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Genfit Sa — Investor Day (November 2016)

67 slides from Genfit Sa's investor day presentation, Nov 14, 2016

  1. Slide 1: AASLD 2016 Analyst Investor Presentation

    2016.11.14 AASLD 2016 ANALYST INVESTOR PRESENTATION November 14, 2016 CONFIDENTIAL 1

  2. Slide 2: Disclaimer

    Disclaimer Important informa?on and forward looking statements • THIS PRESENTATION HAS BEEN PREPARED BY GENFIT AND IS FOR INFORMATION PURPOSES ONLY. • THE INFORMATION, OPINIONS AND FORWARD LOOKING INFORMATION CONTAINED IN THIS PRESENTATION SPEAK ONLY AS OF THE DATE OF THIS DOCUMENT, UNLESS OTHERWISE

  3. Slide 3: GENFIT: Innovative Company in Diagnostic & Treatment of Metabolic & Inflammatory Diseases

    GENFIT: Innova?ve Company in Diagnos?c & Treatment of Metabolic & Inflammatory Diseases • Public company focused on metabolic diseases & associated complicaAons, including liver related disorders › Elafibranor (GFT505) lead program Phase 2b completed, first-in-class PPAR α/δ candidate for NASH › Biomar

  4. Slide 4: GENFIT's Pipeline is Well-diversified

    GENFIT’s Pipeline is Well-diversified, With R&D Efforts Well Distributed between Late Stage and Early Stage Programs IndicaAon Program MOA Program Maturity Elafibranor PPAR α/δ End of Enrollment Phase 3 (GFT505) agonist H1 2017 NASH Biomarker ValidaAon Steps DiagnosAc Q1 2017 Lead Elafibranor PPARα/δ Ph

  5. Slide 5: Agenda

    Agenda NAFLD, Scale of the Problem Dr. Stephen A. HARRISON, MD, FACP, FAASLD, COL (ret.), USA, MC – Visi=ng Professor of Hepatology, Radcliffe College of Medicine, University of Oxford (USA) Medical Director, Pinnacle Clinical Research Member of the Interna=onal Steering CommiOee for the RESOLVE-IT P

  6. Slide 6: NAFLD- Scale of the Problem

    NAFLD- Scale of the Problem Stephen A. Harrison, MD, FACP, FAASLD COL (ret.), USA, MC Visi?ng Professor of Hepatology Radcliffe College of Medicine, University of Oxford Medical Director, Pinnacle Clinical Research

  7. Slide 7: Disclosure Information

    Disclosure Informa?on (Relevant Speaker Financial Rela=onships) • Dr. Stephen Harrison discloses the following relevant financial rela?onships with commercial interests within the past twelve months: – Gilead, Abbvie, Alexion, Merck: Speakers’ Bureau – Fibrogen, Genfit, Pfizer, BMS, Merck, NGM Biopharm

  8. Slide 8: Epidemiology and Natural History

    Epidemiology and Natural History

  9. Slide 9: Global Epidemiology of NAFLD

    Global Epidemiology of NAFLD Systema?c literature search • 729 studies evaluated, 86 studies included • 57 studies analysed NAFLD prevalence, 15 studies analysed for NASH prevalence Abbreviations: N, North; NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis; S, South. Younos

  10. Slide 10: NAFLD Prevalence in Prospective US Studies

    NAFLD Prevalence in 2 Prospec?ve US Studies San Antonio Dallas Heart Study Study NAFLD Overall 46% 30% Hispanic 58.3% 45% Caucasian 44.4% 33% African American 35.1% 24% NASH Overall 12.2% – Among NAFLD 29.9% – Abbreviations: NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis

  11. Slide 11: Prevalence of NAFLD in South Texas

    Prevalence of NAFLD in South Texas 75% 80 (42/56) 70 60.8% (48/79) 60 % Prevalence 50 40.7% 40.5% (158/388) (83/205) 40 27.1% (19/70) 23.5% 30 (4/17) 16.7% 19% (1/6) (30/158) 20 7.7% 10 (30/388) 0 Paredes et al, AASLD 2016

  12. Slide 12: NAS breakdown for NASH patients

    NAS breakdown for NASH pa?ents n=1 NAS 3 3.4% n=5 17.24% n=8 NAS 4 27.6% NAS 5 n =10 n=6 31.0% NAS 6 20.7% NAS 8 NAS 7 n=0 NAS 8 Roberts et al, AASLD 2016

