TODAY’S SCIENCE TARGETING TUMOR DNA FUNCTIONS

TOMORROW’S NEW HOPE AGAINST RESISTANT CANCER LISTED EURONEXT │ Paris NASDAQ │ Copenhagen

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July 2020 Developing disruptive therapies in the field of DNA Damage Response (DDR) to address unmet needs in oncology

STRONG MANAGEMENT & OPERATIONAL TEAM DIFFERENTIATED SCIENCE IN A highly skilled team of 30, with strong translational DNA DAMAGE RESPONSE & clinical expertise, led by experienced management PlatON™, proprietary chemistry platform of and board of directors with demonstrated track oligonucleotides, generating new compounds record in product & business development AsiDNA™, lead candidate at clinical stage, a first-in-class decoy agonist with a unique ability to abrogate resistance to targeted therapies OX401, a newly optimized PARP agonist with NEXT KEY MILESTONES FUNDED potent activity on tumor control and immune Financial visibility to Q1 2022 supports response strategic plan to deliver key near-term clinical milestones

LISTED A WELL-DEFINED BUSINESS MODEL EURONEXT │ Paris Create value by bringing drug candidates from NASDAQ │ Copenhagen preclinical stage to proof-of concept in man, EPA: ONXEO the best inflection points to monetize these assets and generate revenues.

July 2020 3 Experienced management team with demonstrated track record in product & business development

JUDITH GRECIET (PHARM.D) (Pharmacia, Wyeth (Pfizer), Eisai) Formerly President of Eisai France CEO

FRANCOISE BONO (PHD) NICOLAS FELLMANN CSO CFO (Sanofi, Evotec) (Ernst & Young, Pfizer) Formerly Executive Vice-President Oncology Formerly Director of Treasury, Tax & of Evotec Audit of Pfizer France

OLIVIER DE BEAUMONT (MD) PHILIPPE MAITRE CMO EVP of Onxeo US, CBDO (Aventis, Quintiles, Stallergenes Greer) (Aventis, PPD, Oscient, mAbRx) Formerly Senior Vice President, Head of Global Formerly Chief Executive Officer and Co- Clinical Development, Pharmacovigilance and Founder of mAbRx Medical Affairs of Stallergenes Greer

July 2020 4 platON™-derived compounds share a decoy-agonist mechanism of action providing a radically disruptive approach to cancer treatment

platON™, a versatile library of decoy-agonist oligonucleotides generating disruptive drug candidates

All candidates based on this mechanism of action  Active component hijack (decoy effect) and hyper-activate (agonist Double-stranded ADN fragment (oligonucleotide) effect) their therapeutic targets, leading to ineffective Variable sequence and length to optimize target binding & activation DNA functions, without inducing any resistance 2 compounds already derived from platON™, each very differentiated in terms of target and activity  AsiDNA™, first-in-class front runner, DNA repair inhibitor acting Linker upstream of the DDR cascade, with a unique ability to abrogate Tethered loop  acquired resistance to targeted therapies to prevent dissociation Vector When appropriate, OX401, next-generation compound targeting PARP and activating to facilitate tumoral & the immune response via the STING pathway nuclear uptake Other platON™-derived compounds under evaluation

July 2020 5 Current cutting-edge R&D pipeline with unique mechanisms of action in DDR

Programs OPTIMIZATION PRECLINICAL PHASE I PHASE Ib PHASE II

platON™ Proprietary Platform of GENERATION OF NEW COMPOUNDS TARGETING DNA FUNCTIONS Decoy Oligonucleotides

OX401 In-vivo proof-of efficacy

Next-gen PARPi + STING pathway activation

+ IO + DDR DDR OX401 + immunotherapy In-vivo proof-of concept

AsiDNA™ DRIIV Safety / Activity AsiDNA™ + chemotherapy DRIIV -1b Safety in combo/ Synergistic efficacy AsiDNA™ + PARPi Response REVOCAN DNA Damage Damage DNA Resistance abrogation AsiDNA™ + other targeted tx In vivo proof of concept Resistance abrogation/ prevention

