Non-alcoholic Steatohepatitis (NASH) is the result of a fatty liver that starts to undergo fibrosis whose scarring can eventually lead to a liver that is non-functional. The increasing global incidence of NASH may be linked to the concomitant rise in diabetes, obesity and other metabolic disorders all over the world. No pharmaceutical treatment yet exists for NASH, but it is an area of active research and industry focus, with several treatments in late-stage clinical trials. However, many translational challenges remain, such as non-invasive ways to measure disease progression and response to treatment and best ways to model the disease outside of the patient. Join fellow drug discovery researchers working in the area of liver disease and/or fibrosis to stay abreast of clinical and preclinical advances in the field and share insights on translational tools and approaches for spurring drug development progress.

Final Agenda


Recommended All Access Package:

27 November: Organ-on-a-Chip and MicroPhysiological Systems

27 November Dinner Course: SC1: Immunology Basics for Drug Discovery, Part 1: Immune System Overview

28-29 November: NASH and Fibrosis: Translational Research and Strategies

29-30 November: Induced Pluripotent Stem Cells

29 November Dinner Course: SC4: Immunology Basics for Drug Discovery, Part 2: Immune-Oncology and Autoimmunity

Wednesday 28 November

7:00 Registration and Morning Coffee


8:50 Welcome Remarks

Anjani Shah, PhD, Conference Director, Cambridge Healthtech Institute

8:55 Chairperson’s Remarks

Rebecca Taub, MD, CMO & Executive Vice President, R&D, Madrigal Pharmaceuticals

9:00 Development of Elafibranor - a Dual PPARα/δ Agonist for the Treatment of NASH

Robert Walczak, PhD, EVP, Head of Research, Genfit

Elafibranor is a first-in-class PPARα/δ agonist which has demonstrated in a Phase IIb study NASH resolution without the worsening of fibrosis while also improving cardio-metabolic risk. Furthermore, NASH resolution correlated with fibrosis improvement. Elafibranor is safe, tolerable and is now being investigated in Phase III. NASH is a multifactorial disease and it is increasingly acknowledged that combination therapies with drugs with complementary mechanisms of action will be required to increase the proportion of patients that reach all treatment goals. Recent data from studies in disease models indicate that Elafibranor is a universal backbone for combination drug therapies in NASH.

Metabolon 9:30 Metabolomic Profiling to Identify Molecular Determinants of Liver Disease

Schauer_NicolasNicolas Schauer, PhD, Managing Director Metabolon, Inc.

A diverse set of disease drivers including genetics, environmental cues, microbiota metabolism and lifestyle influences come together resulting in an uncertain natural history of NAFLD/NASH. Metabolomics provides a comprehensive picture of the metabolome and maps metabolites to their key biochemical pathways providing a holistic assessment of complex diseases.

10:00 Grand Opening Coffee Break in the Exhibit Hall with Poster Viewing


10:45 Thyroid Hormone Receptor Agonists

Rebecca Taub, MD, CMO & Executive Vice President, R&D, Madrigal Pharmaceuticals

I will present topline public data from our latest clinical study on MGL-3196, a β-selective thyroid hormone receptor (THR) agonist. MGL-3196 is an orally administered, small-molecule, liver-directed compound that is currently in Phase II development for NASH. The data show highly significant reduction of liver fat and biomarkers of inflammation and fibrosis at 12 weeks in a 36 week serial liver biopsy study.


Conde-Knape_KKarin Conde-Knape, PhD, Corporate Vice President, Cardiovascular and Liver Disease Research, Novo Nordisk

GLP1 receptor agonists have been successfully positioned for the treatment of diabetes and obesity.  It has been documented that weight loss either by dietary or surgical intervention leads to improvement in NASH and fibrosis.  Initial clinical data suggests a beneficial effect of GLP1 receptor agonists in NASH clinical trials.  An overview of GLP1 receptor agonism in the treatment of NASH and future directions will be provided.

11:45 Enjoy Lunch on Your Own


13:45 Chairperson’s Remarks

Diane Shevell, PhD, Director, Clinical Biomarkers and Innovative Medicines Development, Bristol-Myers Squibb

13:50 Animal Models of NASH in Preclinical Drug Development

Iwona Ksiazek, PhD, Senior Investigator I, Chemical Biology & Therapeutics, Novartis Institutes for Biomedical Research

Despite the tremendous progress in development and characterization of animal models of NAFLD/NASH made over the last years, we still lack robust and appropriately validated preclinical models with proven clinical translatability. Advantages and limitations of selected mouse NASH models used to test pharmacological agents will be discussed and a newly developed diet-induced obesity model of NASH with fibrosis will be presented, covering the diet, systemic metabolic and inflammatory milieu, as well as the histological spectrum of human NASH disease and its application in drug discovery, including validation with drugs currently in clinical development for NASH.

