ADVANCING INNOVATION TOWARDS BREAKTHROUGH CANCER THERAPIES

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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. 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3 INVESTMENT CASE

4 From cutting-edge science to breakthrough products 4 DIFFERENTIATED SCIENCE AND BUSINESS MODEL targeting unique mechanisms of action in DNA-targeting and strategy to partner post proof-of-concept ROBUST TRANSLATIONAL & CLINICAL CAPACITY including preclinical and clinical platforms and important academic scientific collaborations PROMISING PIPELINE Including two product candidates & proprietary chemistry platform PlatON MULTIPLE NEAR-TERM CATALYSTS with clinical data from Phase I trials expected in 2018 Developing disruptive DNA-targeting therapies for unmet treatment needs in oncology

5 Differentiated science and business model 5 Develop products to proof-of-concept/optimal inflection points, compelling to pharma partners, to optimize value and time to assets monetization Build a diversified pipeline with first-in-class programs Innovative programs in DNA Repair and epigenetics, two of the most sought-after areas in oncology platon, a unique chemistry platform of decoy oligonucleotides generating new DNA-targeting compounds Leverage deep translational expertise to minimize time and risks from preclinical to clinical Proven track record in executing value-creating business development-related transactions

6 A complementary and experienced management team 6 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, Evotec Evotec s EVP until 2016 Philippe MAITRE EVP Onxeo Inc., CBDO Leads the US subsidiary Formerly Aventis, PPD, mabrx Olivier DE BEAUMONT (MD) CMO Formerly Senior VP Stallergenes Greer, Quintiles, Aventis Demonstrated track record in product development and business development

7 BD Epigenetics DNA Break repair Inhibition Platform Leading-edge R&D Pipeline in DNA-targeting 7 Programs INDICATION PRECLINICAL PHASE I PHASE II PHASE III UPCOMING MILESTONES platon Proprietary chemistry platform of decoy oligonucleotides GENERATION OF NEW DNA-TARGETING COMPOUNDS Next compound H AsiDNA IV 1 Solid tumors Phase I filing Q4 17 Proof-of-Mechanism (PoM) in man end 2018 AsiDNA + PARPi Solid tumors Ready to initiate Proof-of-Concept (PoC) in man in 2018 AsiDNA + chemo/radio Solid tumors IT 1 PoC confirmed (DRIIM phase I study) Ongoing for IV AsiDNA + belinostat /HDACi Solid tumors Ready to initiate PoC in man in 2018 Oral belinostat Liquid & solid tumors Ready for clinical phase I 2018 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 Livatag Hepatocellular carcinoma Looking for a partner to explore other options (HBV, 1st line, combo ) 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

8 DNA Repair and Epigenetics 2 of the most sought-after mechanisms of action in oncology 8 $m total deal value 1,2 1, AsiDNA belinostat 3 rd quartile Median 1 st quartile $m total deal value Mean upfront payment ($m) Ph1 Ph2 Ph Number of deals: IO DNA Repair Epigenetics KI ADCC Reformulation Hormonal Other Nb. of deals in Oncology Deals with published financials / upfront 7/ 5 14/ 12 8/8 Phases I and II drive the highest deal values IO: immuno-oncology KI : Kinase inhibitors ADDC : antibody-dependent cellular cytotoxicity Onxeo s analysis based on Clarivate Cortellis (only licensing deals with publicly available financial information, excluding M&A /2017): ):

