ± 16 224 ± 33

Low IFNα signature = less severe disease High IFNα signature= more severe disease

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IFNα-Kinoid in Systemic Lupus Erythematosus (Lupus)

HIGH IFNα SIGNATURE

LOW IFNα SIGNATURE

Healthy

Monoclonal Ab (ROSE)

Polyclonal Ab (Phase I-II IFN-Kinoid)

MAb: Clinical Efficacy

MAb: No clinical efficacy

IFNα-Kinoid: complete neutralisation of IFNα signature

POLYCLONAL ANTIBODIES NEUTRALIZE BETTER THE IFNα GENE SIGNATURE THAN MONOCLONAL ANTIBODIES, EVEN FOR SEVERE FORMS OF LUPUS

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IFNα-Kinoid in Systemic Lupus Erythematosus (SLE)

Polyclonal neutralizing anti-IFNα antibodies

IFNα

IFNα

IFNα

IN CONCLUSION: • Very strong antibody response (40x>TNF-Kinoid)

• Strong response neutralizing antibodies

• Those antibodies neutralize all 13 subtypes of IFNα, in contrast with monoclonal anti-IFNα antibodies (2 subtypes only are completely neutralized) • Higher production of binding and neutralizing antibodies in patients with more severe lupus • Improvement of disease biomarkers is correlated with the intensity and duration of the neutralizing response

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2014-2015 2016 2017

IFNα-Kinoid : Planned clinical studies

IFNα-Kinoid Phase IIb in lupus : EU, Asia and Latin America • Objectives : biomarkers and clinical efficacy • N = ~150 ; IFNα-Kinoid versus Placebo ; Double-blind, Randomized • FPI : Q3 2015 – Results end of 2016

2018

IFNα-Kinoid Phase I/IIa in lupus : USA • Objectives : Safety, Dose, Immunogenicity • N = 60 ; IFNα-Kinoid 60-360 µcg • FPI : Q1 2016 ; Results : Q1 2017

Launch of clinical studies with IFNα-Kinoid in other indications currently under evaluation

STRONG CLINICAL PORTFOLIO WITH IFNα-KINOID

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Comparison between TNF-Kinoid and IFNα-Kinoid: two different products

100

5100

10100

15100

20100

25100

30100

35100

40100

0 20 40 60 80 100 120 140 160 180

Mo

yen

ne

gé

om

étr

iqu

e d

es

titr

es

(Dil

-1)

Study Day

TNF-K-006540µg; 5 inj.

TNF-K-003360µg; 3 inj.

TNF-K-003360µg; 2 inj.

TNF-K-003180µg; 3 inj.

IFN-K-001240µg

Comparison of antibody levels induced by TNF-Kinoid in RA And by IFNα-Kinoid in Lupus

SIGNIFICANT SUPERIORITY OF IFNα-KINOID IN TERMS OF ANTIBODY RESPONSE AND NEUTRALIZING ACTIVITY

IFN-K

TNF-K

26

Preclinical studies of TNF-Kinoid in Rheumatoid Arthritis:

Proof of efficacy in mice with arthritis

No safety issue

Highly specific response to TNF

2003 – 2008

TNF-Kinoid: development strategy

2008 – 2010 Phase I/II study of TNF-Kinoid in Crohn’s Disease: establish POC in Crohn’s

N= 21 patients. Completed

2011 – 2012 Phase IIa study of TNF-Kinoid in Crohn’s Disease

N= 66 patients.

