Developing breakthrough therapies in NASH and ... · Non-confidential – Property of Inventiva │ 2. DISCLAIMER. This document has been prepared by Inventiva (the "Company") solely

Developing breakthrough therapies inNASH and mucopolysaccharidosis

Corporate PresentationJune 2019

Non-confidential – Property of Inventiva │ 2

DISCLAIMER

This document has been prepared by Inventiva (the "Company") solely for the purpose of this presentation. This presentation includes only summary information and does not purport to be comprehensive. Any information in this presentation, whether from internal or from external sources, is purely indicative and has no contractual value. The information contained in this presentation are provided as at the date of this presentation. Certain information included in this presentation and other statements or materials published or to be published by the Company are not historical facts but are forward-looking statements. The forward-looking statements are based on current beliefs, expectations and assumptions, including, without limitation, assumptions regarding present and future business strategies and market in which the Company operates, and involve known and unknown risk, uncertainties and other factors, which may cause actual results, performance or achievements, or industry results or other events, to be materially different from those expressed or implied by these forward-looking statements. These risks and uncertainties include those discussed or identified under Chapter “Risk factors” in the Company’s registration document (document de reference) filed with the French Financial markets authority (AMF – Autorité des marchésfinanciers), available on the Company’s website (www.inventivapharma.com) and on the website of the AMF. The Company may not actually achieve the plans, intents or expectations disclosed in its forward-looking statements and you should not place undue reliance on the forward-looking statements contained herein. There can be no assurance that the actual results of the Company’s development activities and results of operations will not differ materially from the Company’s expectations. Factors that could cause actual results to differ from expectations include, among others, the Company’s ability to develop safe and effective products, to achieve positive results in clinical trials, to obtain marketing approval and market acceptance for its products, and to enter into and maintain collaborations; as well as the impact of competition and technological change; existing and future regulations affecting the Company’s business; and the future scope of the Company’s patent coverage or that of third parties.

The information contained in this presentation has not been subject to independent verification. No representation or warranty, express or implied, is made by the Company or any of its affiliates, advisors, representatives, agents or employees as to, and no reliance should be placed on, the fairness, accuracy, completeness or correctness of the information, or opinions contained herein. Neither the Company, nor any of its respective affiliates, advisors, representatives, agents or employees, shall bear any responsibility or liability whatsoever (for negligence or otherwise) for any loss howsoever arising from any use of this presentation or its contents or otherwise arising in connection with this presentation. Such information is subject to modification at any time, including without limitation as a result of regulatory changes or changes with respect to market conditions, and neither the Company, nor any of its affiliates, advisors, representatives, agents or employees, shall, nor has any duty to, update you.

Corporate Presentation | 2019

Non-confidential – Property of Inventiva │ 3Corporate Presentation | 2019

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


Validated oral small molecule-focused discovery engine targeting nuclear receptors, transcription factors and epigenetic modulation


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

Library of ~240,000 compounds of which 60% proprietary

Wholly-owned 129,000 square foot pharma-like R&D facilities

Expertise: nuclear receptors, transcription factors, epigenetic targets

Strong scientific team of ~90 people

https://www.google.com/url?sa=i&rct=j&q=&esrc=s&source=images&cd=&cad=rja&uact=8&ved=2ahUKEwjIydv124vfAhUnyYUKHb7DAfEQjRx6BAgBEAU&url=https://thenounproject.com/term/test-tube/2329/&psig=AOvVaw2RFyTFuCQE-eNdNCSFWct2&ust=1544203325385958


Deep pipeline approaching major near term value inflection points


Candidate / Program Indication Discovery IND

Enabling Phase I Phase II Phase III Commercial Rights

Lanifibranor NASHPhase IIb

results: H1 2020

Odiparcil MPS VIPhase IIa

results: H2 2019

ABBV-157 Moderate to severepsoriasis

SAD phase I completed(1)

HippoNon-small cell

lung cancer and mesothelioma

Candidate Selection: 2019

TGF-β Idiopathic pulmonary fibrosis (IPF)