  13. Slide 13: Prevalence of NAFLD in South Texas

    Prevalence of NAFLD in South Texas • 172 biopsies completed. We have – 30 NASH • 5 stage 0 • 13 stage 1 • 9 stage 2 • 3 stage 3 • 0 stage 4 • Caveat: Remember these are asymptoma?c pa?ents with no previous h/o liver disease Roberts et al, AASLD 2016

  14. Slide 14: Natural History of NAFLD

    Natural History of NAFLD Isolated • None to very minimal Faiy Liver progression to fibrosis • No ↑ risk of death compared >80% with the general populaAon Faiy Liver with Mild InflammaAon NAFLD Possible sampling variability with some risk of progression ~7% over 6.5 years ~11% over 15 years, but NASH s

  15. Slide 15: Risk Stratification in NASH

    Risk Stra?fica?on in NASH Clinical Histologic7 • Older age1 • Advanced fibrosis • Male gender2 • Fibrosis • Metabolic syndrome1 • Portal inflamma?on • Diabetes mellitus (DM) 1 • NASH • Family history of DM3 • Ballooning • AST/ALT ra?o4 • Low platelets5 • PNPLA3 genotype6 Abbreviations: ALT, alanine ami

  16. Slide 16: Predictive Value of Liver Aminotransferases in NAFLD

    Predic?ve Value of Liver Aminotransferases in NAFLD Serum ALT can be normal in up to nearly 60% of NAFLD pa?ents with NASH1 Serum ALT can be increased in up to 53% of NAFLD pa?ents with no NASH2,3 Therefore, serum ALT level alone is not predic?ve of NASH or fibrosis level1-3 • Normal ALT cannot rule

  17. Slide 17: Metabolic Comorbidities Associated with NASH

    Metabolic Comorbidi?es Associated with NASH Obesity 81.83% (95% CI, 55.16–94.28) Diabetes 43.63% (95% CI, 30.28–57.98) Metabolic 70.65% (95% CI, 54.64–82.79) syndrome Dyslipidemia 72.13% (95% CI, 54.59–84.78) Hypertension 67.97% (95% CI, 56.31–77.74) Abbreviation: NASH, nonalcoholic steatohepatitis.

  18. Slide 18: The Association Between Metabolic Syndrome and NASH

    The Associa?on Between Metabolic Syndrome and NASH P <.0001 • Patients with NAFLD, no overt diabetes (N = 304) • NASH confirmed in 120/304 patients • Metabolic syndrome* was independently associated with – Histologic NASH (OR, 3.2; 1.2–8.9) – Severe fibrosis (OR, 3.5; 1.1–11.2) NASH Non-NASH *Metabo

  19. Slide 19: Clinical Predictors of Advanced Fibrosis in NAFLD

    What Are the Clinical Predictors of Advanced Fibrosis in NAFLD? Hypertension OR 1.61 (95% CI, 1.21–2.01; P = .0374) Diabetes OR 1.64 (95% CI, 1.13–2.17; P = .0258) Hypertension + OR 1.69 (95% CI, 1.11–2.28; P = .0246) Diabetes Hypertension + Diabetes + OR 1.72 (95% CI, 1.13–2.31; P = .0205) Visceral

  20. Slide 20: NASH and Hepatocyte Ballooning are Clear Risk Factors

    NASH and Hepatocyte Ballooning are Clear Risk Factors, and Appropriate Targets to Prevent Disease Progression NASH Ballooning › NASH and hepatocyte ballooning iden?fied as histological features correlated with clinical outcomes and mortality. › In-line with the clinical use of Elafibranor. Angulo, Gas

  21. Slide 21: The PRELHIN Study—Prognostic Relevance of Liver Histology in NAFLD

    The PRELHIN Study—Prognos?c Relevance of Liver Histology in NAFLD • Interna?onal study of NAFLD (N = 619; diagnosed between 1975 and 2005) • Biopsies read centrally; median follow-up 12.6 years Death or OLT 193 pa?ents Death due to CV disease 74/193 (38.3%) Key Outcomes Death due to nonliver cancer

