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1 ADVANCING INNOVATION TOWARDS BREAKTHROUGH CANCER THERAPIES LISTED EURONEXT Paris NASDAQ Copenhagen EPA: ONXEO

2 Important Information IMPORTANT: You must read the following before continuing. In accessing this document, you agree to be bound by the following terms and conditions. This document has been prepared by Onxeo SA (together with its subsidiaries, the "Group") and is for information purposes only. The content of this document is provisional and for information purposes only and is not to be construed as providing investment advice. The information, statements and opinions contained in this document (the Information ) are provided as of the date of this document only and may be subject to significant changes at any time without notice. Neither the Group, nor its advisors, nor any other person is under any obligation to update the Information. Subject to applicable law, none of the Company or its advisors accepts any responsibility whatsoever and makes no representation or warranty, express or implied, as to the fairness, accuracy, completeness or correctness of the Information. The Information has not been subject to independent verification and is qualified in its entirety by the business, financial and other information that the Group is required to publish in accordance with the rules, regulations and practices applicable to companies listed on Euronext Paris, including in particular the risk factors in the Company s Registration Document filed with the French Financial Markets Authority (Autorité des marchés financiers) under number D on April 24, 2017, in any other periodic report and in any other press release, which are available free of charge on the websites of the Group ( and/or the AMF ( This document contains information on the use of the Group's products and its competitive position. Some of the Information is from third parties. While this third party information has been obtained from sources believed to be reliable, there is no guarantee of the accuracy or completeness of such data. In addition, certain of the industry and market data comes from the Group's own internal research and estimates based on the knowledge and experience of the Group's management. While the Group believes that such research and estimates are reasonable and reliable, they, and their underlying methodology and assumptions, have not been verified by any independent source for accuracy or completeness and are subject to change without notice. Accordingly, undue reliance should not be placed on any of the industry, market or competitive position data contained in the Information. The Information is not directed to, or intended for distribution to or use by, any person or entity that is a citizen or resident of, or located in, any locality, state, country or other jurisdiction where such distribution or use would be contrary to law or regulation or which would require any registration or licensing within such jurisdiction. 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All statements in this document other than statements of historical fact are or may be deemed to be forward looking statements. These statements are not guarantees of the Group's future performance. These forward-looking statements relate without limitation to the Group's future prospects, developments, marketing strategy regulatory calendar, clinical milestones, assumptions and hypothesis, clinical development approach and financial requirements and are based on analyses of earnings forecasts and estimates of amounts not yet determinable and other financial and nonfinancial information. Forward-looking statements are subject to a variety of risks and uncertainties as they relate to future events and are dependent on circumstances that may or may not materialize in the future. Forward-looking statements cannot, under any circumstance, be construed as a guarantee of the Group's future performance as to strategic, regulatory, financial or other matters, and the Group s actual performance, including its financial position, results and cash flow, as well as the trends in the sector in which the Group operates, may differ materially from those proposed or reflected in the forward-looking statements contained in this document. Even if the Group s performance, including its financial position, results, cash-flows and developments in the sector in which the Group operates were to conform to the forward-looking statements contained in this document, such results or developments cannot be construed as a reliable indication of the Group's future results or developments. The Group expressly declines any obligation to update or to confirm projections or estimates made by analysts or to make public any correction to any prospective information in order to reflect an event or circumstance that may occur after the date of this document.

3 Bringing differentiated and disruptive DNA-targeting therapies through to Proof-of-Concept 3 DIFFERENTIATED SCIENCE AND BUSINESS MODEL targeting unique mechanisms of action in DNA-targeting and strategy to partner post proof-of-concept ROBUST IN-HOUSE TRANSLATIONAL & CLINICAL EXPERTISE including preclinical and clinical platforms ; important academic scientific collaborations PROMISING & GROWING PIPELINE including two product candidates & proprietary chemistry platform PlatON MULTIPLE NEAR-TERM CATALYSTS with preliminary clinical data expected in 2018 Developing disruptive DNA-targeting therapies for unmet treatment needs in oncology

