Developing breakthrough therapies in NASH and mucopolysaccharidosis

Corporate Presentation June 2019 DISCLAIMER

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Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 2 Inventiva investment highlights

Clinical stage biotech with focus on oral small molecules for high unmet need in fibrosis, lysosomal storage disorders and oncology

Two unencumbered late stage assets in two high value indications – Lanifibranor – only pan-PPAR agonist in clinical development for NASH, Phase IIb data due H1 2020 – Odiparcil – first orally available therapy for MPS, Phase IIa data due H2 2019

State of the art R&D capabilities including wholly owned ‘pharma scale’ discovery facilities

Portfolio underpinned by discovery engine focused on nuclear receptors, transcription factors and epigenetic targets with a 240,000 compound library, 60% of which are proprietary

Compelling early stage pipeline leveraging power of discovery engine in fibrotic disease and oncology, supported by validating partnerships with AbbVie and Boehringer Ingelheim – ABBV-157 RORγ program: first phase I completed and second one in 60 healthy volunteers and patients with chronic plaque psoriasis due to start in May 2019 – YAP-TEAD program in late pre-clinical stage, clinical candidate selection expected in 2019

Strong US and European shareholder base and experienced senior management team with a track record of operational and scientific excellence

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 3 Validated oral small molecule-focused discovery engine targeting nuclear receptors, transcription factors and epigenetic modulation

Expertise: nuclear receptors, transcription Library of ~240,000 factors, epigenetic compounds of which Wholly-owned targets 60% proprietary 129,000 square foot pharma-like R&D facilities

Strong scientific team of ~90 people

Power of discovery engine underpins deep pipeline of clinical and discovery stage assets

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 4 Deep pipeline approaching major near term value inflection points

Candidate / IND Commercial Indication Discovery Phase I Phase II Phase III Program Enabling Rights

Phase IIb Lanifibranor NASH pan-PPAR results: H1 2020

Phase IIa Odiparcil MPS VI GAG clearance results: H2 2019

Moderate to ROR  SAD phase I ABBV-157 severe completed(1) psoriasis 𝛾𝛾

 Non-small cell YAP/TEAD Candidate lung cancer Hippo Selection: and mesothelioma 2019

 Idiopathic Lead Op(2) TGF-β pulmonary fibrosis (IPF)

(1) SAD: Single Ascending Dose; (2) Lead optimization means refining molecules in advance of selecting candidates Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 5 Key financials and shareholder base

Key financials Shareholder base

Free float* 22.1% *Including ISIN code FR0013233012 Perceptive Founders Advisors 43.9% Market Euronext Paris BVF Shares outstanding 22.294.677 15.0%

Market cap €54m (May 24 2019) Novo 8.8% Employees & Others €47,3m compared to €56,7m 3.1% Sofinnova 7.1% as of December 2018. Cash position Successful €48.5m Euronext Analyst coverage (March 31 2019) IPO (February 2017) and HC Wainwright Ed Arce €35.5m private placement (April 2018) LifeSci Capital Patrick Dolezal Jefferies Peter Welford Revenues €3.2m compared to €4.8m in (December 31 2018) 2017 KBC Lenny Van Steenhuyse Société Générale Delphine Le Louët R&D expenditures €31,6m compared to €26,7m Gilbert Dupont Jamila El Bougrini (December 31 2018) in 2017 Kepler Chevreux Arsene Guekam

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 6 Lanifibranor in Nonalcoholic Steatohepatitis (NASH) Lanifibranor is a differentiated pan-PPAR agonist with moderate and well balanced activity on the 3 PPAR isoforms Lanifibranor human dose response curves and EC50s for various PPAR agonists PPARα PPARδ PPARγ Compound EC50 (nM) EC50 (nM) EC50 (nM) 150 α hPPAR  Lanifibranor(1) 1630 850 230 125 hPPARδ γ 100 hPPAR  2400 - - 75  - - 263 50

%Activation  - - 13 25  (2) 0 10 100 - -10 -8 -6 -4 (3) Lanifibranor (M)  Seladelpar - 2 - Lanifibranor binds differently than rosiglitazone to PPARγ inducing different coactivator recruitment(4)