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

10 AsiDNA - A first-in-class compound in DNA break repair inhibition bp DNA duplex with a 5 -Chol-TEG & a non-nucleotidic loop Cholesterol: Vector to promote cellular uptake Active 32-bp DNA duplex Binds and activates DNA-PK and PARP signaling enzymes Sequence not specific, chosen to be non-homologous Genomic DNA length optimize Loop: Coupling Agent 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 Simple, elegant, unique and safe 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 - A mechanism of action unlike any other: DNA break repair inhibition through an agonist mechanism 11 Recruitment of DNA damage signaling and repair proteins to the sites of genomic damage is one of the early events in tumors DNA repair AsiDNA is a double stranded DNA molecule (decoy oligonucleotide) that mimics double stranded DNA breaks to interfere with tumor DNA repair, redirecting repair enzymes away from sites of tumor DNA damage 1,2,3 Tumoral cells (deficient cell cycle control) keep dividing with damaged DNA leading to DNA fragmentation and loss and then mitotic death. Healthy cells (proficient cell cycle control) stop dividing and reduce transcription then resume division once false signals disappear 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 Survival (%) AsiDNA anti-tumoral efficacy - Proof of concept studies 12 Proof of concept established in Phase I clinical trial : Intra-tumoral administration for metastatic melanoma + radiotherapy Overall response rate = 59% Complete response = 30% (CR from low-dose radiotherapy alone less than 10% 2 ) Partial response = 29% Durable response (up to 12-months follow-up period Before treatment 90 days after treatment *as measured by gh2ax phosphorylation AsiDNA therapeutic efficacy demonstrated after intravenous injection in a murine model of Triple Negative Breast Cancer Time post treatment (days)

13 AsiDNA - a potent enhancer of the anti-tumoral activity of double-strand DNA damaging agents 13 DNA damaging agents/epigenetic drugs Radiotherapy DNA targeting chemotherapies PARPi HDACi Genetic instabilities DNA damage DNA damage signaling AsiDNA ATM CHK1 PARP RAD51 ATR CHK2 MRN DNA-PK CANCER CELL CANCER CELL DEATH

14 Tumor volume (mm3) % of survival Synergistic effect of AsiDNA + olaparib combined treatment on TNBC HR proficient tumor xenograft model in mice 14 d-xx graft Endpoint XXmm3 Xenograft mice - HR proficient Breast Cancer model - AsiDNA (IT + SC, n=9) - olaparib (PO, n=8) - AsiDNA + Olaparib (n=9) - NT (n=8) Group I: NT Group II : AsiDNA (2x1mg IT+SC) Group III : olaparib (100mg/Kg PO) Group IV : AsiDNA (2x1mg IT+SC) + olaparib (100mg/Kg PO) Week 1 Week 2 Week 3 Week AsiDNA + olaparib AsiDNA Vehicle Olaparib 0 Treatment period Days post treatment Days after treatment Source: AACR 2017 AsiDNA induce tumor sensitivity to PARP inhibitors in homologous recombination proficient breast cancer, Wael Jdey et al.

15 Number of gh2ax Foci/cell Number of gh2ax Foci/cell % cells with MN % cells with MN AsiDNA and HDACi, a 2-way synergistic mechanism 15 HDAC inhibitors are potent DNA-damaging agents HDAC inhibitors induce histone hyperacetylation and ROS generation causing structural alterations in chromatin and thus exposing portions of DNA normally protected by heterochromatin from DNA damages belinostat induces a strong increase of DNA breaks and genetic instability on tumor cells, but not on healthy cells **** DNA breaks gh2ax quantification **** **** Genetic instability Micronucleus quantification **** 0 24h 48h 72h Time post Belinostat treatment (h) Tumor cell line MDA-MB ns ns ns 0 24h 48h 72h Time post Belinostat treatment (h) Healthy cell line MCF-10A *** **** 0 24h 48h 72h Time post Belinostat treatment (h) Tumor cell line MDA-MB ns ns ns 0 24h 48h 72h Time post Belinostat treatment (h) Healthy cell line MCF-10A AsiDNA increases belinostat-induced histone 4 acetylation in both tumor cell lines U937 MDAMB231