Legend Completed or ongoing Planned short-term

July 2020 6 AsiDNA™

Unique Decoy-Agonist Mechanism of Action in DNA Damage Response AsiDNA™: a first-in-class product in DNA Damage Response (DDR)

A purpose-designed cholesterol-oligonucleotide conjugate

IP Active 32 bp DNA duplex Cholesterol Patent Protection Binding and activating DNA-PK and PARP (Composition of signaling enzymes 3’ 5’ Tumoral and nuclear uptake of the Matter on AsiDNA™ & Phosphorothioate substitutions at the 5’ and DNA mediated via a covalently 1 related compounds) 3’ ends to prevent degradation1 linked cholesterol molecule until 2031. Sequence non-homologous and not Extendable to 2036 immunogenic (CpG-free) with SPC & PTE. AsiDNA is not an RNAi therapy, thus avoiding 5’ 3’ Combination the toxicity issues of this class Loop patents up to 2040 Double-stranded 32 bp DNA is tethered with a loop to prevent dissociation2

1 Berthault N, et al. Cancer Gene Therapy (2011), 1-12, doi: 10.1038/cgt.2011.3 July 2020 2 Quanz M, et al. PLoS ONE. 2009 4(7), doi: 10.1371/journal.pone.0006298 8 AsiDNA™: a differentiated product in the clinically-validated field of DDR

AsiDNA™ mimics DNA breaks in the tumor cell (decoy), binds and hyperactivates the proteins (agonist) involved in the DDR cascade (sensing, signaling and repairing) …

… diverts them away from the true damage …., … leading to cellular death.

DDR inhibition is clinically-validated in oncology (PARPi*) Decoy-agonist mode of action avoids compensatory mechanisms, blocking the induction of resistance AsiDNA™ acts upstream of the DDR, enabling cytotoxic activity regardless of genetic context Cytotoxic activity is restricted to cancer cells, translating into an outstanding safety profile

Source : Quanz M, et al. Clin Cancer Res 2009 15:1308-1316; Quanz M, et al. PLoS ONE. 2009 4(7), doi: 10.1371/ journal.pone. 0006298; Jdey W, et al. Clin Can Res. 2016;22:DOI: 10.1158/ 1078-0432.CCR-16-1193 July 2020 * PARP inhibitors (PARPi) are a leading class of targeted therapies, the first approved and marketed in the field of DDR 9 An extensive preclinical program paves the way to ambitious clinical translation

In vitro data In vivo data

Safety profile  No cytotoxic activity in healthy cells  Very favorable data in tox. study (monkey)

Autosensitization and no  Confirmed resistance observed  In multiple cell lines

 In multiple PARPi sensitive & resistant cell lines  AsiDNA™ increases survival & responders Efficacy synergy with PARPi  No restriction to specific genetic context to PARPi

Efficacy synergy with chemo  In multiple cell lines  AsiDNA™ increases efficacy & survival

Abrogation of resistance to PARPi  In multiple cell lines  AsiDNA™ stops resistance to PARPi

Abrogation/ prevention of Prelim. data confirmed prolongation of Ongoing validation with several TKI, KRASi, … resistance to other targeted tx anti-EGFR, anti-ALK efficacy

July 2020 PARP inhibitors (PARPi) and tyrosine kinase inhibitors (TKI) are leading, approved targeted therapies in oncology 10 AsiDNA™ full clinical potential overview

Potential indications Market size1 (incidence 2020)

 S Combo with carboplatin Neoadjuvant treatment for locally advanced triple TNBC local/regional disease : 116 000 pts negative breast cancer y • Improve response / dur. of response  N 1L / 2L (platinum-sensitive) treatment of advanced Advanced OC : 42 000 pts (*) • Preserve sensitivity to platinum ovarian cancer E  1L advanced Non-small cell lung cancer treated with R platinum Advanced NSCLC, w/o mutations : 179 000 pts G Combo with PARPi  1L/2L treatment of gBRCAm, HER2-, metastatic Advanced HER2- BC : 119 000 pts • Improve response / dur. of response breast cancer (w/ ola and/or Talazo)  gBRCAm = 11 000 pts Y • Enlarge addressable population  2L treatment of metastatic castration-resistant mCRPC : 98 000 pts (BRCAwt) prostate cancer, HRR gene mutated (w/ olaparib) E  gBRCAm = 13 000 pts C N  1L / 2L maintenance of advanced ovarian cancer (w/ Advanced OC : 42 000 pts A Combo with PARPi ola/ nira/ rucaparib) • Delay time to progression under T  1L maintenance of gBRCAm metastatic pancreatic mPaC : 119 000 pts (*) S PARPi (maintenance) cancer (w/ olaparib)  gBRCAm = 6 000 pts I Combo with targeted therapies S  1L treatment of EGFR+ Non small cell lung cancer (w/ E • Delay time to progression Advanced NSCLC, EGFR+ : 111 000 pts R anti-EGFR TKI and/or other TT)