Potency scale: red 10 nM; grey: 500 nM; green 5 000 nM

Source: (1) Company data (2) Hanf R et al, Diabetes & Vascular Dis Res 2014 (3) Cymabay company presentation (4) J Med Chem. 2018 Feb 15. doi: 10.1021/acs.jmedchem.7b01285

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 8 Favorable safety profile differing from previously developed PPARs

PPAR isoforms Reported Lanifibranor Organ activated PPAR liabilities effects

 Fluid retention Heart  PPARγ  Cardiac hypertrophy Not observed

Skeletal  PPARα  Myofiber degeneration muscle Not observed  > 50% increases in creatinine, Kidney  PPARα degenerative changes Not observed in renal tubules

Urinary  Proliferative changes  PPARγ bladder in bladder epithelium Not observed

Lanifibranor not associated with typical single or dual PPAR liabilities

Source: Company data Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 9 In long-term toxicological studies lanifibranor presents a safe and differentiating profile

No carcinogenic effect relevant to humans, contrasting with some other PPARγ and PPARα/γ agonists

 Lanifibranor shows a very favorable profile in 12 month monkey study … − No adverse clinical signs were observed at any dose-level tested − No effects on body weight and heart weight, no haemodilution or creatinine increase − Electrocardiography and clinical pathology investigations did not reveal any undesirable effects  … and in two-year carcinogenicity studies performed in rat and mice − Rat: no neoplastic changes and increase in tumor types commonly associated with single PPARγ and dual PPARα/γ agonists: liver, adipose, bladder, renal and skin − Mice: no neoplastic changes and increase in tumor types of human relevance

After review of carcinogenicity studies, FDA has lifted PPAR class clinical hold and allowed long-term clinical studies in NASH with lanifibranor

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 10 Phase I and Phase IIa clinical studies(1) demonstrated lanifibranor beneficial effects on key metabolic markers

Lanifibranor has beneficial effects on key metabolic markers in type II diabetic patients

Adiponectin (PPARγ) HDL Cholesterol (PPARα/δ) Triglycerides (PPARα/δ)

300 p=0.05 40 0

p<0.05 p=0.05 -10 30 200 p<0.05 -20

p=0.08 20 p=0.13 -30 p=0.08 100 10 p<0.05 -40 p<0.05 Percent change from baseline Percent change from baseline Percent change from baseline Percent change of baseline Percent change of baseline 0 0 Percent change of baseline -50 Placebo 400 mg 800 mg 1400 mg Placebo 400 mg 800 mg 1400 mg Placebo 400 mg 800 mg 1400 mg IVA337 IVA337 IVA337 IVA337 IVA337 IVA337 IVA337 IVA337 IVA337 lanifibranor lanifibranor lanifibranor lanifibranor lanifibranor lanifibranor lanifibranor lanifibranor lanifibranor

Adiponectin fold: HDL increase: TG decrease:  Lanifibranor (800/1400mg): +2.8/+3.2 Lanifibranor (800/1400mg): +18%/28% Lanifibranor (800/1400mg): -24%/28%  Pioglitazone(2) (45mg): +2.3 Elafibranor(3) (80mg): +7,8% Elafibranor (80mg)(3): -16,7% Homa-IR: Seladelpar(4) (50mg): +9,9%  Seladelpar(4) (50mg): -32,4%  Lanifibranor (800/1400mg): -20%/-44%

Source: Company data ; (1) Conducted by Abbott (2) A placebo controlled trail of Pioglitazone in subjects with nonalcoholic steatohepatitis Belfort et Al; N Engl J Med 355;22 November 30, 2006; 6 month treatment (3) Effects of the new dual PPAR α/δ agonist GFT505 on lipid and glucose homeostasis in abdominally obese patients with combined dyslipidemia or impaired glucose metabolism ; Diabetes Care. 2011 Sep;34(9):2008-14. doi: 10.2337/dc11-0093. Epub 2011 Aug 4. 4 week treatment study 1 (4) A Novel Peroxisome Proliferator Receptor-δ Agonist: Lipid and Other Metabolic Effects in Dyslipidemic Overweight Patients Treated with and without Atorvastatin The Journal of Clinical Endocrinology & Metabolism, Volume 96, Issue 9, 1 September 2011, Pages 2889–2897, https://doi.org/10.1210/jc.2011-1061; 8 week treament