16 Survival (%) Survival (%) Survival (%) HDAC inhibitors demonstrate strong synergy in combination with DNA break repair inhibitor AsiDNA 16 Synergistic effect of belinostat combined with AsiDNA : Increased cell lethality in different tumor cell lines (MDAMB 231 and U937), no lethality observed in healthy cells (MCF-10A) MDAMB AsiDNA Belinostat AsiDNA + Belinostat % of cell survival [x IC50] AsiDNA Belinostat 80 AsiDNA + Belinostat U MCF [x IC50] AsiDNA Belinostat 100 AsiDNA + Belinostat Solid tumor cell line Liquid tumor cell line Healthy cell line AsiDNA Belinostat AsiDNA + Belinostat Same results obtained with vorinostat, entinostat and romidepsin [x IC50]

17 AsiDNA Development Strategy 17 IP Proprietary technology (Method of Use) patent until 2024 Drug product and related compounds protected until 2031 Confirm AsiDNA activity via systemic administration (IV) Biomarkers activity and stratification (micronuclei, g H2AX) Ongoing in vivo preclinical study in several tumors/combo (PARPi, HDACi ) First-in-man Phase I AsiDNA IV in advanced malignancies Confirm proof of mechanism in man, determine optimal clinical dose Translational clinical outcomes, relationship between exposure, activity & safety Clinical development program extension in solid / liquid tumors Phase I/II AsiDNA IV in combination with DNA damaging agents (PARPi, HDACi ) AsiDNA IV alone for genetically unstable tumors H CTA Filing Q First data in 2018 CTA filing in 2018 First data for end 2018 / early 2019

18 Scientific Advisory Board with International Experts in DNA-targeting 18 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 to provide expertise, challenge and guidance and support Onxeo s goal of establishing a new paradigm for cancer treatment

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

20 platon : Proprietary Chemistry Platform of Decoy Oligonucleotides 20 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 Trademark pending

21 platon : a broad potential beyond AsiDNA 21 Properties of AsiDNA 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 platon future products Target the regulation of tumor DNA functions through a decoy mechanism Generate decoy oligonucleotides able to induce cancer cell death and trigger immune response within the tumor without any effect on healthy cells platon upcoming products having a clinical positioning differentiated from AsiDNA 1 Oligonucleotide 2 Linker 3 Vector

22 platon : expanding Onxeo s ability to feed the pipeline with new candidates 22 Dedicated screening platform Decoy oligonucleotides library DRUG DEVELOPMENT AsiDNA, first drug candidate from platon to enter Phase 1 in Q DNA binding proteins Translational capabilities Best-in-class drug candidates Next compounds planned from H onwards Combine deep biology insight with leading translational expertise and capabilities in oncology to deliver new, best-in-class drugs

23 BELINOSTAT (BELEODAQ ) HDAC INHIBITOR

24 Beleodaq (belinostat IV ) already approved and marketed in Peripheral T-Cell Lymphoma (PTCL) 24 Peripheral T-cell lymphoma A subtype of non-hodgkin s lymphoma (NHL) which affects T-cells with 17,000 to 27,000 incident cases (1) in key pharmaceutical markets Regulatory status Beleodaq in PTCL Fast Track / Orphan Drug Designation (US & EU) ; FDA conditional approval in 2nd line PTCL in 2014 following successful Phase II Belief Study Commercialized in the US by Spectrum Pharma (SPPI) since July 2014 Clinical development Successful Phase II Belief Study (n = 129) (2) Pivotal for FDA conditional approval Favorable safety profile Successful Phase I study of Beleodaq + CHOP* (n=23) in 1 st line PTCL Next: Phase III clinical study of Beleodaq + CHOP in PTCL 1 st line FDA requirement post conditional approval in 2 nd line Under preparation by SPPI** (as market authorization holder in the US) Beleodaq is the brand name of belinostat via intravenous (IV) administration in PTCL in the US 1 International Peripheral T-Cell and Natural Killer/T-Cell Lymphoma Study, (J Clin Oncol 26 : ) and GLOBOCAN 2012, IARC data. 2 Lee et al (FDA approval) Clin. Cancer Res. March * CHOP: Cyclophosphamide, Vincristine, Doxorubicine, Prednisone ** Spectrum Pharmaceuticals

