developing breakthrough therapies in nash and ...2).… · non-confidential –property of...

Developing breakthrough therapies in

NASH and mucopolysaccharidosis

Corporate PresentationNovember 2019

Non-confidential – Property of Inventiva │ 2

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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

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Corporate Presentation | 2019

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

Inventiva: 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

A clinical stage partnership with AbbVie

– ABBV-157 RORg program with potential in several auto-immune indications: first phase I

completed and second one in 60 healthy volunteers and patients with chronic plaque

psoriasis ongoing

Compelling early stage pipeline

– YAP-TEAD program in late pre-clinical stage, clinical candidate selection expected in 2019

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

Strong US and European shareholder base and experienced senior management team

with a track record of operational and scientific excellence

Cash position allowing a runway until end of Q3 2020 post Phase IIb results in NASH


Validated oral small molecule-focused discovery engine targeting

nuclear receptors, transcription factors and epigenetic modulation


Power of discovery engine underpins deep pipeline

of clinical and discovery stage assets

Library of ~240,000

compounds of which

60% proprietaryWholly-owned

129,000 square

foot pharma-like

R&D facilities

Expertise: nuclear

receptors,

transcription

factors, epigenetic

targets

Strong

scientific team

of ~70 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 /

ProgramIndication Discovery

IND

EnablingPhase I Phase II Phase III

Commercial

Rights

Lanifibranor NASH

Phase IIb

results: H1

2020

Odiparcil MPS VI

Phase IIa

results: H2

2019

ABBV-157 Moderate to

severe psoriasis

Next

milestone:

H1 2020

HippoNon-small cell

lung cancer and

mesothelioma

Candidate

Selection:

2019

TGF-β Idiopathic

pulmonary

fibrosis (IPF)

Lead Op(1)

GAG clearance

ROR𝛾

pan-PPAR

YAP/TEAD

(1) Lead optimization means refining molecules in advance of selecting candidates


Key financials and shareholder base

ISIN code FR0013233012

Market Euronext Paris

Shares outstanding 26.846.112

Market cap(Nov. 4 2019)

€77m

Cash position(September 30 2019)

35,3m compared to €56,7m as

of December 2018. Runway to

end of Q3 2020 post NASH

phase IIb results

Revenues in H1

2019(September 30, 2019)

€3,4m compared to €2,2m in

2018 (9 months period)

R&D expenditures

in H1 2019(June 30, 2019)

€19,6m compared to €15,9m

in H1 2018

Key financials Shareholder base

Analyst coverage

HC Wainwright

LifeSci Capital

Jefferies

KBC

Société Générale

Gilbert Dupont

Ed Arce

Patrick Dolezal

Peter Welford

Lenny Van Steenhuyse

Delphine Le Louët

Jamila El Bougrini

Free float*13,3%

BVF20.2%

NEA11.6%

Novo 8.7%Sofinnova 7.0%

Employees & others 2.8%

Founders36.4%

* Including

Perceptive Advisors


Lanifibranor in Nonalcoholic

Steatohepatitis (NASH)


Lanifibranor is a differentiated pan-PPAR agonist with moderate and

well balanced activity on the 3 PPAR isoforms


CompoundPPARa

EC50 (nM)

PPARd

EC50 (nM)

PPARg

EC50 (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

cti

vati

on

hPPARa

hPPARd

hPPARg

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


OrganPPAR isoforms

activated

Reported

PPAR liabilities

Lanifibranor

effects

Heart PPARg Fluid retention

Cardiac hypertrophyNot observed

Skeletal

muscle PPARa Myofiber degeneration Not observed

Kidney PPARa

> 50% increases in

creatinine,

degenerative changes

in renal tubules

Not observed

Urinary

bladder PPARg

Proliferative changes

in bladder epitheliumNot observed

Source: Company data

Lanifibranor not associated with typical single or dual PPAR liabilities


Lanifibranor favorable safety profile supported by long and extensive

studies


6 month tox in rodents

6 month tox data in primates

12 month tox data in primates

2 year carcinogenicity studies in rats and mice

200+ healthy volunteers treated in Phase I trials

47 T2DM patients treated in Phase IIa study

97 SSc patients treated in a Phase IIb

Safety package

Recently generated safety data

Fourth and last DSMB for NATIVE trial in NASH recommending to continue the trial as

planned based on safety data from 228 patients, including 139 patients treated for

the whole study period

After review of carcinogenicity studies, FDA has lifted PPAR class clinical hold and

allowed long-term clinical studies in NASH with lanifibranor


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

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

Pe

rce

nt

ch

an

ge

of

base

lin

e

Adiponectin (PPARg)