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 11 Phase I and Phase IIa clinical studies(1) confirmed lanifibranor safety

Clinical findings underline the favorable tolerability of lanifibranor  Good overall tolerance and no major safety findings – No increases of creatinine, liver function test (LFT) or creatine phosphokinase (CPK) – No changes in blood pressure – No signal of fluid overload or hemodilution – No clinically relevant weight gain  No significant differences in SAE and AE between placebo and lanifibranor in the phase IIa

Source: Company data and * Ohashi, Endocr Metab Immune Disord Drug Targets. 2015. Note: (1) Conducted by Abbott ; (2) Pioglitazone data obtained after 6 month treatment (Belfort 2006); elafibranor after 4 week and seladelpar after 8 week

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 12 NASH overview

A severe disease with no currently approved treatment

Healthy 15-20% Liver Cirrhosis

Hepato- NASH Death NAFLD NASH with carcinoma 2-3% per year fibrosis 30-40% Severe liver Reversible damage 40-50% Liver transplant

The overall NASH prevalence in the adult population of the United States is believed to be approximately 12%

Source: NASH Market, Allied Market Research 2016 ; Deutsche Bank Markets Research; Intercept website.; Epidemiology and natural history of non-alcoholic steatohepatitis.Clinical Liver Disease.2009 Nov;13(4):511-31.

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 13 Lanifibranor’s mechanism of action addresses all the key features of NASH

Metabolism Steatosis

Insulin sensitivity FA uptake α,δ,γ α γ PPAR HDLc PPAR , FA catabolism TG Lipogenesis

Inflammation and Ballooning Fibrosis Stellate cell NFkB-dependent proliferation and gene activation PPARα,δ,γ PPARγ activation Inflammasome Collagen and Ballooning fibronectin production

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 14 Pioglitazone PPARγ NASH resolution efficacy results are still unmatched

Resolution of NASH without worsening of fibrosis

60%

50%

40%

30%

51%

20%

27% pbo 10% 19% 19%

Patients withPatients % improvement, 19% pbo pbo 12% 12% pbo 8% pbo pbo 8% 6% 6% 7% 0% Pioglitazone Ocaliva Elafibranor CVC MGL-3196 Aramchol

Pioglitazone Cusi study (45 mg, 18 month), Annals of Internal Medicine, 2016 ; Ocaliva Regenerate Phase III study (25 mg, 18 months), press release Feb. 19, 2019 CVC Centaur Phase II study (150 mg, 12 months), Hepatology 2017 ; Elafibranor Golden 505 Phase II study (120 mg, 12 months), Gastroenterology. 2016 MGL-3196 Phase II study (100mg, 8 months), press release May 31, 2018 ; Aramchol Arrest Phase II study (600 mg, 12 months) – press release June 12, 2018

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 15 Overview of NATIVE trial design (I/II)

Trial design Principal investigator Inclusion criteria  Prof. Francque (Universitair Ziekenhuis,  Severe patients with an inflammation and Antwerpen, Belgium) ballooning score of 3 or 4  Prof. Manal Abdelmalek (Duke University,  Steatosis score ≥ 1 and fibrosis score < 4 (no USA) cirrhosis) Status Primary endpoint  Trial enrolling  Decrease from baseline ≥ 2 points of the  Results expected first-half 2020 inflammation and ballooning score without worsening of fibrosis Clinicaltrials.gov identifier: NCT03008070 225 patients 24 week treatment Double blind randomized placebo controlled

Screening Placebo, 75 patients End of treatment  Liver biopsy  Liver biopsy Lanifibranor, 800 mg once daily, 75 patients Lanifibranor, 1200 mg once daily, 75 patients

More information on: http://www.native-trial.com/ Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 16 Overview of NATIVE trial design (II/II)

