Developing breakthrough therapies in NASH and mucopolysaccharidosis - - PowerPoint PPT Presentation
Developing breakthrough therapies in NASH and mucopolysaccharidosis - - PowerPoint PPT Presentation
Developing breakthrough therapies in NASH and mucopolysaccharidosis Corporate Presentation April 2019 DISCLAIMER This document has been prepared by Inventiva (the "Company") solely for the purpose of this presentation. This
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 marchés financiers), 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 │ 3 Corporate 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 ROR program in phase I with AbbVie, Phase I data due in 2019 – YAP-TEAD program in late pre-clinical stage, clinical candidate selection expected in 2019 Strong balance sheet and experienced senior management team with a track record of
- perational and scientific excellence
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Validated oral small molecule-focused discovery engine targeting nuclear receptors, transcription factors and epigenetic modulation
Corporate Presentation | 2019
Power of discovery engine underpins deep pipeline of 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
- f ~90 people
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Deep pipeline approaching major near term value inflection points
Corporate Presentation | 2019
Candidate / Program Indication Discovery IND Enabling Phase 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
Phase I results: 2019 Hippo
Non-small cell lung cancer and mesothelioma
Candidate Selection: 2019 TGF-β
Idiopathic pulmonary fibrosis (IPF)
Lead Op(1) GAG clearance ROR pan-PPAR
YAP/TEAD
(1) Lead optimization means refining molecules in advance of selecting candidates
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Strong cash position and shareholder base
ISIN code FR0013233012 Market Euronext Paris Shares outstanding 22.294.677 Market cap
(February 26 2020)
€84m Cash position
(December 31 2018)
€56,7m compared to €59.1m as of December 2017. 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
Jefferies HC Wainwright KBC Société Générale Gilbert Dupont Kepler Chevreux LifeSci Capital Peter Welford Ed Arce Lenny Van Steenhuyse Delphine Le Louët Jamila El Bougrini Arsene Guekam Patrick Dolezal
Corporate Presentation | 2019
Free float* 22.1% BVF 15,0% Novo 8,8% Sofinnova 7,1%
Employees & Others 3,1%
Founders 43,9%
*Including Perceptive Advisors
Lanifibranor in Nonalcoholic Steatohepatitis (NASH)
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Lanifibranor is a differentiated pan-PPAR agonist with moderate and well balanced activity on the 3 PPAR isoforms
Corporate Presentation | 2019
Compound PPAR EC50 (nM) PPAR EC50 (nM) PPAR 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
- 4
25 50 75 100 125 150
%Activation
hPPAR hPPAR hPPAR
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
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Favorable safety profile differing from previously developed PPARs
Corporate Presentation | 2019
Organ PPAR isoforms activated Reported PPAR liabilities Lanifibranor effects
Heart PPAR
Fluid retention Cardiac hypertrophy
Not observed
Skeletal muscle PPAR
Myofiber degeneration
Not observed
Kidney PPAR
> 50% increases in creatinine, degenerative changes in renal tubules
Not observed
Urinary bladder PPAR
Proliferative changes in bladder epithelium
Not observed Plasma volume and heart weight after administration of PPAR agonists
Source: Company data
Plasma Volume Heart Weight
20 40 60
* * * *
Rosi Mura IVA337 Tesa Plasma volume (mL)
0.0 0.2 0.4 0.6
* * * *
Rosi Mura IVA337 Tesa Heart weight (% BW)
Control Rosi (3 mg/kg/d) Rosi (10 mg/kg/d) Mura (10 mg/kg/d) Mura (100 mg/kg/d) IVA337 (100 mg/kg/d) IVA337 (1000 mg/kg/d) Tesa (1 mg/kg/d) Tesa (10 mg/kg/d)
Lani Lani
Lani Lani
mg/kg/day; 9 W rat study
Single PPAR Dual PPAR Dual PPAR Pan PPAR Single PPAR Dual PPAR Dual PPAR Pan PPAR
Lanifibranor not associated with plasma volume expansion or heart weight increase
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Phase IIb study in systemic sclerosis confirmed favorable safety profile of lanifibranor
Well conducted 48 week phase IIb clinical trial in early diffuse systemic sclerosis adult patients The primary endpoint on skin score was not met, nor secondary efficacy endpoints Lanifibranor showed a favorable trend in patients’ global assessment of disease activity indicating a perceived benefit by patients Within this fragile and poly-medicated population, lanifibranor was observed to be associated with a favorable safety profile without apparent adverse interactions with immunosuppressive background therapies, and no cardiac or renal safety concerns Presence of mostly mild or moderate edema maybe due to twice daily administration of lanifibranor possibly leading to higher PPAR pathway activation reflected by high adiponectin levels in a systemic sclerosis population prone to present edema Adiponectin levels in NATIVE NASH patients significantly lower compared to FASST systemic sclerosis patients
Corporate Presentation | 2019