25 Belinostat Plasma concentration (ng/ml) Percent % Belinostat Oral Formulation Development 25 New formulation technology (Amorphous spray dried dispersion) Improved bioavailability by x4 increase patients access (outpatients) U DOG PK study 50mg/dog Oral solution API in capsule Spray Dried Dispersion Time (hours) MDAMB Bioavailability F% [AUC 0-12h ] 26% 7% 28% Oral Solution API in Capsule Spray dried dispersion IP belinostat oral formulation will extend IP protection until 2038 Significant potential competitive advantages over IV formulations

26 Belinostat Development Strategy 26 Confirm belinostat and AsiDNA combination synergistic efficacy In vivo preclinical testing in several tumor types PK/PD relationship in vivo First-in human Phase I belinostat + AsiDNA IV in advanced malignancies First phase I/II to assess safety and synergistic activity in man Confirm proof of mechanism, determine optimal clinical dose Translational clinical outcomes, relationship between exposure, activity & safety H CTA filing in 2018 First data end 2018 /early 19 Pursue oral formulation development once synergistic activity in combination is demonstrated Bridge between the oral form and the current IV one

27 FINANCIALS AND NEXT MILESTONES

28 Financials 28 Shares Dual listing Euronext Paris & Nasdaq Copenhagen - Ticker: ONXEO SHARES OUTSTANDING (10/31/17) Fully diluted AVERAGE DAILY STOCK TURNOVER (9 months 2017) MARKET CAP 50.7M 53,1M shares 1.6M +/-60M Financials CASH POSITION (09/30/17) 27.5M

29 Multiple near to mid-term value-creating R&D milestones 29 AsiDNA (IV) End 2017 Filing for a Phase I as monotherapy in solid tumors Early 2018 Results of ongoing in-vivo preclinical studies in other tumors/ combinations From H onwards Intermediate findings from phase I monotherapy Intermediate findings from phase I/II in combination (end 2018) End 2018 Phase I Proof-of-mechanism in man belinostat Early 2018 Results of ongoing preclinical studies in other tumors/ combinations 2018 Initiation of a phase I/II study in combination From H onwards Intermediate findings from phase I/II combo Development of belinostat oral platon platform From 2018 onwards New compounds targeting DNA functions through a decoy mechanism and their potential applications

30 Onxeo - Advancing innovation towards breakthrough cancer therapies 30 A clear value-creation strategy : drive innovative programs to best inflexion points and generate deals A robust translational expertise to drive optimal compounds development R&D programs based on 2 of the most promising mechanisms of action, with multiple development paths and wide potential of applications A proven capacity to generate transactions and enrich the pipeline

31 Appendices

32 AsiDNA Publications (1/2) 32 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:

33 AsiDNA Publications (2/2) 33 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.

34 belinostat/beleodaq Publications 34 Belinostat in Patients With Relapsed or Refractory Peripheral T-Cell Lymphoma: Results of the Pivotal Phase II BELIEF (CLN-19) Study. (O Connor, O.A., et al., 2015, J Clin Onc, 33(23), Safe and Effective Treatment of Patients with Peripheral T-cell Lymphoma (PTCL) with the Novel HDAC Inhibitor, Belinostat, in Combination with CHOP: Results of the Bel- CHOP Phase 1 Trial. (Johnston, P., et al., ASH 2015). A Phase II trial of Belinostat (PXD101) in patients with relapsed or refractory peripheral or cutaneous T -cell lymphoma. (Foss, F., et al., 2014, BJH) A phase 1 pharmacokinetic and pharmacodynamic study of the histone deacetylase inhibitor belinostat in patients with advanced solid tumors. (Steele, N. L. et al, Clin Cancer Res, 2008; 14(3): ) A Phase I clinical trial of the histone deacetylase inhibitor belinostat in patients with advanced hematological neoplasia. (Gimsing, P., et al., 2008, Eur J Haematol, 81: ) Phase II activity of belinostat (PXD-101), carboplatin, and paclitaxel in women with previously treated ovarian cancer. (Dizon, D.S, et al., Int J Gynecol Cancer, 2012) A Phase I/II Clinical Trial of Belinostat (PXD101) in Combination with Doxorubicin in Patients with Soft Tissue Sarcoma. (Vitfell-Rasmussen, J., et al., 2016, Sarcoma) Paclitaxel/Carboplatin With or Without Belinostat as Empiric First-Line Treatment for Patients With Carcinoma of Unknown Primary Site: A Randomized, Phase 2 Trial. (Hainsworth, J.D., et al., 2015, Cancer, 121(10), ).