July 2020 1: source GlobalData for 8MM countries (US, 5EU, JPN, CHN) except (*) without CHN. Current clinical program: delivering the promises of AsiDNA™ to patients

Safety Validation / Proof-of-Mechanism in man DRIIV-1 Phase 1  Favorable safety via I.V. First IV administration in solid tumors  Proof of mechanism in tumors Safety Validation in Combo / Efficacy with Chemotherapies

Excellent safety in combination with carboplatin DRIIV-1b Phase 1b (IV)  Ongoing: Safety in combination with carbo + pacli Combo with carboplatin +/- paclitaxel   Ongoing: Preliminary signals of efficacy Abrogation of Acquired Resistance to Targeted Therapies

REVOCAN Phase 1b/2 (IV)  Ongoing: Abrogation of resistance to PARPi Relapsed ovarian cancer in addition to PARPi niraparib FPI expected Q3 2020 Under exploration Phase 1b/2 (IV) Non small cell lung cancer in addition to  Abrogation of resistance to targeted therapies other targeted tx (TKIs, …)

July 2020 12 DRIIV-1 Phase 1: Favorable safety profile & demonstrated proof-of- mechanism

Phase 1 study via IV route Proof-of-mechanism : Strong activation of γH2AX at Open-label, 3+3 dose escalation from 200mg to 1800mg cell level, reflecting DNA-PK pathway engagement 22 patients; 5 doses Study coordinator: Pr. C. Le Tourneau (Institut Curie) Objectives: to determine the safety and PK/PD profile of AsiDNA™ Activity, pharmacodynamic biomarkers (on tumor biopsies)

Primary objective reached: favorable safety outcome Pre-treatment Post-treatment AsiDNA™ 200mg, 400mg, 600mg: No drug-related serious adverse event (SAE) and no dose-limiting toxicity (DLT)

AsiDNA™ 900mg & 1300mg: 3 related SAEs, including 2 DLTs per dose

MTD was not reached 1 22 (11%) γH2AX: Readout of DNA-PK target engagement Non-related Patient 003-001 95% Adverse Events

Grade 1/2 Grade 3 Non-related 77% Grade 4

181 (89%) July 2020 DRIIV-1 results were presented at EORTC-NCI-AACR on 10/27/19 13 DRIIV-1b Phase 1b: Preliminary data confirm safety and efficacy signals

Cohort 1 AsiDNA™ 600 mg + carboplatin 3 pts Heavily treated patients with advanced solid tumors, progressing at inclusion No DLT and very good tolerance of the combination Disease stabilized (SD) in 2/3 patients for 5.5 mo. (TNBC 6th L) and 10 mo. (NSCLC 3rd L) Disease controlled with AsiDNA™ for significantly longer than with any of the prior treatment lines

Cohort 2 AsiDNA™ 600 mg + carboplatin + paclitaxel 6 pts Ongoing, 3 patients treated DSMB approved the next 3-patient step after reviewing the safety profile of the combination Topline results expected end 2020*

July 2020 * Timelines include Covid-19 impact to date, and may be further reviewed 14 AsiDNA™ ability to abrogate resistance to targeted therapies is a unique feature

“Resistance is the biggest challenge in cancer biology” (Paul Workman – ICR) AsiDNA™ abrogated acquired resistance to PARPi in preclinical studies, which supports its next clinical development in ovarian cancer in addition to niraparib Other applications are under exploration in indications with high unmet needs