4 A complementary and experienced management team 4 Judith GRECIET (Pharm.D) CEO since 2011 Formerly Wyeth, Eisai Eisai France President until 2011 Nicolas FELLMANN CFO Formerly Pfizer, Ernst & Young Françoise BONO (PhD) CSO Sanofi Oncology Evotec s EVP Oncology until 2016 Philippe MAITRE EVP Onxeo Inc., CBDO Leads the US subsidiary Formerly Aventis, PPD, mabrx Demonstrated track record in product development as well as business development Olivier DE BEAUMONT (MD) CMO Aventis, Quintiles Former SVP, Head of clinical development and medical affairs, Stallergenes Greer

5 Scientific Advisory Board : international experts in DNA-targeting 5 Marie Dutreix Ph.D., Director of Research (CNRS Institut Curie), Paris, France, co-founder of DNA Therapeutics and inventor of the signalinterfering DNA technology (sidna). Penny Jeggo Ph.D., Professorial Fellow at the Genome Damage and Stability Centre - University of Sussex, Brighton, United Kingdom. Josef Jiricny Ph.D., Emeritus Professor at the Institute of Biochemistry of the Swiss Federal Institute of Technology (ETH), Zurich, Switzerland. Tomas Lindahl Chair of Onxeo Scientific Advisory Board, FRS, FMedSci, Emeritus Professor at the Francis Crick Institute, London, United Kingdom. Joint recipient of the 2015 Nobel Prize in chemistry for his pioneering work on DNA repair mechanisms. Yves Pommier M.D., Ph.D., Chief of the Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, NHS- NCI, Bethseda, MD, USA. Sebastian Amigorena Ph.D., Head of the Immunology Department (INSERM U932, Cancer Immunity ) at the Institut Curie. Robert Bristow M.D., PhD., formerly Professor of the Departments of Radiation Oncology at the University of Toronto, Canada and recently appointed Director of the Manchester Cancer Research Centre, United Kingdom. Key scientific resource providing expertise, guidance and supporting Onxeo s goal of establishing a new paradigm for cancer treatment

6 Epigenetics DNA Break repair Inhibition Platform Leading-edge R&D Pipeline in DNA-targeting 6 Programs LEAD OPTIMIZATION PRECLINICAL PHASE I PHASE II PHASE III UPCOMING MILESTONES platon Proprietary chemistry platform of decoy oligonucleotides GENERATION OF DISRUPTIVE DNA-TARGETING COMPOUNDS New optimized compound to enter preclinical stage by end 2018 AsiDNA IV 1 Solid tumors April 2018 : FPI Phase I study Preliminary safety & activity results Q Final results H AsiDNA + PARPi Solid tumors Phase Ib/II PoC study in combination with PARPi ready to start Q AsiDNA + chemotherapy Solid tumors Phase Ib/II PoC study in combination with chemo ready to start Q AsiDNA IT 1 + radiotherapy Metastatic melanoma IT 1 proof-of-concept confirmed in DRIIM phase I study, combined w/ radiotherapy Oral belinostat + platon Solid tumors Considering combination with a new compound from platon with matching PK properties Beleodaq 2 + CHOP 3 PTCL 4 1 st line Phase III required by the FDA from SPPI 5 as MA holder in 2 nd line PTCL 4 1 IT: intratumoral IV: intravenous 2 Beleodaq : commercial brand name of belinostat (IV form) in the US in r/r PTCL 3 CHOP: Cyclophosphamide, Vincristine, Doxorubicine, Prednisone 4 PTCL : Peripheral T-cell lymphoma a rare form of blood cancer 5 SPPI : Spectrum Pharmaceuticals, Onxeo s partner and Market Authorization holder in the US for the use of Beleodaq in the treatment of PTCL in 2 nd line