Perc

en

t ch

an

ge f

rom

baselin

e

lanifibranor lanifibranor lanifibranor

Placebo 400 mg 800 mg 1400 mg 0

10

20

30

40

IVA337 IVA337IVA337

p=0.13

p<0.05

p<0.05

Pe

rce

nt

ch

an

ge

of

base

lin

e

HDL Cholesterol (PPARa/d)

Perc

en

t ch

an

ge f

rom

baselin

elanifibranor lanifibranor lanifibranor

Placebo 400 mg 800 mg 1400 mg -50

-40

-30

-20

-10

0

IVA337 IVA337IVA337

p=0.08

p<0.05

p<0.05

Pe

rce

nt

ch

an

ge

of

base

lin

e

Triglycerides (PPARa/d)

Perc

en

t ch

an

ge f

rom

baselin

e

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): +2.3

Homa-IR:

Lanifibranor (800/1400mg): -20%/-44%

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

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


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-

carcinomaDeath

Liver transplant

Reversible

40-50%

15-20%

Severe liver

damage

Healthy

Liver

NASHNAFLD

Cirrhosis

NASH

with

fibrosis2-3% 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

PPARa,d,g

Metabolism

FA uptake

FA catabolism

Lipogenesis

PPARg

Steatosis

Inflammation and Ballooning

NFkB-dependent gene

activation

Inflammasome

Ballooning

PPARa,d,g

Stellate cell proliferation

and activation

Collagen and fibronectin

production

PPARg

Fibrosis

Vascular

Portal pressure

LSEC capillarization

Intrahepatic vascular

resistance

PPARa,g


Lanifibranor shows consistent improvements in metabolic

parameters and histology while displaying anti-fibrotic activity


Methionine Choline

Deficient diet (MCD)

Choline-deficient amino-acid and

high fat diet

Foz / Foz

Carbon tetrachloride

(CCL4)Thiocetamide (TAA)

Diet induced obesity

high fat / high sucrose

HSC biologyMacrophages biologyHepatoma and muscle

cells biology

Endothelial biology

Metabolic models

NASH & NAFLD

models Fibrosis models Cirrhosis models

Lanifibranor improves

Insulin resistance

Non fasting glucose

Homa-IR

Lipid profile

Lanifibranor maintains

body weight

Lanifibranor reduces

Steatosis

Inflammation

Ballooning

Lanifibranor improves

NAS score


fibrosis

Lanifibranor inhibits

stellate cell activation

Lanifibranor reverses

NASH


Portal pressure

Established fibrosis

In Vivo

In Vitro


Pioglitazone PPARg 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), corporate presentation March 2019 page 14 ; Aramchol Arrest Phase II study (600 mg, 12 months) – press release June 12, 2018

pbo

19%

pbo

8%

pbo

12% pbo

6%pbo

6%

pbo

7%

51%

12%

19%

8%

25%

19%

0%

10%

20%

30%

40%

50%

60%

Pioglitazone Ocaliva Elafibranor CVC MGL-3196 Aramchol

Pati

en

ts w

ith

im

pro

vem

en

t, %

Resolution of NASH without worsening of fibrosis


NATIVE phase IIB study


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

Trial design

225 patients treated for 24 week + 4 week safety follow-up

Double blind randomized placebo controlledEnd of treatment Liver biopsyPlacebo, 75 patients

Lanifibranor, 800 mg once daily, 75 patients


Screening Liver biopsy

Principal investigators

Prof. Sven Francque (Antwerp University, Belgium)

Prof. Manal Abdelmalek (Duke University, USA)

Randomisation

1/1/1, stratification on T2DM patients

Study powered with 75 patients per group

Central reading

Status

Recruitment completed with 247 patients

randomized

4 positive DSMB reviews recommending to

continue the study without any changes

Clinicaltrials.gov identifier

NCT03008070

Inclusion criteria

Liver biopsy

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

Key secondary endpoints

Decrease of at least 2 points in NAS

Resolution of NASH (to NAFLD: steatosis ± mild inflammation)

Change in fibrosis score

Change in liver enzymes, inflammatory markers, glucose

metabolism parameters, plasma lipids parameters, adiponectin, …

Safety

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


NATIVE trial in NASH is fully recruited and results

are expected for first-half 2020


17 countries

►13 in EU

►United States

►Canada, Australia

►Mauritius

>70 sites

recruited

patients

14 sites in the

United-States

247 patients randomized, exceeding the initial target of 225 patients

Patients with moderate/severe NASH recruited: ~72% with NAS ≥ 6 and ~76% F2 or F3

~40% have type 2 diabetes allowing to conduct the planned sub-analyses

167 patients(1) had already completed the six-month study confirming that the treatment is

well tolerated

Results expected first-half 2020(1) Database extraction October 8 2019

CountryPatients

randomized

Europe 183 (74%)

US 36 (15%)

Australia 13 (5%)

Canada 8 (3%)

Mauritius 7 (3%)