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No cardiac or renal safety concern observed in the phase IIb study in systemic sclerosis study after one year of treatment
Corporate Presentation | 2019
Description of fold in creatinine over time – observed cases under treatment - mITT population Description of fold in NT-ProBNP over time– observed cases under treatment - mITT population
Value (Mean ± 95% CI) Week 12 Week 24 Week 48 Week 12 Week 24 Week 48 Value (Mean ± 95% CI)
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Phase I and Phase IIa clinical studies(1) demonstrated beneficial effects on key metabolic markers
Corporate Presentation | 2019
Insulin resistance (HOMA-IR, adiponectin) Dyslipidemia (increase in HDL-C, reduction of TG) Lanifibranor metabolic markers in type II diabetic patients Good overall tolerance and no major safety findings No increases of creatinine, LFTs, or CPK No changes in blood pressure No signal of fluid overload or hemodilution No clinically relevant weight gain 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
Placebo 400 mg 800 mg 1400 mg
100 200 300
IVA337 IVA337 IVA337
p=0.08 p=0.05 p=0.05
Percent change of baseline
Adiponectin (PPAR)
Percent change from baseline
lanifibranor lanifibranor lanifibranor
Placebo 400 mg 800 mg 1400 mg
10 20 30 40
IVA337 IVA337 IVA337
p=0.13 p<0.05 p<0.05
Percent change of baseline
HDL Cholesterol (PPAR)
Percent change from baseline
lanifibranor lanifibranor lanifibranor
Placebo 400 mg 800 mg 1400 mg
- 50
- 40
- 30
- 20
- 10
IVA337 IVA337 IVA337
p=0.08 p<0.05 p<0.05
Percent change of baseline
Triglycerides (PPAR)
Percent change from baseline
lanifibranor lanifibranor lanifibranor
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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.
Corporate Presentation | 2019
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 Reversible 40-50% 15-20% Severe liver damage
Healthy Liver NASH NAFLD Cirrhosis
NASH with fibrosis 2-3% per year 30-40%
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Lanifibranor’s mechanism of action addresses all the key features of NASH
Corporate Presentation | 2019
Insulin sensitivity HDLc TG PPAR Metabolism FA uptake FA catabolism Lipogenesis PPAR, Steatosis Inflammation and Ballooning NFkB-dependent gene activation Inflammasome Ballooning PPAR Stellate cell proliferation and activation Collagen and fibronectin production PPAR Fibrosis
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Overview of NATIVE trial design (I/II)
Corporate Presentation | 2019
More information on: http://www.native-trial.com/
Trial design 225 patients 24 week treatment Double blind randomized placebo controlled End of treatment Liver biopsy Placebo, 75 patients Lanifibranor, 800 mg once daily, 75 patients Lanifibranor, 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
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Overview of NATIVE trial design (II/II)
Corporate Presentation | 2019
17 countries worldwide ► 13 in EU ► US ► Canada ► Australia ► Mauritius 92 sites involved 78 sites activated 68 sites screening Status March 23, 2019: 594 patients screened, 164 patients randomized 3 positive DSMB reviews Results expected first-half 2020 14 sites selected in the US
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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
Corporate Presentation | 2019
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 Principal investigator Prof. Kenneth Cusi (University of Florida) Randomisation N=64 assuming a 35% reduction of IHGT(1) Status IND approved First Patient First Visit: August 2018 Results expected first-half of 2020 Primary endpoint Change from baseline to week 24 in IHTG Key secondary endpoints Proportion of responders; change in hepatic fibrosis (MRE(2), biomarkers); change in metabolic outcomes Safety Clinicaltrials.gov identifier: NCT03459079 Trial design
Odiparcil – MPS
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Mucopolysaccharidoses (MPS) are devastating diseases with high unmet medical need
Corporate Presentation | 2019
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: – MPS I: 1/100,000(1) – MPS II: 1/100,000(1) – MPS IV type A: 1/40,000 to 1/200,000(1) – MPS VI: 1/240,000 to 1/400,000 (1) – MPS VII: very rare (1)
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 VI Consequences
(1) Retinal degeneration with no corneal clouding
Odontoid hypoplasia Kyphoscoliosis, genu valgum Pebbled skin Diarrhoea
(1)
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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
Corporate Presentation | 2019
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
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Unique mechanism of action potentially synergistic with ERT
Corporate Presentation | 2019
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
- f soluble
DS and CS
Odiparcil
Odiparcil
Galactosyl transferase I (GTI)
MPS VI fibroblasts GAG overloaded cells Intracellular CS storage Extracellular GAG
5 10 15 20 25 10- 8 10- 7 10- 6 10- 5
MPS VI (IC50=3 µM)
Veh.