Lead Op(2)

GAG clearance

ROR𝛾𝛾

pan-PPAR

YAP/TEAD

(1) SAD: Single Ascending Dose; (2) Lead optimization means refining molecules in advance of selecting candidates


Key financials and shareholder base

ISIN code FR0013233012

Market Euronext Paris

Shares outstanding 22.294.677Market cap(May 24 2019)

€54m

Cash position(March 31 2019)

€47,3m compared to €56,7m as of December 2018.Successful €48.5m Euronext IPO (February 2017) and €35.5m private placement (April 2018)

Revenues(December 31 2018)

€3.2m compared to €4.8m in 2017

R&D expenditures(December 31 2018)

€31,6m compared to €26,7m in 2017

Key financials Shareholder base

Analyst coverage

HC WainwrightLifeSci CapitalJefferiesKBCSociété GénéraleGilbert DupontKepler Chevreux

Ed ArcePatrick DolezalPeter WelfordLenny Van SteenhuyseDelphine Le LouëtJamila El BougriniArsene Guekam


Free float*22.1%

BVF15.0%

Novo 8.8%

Sofinnova 7.1%Employees & Others

3.1%

Founders43.9%

*Including Perceptive Advisors

Lanifibranor in NonalcoholicSteatohepatitis (NASH)


Lanifibranor is a differentiated pan-PPAR agonist with moderate and well balanced activity on the 3 PPAR isoforms


Compound PPARαEC50 (nM)

PPARδEC50 (nM)

PPARγEC50 (nM)

Lanifibranor(1) 1630 850 230 Fenofibrate 2400 - -

Pioglitazone - - 263

Rosiglitazone - - 13

Elafibranor(2) 10 100 -

Seladelpar(3) - 2 -

Lanifibranor human dose response curves and EC50s for various PPAR agonists

-10 -8 -6 -40

25

50

75

100

125

150

%A

ctiv

atio

n

hPPARα

hPPARδhPPARγ

Lanifibranor (M)

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

Lanifibranor binds differently than rosiglitazone to PPARγ inducing different coactivator recruitment(4)

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


Favorable safety profile differing from previously developed PPARs


Organ PPAR isoforms activated

ReportedPPAR liabilities

Lanifibranoreffects

Heart PPARγ Fluid retention Cardiac hypertrophy Not observed

Skeletalmuscle PPARα Myofiber degeneration Not observed

Kidney PPARα

> 50% increases in creatinine,degenerative changes in renal tubules

Not observed

Urinarybladder PPARγ Proliferative changes

in bladder epithelium Not observed

Source: Company data

Lanifibranor not associated with typical single or dual PPAR liabilities


In long-term toxicological studies lanifibranor presents a safe and differentiating profile

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


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

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


Phase I and Phase IIa clinical studies(1) demonstrated lanifibranorbeneficial effects on key metabolic markers


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

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

Placebo 400 mg 800 mg 1400 mg 0

100

200

300

IVA337 IVA337IVA337

p=0.08

p=0.05

p=0.05

Perc

ent c

hang

e of

bas

elin

e

Adiponectin (PPARγ)

Perc

ent c

hang

e fr

om b

asel

ine

lanifibranor lanifibranor lanifibranorPlacebo 400 mg 800 mg 1400 mg

0

10

20

30

40

IVA337 IVA337IVA337

p=0.13

p<0.05

p<0.05

Perc

ent c

hang

e of

bas

elin

e

HDL Cholesterol (PPARα/δ)

Perc

ent c

hang

e fr

om b

asel

ine

lanifibranor lanifibranor lanifibranorPlacebo 400 mg 800 mg 1400 mg

-50

-40

-30

-20

-10

0

IVA337 IVA337IVA337

p=0.08

p<0.05p<0.05

Perc

ent c

hang

e of

bas

elin

e

Triglycerides (PPARα/δ)