  22. Slide 22: Cardiovascular mortality due to NASH and isolated hepatic steatosis

    Cardiovascular mortality due to NASH and isolated hepa?c steatosis NASH Isolated hepatic steatosis NASH Steatosis Reference population Reference population Time (years) Time (years) Ekstedt M, et al. Hepatology. 2006;44:865-73

  23. Slide 23: NAFLD and Liver Transplantation

    NAFLD and Liver Transplanta?on NASH 4000 HCV +14% ALD 3500 HCV / ALD New waitlist registrations 3000 2500 +170% 2000 +45% 1500 -9% 1000 500 0 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 Annual trends in new liver transplant waitlist registrations Wong RJ, et al. Gastroenterology. 2015;148:547-

  24. Slide 24: Disease Definitions

    Disease Defini?ons • NASH – >5% steatosis on biopsy – Evidence of ballooning degenera?on – Evidence of lobular inflamma?on • NASH Resolu?on – Resolu?on of ballooning degenera?on – Resolu?on or improvement of lobular inflamma?on to a score of 0 or 1 – Gestalt diagnosis of pathologist that NASH is no lon

  25. Slide 25: Thank You

    THANK YOU

  26. Slide 26: Elafibranor, First-in-class, has Pluripotent Activities

    Elafibranor, First-in-class, has Pluripotent Ac?vi?es Elafibranor, Fast-track Treatment for the Resolu?on of NASH PPARα and δ Regulate Mul?ple Pathways Essen?al in NASH Professor Vlad Ratziu Professor of Hepatology Hôpital PiAé Salpêtrière and Université Pierre et Marie Curie Paris, France Principal I

  27. Slide 27: Elafibranor Treatment for Resolution of NASH

    ELAFIBRANOR TREATMENT FOR RESOLUTION OF NASH 27

  28. Slide 28: Elafibranor, First-in-class, has Pluripotent Activities

    Elafibranor, First-in-class, has Pluripotent Ac?vi?es PPARα and δ Regulate Mul?ple Pathways Essen?al in NASH i Fibrogenesis (TGFβ1, αSMA, Col1α1) i OxidaAve stress (CAT, SOD) i InflammaAon(MCP-1, IL-6, TNFα) i steatosis (h lipid uAlizaAon) FIBROSIS i OxidaAve stress (CAT, SOD) i Atherogenic lipid profi

  29. Slide 29: Elafibranor Phase 2b in NASH

    Elafibranor Phase 2b in NASH GOLDEN505 study Trial design Updated definiAon of NASH resoluAon without worsening of fibrosis 9 countries 274 (more stringent) 56 centers Randomized pa?ents Score of 0 for ballooning Score of 0 or 1 for inflammaAon TREATMENT PERIOD No score objecAve for steatosis Placebo (N

  30. Slide 30: Elafibranor 120mg has significant effect vs placebo

    Elafibranor 120mg has significant effect vs placebo in both global and NAS≥4 popula?ons GOLDEN-505: The first internaAonal Phase 2 clinical trial with “ResoluAon of NASH without worsening of fibrosis” as the Primary endpoint (56 centers, 9 countries, 52 weeks) (ITT) 30

  31. Slide 31: Elafibranor responders have significant histological responses

    Elafibranor responders have significant histological responses on NASH and Fibrosis Elafibranor 120mg Responders vs Elafibranor 120mg Non-Responders 1 0.5 0 Mean change versus baseline -0.5 -1 # ### -1.5 # ### -2 -2.5 Pa?ents who resolved their NASH showed significant reduc?on in liver fibrosis while non-

  32. Slide 32: Changes in Hepatocyte Ballooning and Lobular Inflammation Drive Fibrosis Response

    Changes in Hepatocyte Ballooning and Lobular Inflamma?on Drive Fibrosis Response Ballooning InflammaAon Steatosis Fibrosis Improvers Fibrosis Worseners Fibrosis Improvers Fibrosis Worseners Fibrosis Improvers Fibrosis Worseners 100 100 100 90 90 90 80 N=7 N=78 N=129 N=23 80 N=9 N=72 N=138 N=18 80 N=5

  33. Slide 33: Activity Index Correlates with Change in Fibrosis Score and Response

    Ac?vity Index Correlates with Change in Fibrosis Score and Response AcAvity Index = Ballooning Score + InflammaAon Score Fibrosis Improvers Fibrosis Worseners ∆ fibrosis score Mean±SE 1.5 70 N=39 N=77 N=27 N=5 N=7 N=82 60 1 R² = 0.94595 50 % Improvers/worseners 0.5 40 ∆ AcAvity Index 30 0 -4 -3 -2 -1