7 ASIDNA A FIRST-IN-CLASS COMPOUND TARGETING TUMOR DNA BREAK REPAIR PATHWAYS

8 Targeting the tumor DNA Damage Response (DDR) to overcome resistance to DNA-damaging treatments 8 Endogenous DNA damage Tumoral genetic instability Exogenous DNA damage Chemo & Radiotherapy Many cancer treatments, or even tumor innate genetic instability, induce tumor DNA damage, which in turn leads to tumor cell death but tumor cells survive by repairing lesions to their DNA and overcoming the cell cycle checkpoints, leading to resistance. Tumor DNA Damage Response is a robust system with multiple & redundant repair pathways Single strand breaks Double strand breaks DNA-PK PARP ATR CHK1 CHK2 WEE1 cdc7 ATM DNA Damage Response proteins DNA Damage Response inhibitors (DDRi) Inhibition of one of the major DNA repair enzymes : PARPi, CHK1i, ATRi or Today, only targeted DDR therapies (targeting a single DDR pathway or protein) are developed: cancer is able to resist treatment by using an alternate pathway Repaired DNA : tumor cell survives & multiplies Tumor cell dies Tumor cell resists, survives & multiplies

9 AsiDNA : Unique approach to tumor DNA Damage Response (DDR) 9 Acquisition of a spin-off from the Curie Institute (2016) Acquired at the right time and at a low price for the tremendous potential of the acquired assets in the DDR field Lead product AsiDNA had already completed a successful phase I in patients with metastatic melanoma (local administration) and benefits from a strong intellectual property protection CHRISTOPHE LE TOURNEAU Head of Clinical Research, Department of Medical Oncology at the Curie Institute, Paris, Principal Investigator of the DRIIV phase 1 study of AsiDNA AsiDNA has a unique mechanism of action and the potential to provide patients with an attractive therapeutic option. DDR is a leading-edge research area, subject of the 2015 Nobel Prize in Chemistry; its joint recipient, Thomas Lindahl, chairs Onxeo s Scientific Advisory Board TOMAS LINDAHL Joint recipient of the 2015 Nobel Prize in Chemistry for his work on DNA repair, Emeritus Professor at the Francis Crick Institute, London. AsiDNA has a new and unique mechanism of action with the potential to bypass cancer cells resistance to treatment while sparing healthy cells. AsiDNA is currently developed for intravenous administration to harvest its full potential in the treatment of multiple solid tumors

10 AsiDNA : first-in-class product in DNA Damage Response base pairs DNA duplex with a 5 -Chol-TEG & a non-nucleotidic loop Cholesterol: Vector to promote cellular uptake IP Active 32 bp DNA duplex 3 5 Patent Protection (Composition of Matter on AsiDNA and related compounds) until Extendable to 2036 with SPC & PTE. Binds and activates DNA-PK and PARP signaling enzymes Sequence not specific, but chosen to be non-homologous and not immunogenic (CpG-free) Genomic DNA length optimized 5 Double-stranded 32 bp DNA is tethered with a loop to prevent disassociation 1 Phosphorothioate substitutions at the 5 and 3 ends to prevent degradation 1 Efficient nuclear uptake of the DNA is mediated via a covalently linked cholesterol molecule 2 Robust GMP manufacturing process scaled up to 1,7kg, long shelf stability 3 Loop: Coupling Agent No formulation needed to achieve sufficient plasmatic and tumor exposure in vivo after intravenous administration 1. Quanz M, et al. PLoS ONE (7), doi: /journal.pone Berthault N, et al. Cancer Gene Therapy (2011), 1-12, doi: /cgt

11 AsiDNA : The only agonist in development that disrupts and exhausts the ability of a tumor cell to repair its damaged DNA 11 AsiDNA is a fragment of double-strand DNA (oligonucleotide) acting as a decoy and an agonist of the DDR It mimics DNA breaks in the tumor cell, hyperactivates and then binds the DDR cascade of cellular events (sensing, signaling and repairing), diverting DDR proteins away from the true damage. 1,2,3 1 AsiDNA sends false alarms throughout the tumor cell nucleus and then activates and binds key components of the DNA Damage Response. 3 Actual tumor DNA damage is not repaired and accumulates: cancer cells die when dividing with a damaged DNA. 2 This sustained artificial DNA damage signaling (agonist effect) leads to exhaustion of the tumor DNA repair machinery However, AsiDNA is safe for healthy cells which stop dividing until the false alarm disappears. AsiDNA acting upstream of the DDR cascade, interferes with multiple DNA repair pathways 1. Quanz M, et al. Clin Cancer Res : ; 2. Quanz M, et al. PLoS ONE (7), doi: / journal.pone ; 3. Jdey W, et al. Oin Can Res. 2016;22:DOI: / CCR