Approval / Strategic objectives Targeted Indications Opportunity Full Market Size ❶ REVOCAN Optimal market access 2L with niraparib (PARPi) Short endpoint: PFS Combo w/ PARPi (fast, favorable P&R*) in ovarian cancer 2025/26 $6,7B (1)

❷ Combo w/ other Access large WW E.g. 1L with TKI or other Target specific population e.g. targeted therapies markets targeted tx in non-small with high risk of $16,9B (1) cell lung cancer progression for 1L NSCLC

July 2020 * P&R : pricing & reimbursement - (1) GlobalData (8MM) 15 Acquired resistance to PARP inhibitors evolves from drug-tolerant cells (DTC) vulnerable to AsiDNA™

Onxeo showed that resistance to PARPi evolves from DTC1 AsiDNA™ prevents resistance to PARP inhibitors by acting on DTC1 AsiDNA™ is dramatically more efficient on DTC than on parental* cells

olaparib AsiDNA™ Olaparib AsiDNA™ Drug Drug-tolerant cells Reactivation No activity pressure (dormant/quiescent/ (tumor recurrence) on DTC tolerant/persister… cells)

DTC eradication

 TME IC50 olaparib – parental cells: 5 M IC50 AsiDNA™ – DTC: 17nMM Tumor microenvironment (TME) TNBC model BC227 BRCA2 -/-

DTC are already an established cause2 of resistance to TKI** AsiDNA™ could effectively counter DTC-driven acquired resistance to a wide range of targeted therapies

* Parental cell: primary tumor cell - ** TKI : tyrosine kinase inhibitors 1 AACR 2020 - Acquired resistance to PARP inhibitors evolves from drug-tolerant persister cells vulnerable to AsiDNA™ July 2020 2 Sharma VS et al. Cell, 2010, 141-1: 69-80 16 AsiDNA™ abrogates acquired resistance to PARP inhibitors (class effect)

AsiDNA™ leads to niraparib-resistant cells eradication in ovarian cancer model, even if introduced only once resistance emerges (CA 125 increase) The REVOCAN study (REVersion of resistance in Ovarian Cancer with AsiDNA™ and Niraparib) was designed on the basis of these results

niraparib Introduction at CA125 increase 6×106 150 6 Emergence of (REVOCAN study protocol) 5×10 120 4×106 Resistant cells 6 Start of AsiDNA™ 90 3×10 Start of AsiDNA™ r 6 60 e 2×10 administration b 1×106 administration

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p ( 4 C e 8×10 Nira+Asi continuous 15 C 6×104 10 4 Nira+Asi at D34 4×10 5 2×104 0 0 Cell death 17 24 31 40 17 24 31 40 0 20 40 60 D D D D D D D D Days post treatment

UWB1.289 (Ovarian Cancer model – BRCA1-/-)

July 2020 Source: Onxeo, data on file 17 AsiDNA™ abrogates acquired resistance to PARP inhibitors

Results confirmed in vivo in a triple negative breast cancer model

MDAMB-436 (TNBC HR deficient - PARPi sensitive)

July 2020 Source: Onxeo, data on file 18 REVOCAN Phase 1b/2: Abrogation of resistance to PARPi niraparib in Ovarian Cancer

REVOCAN REVersion of resistance in Ovarian Cancer with AsiDNA™ and Niraparib

Collaboration with Gustave Roussy, PI Dr Patrica Pautier, supported by the Arcagy Gineco Network n= up to 26 patients, platinum-sensitive relapsed ovarian cancer under 2nd line of maintenance with niraparib > 6 months Inclusion at CA 125 increase (well established predictive biomarker of resistance in OC)

Primary objective: Safety run & CA125 decrease (GCIG criteria) Secondary objective: Efficacy: PFS (RECIST criteria) - OS

Study approved by the regulatory authorities in late May 2020 FPI expected from H2 2020 => Preliminary data by end 2020/early 2021 *

July 2020 * Timelines include Covid-19 impact to date, and may be further reviewed 19 AsiDNA™: First-in-class therapy designed to address a major challenge in oncology: resistance to treatment