Study not conclusive due to interferences

2011 – 2012 Phase IIa study of TNF-Kinoid in RA: determine best dose and administration schedule

N= 40 patients.

completed

2013 – 2014

Phase IIb study of TNF-Kinoid in RA: demonstrate clinical efficacy of TNF-Kinoid in RA

N=140 patients

Study completed; results made available Q4 2014; primary end point not reached due to absence of neutralizing antibodies

2015 – 2016 Product back to bench

Understanding of reasons for failure

Depending upon findings, development of new formulation

Phase IIb in Rheumatoid Arthritis : Study Design & Main Features

Phase II, double blind, placebo controlled

Multicenter in Europe, 11 countries, 46 sites

140 RA patients will be enrolled in a 1:1 ratio

CRP>10, active disease

TNF K 540 mcg or placebo

Schedule: days 0, 7, 28, 49, 70

Stratification by age (18-50 and 51-75 ) and study site

Expected high screen failure rate about 60% Projected No of screened patients – 350

28

TNF-K-006 Study: Results & Conclusions

Good safety profile

There is an anti-TNF antibody response, moderate and transient

But no clinical efficacy is detected. no association between antibody level and clinical effect

Unequivocal result: balanced groups, no treatment interference, no undue placebo effect

No neutralizing activity of antibodies

Visit 7 (D 85) Visit 8 (D 113) Visit 9 (D 169)

DAS28-CRP (change from baseline)

TNF-Kinoid -1.42 -1.46 -1.78

Placebo -1.54 -1.51 -1.89

Visit 7 (D 85) Visit 8 (D 113) Visit 9 (D 169)

Number of patients at ACR20 (week 24)

TNF-Kinoid 47.8% 50.7% 57.8%

Placebo 46.5% 42.9% 52.4%

Conclusion

STUDY DOES NOT MEET EFFICACY IN SPITE OF ANTIBODY RESPONSE AND GOOD SAFETY

29

Lessons Learned from TNF-Kinoid Studies for IFNα-Kinoid Program

- IFNα animal model relevant - Much higher anti-IFNα antibody response: 20x higher than TNF-K - Neutralizing antibodies, dose dependent, in human - Neutralization of 13 subtypes of IFNα vs 2-7 with Mabs - Neutralization of IFN gene signature - Correlation between antibody levels and neutralization of IFN gene signature

TNF-KINOID STUDY RESULTS DO NOT PREDICT OUTCOME FOR IFNα-KINOID STUDY

Learning curve on active immunotherapy

- Good safety and tolerability of the product (5 clinical trials to date) - Highest antibody response obtained at highest dose + boost (TNF-K-003, 005 and IFN-K-001) - Possible interference of Kinoid with residual antibodies (TNF-K-005) - Neutralizing antibodies necessary to obtain clinical response ; simple presence of binding

antibodies not sufficient (TNF-K-006)

30

Programs of Preclinical Development

VEGF-Kinoid in Age-related Macular Degeneration (AMD)

– Very encouraging results had been obtained with a preliminary VEGF Kinoid

– Prevention of laser induced neo vascularization in mice

– Results presented at EVER conference in 20093

VEGF-Kinoid in solid tumors

– Very encouraging results had been obtained with a preliminary VEGF Kinoid

IL-4-Kinoid in allergies

– Preliminary studies indicate the potential to control allergic reactions thanks to a Kinoid targeting IL-44.

Note : 1Gringeri, 1999 2Teijaro et al. 2013 ; Wilson et al. 2013, 3 European Association for Vision and Eye Research (EVER) 2009, September 30-October 3, Portoroz, Slovenia. Abstract 4352 4 Le Buanec, 2007

Preclinical POC with VEGF-Kinoid: In Vivo Qualitatives Analyses of CNV

D 6

140 ‘’

40 ‘’ 150 ‘’

50 ‘’

D 13

Placebo VEGF-Kinoid

IMMUNIZATION WITH VEGF-KINOID REDUCES LASER INDUCED CHOROID NEOVASCULARISATONS

European Association for Vision and Eye Research (EVER) 2009, September 30-October 3, Po

VEGF-Kinoid in Tumor Growth Inhibition

Tu

mo

r vo

lum

e (c

m3)

0

0,5

1

1,5

2

D 21 D28 D 35 D42

bevacizumab + Paclitaxel

PBS

Anti-VEGF IgGs + Paclitaxel

Ab-induced inhibition of tumor growth in xenografted immunodeficient mice. Effect of anti-VEGF IgGs (8 mg/kg) combined with paclitaxel (10 mg/kg) on HT29 tumor growth in NOD/SCID mice (2 × 105 cells; 10 mice per group, compared with effect of bevacizumab (5 mg/kg) combined with paclitaxel (10 mg/kg).