12 AsiDNA IV route : Validated for clinical program expansion 12 Favorable safety profile Proof-of-mechanism and activity in man Preclinical package* indicating unique properties of AsiDNA alone and in combination Repeated treatment with AsiDNA leads to sensitization to AsiDNA and does not generate resistance Resistance to PARPi is prevented by co-treatment with AsiDNA Strong synergy of AsiDNA in combination with PARPi Strong synergy of AsiDNA in combination with carboplatin *Data submitted for publication to peer-reviewed journals

13 Mean volumes (mm3) Mean volumes (mm3) Comparison of the efficacy of single and combined treatments in MDA-MB-231 xenograft mice model (TNBC HR proficient tumor cells) Vehicle (NaCl 0.9%) AsiDNA TM (ip 25 mg) Carboplatin (ip) AsiDNA in combination with carboplatin: synergy in resistant Triple Negative Breast Cancer Randomization AsiDNA TM + Carboplatin Week 1 Week 4 Week 7 Endpoint 1500 mm Vehicle mean of volume vehicle mean volume DT01 mean AsiDNA volume carboplatin mean volume DT01+carboplatin* Carboplatin AsiDNA + Carboplatin Mean volume Mean volume Time after treatment (days) mean of volume vehicle mean volume DT01 mean volume carboplatin mean volume DT01+carboplatin* Time after treatment (days) 13 Synergy with mainstream DNA-damaging agents may improve therapeutic options in difficult-to-treat cancers

14 Repeated treatment with AsiDNA leads to sensitization to AsiDNA and does not generate resistance 14 Triple negative breast cancer - HR proficient (PARPi are ineffective on this cell line) AsiDNA Triple negative breast cancer - HR BRCA1 mutated BC227 AsiDNA Talazoparib Olaparib Small cell lung cancer NCI-H446 AsiDNA Talazoparib Auto-sensitization and no resistance with AsiDNA Survival (%/NT) Resistance 1 st cycle 2 nd cycle 3 rd cycle 4 th cycle Survival (%/NT) Resistance with PARPi Suggests a compelling opportunity as a maintenance therapy 0 Resistance 1 st cycle 2 nd cycle 3 rd cycle 4 th cycle * Source: Onxeo, data on file

15 Synergistic effect of AsiDNA + olaparib combined treatment in a Triple Negative Breast Cancer mice model 15 Comparison of the efficacy of single and combined treatments in MDA-MB-231 xenograft mice model (TNBC HR proficient tumor cells) olaparib 5x100mg/Kg/PO (6Ax) AsiDNA 3x15mg/IP + 3x25mg (10Ax) olaparib 5x100mg/Kg/PO & AsiDNA 3x15mg/IP + 3x25mg (10Ax) NT (6ax) Idem. CTL MD20 Randomization 1 week 2 weeks 3 weeks 4 weeks Endpoint 2000 mm 3 NT olaparib AsiDNA AsiDNA + olaparib CR=0/6 CR=2/6 CR= 4/8 CR= 5/7 CR rate 0% CR rate 33% CR rate 50% CR rate 71% CR : Complete Response Complete response more than doubled with combination treatment

16 AsiDNA : a very innovative compound that offers promising prospects in mono and combo-therapies to fight resistance 16 AsiDNA : a unique mechanism of action enabling a new approach to cancer treatment Innovative and very differentiated mechanism of action : agonist of DDR through decoy, impacting multiple DDR pathways Agonist effect that triggers DNA repair exhaustion in tumor cells leading to tumor cell auto-sensitization to AsiDNA Capacity to target cancer cells while sparing healthy ones Exhaustive and robust preclinical package showing product wide potential Potential as monotherapy supported by data on patients stratification, long-term effect, no occurrence of resistance Huge interest in combination with other therapies showing synergistic effect in terms of efficacy, prevention & reversion of resistance ( with chemotherapies, PARPis...) Potential to address multiple indications with high unmet needs (e.g. OC, TNBC...) Established proof-of-concept in patients Successful DRIIM* Phase 1 study of AsiDNA via intratumoral administration in combination with radiotherapy in patients with metastatic melanoma On-going DRIIV-1 Phase 1 study of AsiDNA via intravenous administration in patient with advanced solid tumors Source: * Le Tourneau et al. Br J Cancer May 24;114(11): ;