Differentiated Decoy Agonist MoA in the clinically-validated field of DNA Damage Response Decoy Agonist MoA does not induce resistance

Clinical-stage asset Collaborations with top-academic centers Favorable safety profile incl. in combination (Institut Curie - Gustave Roussy – Oncopole Toulouse…) Proof of mechanism / signals of efficacy

Long IP (up to 2040) Depletes the drug-tolerant cells from which resistance to targeted therapies emerge

REVOCAN Phase 1b/2 to evaluate the addition of AsiDNA™ on the abrogation of acquired resistance to niraparib (to start Q3 2020)

July 2020 20 OX401

Next-generation compound targeting PARP with strong immune response activation

21 OX401 is a PARP agonist that triggers the immune response

OX401 binds PARP (decoy) and then hyperactivates the protein (agonist), diverting it away from its role in tumor DNA Damage Response and leading to a significant immune response

Untreated OX401 Potent PARP activation after OX401 treatment

PARylation (fluorescence microscopy)

Active 16 bp DNA duplex IP nd The 2 purpose-designed oligonucleotide from platON™ Patent Protection Double-stranded 16 bp DNA tethered with a loop to prevent dissociation until 2038 Genomic DNA length optimized to specifically bind and activate PARP (Composition of Matter of OX401 & enzymes related compounds) Optimized to be non-homologous and non- immunogenic (CpG-free) Extendable to 2043 Modified to enhance intracellular stability with SPC & PTE

PARP Inhibitors and DDR Summit 2020 : Introducing OX401, a Next Generation PARP Inhibitor Able to Exploit July 2020 Metabolic Vulnerabilities of Cancer Cells and Inducing a Potent STING Response 22 OX401 has a strong cytotoxic effect on cancer cells and does not induce any resistance

Lymphoma Based on a similar decoy agonist mechanism, U937 cell line Emergence of resistance to PARPi OX401 displays the same features as AsiDNA™ in terms of tolerance and absence of resistance

OX401 is as potent as a PARPi at short term BUT does not induce acquired resistance No resistance with OX401 High selectivity for tumor cells suggests a favorable tolerability profile in the clinical setting

Quantification of cancer cell survival

July 2020 23 OX401 has confirmed its potent anti–tumor efficacy in vivo

OX401 is more effective on tumor control than a reference PARP inhibitor, olaparib

Syngenic mouse breast cancer model - EMT6 (PARP)

July 2020 24 OX401 potentiates the antitumoral immune response in vivo

Strong activation of key markers of the immune response

Robust adaptive and innate immune response through the activation of the STING pathway

Next step : in vivo proof of efficacy in combination with checkpoint inhibitors

Syngenic mouse breast cancer model - EMT6 (PARP)

July 2020 25 *TILs : Tumor infiltrating lymphocytes Outlook

26 Short-term key clinical catalysts in 2020/ 2021

H1 2020 H2 2020 H1 2021 H2 2021

DRIIV-1b Tolerance in combination + first signals of efficacy AsiDNA™ + DRIIV-1b DRIIV-1b * * DRIIV-1b carboplatin +/- Enrolment resumed cohort 2 Final data paclitaxel (post Covid-19) Topline data

Reversion of Resistance REVOCAN Reg. REVOCAN phase 1b/2 * * REVOCAN approvals First data set Top line data AsiDNA™ + niraparib /FPI (1b part)

AsiDNA™ + TKI or Abrogation of resistance other targeted tx * In vivo validation Preclinical to support clinical proof-of-concept translation

PARP agonist + activation of immune response OX401 In-vivo Reg. tox study and full Preclinical proof of In-vivo validation validation of translational profile efficacy of combo w/ CPI OX401 profile Ready for FIM

July 2020 * Timelines include Covid-19 impact to date, and may be further reviewed 27 Financial resources in line with key development milestones objectives

Cash position of €7.3m at 03/31/2020 + €6m from transaction with Acrotech on 04/06/2020 + €7.3m from private placement on 06/09/2020 to Invus, new long-term shareholder, & Financière de la Montagne, historical shareholder Cash runway to Q1 2022

Dual listing Euronext Paris & Nasdaq Copenhagen Financière de la Montagne 13% ISIN: FR0010095596