Proc Natl Acad Sci U S A. 2007 Feb 20;104(8):2837-42. Epub 2007 Feb 14. VEGF kinoid vaccine, a therapeutic approach against tumor angiogenesis and metastases. Rad FH, Le Buanec H, Paturance S, Larcier P, Genne P, Ryffel B, Bensussan A, Bizzini B, Gallo RC, Zagury D, Uzan G.

Abstract Tumor growth depends on blood supply, requiring the development of new vessels, and vascular endothelial growth factor (VEGF) plays a central role in neoangiogenic processes. For this reason, VEGF represents a target for the development of new therapeutic antiangiogenic molecules. Clinical trials using anti-VEGF mAbs such as bevacizumab have validated the efficacy of this therapeutic approach but have also revealed adverse effects. Here we report that a VEGF-derived immunogen, consisting of a heterocomplex of a murine (m)VEGF and keyhole limpet hemocyanin, called "mVEGF kinoid," triggered a strong Ab immune response in mice. The anti-VEGF Abs inhibited both the proliferation of human umbilical vein endothelial cells cultured in the presence of mVEGF and the binding of mVEGF to its receptor-2 Flk-1. In mVEGF kinoid-immunized BALB/c mice challenged with syngeneic CT26 colorectal tumor cells, the number and size of lung metastases were significantly decreased. In human (h)VEGF kinoid-immunized BALB/c mice, high levels of serum Abs to hVEGF were present, and purified IgG from these mice decreased by > or =50% the tumor growth of human A673 rhabdomyosarcoma cells and HT29 colon carcinoma xenografted in Swiss nude and NOD/SCID mice, respectively. Tumor cell growth inhibition was similar to that observed in mice receiving therapeutic doses of bevacizumab. These experiments suggest that a therapeutic vaccine containing VEGF kinoid may represent a strategy for safely combating VEGF-dependent neovascularization and metastases occurring in malignant tumors.

33

Shareholding structure and Stock information

NYSE Alternext Paris

ISIN code: FR0004032746

1.20 € (Closing January 30, 2015)

– Market cap: 28 M€

– Average Vol.: 748K shares / per day

– Number of shares outstanding: 23,006,310

7%

5%

77%

5% 3% 2%

Truffle Capital

Novartis Venture Fund

Free Float

OTC AM

Other historical investors

Founders

SHAREHOLDERS December 2014

Date Reco. Target price Upside

Kepler L. Labourdette 12/16/14 Reduce 1,80 € 50%

Invest Sec. M. Descoutures 01/05/15 Reduce 1,80 € 50%

CIC A Guekam 12/16/14 Sell 2,10 € 75%

Portzamparc A Guerin 12/16/14 Reduce 2,60 € 117%

Alpha Value A Moulin 01/11/15 Buy 1,71 € 43%

Edison J. Savin 07/11/14 - 1,70€ 42%

Consensus 01/30/15 1,95 € 63%

34

Financing

Cash and cash equivalents as of 06/30/2014: €2.8 million

Equity line arranged with Kepler Cheuvreux: up to €20 million in financing available

– 1st tranche : up to €7 million over the next 12 months (~9.9% of capital)

– 2nd and 3rd tranches : 2* €6.5 million from November 2015 onwards and over 18 months – to be drawn down only if needed

Other resources

– French Research Tax Credit – Q2 2015

– Possible Grants and subsidies

COMPANY FINANCING INSURED BEYOND S1 2015

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Investment Highlights

• Conjugate of inactivated cytokine attached to carrier protein, which acts to stimulate patient’s immune system to produce targeted polyclonal antibodies and block pathologic cytokine

• Major unmet need emerging from resistance to current treatments and high-price treatments