  34. Slide 34: Elafibranor Significantly Improves Cardiometabolic Parameters

    In Addi?on to Improvement on Histology, Elafibranor Significantly Improves Cardiometabolic Parameters Elafibranor 120mg vs placebo on Elafibranor 120mg vs Placebo lipid markers on HbA1c 0 -0.06 -0.1 -0.2 Effect size vs placebo (%) -0.3 -0.4 -0.5 -0.6 -0.7 # -0.8 HbA1c GFT-80 FDA/AASLD recommandaAon “It

  35. Slide 35: Histological Efficacy of Elafibranor Combined with Cardiometabolic Improvement

    Histological Efficacy of Elafibranor Combined with Cardiometabolic Improvement } Significant effect of Elafibranor 120mg on resoluAon of NASH without worsening of fibrosis (new recommended definiAon) : • Elafibranor is the only NASH drug candidate to demonstrate efficacy on the regulatory endpoint of resolu?on

  36. Slide 36: Elafibranor Phase 3 Design in NASH: Details and Timing

    Elafibranor Phase 3 Design in NASH: Details and Timing ~ 250 centers ~ 1000 paAents ~ 2000 paAents (worldwide) SUBPART H ANTICIPATED MARKET AUTHORIZATION FIRST TREATMENT PERIOD EXTENSION PERIOD Placebo Placebo Elafibranor 120mg Elafibranor 120mg 2:1 2:1 TRIAL INITIATION Q1 2016 72-WEEK INTERIM ANALYSIS

  37. Slide 37: Pediatric Nonalcoholic Steatohepatitis and Unmet Needs for Treatment

    Contributing Authors Pediatric Nonalcoholic Steatohepatitis and Unmet Needs for Treatment Professor & Vice-Chair (Research) Department of Pediatrics Chief, Pediatric GI /Hepatology/Nutrition Columbia University Genfit Conference, November, 2016

  38. Slide 38: Pediatric NAFLD

    Pediatric NAFLD What is it? An alcohol-like disease of the liver that develops in children who drink no or little alcohol

  39. Slide 39: All the News

    All the News 's Fit to Print” | VOL. CLXII... No. 56,532 + Thee ¢ New York Cimes © NEW YORK, SATURDAY, JUNE 14, 2014 Late Edition By ANAHAD O’CONNOR Despite major gains in fighting hepatitis C and other chronic liv- er conditions, public health offi- cials are now faced with a grow- ing epidemic of

  40. Slide 40: Why Is It Important?

    Why Is It Important? • Most common liver disease • Usually asymptomatic • Under-recognized • Cumulative injury, early onset • Non-liver morbidity • Health disparity • Compounded damage with drugs/viruses/alcohol • Cirrhosis, liver cancer, transplant

  41. Slide 41: Overall, 9-10% children have NAFLD in SD

    Estimated Prevalence of Fatty Liver in Obese Children Hispanic Hispanic BOYS GIRLS black black Overall, 9-10% children have NAFLD in SD Obese>normal; older>younger; Hispanic>non-Hispanic; boys>girls Pediatrics. 2006. 118;1388-93

  42. Slide 42: How Is NAFLD Suspected?

    How Is NAFLD Suspected? • Usually obese • Hepatomegaly • Elevated ALT (and ALT>AST) • Liver imaging (MRI>U/S) • Family history of NAFLD • Other metabolic syndrome concomitants • RUQ pain (+/-) • Lack of abnormal tests indicaAng other cause

  43. Slide 43: Practice Guideline for Diagnosis and Management of NAFLD

    GASTROENTEROLOGY 2012;142:1592-1609 AGA The Diagnosis and Management of Non-alcoholic Fatty Liver Disease: Practice Guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology NAGA CHALASANI, MD, FACG,* ZOB