Odiparcil concentration (M) Total sulfated GAGS (µg/mL)
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) Fluorescence intensity
Odiparcil observed to reduce GAG accumulation in MPS VI patient cells
Odiparcil
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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
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-Lamy syndrome
MPS VII Sly syndrome
Corporate Presentation | 2019
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Odiparcil decreases GAG content in vivo and improves mobility in a MPS VI model
Corporate Presentation | 2019
Source: Company data
10 20 30 40 p<0.001
WT MPS VI MPS VI + Odi
p<0.05
time on pole [sec]
In vivo in MPS VI affected mice Odiparcil decreases GAG accumulation in various tissues and intracellular GAG accumulation in lymphocytes Odiparcil decreases GAG accumulation in cornea, restores corneal structure and decreases GAG accumulation in cartilage Odiparcil restores mobility
GAG Granules: 1 -1 0 > 1 0 WT 40.4 45.8 9.4 MPS VI 15.1 32.6 51.3 MPS VI + Odi 19.7 47.4 21.5
10 20 30 40 p<0.001
WT MPS VI MPS VI + Odi
p<0.001
GAG in liver [Area * Index]
± Odiparcil* Given in food 6 months Wild-type and MPS VI mice Treatment 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
- 100%
Odiparcil decreases intra-cellular GAG Odiparcil improves animal mobility
Chow diet Odiparcil : 4.5 g/kg in food Chow diet Odiparcil : 4.5 g/kg in food
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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
Corporate Presentation | 2019
Odiparcil is well distributed in tissues and organs poorly penetrated by recombinant enzymes
Heart Cornea Bone Cartilage
Odiparcil(1) rhASB(2) Not detected Not tested Not detected
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Odiparcil shows promising results in poorly vascularized tissues not treated by ERT
Corporate Presentation | 2019
Source: Company data
Decreases in GAG accumulation and improvements in corneal structure expected to improve corneal function and ocular impairment
WT control MPSVI
epithelium stroma
MPS VI + Odi
10 20 30 40 p<0.001
WT MPS VI
p<0.0001
MPS VI + Odi thickness (µm)
Odiparcil effect on corneal structure and epithelium thickness
Chow diet Odiparcil : 4.5 g/kg in food
Odiparcil decreases trachea and knee cartilage thickness
20 40 60 80 100 p<0.0001
- 31%
Trachea cartillage thickness in µm
MPS VI MPS VI + Odi WT
Chow diet Odiparcil : 4.5 g/kg in food 100 200 300 p<0.0001
- 26%
WT MPS VI
p<0.0001
MPS VI + Odi Distal femoral growth plate thickness [µm]
Chow diet Odiparcil : 4.5 g/kg in food
By decreasing GAG storage in cartilage, odiparcil improves cartilage- linked disease manifestations
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Odiparcil has the potential to positively differentiate versus current MPS treatment options
Corporate Presentation | 2019
Source: Company evaluation
Effect on mobility Effect on eye, cartilage, bones, heart valves, spinal cord compression Distribution type Oral Intravenous Infusion Transplantation Odiparcil Aldurazyme, Elaprase, Naglazyme, Vimizim, Mepsevii HSCT (Hematopoietic stem cell transplantation)
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Odiparcil overall development plan in MPS VI
Corporate Presentation | 2019 (1) leukoGAG: GAG levels in circulating leukocytes; UGAG: urinary GAG)
Biomarker Study 12 MPS VI patients Phase IIa, 6-month treatment 24 MPS VI adults Add on to ERT and Naïve Phase Ib/II, 6-month treatment 9 MPS VI children Add on to ERT Phase III MPS 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
R&D collaborations and Hippo pathway program update
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Key validating collaborations with AbbVie and Boehringer Ingelheim
Corporate Presentation | 2019
ABBV-157: Phase I studies initiated RORγ collaboration in inflammatory disease RORγ program addresses large markets currently dominated by biologics and could prove to be superior to biologics AbbVie has started Phase I study with ABBV-157 Inventiva remains 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 Inventiva eligible to up to ~€170m in milestones plus royalties Program progressing as planned with first screening performed
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YAP-TEAD program: significant progress achieved and clinical candidate selection planned in 2019
The program is expected to enter into Phase I/II enabling preclinical development in 2019
Corporate Presentation | 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
- ngoing
Clinical candidate selection in 2019 Phase I/II start planned in 2020 In vitro evidence for synergies with standard of care and suppression of tumor resistance In vivo efficacy shown (alone and in combination with standard of care) First in class YAP-TEAD program
Near-term catalysts
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Recent achievements and upcoming expected milestones
Corporate Presentation | 2019
2018
Lanifibranor Odiparcil Collab.
Phase IIa MPS VI results - H2 2019 Launch Phase Ib/II in children – H2 2019 Rare pediatric disease designation MPS VI
Discovery Finance
Last patient Phase IIb NASH Last patient Prof. Cusi study in NAFLD patients with TD2M
2019
Start Phase I with ABBV-157 Clinical candidate selection
MPS VI biomarker study results
Juvenile tox results Capital increase
YAP/TEAD: In vivo POC
2 year carcinogenicity study results
US fibrosis indication patent US IND First patient in NAFLD Phase II
Phase I ABBV-157 results - 2019
Contacts Inventiva Frédéric Cren CEO info@inventivapharma.com +33 (0)3 80 44 75 00 Brunswick Julien Trosdorf / Yannick Tetzlaff Media relations inventiva@brunswickgroup.com + 33 1 53 96 83 83 LifeSci Advisors Monique Kosse Investor relations monique@lifesciadvisors.com