17 countries worldwide ► 13 in EU 14 sites selected ► United States in the United- ► Canada States ► Australia ► Mauritius 92 sites involved 91 sites activated Status 82 sites screening  756 patients screened and 192 patients randomized (85%) at end of May 2019  3 positive DSMB reviews recommending to continue the study without any changes  Limited number of edema (blinded data): 7 patients treated with placebo or lanifibranor reported mild or moderate edemas of short duration and which did not require treatment discontinuation  Results expected first-half 2020

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 17 NATIVE study results will also be backed by the Phase II trial in T2DM patients with NAFLD Trial design Principal investigator Primary endpoint  Prof. Kenneth Cusi (University of Florida)  Change from baseline to week 24 in IHTG Randomisation Key secondary endpoints  N=64 assuming a 35% reduction of IHGT(1)  Proportion of responders; change in hepatic Status fibrosis (MRE(2), biomarkers); change in  IND approved metabolic outcomes  First Patient First Visit: August 2018  Safety  Results expected first-half of 2020 Clinicaltrials.gov identifier: NCT03459079 64 patients 24 week treatment Double blind randomized placebo controlled

Healthy non-obese control group, 10 subjects Placebo, 32 patients Lanifibranor, 800 mg once daily, 32 patients

A positive study result would further reinforce lanifibranor’s profile in NAFLD and NASH patients with type 2 diabetes

(1) Intrahepatic triglycerides (2) Magnetic resonance elastography (3) De-novo lipogenesis Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 18 Odiparcil – MPS Mucopolysaccharidoses (MPS) are devastating diseases with high unmet medical need MPS is a group of inherited lysosomal storage disorders  Autosomal recessive disorders characterized by accumulation of glycosaminoglycan(s) (GAGs) due to deficient lysosomal enzymes  Seven distinct clinical types based on the enzyme affected: odiparcil could be the first substrate reduction therapy for five forms of MPS with the following incidences: Kathleen (MPS I)

MPS has devastating clinical consequences: example MPS I, II and VI

Consequences MPS I MPS II MPS VI  Mental retardation    Coarse facies, short stature    Scotty (MPS II)  Dysostosis multiplex     Joint stiffness     Spinal cord compression     Organomegaly     Poor vision (corneal clouding)  (1)   Hearing loss     Cardiac/respiratory disease    (1) Retinal degeneration with no corneal clouding  Pebbled skin  Odontoid hypoplasia  Diarrhoea  Kyphoscoliosis, genu valgum Karima (MPS VI)

Source: (1) Source: Rheumatology 2011 Therapy for mucopolysaccharodises; Vassili Valayannopoulos and Frits A. Wijburg

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 20 Enzyme replacement therapy (ERT) is commercially successful, but with limited therapeutic efficacy Enzyme replacement therapies are standard of care in MPS  Recombinant human enzymes, weekly intravenous infusion over 4 hours  Approx. 50% of patients experience infusion reactions initially, some can be life threatening  Limited penetration into protected or poorly vascularized tissues such as cornea or cartilage

Product Company MPS Est. yearly cost 2018 sales  MPS I  $ 217K  $ 206M

 MPS II  $ 522K  $ 616M(1)

 MPS IVA  $ 578K  $ 482M

 MPS VI  $ 476K  $ 345M

 MPS VII  $ 550K  $ 8M

Source: Sales - Company annual reports 2017; WAC without discounts for a 25-kg patient - BioCentury “Making of MEPSEVII” Dec 11, 2017 ; (1) 2017 sales

ERT is expensive and usually requires outpatient administration. Significant unmet need remains in addressing symptoms in organs where ERT fails to penetrate

Source: (1) H. Noh, J. I. Lee; Current and potential therapeutic strategies for mucopolysaccharidoses; Journal of Clinical Pharmacy

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 21 Unique mechanism of action potentially synergistic with ERT

Odiparcil diverts endogenous protein-bound GAG synthesis to soluble odiparcil-bound chondroitin sulfate (CS) and dermatan sulfate (DS) synthesis

Galactosyl transferase I (GTI) Galactosyl transferase I (GTI) Synthesis Synthesis of Odiparcil of soluble proteoglycans DS and CS (HS, CS, DS)