Perc

ent c

hang

e fr

om b

asel

ine

lanifibranor lanifibranor lanifibranor

HDL increase:Lanifibranor (800/1400mg): +18%/28%Elafibranor(3) (80mg): +7,8%Seladelpar(4) (50mg): +9,9%

TG decrease:Lanifibranor (800/1400mg): -24%/28%Elafibranor (80mg)(3): -16,7%Seladelpar(4) (50mg): -32,4%

Adiponectin fold: Lanifibranor (800/1400mg): +2.8/+3.2 Pioglitazone(2) (45mg): +2.3Homa-IR: Lanifibranor (800/1400mg): -20%/-44%

https://www.ncbi.nlm.nih.gov/pubmed/21816979

https://doi.org/10.1210/jc.2011-1061


Phase I and Phase IIa clinical studies(1) confirmed lanifibranor safety


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

Clinical findings underline the favorable tolerability of lanifibranor

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


NASH overview

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.


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

A severe disease with no currently approved treatment

Hepato-carcinoma Death

Liver transplant

Reversible40-50%

15-20%

Severe liverdamage

HealthyLiver

NASHNAFLD

Cirrhosis

NASHwith

fibrosis 2-3% per year 30-40%

http://www.ncbi.nlm.nih.gov/pubmed/19818302


Lanifibranor’s mechanism of action addresses all the key features of NASH


Insulin sensitivity

HDLc

TG

PPARα,δ,γ

Metabolism

FA uptake

FA catabolism

Lipogenesis

PPARα,γ

Steatosis

Inflammation and Ballooning

NFkB-dependent gene activation

Inflammasome

Ballooning

PPARα,δ,γ

Stellate cell proliferation and activation

Collagen and fibronectin production

PPARγ

Fibrosis


Pioglitazone PPARγ NASH resolution efficacy results are still unmatched


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

pbo19%

pbo8%

pbo12% pbo

6%pbo6%

pbo7%

51%

12%19%

8%

27%

19%

0%

10%

20%

30%

40%

50%

60%

Pioglitazone Ocaliva Elafibranor CVC MGL-3196 Aramchol

Patie

nts

with

impr

ovem

ent,

%

Resolution of NASH without worsening of fibrosis


Overview of NATIVE trial design (I/II)


More information on: http://www.native-trial.com/

Trial design

225 patients24 week treatment

Double blind randomized placebo controlled

End of treatment Liver biopsy

Placebo, 75 patientsLanifibranor, 800 mg once daily, 75 patientsLanifibranor, 1200 mg once daily, 75 patients

Principal investigator Prof. Francque (Universitair Ziekenhuis,

Antwerpen, Belgium) Prof. Manal Abdelmalek (Duke University,

USA)Status Trial enrolling Results expected first-half 2020

Clinicaltrials.gov identifier: NCT03008070

Inclusion criteria Severe patients with an inflammation and

ballooning score of 3 or 4 Steatosis score ≥ 1 and fibrosis score < 4 (no

cirrhosis)Primary endpoint Decrease from baseline ≥ 2 points of the

inflammation and ballooning score without worsening of fibrosis

Screening Liver biopsy

http://www.native-trial.com/


Overview of NATIVE trial design (II/II)


17 countries worldwide

► 13 in EU► United States► Canada► Australia► Mauritius

92 sites involved91 sites activated82 sites screening

14 sites selected in the United-States

Status

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


NATIVE study results will also be backed by the Phase II trial in T2DM patients with NAFLD

(1) Intrahepatic triglycerides (2) Magnetic resonance elastography (3) De-novo lipogenesis

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


64 patients24 week treatment

Double blind randomized placebo controlled

Healthy non-obese control group, 10 subjectsPlacebo, 32 patientsLanifibranor, 800 mg once daily, 32 patients

Principal investigator Prof. Kenneth Cusi (University of Florida)Randomisation N=64 assuming a 35% reduction of IHGT(1)