17 DRIIV-1 study Design & Cohort Status DNA Repair Inhibitor administered IntraVenously in patients with advanced solid tumors 17 PHASE I Open-label, dose escalation, phase I study Max. 36 patients 2 European countries: FR, BE 5 centers: Paris(2),Toulouse, Lyon, Brussels Study coordinator: Pr. C. Le Tourneau (Institut Curie) DSMB APRIL 2018 FPI 200 mg Dose Level 1 3 patients* 1-hour IV infusion 400 mg Dose Level 2 3 patients* Q PRELIMINARY RESULTS TOLERANCE, PK/PD, ACTIVE DOSE FINDING (TARGET ENGAGEMENT) COMPLETED 600 mg Dose Level 3 3 patients* 900 mg Dose Level 4 3 patients* 1800 mg 1200 mg Dose Level 6 Dose Level 5 3 patients* 3 patients* 5 Nov 2018: DL4 ongoing H FINAL RESULTS TREATMENT SCHEDULE OBJECTIVE - To assess the safety, pharmacokinetics and pharmacodynamics of AsiDNA DAY CYCLE 1 1-hour I.V. infusion ; cycle 1 : loading dose (day 1, day 2, day 3) then weekly dosing day 8 and day 15; cycle 2 & beyond : weekly dosing; 21-day cycles To determine dose-limiting toxicities (DLTs) and the maximum tolerated dose (MTD) To evaluate the pharmacokinetics/pharmacodynamics (PK/PD) effects of AsiDNA based on biomarkers of activity in blood and in tumor tissue (MN, УH2AX, phsp90, PARP activation) To assess the preliminary efficacy of AsiDNA CYCLE 2 and beyond : once a week * 3 additional patients if a dose limiting toxicity is found Compelling safety & activity results as early as dose 2

18 Mid-study results of DRIIV-1 : Favorable safety profile () 18 In DRIIV-1 ongoing study 10 patients - 200mg, 400 mg & 600 mg Dose proportionality for both Cmax and AUC No drug-related serious adverse events No dose-limiting toxicity Maximum tolerated dose not reached Only grade 1 & 2 drug-related adverse events Drug-related AE Grade 1 Grade 2 Favorable safety profile confirms positive regulatory toxicity studies No in-vitro genotoxicity Positive repeated in-vivo regulatory toxicity studies, incl. 4-week study in animal Maximum tolerated dose not reached Favorable safety profile at active doses providing a comfortable therapeutic window

19 Mid-study results of DRIIV-1 : Proof-of-Mechanism in man () 19 Analysis of the first 3 dose levels out of 6 planned 10 patients 4 biopsies available at baseline and end of cycle 2 Activity Target engagement confirmed by significant increase of activity biomarkers from dose level 2 and 3 = Proof-of-Mechanism of AsiDNA in man DL2 : 400mg Tumor proliferation biomarker KI67 DL3 : 600mg Tumor proliferation biomarker KI67 Activity biomarkers DL2 : 400mg gh2ax phsp90 Patient 0106 Activity biomarkers DL3 : 600mg gh2ax phsp90 Patient 0202 Patient 0106 Patient 0202 Patient 0109 Patient 0301 Patient 0109 Patient 0301 Significant increase after treatment with AsiDNA Major increase after treatment with AsiDNA Decrease or stabilization of tumor proliferation rate from dose level 2 and 3 Tumor status Robust target engagement in patients tumors demonstrates AsiDNA activity via IV route

20 AsiDNA : a highly differentiated molecule with promising prospects for development 20 AsiDNA : a unique mechanism of action enabling a new approach to cancer treatment Exhaustive and robust preclinical package indicating product wide potential Established proof-ofmechanism in man, strong activity, favorable safety Ready for expanded clinical development in combination H Initiation of Phase 1b/2 in combination with PARP inhibitors an/or DNA-damaging agents (chemotherapies) H Initiation of IND filing in the US