14:20 LXR Inverse Agonists for the Treatment of NASH

Kremoser_CClaus Kremoser, PhD, CEO, Phenex

Nuclear Receptor targeted drugs such as FXR, TRbeta or PPAR agonists have emerged as effective approaches to combat NASH but they all come with limitations. LXR is known as a functional counterplayer of FXR and as such, inhibiting LXR function by inverse agonist ligands should yield similar effects than activating FXR. Animal data show that beyond strong anti-steatotic properties, LXR inverse agonists demonstrate novel, unprecendeted antidiabetic effects.

14:50 Interactive Breakout Discussion Groups

This session features various discussion groups that are led by a moderator/s who ensures focused conversations around the key issues listed. Attendees choose to join a specific group and the small, informal setting facilitates sharing of ideas and active networking. Details on the topics and moderators are available on the conference website.

Animal Models for Fibrosis

Moderator: Iwona Ksiazek, PhD, Senior Investigator I, Chemical Biology & Therapeutics, Novartis Institutes for Biomedical Research

  • Who has used what?
  • Pros and cons of different models
  • What looks promising

NASH Drug Development Challenges

Moderator: Rebecca Taub, MD, CMO & Executive Vice President, R&D, Madrigal Pharmaceuticals

  • Role of biomarkers
  • European v. FDA guidance
  • Defining target population

16:00 Refreshment Break in the Exhibit Hall with Poster Viewing

16:45 NEW: Report-Back from Breakout Discussions

17:15 Navigating Liver-Derived Omics Data for Translational Research

Florian Nigsch, PhD, Senior Investigator I, Chemical Biology and Therapeutics, Data Science,Novartis Institutes for BioMedical Resesarch, Basel

Translational research is of paramount importance for drug discovery, and computational techniques can play a major role. This talk will focus on common challenges of computational translational liver research, and then provide some insights with specific examples based on omics datasets of disease models, in vitro and in vivo, including single cell analyses of human liver tissue.

17:45 MTBL0036, a Promising, New Anti-NASH and Antifibrotic Candidate

Baverel_GGabriel Baverel, PhD, President, Founder, CSO, Metabolys, Inc.

MTBL0036 is a small molecule, orally active with favorable PK characteristics, and safe. In the STAM mouse model of NASH, it greatly diminished the NAFLD Activity Score by drastically reducing inflammation and ballooning, the major drivers of fibrosis. In mice fed a choline deficient amino acid defined high fat diet, it greatly ameliorated liver fibrosis. Unlike that of most anti-NASH candidates in development, its molecular target is not nuclear.

18:15 Welcome Reception in the Exhibit Hall with Poster Viewing

19:15 Close of Day


Thursday 29 November

8:00 Registration and Morning Coffee


8:55 Chairperson’s Remarks

Iwona Ksiazek, PhD, Senior Investigator I, Chemical Biology & Therapeutics, Novartis Institutes for Biomedical Research

9:00 KEYNOTE PRESENTATION: Biomarkers to Assess the Impact of Therapeutics on Patients with Liver Fibrosis

Shevell_DDiane Shevell, PhD, Director, Clinical Biomarkers and Innovative Medicines Development, Bristol-Myers Squibb

Non-alcoholic steatohepatitis (NASH), the most advanced form of non-alcoholic fatty liver disease (NAFLD), is characterized by steatosis with inflammation and liver cell injury, which can lead to liver fibrosis.  Non-invasive, accurate biomarkers are needed to identify patients at high risk for NASH and to monitor disease progression.  The potential use of non-invasive biomarkers to characterize patients with NASH and their response to an investigational therapy will be presented.

9:30 Identification of NAFLD in Primary Care: Can Algorithms and Transient Elastography (TE) Predict Fibrosis? 

Helena Cortez-Pinto, MD, PhD, Professor, Department of Gastroenterology, Faculty of Medicine of Lisbon 

NAFLD is extremely frequent in primary care. However it is generally unrecognized or devalued by general practitioners. Although screening in the general population is not recommended, the rules of referral to specialists and the population to be screened needs better definition. Definition of these groups, what are the best algorithms and role of TE to predict fibrosis severity will be presented.

10:00 Coffee Break in the Exhibit Hall. Last chance for poster viewing.


10:45 IL-1 beta Small Molecule Inhibitors for the Treatment of NASH 

Juan J. Perez, PhD, Professor, Department of Chemical Engineering, Universitat Politecnica de Catalunya-BarcelonaTech

11:15 Modelling of NAFLD/NASH with Patient-Derived iPS Cells

Adjaye_JJames Adjaye, PhD, Professor,Director, Institute for Stem Cell Research and Regenerative Medicine, Heidrich Heine University, Dusseldorf, Germany

Steatosis leading to NAFLD and NASH should be considered as a multifactorial metabolic disease. Studies based on rodents, patient liver-biopsies and serum have provided useful insights into the etiology of steatosis. Though useful, a better understanding of disease mechanisms, biomarker discovery and drug development necessitates the use of hepatocyte-like cells differentiated from patient derived induced pluripotent stem cells. My talk will focus on genes and associated pathways implicated in disease progression.

11:45 NEW: Close of Conference