35 Livatag : Publications 35 Doxorubicin-loaded nanoparticles: increased efficiency in murine hepatic metastases. (Chiannilkulchai, N et al. Sel Cancer Ther, (1): p ) Doxorubicin-loaded nanospheres bypass tumor cell multidrug resistance. (Cuvier, C., et al. Biochem Pharmacol, (3): p ) Phase I clinical trial and pharmacokinetic evaluation of doxorubicin carried by polyisohexylcyanoacrylate nanoparticles. (Kattan, J. et al. Investigational New Drugs 10: , 1992.) Enhanced cytotoxicity and nuclear accumulation of doxorubicin-loaded nanospheres in human breast cancer MCF7 cells expressing MRP1. (Aouali, N., et al. Int J Oncol, (4): p ) Increase of doxorubicin sensitivity by doxorubicin-loading into nanoparticles for hepatocellular carcinoma cells in vitro and in vivo. (Barraud, L., et al. J Hepatol, (5): p ) A randomized phase II trial of Doxorubicin-Transdrug (Livatag ) demonstrates significant overall survival increase in inoperable hepatocellular carcinoma (HCC) patients. Merle, P. et al (In Book of abstracts) Doxorubicine-Transdrug (Livatag ) apporte un bénéfice significatif sur la survie des patients porteurs d'un carcinome hépatocellulaire (CHC) palliatif : essai de phase 2 randomisé. Merle, P. et al (In Book of abstracts) A randomized phase II trial of Doxorubicin-Transdrug (Livatag ) demonstrates significant overall survival increase in inoperable hepatocellular carcinoma (HCC) patients. Merle, P. et al Hepatology. Dose and infusion rates drive lung toxicity of Doxorubicin Transdrug (DT) in rats. Merle, P. et al (In Book of abstracts) A multicentre, randomised, open-label study comparing the efficacy and safety of two doses of Doxorubicin Transdrug to Best Standard of Care in patients with advanced Hepatocellular Carcinoma (HCC) after sorafenib. The ReLive study. Merle, P. et al. J Hepatol, Supp.2 Vol. 62(P1334): S856 Efficacy and safety of intra-arterial hepatic infusion of doxorubicin transdrug nanoparticules in hepatocellular carcinoma. Merle, P. et al. Ongoing. Annals of Oncology Mechanistic study of the relative cytotoxicity of doxorubicin loaded nanoparticle formulation compared to free doxorubicin in hepatocellular carcinoma (HCC) cell lines. Trochon- Joseph, V et al. AACR 2016, Abstr nr 2143 A novel nanoparticle formulation of doxorubicin is clearly differentiated from free doxorubicin in overcoming resistance mechanism in chemo-resistant tumors. Trochon-Joseph, V et al. AACR 2017, Abstr nr 3076 Safety and efficacy results from the phase 3 relive study of doxorubicinloaded nanoparticles versus best standard of care in patients with advanced hepatocellular carcinoma after failure or intolerance to previous treatment including sorafenib, P. Merle et al, (O-020) (Summary of key findings on Onxeo s website - )

36 CONTACTS Judith Greciet CEO Nicolas Fellmann CFO Tel: contact@onxeo.com COMPANY INFORMATION