21 PLATON CHEMISTRY PLATFORM OF DECOY OLIGONUCLEOTIDES Leverage proprietary decoy oligonucleotides technology to generate new breakthrough compounds in oncology

22 platon : proprietary chemistry platform of decoy OligoNucleotides 22 All three components of the platform can be acted upon to obtain new compounds with different properties and/or activities 1 Oligonucleotide* 3 Vector 2 Linker Active component of the molecule Prevention of strand dissociation Spontaneous uptake by cells, no need for a transfection vector A powerful and versatile platform to generate disruptive compounds acting on intracellular DNA-binding targets * oligonucleotide: ADN fragment

23 platon : broad potential beyond AsiDNA with the opportunity to feed the pipeline with differentiated new drug candidates 23 Properties of AsiDNA, lead product from platon Unique mechanism of action (decoy role & agonist effect): blocks multiple repair pathways without inducing resistance mechanisms Enhancer of the antitumoral properties of DNA damaging agents Objectives for upcoming products from platon Regulation of tumor DNA functions through a decoy mechanism Decoy oligonucleotides able to induce cancer cell death and trigger immune response within the tumor, without any effect on healthy cells Clinical positioning clearly differentiated from the one of AsiDNA 1 Oligonucleotide Linker 2 3 Vector Evaluation of several compounds ongoing, some already under manufacturing Next candidate readiness for preclinical stage expected end 2018

24 FINANCIAL HIGHLIGHTS

25 Competitive landscape: DDR inhibition is gaining momentum MoA (Targeted Therapies) Name Company Phase 1 Phase 2 Phase 3 Launched Olaparib AstraZeneca PARP inhibitor Approved indications: Ovary, breast Chk1/2 inhibitor Combo: Chemo, RT, PARPi, IO ATR inhibitor Combo: Chemo, RT, PARPi, TKI DNA-PK inhibitor Combo: Chemo, RT ATM inhibitor Combo: Chemo, RT, PARPi Wee1 inhibitor Combo: Chemo, RT, PARPi Rucaparib Niraparib Talazoparib Veliparib Pamiparib Clovis Oncology Tesaro Pfizer AbbVie Beigene 2X-121 Oncology Ventures Fluzoparib MK-8776 Prexasertib GDC-0575 SRA737 ESP-01 AZD-6738 Jiangsu Hengrui Med. Merck & Co Eli Lilly Roche (Genentech) Sierra Oncology Esperas Pharma AstraZeneca M-6620 Merck KGaA M-4344 Merck KGaA BAY CC115 M9831 M3814 AZD-0156 AZD-1390 Bayer Celgene Merck KGaA Merck KGaA AstraZeneca AstraZeneca M-3541 Merck KGaA Adavosertib AstraZeneca AsiDNA differentiated approach: a decoy with agonist effect impacting multiple DDR pathways & amenable to combinations 25

26 Sustained interest from pharma companies for very innovative and promising early-stage projects in oncology 26 DNA-related projects are the new and upcoming field of interest, with the rarity of quality projects generating high deal values, on par with immuno-oncology 1200 $m total deal value $m total deal value Ph1 Ph2 Ph rd quartile st quartile Mean upfront payment ($m) Nb. of deals in Oncology AsiDNA field Deals with published financials / upfront 7/ 5 14/ 12 8/8 Phases I and II drive the highest deal values Source : Onxeo analysis based on Clarivate Cortellis database on licensing deals

27 All our studies to date support AsiDNA potential in broad indications* and combinations 27 with PARP inhibitors Synergistic efficacy observed in vivo, including in HR proficient tumors Potential indications: OC, TNBC, SCLC * Strong rationale for use as maintenance Pts US + UE with DNA-damaging chemotherapies 10 to 20% of all cancer patients are treated with platin-based chemotherapies Potential indication: SCLC* (ODD) 700,000 Pts US + UE as a monotherapy Selection of the best responding patients with stratification biomarkers 26,000 Pts US + UE with radiotherapy 50-60% of cancer patients treated with radiation therapy during the course of their disease DRIIM phase 1 study clinical signals of efficacy 2.3 Million Pts US + UE Unique mechanism of action positions AsiDNA at the heart of DDR strategies in oncology November 5,2018 * Targeted Population Company s Estimate HR: Homologous recombination - OC : Ovarian cancer TBNC : Triple negative breast cancer SCLC : Small cell lung cancer HCC : Liver cancer mcrpc : Metastatic castration-resistant prostate cancer mcrc : Metastatic colorectal cancer ODD: Orphan Drug Designation