Total 247 (100%)


NATIVE trial: baseline characteristics


Parameters

Patients without

diabetes

(N = 148 ; 60%)

Patients with

diabetes

(N = 99 ; 40%)

Total

(N = 247 ; 100%)

Gender Female 57% 60% 58%

Male 43% 40% 42%

Age Mean ± SD 51.8 ± 13.5 56.3 ± 10.4 53.6 ± 12.5

Median 54.0 57.0 55.0

Min ; Max 20 ; 76 28 ; 77 20 ; 77

Weight (kg) Mean ± SD 93.5 ± 19.0 92.8 ± 18.8 93.2 ± 18.9

Median 91.0 90.0 91.0

Min ; Max 51 ; 142 55 ; 145 51 ; 145

BMI (kg/m²) Mean ± SD 32.8 ± 5.5 33.0 ± 5.3 32.9 ± 5.4

Median 32.2 32.9 32.4

Min ; Max 21 ; 45 23 ; 44 21 ; 45

Male waist

circumference (cm)Mean ± SD 109.6 ± 12.6 112.2 ± 12.2 110.6 ± 12.4

Median 108.0 110.0 110.0

Min ; Max 88 ; 134 89 ; 142 88 ; 142

Female waist

circumference (cm)Mean ± SD 104.8 ± 13.5 105.7 ± 12.0 105.2 ± 12.9

Median 106.0 106.0 106.0

Min ; Max 76 ; 139 75 ; 138 75 ; 139

Fibrosis Score (%) F0 – F1 27% 20% 24%

F2 44% 36% 41%

F3 29% 43% 35%

Non-confidential – Property of Inventiva │ 19Corporate Presentation | 2019

Parameters DSMB # 1 DSMB # 2 DSMB # 3 DSMB # 4

Date of DSMB meeting June 2018 October 2018 March 2019 September 2019

# patients reviewed / % of

total patients in the study52 / 21% 94 / 38% 156 / 63% 227 / 92%

# patients having finished the

study / % of total patients in

the study

18 / 7% 36 / 15% 86 / 35% 139 / 57%

DSMB conclusion: continue

study as planned

NATIVE trial: lanifibranor is well tolerated and safe

as confirmed by four positive DSMBs


Ongoing Phase II trial in type 2 diabetes patients with NAFLD

evaluating the effect of lanifibranor on hepatic insulin sensitivity

(1) Intrahepatic triglycerides (2) Magnetic resonance elastography (3) De-novo lipogenesis ; (4) Levin J., EASL 2018. Bril, F & Cusi, K, 2017 Diabetes Care, 40:419-430. Younossi, Z., et al, 2018. Nat Rev Gastroenterol

Hepatol, 15(1): 11-20

Lanifibranor could be the drug of choice for NASH patients with TD2M: ~48% of NASH

patients have TD2M(4)


64 patients

24 week treatment

Double blind randomized placebo controlled

Healthy non-obese control group, 10 subjects

Placebo, 32 patients


Principal investigator

Prof. Kenneth Cusi (University of Florida)

Randomisation

Randomized (1:1), double-blind, placebo-controlled

Non-obese subject control group for the metabolic

and imaging procedures

N=64 calculated assuming a 35% relative reduction

of IHGT(1)

Status

IND approved

First Patient First Visit: August 2018

Results expected second-half of 2020

Primary endpoint

Change from baseline to week 24 in IHTG

Key secondary endpoints

Proportion of responders (IHTG, NAFLD

resolution)

Change in hepatic fibrosis (MRE(2), biomarkers)

Change in metabolic outcomes (insulin

sensitivity, DNL(3), glycemic control, lipids)

Safety

Clinicaltrials.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)


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)

Synthesis of

proteoglycans

(HS, CS, DS)

Synthesis

of soluble

DS and CS

Odiparcil

Odiparcil

Galactosyl transferase I (GTI)

Normal

GAGs level

Healthy Patient

Normal GAG

degradation

Odiparcil

GAGs level

reduction

Intracellular GAGs

reduction

MPS

GAGs

accumulation

GAG degradation is

defective

Normal

GAGs level

Odiparcil original mechanism of action could provide additive benefit to enzyme

replacement therapies (ERT) in MPS I, II, IVA, VI and VII patients


By producing soluble dermatan and chondroitin sulfates, odiparcil

can address several types of MPS

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

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

MPS VIMaroteaux-Lamy

syndrome

MPS VII Sly syndrome



Odiparcil decreases intracellular GAG accumulation in vitro in MPS

VI patient cells


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

MPS VI fibroblasts

GAG 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)

To

tal su

lfate

d G

AG

S (

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)