StatusIND approved First Patient First Visit: August 2018

Results expected first-half of 2020

Primary endpoint Change from baseline to week 24 in IHTGKey secondary endpoints Proportion of responders; change in hepatic

fibrosis (MRE(2), biomarkers); change in metabolic outcomes

SafetyClinicaltrials.gov identifier: NCT03459079

Trial design

Odiparcil – MPS


Mucopolysaccharidoses (MPS) are devastating diseases with high unmet medical need


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

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)

Scotty (MPS II)

Karima (MPS VI)

MPS is a group of inherited lysosomal storage disorders

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

MPS I

Mental retardation Coarse facies, short stature Dysostosis multiplex Joint stiffness Spinal cord compression Organomegaly Poor vision (corneal clouding) Hearing loss Cardiac/respiratory disease

MPS II MPS VIConsequences

(1) Retinal degeneration with no corneal clouding Odontoid hypoplasia Kyphoscoliosis, genu valgum

Pebbled skin Diarrhoea

(1)


Enzyme replacement therapy (ERT) is commercially successful, but with limited therapeutic efficacy

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


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

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

Enzyme replacement therapies are standard of care in MPS

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


Unique mechanism of action potentially synergistic with ERT


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

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

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

Galactosyl transferase I (GTI)

Synthesis of proteoglycans (HS, CS, DS)

Synthesis of soluble DS and CS

Odiparcil

Odiparcil

Galactosyl transferase I (GTI)

MPS VI fibroblastsGAG overloaded

cells

Intracellular CS storage Extracellular GAG

0

5

10

15

20

25

10- 8 10- 7 10- 6 10- 5

MPS VI (IC50=3 µM)

Veh.Odiparcil concentration (M)

Tota

l sul

fate

d G

AGS

(µg/

mL)

0

100000

200000

300000

10- 8 10- 7 10- 6 10- 5

Control (IC50=2.8 µM)MPS VI (IC50=2.7 µM)

Veh.Odiparcil concentration (M)

Fluo

resc

ence

inte

nsity

Odiparcil observed to reduce GAG accumulation in MPS VI patient cells

Odiparcil


By producing soluble dermatan and chondroitin sulfates, odiparcilcan address several types of MPS

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

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

MPS VI Maroteaux-Lamysyndrome

MPS VII Sly syndrome



Odiparcil decreases GAG content in vivo and improves mobility in a MPS VI model



0

10

20

30

40 p<0.001

WT MPS VI MPS VI + Odi

p<0.05

time

on p

ole

[sec

]

0

10

20

30

40p<0.001

WT MPS VI MPS VI + Odi

p<0.001

GAG

in li

ver

[Are

a *

Inde

x]

± Odiparcil*Given in food

6 monthsWild-type and MPS VI miceTreatment starts when animals are one month old

►Sulfated GAGs in organs/tissues and urine►Mobility test►Corneal structure/clouding

* The doses administered provide exposure levels similar to that to be used in clinic

Liver

Odiparcil decreases GAG accumulation in tissues

Odiparcil improves animal mobility

Chow dietOdiparcil : 4.5 g/kg in food

Odiparcil decreases intra-cellular GAG

0

20

40

60

80%

cells

with

> 1

0 G

AG g

ranu

les

p<0.001p<0.001

MPS VI MPS VI+OdiWT

Leukocytes Pole Test


Odiparcil penetrates tissues that ERT cannot reach

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


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

Heart CorneaBone Cartilage

Odiparcil(1)

rhASB(2) Not detectedNot tested Not detected


Odiparcil shows promising results in poorly vascularized tissues not treated by ERT



Decreases in GAG accumulation and improvements in corneal structure expected to improve corneal function and ocular impairment

WT control MPSVI

epithelium stroma

MPS VI + Odi0

10

20

30

40p<0.001

WT MPS VI

p<0.0001

MPS VI + Odi

thic

knes

s (µ

m)