Proprietary Kinoid technology platform exhibits potential against chronic auto-immune and inflammatory diseases

• Broad therapeutic response ● Convenient treatment

• Long-lived efficacy ● Low cost

• High tolerance

Unique mechanism of action provides significant advantages over conventional treatments

• IFNα-Kinoid Phase IIb for lupus in EU, Latin America and Asia launching 2H 2015

• IFNα-Kinoid Phase I/IIa for lupus in the US launching 1H 2016

• Other clinical trials to be launched in short and mid-term

Lead product entering the clinic mid 2015/2016 with 2 trials in SLE

• Limited pharmaceutical competition

• SLE market to grow as new drug enter the market

• Product to be commercialized as specialty drug

Large commercial opportunity

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An experienced management team

MIGUEL SIELER Chief Executive Officer

• 32 years of an international career for Bayer, in 1998 he became Chairman and C.E.O of the Bayer Group in France until his retirement in 2008.

• Member of the board of Nexity S.A, Stratoz, Plasmaprime and Abivax, a biotech company focused on the development of innovative vaccines and antivirals.

• Master of Law from the University of Tubingen, Germany and graduated from the Institut d’Etudes Politiques de Paris, France.

BERNARD FANGET Vice President Pharmaceutical Development

• Bernard joined Neovacs in 2005, he was previously Senior Vice President, Pharmaceutical Development, of Flamel Technologies and Prior to Flamel was Corporate Vice President, Global Industrialization, at Sanofi Pasteur.

• Degree in biological chemistry from the University of Lyon, France.

OLIVIER DHELLIN Director of Pharmaceutical Development

• Olivier joined Neovacs in 2005. He previously held positions at Anosys (a US/French cell therapy biotech company), and research activities for 7 years at Gustave Roussy Institute (molecular biology and genomics) and Pasteur Institute where he was a post-doctorate fellow in molecular pharmacology. He had previously spent 4 years as a resident in several hospital departments (pediatrics, pharmacology and biochemistry).

• Degree in Pharmacy (Paris XI University, France) and a PhD in Virology (Pierre et Marie Curie University, France).

PIERRE VANDEPAPELIÈRE Chief Medical Officer

• Pierre joined Neovacs in June 2008 after 18 years as Head of Clinical Research and Early Development at GlaxoSmithKline Biologicals in charge of the clinical evaluation of early phase project. Prior to GSK Biologicals, Pierre was at ICI Pharmaceuticals from 1987 to 1990, working on cardiovascular products.

• Medical Doctorate from the Universities of Namur and Louvain-Brussels, a Postgraduate Diploma in Tropical Medicine from the Institute of Tropical Medicine of Antwerp and a PhD in Biomedical Medicine from the University of Ghent.

GERALDINE GROUARD-VOGEL Head of Research and Preclinical Development

• Géraldine joined Neovacs in 2005. She previously worked at Sanofi-Pasteur USA in bacterial vaccine development and as a researcher at the Walter Reed Army Institute of Research at the Seattle University.

• Degree in Pharmacy from Angers University (France) and did her PhD in Immunology with Dr Jacques Banchereau at Schering-Plough Lyon (France).

• She has authored several scientific publications in peer-reviewed journals.

NATHALIE THOMAS-PUJOL Head of Regulatory Affairs

• Nathalie joins Neovacs in 2014 after more than 20 years in the pharmaceutical industry in regulatory affairs and clinical research, such as head of Regulatory Affairs EMEA at Cephalon/Teva. Previously, she worked for 15 years at Sanofi-Aventis R&D.

• Pharmacist Doctorate from the University of Rouen in France and a PhD in toxicology from the University of Paris VII in France.

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Thank you & Contact

Nathalie TREPO IR manager 3/5 impasse Reille 75014 Paris Tel: +33-153-109-314 ntrepo@neovacs.com

Do not hesitate to contact us

Press - IR – U.S. - The Ruth Group Melanie Sollid-Penton 1.646.536.7023 msollid@theruthgroup.com