Flu

ore

scence inte

nsity

Odiparcil observed to reduce GAG accumulation in MPS VI patient cells

Odiparcil


Odiparcil decreases GAG accumulation and restores mobility

in a mouse model of established MPS VI disease



Odiparcil decreases GAG accumulation in tissues

Odiparcil restores mobility

Whole eyeLiver

Knee

(Distal femoral growth plate)

Odiparcil decreases knee

cartilage thickness

Decrease of GAG accumulation was also observed in spleen, kidney, and heart

Age at treatment onset: 12

weeks

Treatment duration: 6 months

0

5

10

15

20***

WT MPS VI MPS VI + Odi

*

GA

G in

liv

er

[Are

a *

Index]

0

10

20

30

40

50***


**

tim

e o

n p

ole

[sec]

0

5 0

1 0 0

1 5 0

2 0 0

2 5 0 * * *

- 3 2 %

W T M P S V I

* * *

M P S V I + O d i

Di

st

al

f

em

or

al

g

ro

wt

h

pl

at

e

th

ic

kn

es

s[

µm

]

-40%

-66%

0

1

2

3

4

5 p<0.001

Sulfate

d G

AG

(µg/m

g o

f w

et tisues)


p<0.001

-67%

p<0.001 p<0.05

p<0.001 p<0.01 p<0.001 p<0.001

Wild-type and MPS VI mice


Odiparcil decreases GAG accumulation in leukocytes which are

excreted through the urine



Odiparcil decreases intracellular

GAG levels in leukocytes

Soluble GAG produced from

Odiparcil are excreted in urine

0

2000

4000

6000 p<0.0001

WT MPS VI MPS VI + OdiSulfa

ted G

AG

(µg/m

g o

f cre

atin

ine)

Wild-type and MPS VI mice

0

20

40

60

80

%cells

with

> 1

0 G

AG

gra

nule

s

p<0.001p<0.001

MPS VI MPS VI+OdiWT


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)


iMProveS Phase IIa trial of odiparcil in MPS VI


More information on: http://www.improves-mpsvi-trial.com/

End of treatment

4 weeks

Placebo + ERT

Odiparcil, 250 mg bid + ERT

Odiparcil, 500 mg bid + ERT

Odiparcil, 500 mg bid and no ERT

Follow up

15 patients double blind + 5 patients open label

26 week treatment 4 weeks

Screening,

baseline and

randomization

6 weeks

Screening

(4w) and

preliminary

safety

assessment

(2w)

Safety

Clinical and biological

assessments (standard tests)

Pharmacokinetics

Odiparcil plasma levels

Efficacy

Leukocyte, skin and urinary GAG content

Activity and mobility tests (6 minute walk test, upper limb function, shoulder mobility

range)

Cardiac, vascular and respiratory functions

Eye impairment, hearing capacity, pain assessment, quality of life questionnaires

Endpoints

≥ 16yo

Phase IIa

► Phase III enabling study with evidence for dose selection

and PK / PD response characterization

► Clinicaltrials.gov identifier: NCT03370653

Population

Status

1st DSMB (Oct 2018): no safety concerns;

recommendation to initiate the core study

Four centers selected: UK, Germany, France, Portugal

Recruitment completed

Results expected second-half of 2019

15 patients

5 patients

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

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

ABBV-157


Key validating collaboration with AbbVie


Successful first Phase I and launch of a new clinical study

(1) Source: clinicaltrial.gov

Inventiva eligible to future milestone payments and sales royalties: next milestone

payment is expected for the first half of 2020

Target Product Profile: Humira in a pill + oral + better safety

Single ascending dose Phase I completed and second clinical study initiated: a randomized, double-blind,

placebo-controlled, multiple-dose study in 60 healthy volunteers and patients with chronic plaque psoriasis

(clinicaltrials.gov identifier: NCT03922607): start date May 2019 and completion September 2020(1)

RORg is a master regulator of Th17

differentiation and IL-17 expression

ABBV-157, a potent RORg, addresses large markets dominated by biologics

• Psoriasis, Rheumatoid Arthritis, Multiple Sclerosis, IBD, Uveitis, …

RORgt = Retinoic acid-related OrphanReceptor, gamma (thymus)

IL approach has been validated by several

successful biologics

ABBV-157 could target several diseases

Brand Name Company TargetSales

(2018, B€)

Stelara Janssen IL-12 and IL-23 4,7

Cosentyx Novartis IL-17A 2,5

Actemra Genentech IL-6 1,9

Taltz Eli Lilly IL-17A 0,8

Upcoming catalysts


Three transformational clinical outcomes expected in the short-term


Results phase IIa in MPS VI - H2 2019

ABBV-157 milestone when first psoriatic patient is treated - H1 2020

Results: phase IIb NASH - H1 2020

Lanifibranor

Odiparcil

ABBV-157

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]



developing breakthrough therapies in nash and ...2).… · non-confidential –property of...

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