Odiparcil effect on corneal structure and epithelium thickness


Odiparcil decreases trachea and knee cartilage thickness

0

20

40

60

80

100p<0.0001

-31%

Trac

hea

carti

llage

thic

knes

s in

µm

MPS VI MPS VI + OdiWT


0

100

200

300p<0.0001

-26%

WT MPS VI

p<0.0001

MPS VI + Odi

Dis

tal f

emor

al g

row

th p

late

thic

knes

s[µ

m]


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


Odiparcil has the potential to positively differentiate versus current MPS treatment options


Source: Company evaluation

Effect on mobility

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

Distribution type Oral Intravenous Infusion Transplantation

OdiparcilAldurazyme, Elaprase,

Naglazyme, Vimizim, Mepsevii HSCT(Hematopoietic stem cell transplantation)


Odiparcil overall development plan in MPS VI


(1) leukoGAG: GAG levels in circulating leukocytes; UGAG: urinary GAG)

Biomarker Study12 MPS VI patients

Phase IIa, 6-month treatment24 MPS VI adults

Add on to ERT and Naïve

Phase Ib/II, 6-month treatment9 MPS VI children

Add on to ERT

Phase IIIMPS VI (5y-adult)

• Validate LeukoGAG(1) assay in human: potential efficacy biomarker

• Safety and tolerability• PK data with pediatric formulation• PD data, biomarkers (uGAG, leukoGAG, skin GAG)

• Identify signals of clinical efficacy

• Safety and tolerability• Identify signals of clinical efficacy and potential as stand-alone therapy

• PK/PD, biomarkers (uGAG(2), leukoGAG, skin GAG)

• Safety and Tolerability• Efficacy

http://www.improves-mpsvi-trial.com/

R&D collaborations and Hippo pathway program update


Key validating collaborations with AbbVie and Boehringer Ingelheim


Inventiva eligible to future milestone payments and sales royaltieson all ROR molecules identified during the collaboration

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 up to ~€170m in milestones and sales royalties

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

(1) Source: clinicaltrial.gov


YAP-TEAD program: significant progress achieved and clinical candidate selection planned in 2019

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


Novel cancer pathway involved in drug resistance, immune evasion, tumor progression and metastases

Relevant in multiple, commercially attractive cancer indications

Proprietary chemistry Lead and back-up compounds

available IP protected

Preclinical candidate screening ongoing

Clinical candidate selection in 2019

Phase I/II start planned in 2020

In vitro evidence for synergies with standard of care and suppression of tumorresistance

In vivo efficacy shown (alone and in combination with standard of care)

First in class YAP-TEAD program

Conclusions


Recent achievements and upcoming expected milestones


2019

Lani

fibra

nor

Odi

parc

ilAB

BV-

157

Rare pediatric disease designation MPS VI Phase IIa in MPS VI: last patient recruited Phase IIa in MPS VI results - H2 2019

YAP-

TEAD

FDA decision to lift lanifibranor clinical hold Last patient Phase IIb NASH Last patient Prof. Cusi study in NAFLD

patients with TD2M

2020

Clinical candidate selection

ABBV-157 multiple-ascending dose in healthy volunteers and psoriatic patients phase I initiation

SAD(1) Phase I with ABBV-157 completed

(1) SAD: Single Ascending Dose

ABBV-157 development in psoriasis

Phase IIb NASH results – H1 2020 Phase II in NAFLD patients with TD2M

results – H1 2020

Launch of phase IB/II in MPS VI children

Launch of Phase I/II in mesotheliomapatients

Contacts

Inventiva

Frédéric Cren

CEO

[email protected]

+33 (0)3 80 44 75 00

Brunswick

Yannick Tetzlaff / Tristan Roquet Montégon

Media relations

[email protected]

+ 33 1 53 96 83 83

LifeSci Advisors

Monique Kosse

Investor relations

[email protected]

mailto:[email protected]



Documents

Developing breakthrough therapies in NASH and ... · Non-confidential – Property of Inventiva │ 2. DISCLAIMER. This document has been prepared by Inventiva (the "Company") solely