28 A sound financial structure and a confirmed capacity to optimize financing options 28 Equity financing - Equity line June 2018 up to 5,4m - Private placement June 2017 ( 15m) Loan Royalty monetization through bond issuance June m Cash position of 13m at 30 September 2018 Grants and subsidies R&D tax credit repaid annually (30% of R&D expenses) 3.6m for 2017 Licensing agreements Signed contracts providing milestone payments in future years 1.6m received in 2018

29 Onxeo and the stock exchange 29 Onxeo share Dual listing Euronext Paris & Nasdaq Copenhagen Shares outstanding Fully diluted* ISIN: FR ,1m 58.6m Share price ( ) Change in the share price (20 months) Livatag US patent + 10th DSMB: anticipation of phase III results Livatag Phase III negative outcome Active market with new portfolio allocations at start of new year Volume (nb. of shares) Average Daily Volume (20 months) shares Mar-17 May-17 Jul-17 Sep-17 Nov-17 Jan-18 Mar-18 May-18 Jul-18 Sep-18 Nov-18

30 OUTLOOK

31 platon AsiDNA Near to mid-term value-creating R&D milestones 31 Q4 18 Predictive biomarkers for patient stratification H1 19 Plan to initiate phases Ib/II in combination (PARPi, platin, ) H Full data from DRIIV on tolerance, PK/PD, activity biomarkers and preliminary efficacy H2 19 Plan to initiate IND in the US Q H H From end-2018 onwards New compound from PlatON ready to enter preclinical

32 Onxeo - Advancing innovation towards breakthrough cancer therapies 32 A clear value-creation strategy based on AsiDNA & PlatON : drive innovative programs to best inflexion points and generate deals A robust in-house translational expertise to drive the development of optimal compounds R&D programs based on a First-in-Class mechanism of action, with multiple development paths and a wide potential of applications A proven capacity to generate transactions and enrich the pipeline

33 ASIDNA PUBLICATIONS

34 AsiDNA Publications (1/2) 34 Small-molecule drugs mimicking DNA damage: a new strategy for sensitizing tumors to radiotherapy. Quanz M, Berthault N, Roulin C, Roy M, Herbette A, Agrario C, Alberti C, Josserand V, Coll JL, Sastre-Garau X, Cosset JM, Larue L, Sun JS, Dutreix M. Clin Cancer Res. 2009, 15: Hyperactivation of DNA-PK by double-strand break mimicking molecules disorganizes DNA damage response. Quanz M, Chassoux D, Berthault N, Agrario C, Sun JS, Dutreix M. PLoS One. 2009, 4:e6298. Comparison of distribution and activity of nanoparticles with short interfering DNA (Dbait) in various living systems. Berthault N, Maury B, Agrario C, Herbette A, Sun JS, Peyrieras N, Dutreix M. Cancer Gene Ther. 2011, 18: Heat shock protein 90 (Hsp90) is phosphorylated in response to DNA damage and accumulates in repair foci. Quanz M, Herbette A, Sayarath M, de Koning L, Dubois T, Sun JS, Dutreix M. J Biol. Chem. 2012, 287: Preclinical study of the DNA repair inhibitor Dbait in combination with chemotherapy in colorectal cancer. Devun F, Bousquet G, Biau J, Herbette A, Roulin C, Berger F, Sun JS, Robine S, Dutreix M. J Gastroenterol. 2012, 47: Pharmacokinetics and toxicity in rats and monkeys of codbait: a therapeutic double-stranded DNA oligonucleotide conjugated to cholesterol. Schlegel A, Buhler C, Devun F, Agrario C, Urien S, Lokiec F, Sun JS, Dutreix M. Mol Ther Nucleic Acids. 2012, 1:e33. Distribution and radiosensitizing effect of cholesterol-coupled Dbait molecule in rat model of 5 glioblastoma. Coquery N, Pannetier N, Farion R, Herbette A, Azurmendi C, Clarencon D, Bauge S, Josserande V, Rome C, Coll JL, Sun JS, Barbier EL, Dutreix M, Remy CC. PLoS One, 2012, e Therapeutic approach of human peritoneal carcinomatosis with Dbait in combination with capnoperitoneum: proof of concept. Solass W, Herbette A, Schwarz T, Hetzel A, Sun JS, Dutreix M, Reymond MA. Surg Endosc. 2012, 26: Kinesin KIFC1 actively transports bare double-stranded DNA. Farina F, Pierobon P, Delevoye C, Monnet J, Dingli F, Loew D, Quanz M, Dutreix M, Cappello G. Nucleic Acids Res. 2013, 41: Inhibition of DNA damage repair by artificial activation of PARP with sidna. Croset A, Cordelières FP, Berthault N, Buhler C, Sun JS, Quanz M, Dutreix M. Nucleic Acids Res. 2013, 41:

35 AsiDNA Publications (2/2) 35 DNA-PK target identification reveals novel links between DNA repair signaling and cytoskeletal Regulation Kotula E, FaigleW, Berthault N, Dingli F, Loew D, Sun JS, DutreixM and Quanz M PLoS One, 2013, 8:e Colorectal cancer metastasis: the DNA repair inhibitor Dbait increases sensitivity to hyperthermia and improves efficacy of radiofrequency ablation. Devun F, Biau J, Huerre M, Croset A, Sun JS, Denys A, Dutreix M. Radiology. 2014, 270: A preclinical study combining the DNA repair inhibitor Dbait with radiotherapy for the treatment of melanoma. Biau J, Devun F, Croset A, Quanz M, Sayarath M, Sun JS, Dutreix M. Neoplasia. 2014, 16: Pressurized intraluminal aerosol chemotherapy with Dbait in the distal esophagus of swine. Khalili-Harbi N, Herath N, Solass W, Giger-Pabst U, Dutreix M, Reymond MA. Endoscopy 2015; 47:1-4. Chemosensitization of hepatocellular carcinoma by the novel DNA repair inhibitor DT01 in mouse and rabbit models. Herath N, et al., Submitted - European radiology (under review) Dbait : un concept innovant pour inhiber la réparation de l ADN et contribuer aux traitements des cancers. J Biau, F Devun, P Verrelle, M Dutreix, Bull Cancer 2016; 103: The DNA Repair Inhibitor DT01 as a Novel Therapeutic Strategy for Chemosensitization of Colorectal Liver Metastasis. Herath NI, Devun F, Lienafa MC, Herbette A, Denys A, Sun JS, Dutreix M. Mol Cancer Ther Jan;15(1): ASCO 2015 annual meeting. Abstract # First-in-human phase I study of the DNA repair inhibitor DT01 in combination with radiotherapy in patients in transit melanoma. Le Tourneau C, Dreno B, Kirova Y, Grob JJ, Jouary T, Dutriaux C, Thomas L, Lebbé C, Mortier L, Saiag P, Avril MF, Maubec E, Joly P, Bey P, Cosset JM, Sun JS, Asselain B, Devun F, Marty ME, Dutreix M. Br J Cancer May 24;114(11): Drug Driven Synthetic Lethality: bypassing tumor cell genetics with a combination of AsiDNA and PARP inhibitors. Jdey W, Thierry S, Russo C, Devun F, Al Abo M, Noguiez- Hellin P, Sun JS, Barillot E, Zinovyev A, Kuperstein I, Pommier Y, Dutreix M. Clin Cancer Res Feb 15;23(4): doi: / CCR Epub 2016 Aug 24. Micronuclei Frequency in Tumors Is a Predictive Biomarker for Genetic Instability and Sensitivity to the DNA Repair Inhibitor AsiDNA. Jdey W, Thierry S, Popova T, Stern MH, Dutreix M. Cancer Res Aug 15;77(16): doi: / CAN Epub 2017 Jun 6.

36 CONTACTS Judith Greciet CEO Nicolas Fellmann CFO Tel: COMPANY INFORMATION