  44. Slide 44: How Is Pediatric NASH Diagnosed?

    How Is Pediatric NASH Diagnosed? Liver Biopsy Is Required -

  45. Slide 45: Treatments for NASH that also treat these co-morbidities are most desirable

    Treatments for NASH that also treat these co-morbidities are most desirable

  46. Slide 46: NEJM 2010 JAMA 2011 Lancet 2015

    NEJM 2010 JAMA 2011 Lancet 2015 Gastro 2016

  47. Slide 47: Adult/Pediatric cases reviewed

    10. Adult/Pediatric cases reviewed Pediatric Total (n=3,447) (n=1,473) (n=4,920) Center (%) No. (%) No. (%) CWRU/CCF/CINC (16) 159 (11) 724 (15) CU/UCSD (10) 615 (42) 957 (19) DUKE/JHU/NWU (13) 152 (10) 614 (12) TU (10) 162 (11) 500 (10) SLU/BCM (13) 185 (13) 638 (13) SMC/UB/VMMC/UW (12) 68 (5) 476

  48. Slide 48: Fibrosis stage in Pediatric Biopsies Can be Considerable

    Fibrosis stage in Pediatric Biopsies Can be Considerable

  49. Slide 49: Clinical Correlates of Histopathology in Pediatric NASH

    GASTROENTEROLOGY 2008;135:1961-1971 Clinical Correlates of Histopathology in Pediatric Nonalcoholic Steatohepatitis HEATHER M. PATTON,* JOEL E. LAVINE,* MARK L. VAN NATTA,® JEFFREY B. SCHWIMMER,* DAVID KLEINER, ' JEAN MOLLESTON,®" and the Nonalcoholic Steatohepatitis Clinical Research Network Table

  50. Slide 50: Treatment Options for Children is Limited

    Treatment Options for Children is Limited • Lifestyle intervention • Diet composition • Exercise • Weight loss • Vitamin E (natural form) 800 IU/day • No other RCT clinical trials in children currently • Failed trials with metformin, cysteamine, omega 3 FA

  51. Slide 51: TONIC trial: Vitamin E increased resolution of NASH

    TONIC trial: Vitamin E increased resolution of NASH (from initial definite or borderline NASH) Vitamin E Placebo Metformin (n=43) (n=38) (n=39) Resolved (%) 58% 28% 41% P-value 0.006 --- 0.23 Lavine et al, JAMA, 2011

  52. Slide 52: Elafibranor in the Pediatric Space

    Elafibranor in the Pediatric Space • Juvenile toxicology studies ongoing • PK/PD studies need to be peformed in children with NAFLD for dose determination • Preliminary preclinical data and phase 2b data in adults encouraging • Phase 2b trial in children with biopsy proven NASH to be done once PK/PD

  53. Slide 53: NAFLD Summary

    NAFLD Summary • Most common pediatric liver disease • Frequent dyslipidemia with other metabolic syndrome features • Cirrhosis found even in 8 year olds • Unique subset of NAFLD histology in children • Treatment should be aimed at NASH with ability to ameliorate metabolic syndrome co-morbidities • E

  54. Slide 54: The Liver's Weighty Problem

    THE LIVER’S WEIGHTY PROBLEM As obesity rates soar, a sometimes fatal liver disease is becoming epidemic sy mitch Lestie Downloaded from

  55. Slide 55: Unmet Needs in Primary Biliary Cholangitis

    Unmet Needs in Primary Biliary Cholangitis Velimir A. Luketic, MD Division of Gastroenterology, Hepatology and Nutrition Virginia Commonwealth University School of Medicine Richmond, VA

  56. Slide 56: PBC is a Rare Disease: 0,05% Prevalence in the General Population

    PBC is a Rare Disease: 0,05% Prevalence in the General PopulaAon (90% Female between 40-60 Years Old), What is PBC ? How is PBC diagnosed and what is the prevalence ? Primary Biliary Cholangitis – PBC PREVALENCE (Primary Biliary Cirrhosis): „ PBC is a rare disease is a chronic cholestatic liver dise

  57. Slide 57: PBC Symptoms

    PBCSymptoms Typical (Primary are Biliary Cholangitis) Pruritus and FaAgue Untreated Strong PBCtoEvolves Rationale to Cirrhosis Enter PBC as Newestand Liver Failure Therapeutic Area What’s the typical paAent journey ? SYMPTOMS „ PRURITUS, a specific symptom of cholestasis: 20-70% „ Fatigue: 78% (no c