Invus Shares outstanding 78.3m 11% Free float 76% Average Daily Volume 555,980 shares

YTD at 06/12/2020 At 06/11/2020

July 2020 HY 2020 results on September 17, 2020 28 Onxeo in 2020/21: Ready for success

platON™ platform generates promising compounds based on unique decoy agonist mechanism of action Each candidate is designed to target specific proteins involved in different DNA functions All display common features: no resistance from cancer cells and favorable safety profile

AsiDNA™, first-in-class DDR inhibitor addressing a major oncology challenge: resistance to targeted therapies Confirmed activity and favorable safety profile in man (DRIIV) REVOCAN phase 1b/2 major catalyst to demonstrate that AsiDNA™ added to niraparib reverses tumor resistance in ovarian cancer ; First study outcomes expected in the short term (end 2020/early 2021)

OX401 preclinical in vivo profile confirmed potent antitumoral activity and strong activation of the immune response Improved preclinical profile vs. PARPi and belongs to the very attractive and promising field of immune oncology Full preclinical package and clinical readiness expected mid 2021

Deep expertise in oligonucleotides and platON™ leading to optimized development plan Financial visibility to Q1 2022, well beyond key clinical catalysts for the Company

July 2020 29 Publications & back-up slides AsiDNA™ Publications (1/2)

Hyperactivation of DNA-PK by double-strand break mimicking molecules disorganizes DNA damage response. Quanz M et al. PLoS One. 2009, 4:e6298. Histone γH2AX and Poly(ADP-Ribose) as Clinical Pharmacodynamic Biomarkers, Redon CE et al. Clin Cancer Res 2010; 16(18) Comparison of distribution and activity of nanoparticles with short interfering DNA (Dbait) in various living systems. Berthault N. et al. Cancer Gene Ther. 2011, 18:695-706. Heat shock protein 90 (Hsp90) is phosphorylated in response to DNA damage and accumulates in repair foci. Quanz M. et al. J Biol. Chem. 2012, 287:8803-15. Preclinical study of the DNA repair inhibitor Dbait in combination with chemotherapy in colorectal cancer. Devun F et al. J Gastroenterol. 2012, 47:266-75. Pharmacokinetics and toxicity in rats and monkeys of coDbait: a therapeutic double-stranded DNA oligonucleotide conjugated to cholesterol. Schlegel A et al. Mol Ther Nucleic Acids. 2012, 1:e33. Distribution and radiosensitizing effect of cholesterol-coupled Dbait molecule in rat model of 5 glioblastoma. Coquery N et al. PLoS One. 2012;7(7):e40567. Resistance to PARP-Inhibitors in Cancer Therapy. Montoni A et al. Front Pharmacol. 2013; 4: 18. Kinesin KIFC1 actively transports bare double-stranded DNA. Farina F et al. Nucleic Acids Res. 2013, 41:4926-37. Inhibition of DNA damage repair by artificial activation of PARP with siDNA. Croset A et al. Nucleic Acids Res. 2013, 41:7344-55. DNA-PK target identification reveals novel links between DNA repair signaling and cytoskeletal regulation. Kotula E et al. PLoS One, 2013: 8(11):e80313. Colorectal cancer metastasis: the DNA repair inhibitor Dbait increases sensitivity to hyperthermia and improves efficacy of radiofrequency ablation. Devun F et al. Radiology. 2014, 270:736-46. A preclinical study combining the DNA repair inhibitor Dbait with radiotherapy for the treatment of melanoma. Biau J et al. Neoplasia. 2014, 16:835-44. An update on PARP inhibitors for the treatment of cancer. Benefif S et al. Dbait: An innovative concept to inhibit DNA repair and treat cancer. Biau J et al. Bull Cancer 2016; 103: 227–235 The DNA Repair Inhibitor DT01 as a Novel Therapeutic Strategy for Chemosensitization of Colorectal Liver Metastasis. Herath NI et al. Mol Cancer Ther. 2016 Jan;15(1):15-22. Targeting DNA Repair in Cancer: Beyond PARP Inhibitors, Brown JS et al. Cancer Discov December 21 2016 DOI: 10.1158/2159-8290.CD-16-0860 Targeting DNA repair by coDbait enhances melanoma targeted radionuclide therapy. Viallard C et al. Oncotarget 2016 Mar 15;7(11): 12927-36. First-in-human phase I study of the DNA repair inhibitor DT01 in combination with radiotherapy in patients in with skin metastases from melanoma. Le Tourneau C et al. Br J Cancer. 2016 June 24;114(11):1199-205. Potentiation of Doxurubicin efficacy in hepatocellular carcinoma by the DNA repair inhibitor DT01 in preclinical models. Herath NI et al. Eur Radiol. 2017 Oct, 27(10):4435-4444. Drug Driven Synthetic Lethality: bypassing tumor cell genetics with a combination of AsiDNA and PARP inhibitors. Jdey W et al. Clin Cancer Res. 2017 Feb 15;23(4):1001-1011 Micronuclei Frequency in Tumors Is a Predictive Biomarker for Genetic Instability and Sensitivity to the DNA Repair Inhibitor AsiDNA. Jdey W et al. Cancer Res. 2017 Aug 15;77(16):4207-4216.