Odiparcil

Odiparcil decreases intracellular GAG accumulation in vitro in MPS VI patient cells

Intracellular CS storage MPS VI fibroblasts Extracellular GAG 300000 GAG overloaded 25 MPS VI (IC50=3 µM) cells 20 200000 Odiparcil 15 10 100000

Control (IC50=2.8 µM) 5 Fluorescence intensity MPS VI (IC50=2.7 µM) 0 -8 -7 -6 -5 0 Veh.10 10 10 10 (µg/mL) GAGS Total sulfated Veh.10 -8 10 -7 10 -6 10 -5 Odiparcil concentration (M) Odiparcil concentration (M)

Odiparcil observed to reduce GAG accumulation in MPS VI patient cells

Source: H. Noh, J. I. Lee; Current and potential therapeutic strategies for mucopolysaccharidoses; Journal of Clinical Pharmacy, company data

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 22 By producing soluble dermatan and chondroitin sulfates, odiparcil can address several types of MPS

Type Name DS CS HS KS

MPS I-H Hurler syndrome  

MPS I-S Scheie syndrome 

MPS I-H/S Hurler-Scheie syndrome  

MPS II Types A & B Hunter syndrome  

MPS IV Type A Morquio syndrome  

Maroteaux-Lamy MPS VI   syndrome

MPS VII Sly syndrome   

Source: Rheumatology 2011 Therapy for mucopolysaccharodises; Vassili Valayannopoulos and Frits A. Wijburg

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 23 Odiparcil decreases GAG content in vivo and improves mobility in a MPS VI model

Wild-type and MPS VI 6 months ►Sulfated GAGs in organs/tissues and urine mice ►Mobility test Treatment starts when ± Odiparcil* ►Corneal structure/clouding animals are one month Given in food old * The doses administered provide exposure levels similar to that to be used in clinic

Odiparcil decreases GAG Odiparcil decreases intra- Odiparcil improves animal accumulation in tissues cellular GAG mobility

Liver Leukocytes Pole Test p<0.001 p<0.05 40 80 40 p<0.001 p<0.001 p<0.001 p<0.001 30 60 30

[Area * Index] 20 40 20

10 20 10 time on pole [sec] on pole time

GAG in liver 0 %cells with > 10 GAG granules >%cells GAG with 10 0 0 WT MPS VI MPS VI + Odi WT MPS VI MPS VI+Odi WT MPS VI MPS VI + Odi Chow diet Odiparcil : 4.5 g/kg in food

Source: Company data

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 24 Odiparcil penetrates tissues that ERT cannot reach

Odiparcil is well distributed in tissues and organs poorly penetrated by recombinant enzymes

Heart Bone Cornea Cartilage

Odiparcil(1) rhASB(2) Not tested Not detected Not detected

Meaningful concentrations of odiparcil observed also in tissues that are poorly vascularized or protected by a barrier: bone, corneal tissue and cartilage

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 25 Odiparcil shows promising results in poorly vascularized tissues not treated by ERT

Odiparcil effect on corneal structure and epithelium thickness

40 p<0.001 p<0.0001 epithelium stroma 30 Chow diet Odiparcil : 4.5 g/kg in food

20

thickness (µm) 10 WT control MPSVI MPS VI + Odi 0 WT MPS VI MPS VI + Odi

Decreases in GAG accumulation and improvements in corneal structure expected to improve corneal function and ocular impairment Odiparcil decreases trachea and knee cartilage thickness

p<0.0001 100 300 -31% p<0.0001 p<0.0001 80 -26%

[µm] 200 60 Chow diet Chow diet Odiparcil : 4.5 g/kg in food Odiparcil : 4.5 g/kg in food 40 100 thickness 20

Distal femoral growthDistal femoral plate 0

Trachea cartillage thickness in µm 0 WT MPS VI MPS VI + Odi WT MPS VI MPS VI + Odi

By decreasing GAG storage in cartilage, odiparcil improves cartilage- linked disease manifestations

Source: Company data

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 26 Odiparcil has the potential to positively differentiate versus current MPS treatment options

Aldurazyme, Elaprase, Odiparcil Naglazyme, Vimizim, Mepsevii HSCT (Hematopoietic stem cell transplantation)