  58. Slide 58: UDCA the First Line Therapy in PBC, Has its Own Limits

    PBCis(Primary UDCA the First Biliary Cholangitis) Line Therapy in PBC, Strong Rationale But HasPBC to Enter its Own LimitsTherapeutic Area as Newest Current limits of first line therapy in PBC UDCA – « bear » bile acid Despite the UDCA treatment… „ Effective dose 13-15 mg/kg/day „In 90% of patients U

  59. Slide 59: Predictive Models - Key Points

    PredicAve Models - Key Points • Predictive survival models for treatment with UDCA - all formulas post treatment ALP and bilirubin - if “response” survival same as population at large • Response to UDCA therapy is suboptimal in 40 – 50% • Disease is not eliminated – progression is slower Regulatory

  60. Slide 60: Obeticholic acid (OCA): A modified bile acid

    ObeAcholic acid (OCA): A modified bile acid What is OCA ? Clinical trial results (Nevens, NEJM, 2016) Modified bile acid (chenodeoxycholic acid) „ Selective FXR agonist „ Impairs bile acid synthesis „ Stimulates choleresis via upregulation of bile acid transporters „ Clinical trial with 5 mg and 10 m

  61. Slide 61: Ongoing Unmet PBC Need

    ONGOING UNMETPBC NEED(Primary Biliary Cholangitis) IN PBC: ParAal/Non-Responders and PaAents Intolerant to Currently Strong Rationale to EnterAvailable Therapies PBC as Newest (UDCA,Area Therapeutic OCA) PopulaAon First line Ursodiol or second line OCA Partial responders PBC population that could be

  62. Slide 62: Beneficial Effects of PPAR Agonism on BA Metabolism and Cycling

    PBC (Primary Biliary Cholangitis) Beneficial Effects of PPAR Agonism on BA Metabolism and Cycling Strong Rationale to Enter PBC as Newest Therapeutic Area Clinical Evidences of PPAR (fibrates) efficacy in PBC S. Lens et al. Liver International 2014, 34:197-203 Y. Zang et al. Drug Design, Development and

  63. Slide 63: Known Effect of PPARα activation on Bile Acids

    PBC (Primary Biliary Cholangitis) Known Effect of PPARα acAvaAon on Bile Acids Strong Rationale to Enter PBC as Newest Therapeutic Area Result of PPARα acAvaAon PPARα activation Increased Decreased Increased Decreased Anti-inflammatory Bile acid detoxification Bile acid synthesis: Bile acid ouput Bil

  64. Slide 64: PPAR Have Shown Effects on ALP, Accepted Surrogate Endpoint for PBC

    PBC PPAR(Primary Have ShownBiliary Cholangitis) Effects on ALP, Accepted Strong Rationale Surrogate to Enter PBC asEndpoint for PBC Newest Therapeutic Area PPAR (Fenofibrate) in PBC (not approved for this indication) C. Levy et al. Aliment. Pharmacol. Ther. 2011; 33:235-242 C. Cheung et al. Aliment.P

  65. Slide 65: Pruritus: OCA exacerbates Pruritus While PPAR Reduces Pruritus

    PBC is Pruritus (Primary a MajorBiliary Cholangitis) CholestaAs Symptom: OCA exacerbates Strong Rationale toPruritus While Enter PBC PPAR Reduces as Newest Pruritus Therapeutic Area Pruritus (major PBC symptom) : DifferenAaAng factor vs. ObeAcholic acid ObeAcholic Acid exacerbates pruritus PPAR (Beza

  66. Slide 66: Elafibranor Has Consistently Shown Effects on ALP in NASH Patients

    PBChas Elafibranor (Primary BiliaryShown Consistently Cholangitis) Effects on ALP in NASH Strong Rationale to Enter PBCPaAents as Newest Therapeutic Area ALP reduction induced by Elafibranor Ph2a Ph2b Ph2b Pre-T2D GOLDEN505 GOLDEN505 Elafibranor in NASH: „Effects on ALP and GGT increase with the level

  67. Slide 67: Unmet need in PBC: Key takeaway

    PBC (Primary Biliary Unmet need in Cholangitis) PBC: KeyPBC Strong Rationale to Enter takeaway as Newest Therapeutic Area „ PBC is a chronic progressive liver disease characterized by immune mediated destruction of the small intrahepatic bile ducts that if untreated progresses to end-stage liver dis

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