July 2020 31 AsiDNA™ Publications (2/2)

The DNA Repair Inhibitor Dbait Is Specific for Malignant Hematologic Cells in Blood. Thierry S et al. Mol Cancer Ther. 2017 Dec;16(12):2817–27. Combining the DNA Repair Inhibitor Dbait With Radiotherapy for the Treatment of High Grade Glioma: Efficacy and Protein Biomarkers of Resistance in Preclinical Models. Biau J et al. Front Oncol. 2019 Jun 19;9:549 Moving From Poly (ADP-Ribose) Polymerase Inhibition to Targeting DNA Repair and DNA Damage Response in Cancer Therapy. Gourley C et al. J Clin Oncol. 2019 June 3 AsiDNA™ treatment induces cumulative antitumor efficacy with a low probability of acquired resistance. Jdey W et al. Neoplasia (2019)21, 863–871 Preclinical studies comparing efficacy and toxicity of DNA repair inhibitors, olaparib and AsiDNA, in treatment of carboplatin resistant tumors. Jdey W et al. Front. Oncol., 12 November 2019 | https://doi.org/10.3389/fonc.2019.01097

Posters Molecular analysis of the mechanism of action of AsiDNA™ brings new clues on DNA damage AACR 2013 response regulation Preclinical study of Dbait, an inhibitor of three DNA repair pathways, in breast cancer AsiDNA™, a novel DNA repair inhibitor to radio-sensitize aggressive medulloblastoma treatment subtypes ASCO 2015 First-in-human phase I study of the DNA repair inhibitor DT01 in combination with EORTC-NCI-AACR 2019 radiotherapy in patients with skin metastases from melanoma Phase I dose escalation study evaluating the safety, pharmacokinetics (PK) and AACR 2017 pharmacodynamics (PD) of AsiDNA™, a first-in-class DNA Repair Inhibitor, administered AsiDNA™ induces tumor sensitivity to PARP inhibitors in homologous recombination intravenously (IV) in patients with advanced solid tumors proficient breast cancer AACR 2018 AACR 2020 Virtual Meeting (Poster and audio online June 22-24, 2020) AsiDNA™ and HDAC inhibitors: A cross-potentiation team work to kill tumor cells Acquired resistance to PARP inhibitors evolves from drug-tolerant persister cells vulnerable Evolution of tumor cells under Dbait (AsiDNA) treatment results in “autosensitization” to AsiDNA™

AACR 2019 AsiDNA™ abrogates acquired resistance to PARP inhibitors Development of a Biomarker-driven patient selection strategy for AsiDNA™ treatment

July 2020 32 OX401 has a cytotoxic effect on cancer cells and no effect on healthy cells

Quantification of cell deaths

High selectivity on tumor cells suggests a favorable tolerability profile in the clinical setting

July 2020 33 CONTACTS Judith Greciet – CEO Nicolas Fellmann – CFO Françoise Bono – CSO Olivier de Beaumont – CMO

Tel: +33 1 45 58 76 00 COMPANY INFORMATION www.onxeo.com [email protected]