Effect on mobility

Effect on eye, cartilage, bones, heart valves, spinal cord compression

Distribution type Oral Intravenous Infusion Transplantation

Source: Company evaluation

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 27 Odiparcil overall development plan in MPS VI

• Validate LeukoGAG(1) assay in human: potential Biomarker Study efficacy biomarker 12 MPS VI patients

• Safety and tolerability Phase IIa, 6-month treatment • Identify signals of clinical efficacy and 24 MPS VI adults potential as stand-alone therapy Add on to ERT and Naïve • PK/PD, biomarkers (uGAG(2), leukoGAG, skin GAG)

• Safety and tolerability Phase Ib/II, 6-month treatment • PK data with pediatric formulation 9 MPS VI children • PD data, biomarkers (uGAG, Add on to ERT leukoGAG, skin GAG) • Identify signals of clinical efficacy

Phase III • Safety and Tolerability MPS VI (5y-adult) • Efficacy

(1) leukoGAG: GAG levels in circulating leukocytes; UGAG: urinary GAG) Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 28 R&D collaborations and Hippo pathway program update Key validating collaborations with AbbVie and Boehringer Ingelheim

RORγ collaboration in inflammatory disease  RORγ program addresses large markets currently dominated by biologics and could prove to be superior to biologics  Single ascending dose phase I completed with ABBV-157, the clinical candidate coming from the partnership  Next step: A randomized, double-blind, placebo-controlled, multiple-dose study to evaluate the pharmacokinetics, safety and tolerability of ABBV-157 in 60 healthy volunteers and patients with chronic plaque psoriasis (clinicaltrials.gov identifier: NCT03922607) – Study start date: May 2019 – Study completion: September 2020(1) Inventiva eligible to future milestone payments and sales royalties on all ROR molecules identified during the collaboration

Fibrosis collaboration

 Multi-year R&D collaboration and licensing partnership. Joint team until pre-CC stage. BI to take full responsibility of clinical development and commercialization  Program progressing as planned with first screening performed

Inventiva eligible to up to ~€170m in milestones and sales royalties

(1) Source: clinicaltrial.gov Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 30 YAP-TEAD program: significant progress achieved and clinical candidate selection planned in 2019

 Novel cancer pathway involved  Proprietary chemistry in drug resistance, immune  Lead and back-up compounds evasion, tumor progression available and metastases  IP protected  Relevant in multiple, commercially attractive cancer indications First in class YAP-TEAD program  Preclinical candidate screening  In vitro evidence for synergies ongoing with standard of care and  Clinical candidate selection in suppression of tumor 2019 resistance  Phase I/II start planned in 2020  In vivo efficacy shown (alone and in combination with standard of care)

The program is expected to enter into Phase I/II enabling preclinical development in 2019

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 31 Conclusions Recent achievements and upcoming expected milestones

2019 2020

 FDA decision to lift lanifibranor clinical hold  Phase IIb NASH results – H1 2020  Last patient Phase IIb NASH  Phase II in NAFLD patients with TD2M  Last patient Prof. Cusi study in NAFLD results – H1 2020

Lanifibranor patients with TD2M

 Rare pediatric disease designation MPS VI  Launch of phase IB/II in MPS VI children  Phase IIa in MPS VI: last patient recruited 

Odiparcil Phase IIa in MPS VI results - H2 2019

 SAD(1) Phase I with ABBV-157 completed ABBV-157 development in psoriasis - 157  ABBV-157 multiple-ascending dose in

ABBV healthy volunteers and psoriatic patients phase I initiation  Clinical candidate selection  Launch of Phase I/II in mesothelioma patients - TEAD YAP

(1) SAD: Single Ascending Dose

Corporate Presentation | 2019 Non-confidential – Property of Inventiva │ 33 Contacts Inventiva Brunswick LifeSci Advisors

Frédéric Cren Yannick Tetzlaff / Tristan Roquet Montégon Monique Kosse

CEO Media relations Investor relations [email protected] [email protected] [email protected]

+33 (0)3 80 44 75 00 + 33 1 53 96 83 83