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April 22-25, 2019 | Boston, MA

57 Expert Speakers ♦ 4 Days  3 Streams ♦ 4 Workshops  Seminar Day ♦ 15+ Hours of Networking

Day One
Tuesday April 23

Day Two
Wednesday April 24

08.20
Chair’s Opening Remarks

  • Laurent Fischer Senior Vice President, Head Liver Therapeutic Area Allergan

Critically Assessing Patient Recruitment Challenges Now & in the Future

08.30
NASH/NAFLD: Does Genotype Connect to Phenotype?

  • Linda Morrow Vice President & Chief Medical Officer , ProSciento

Synopsis

  • The slow rise of individualized medicine
  • Genetic markers of risk for NASH/NAFLD
  • Is NASH the poster child for individualized medicine?

09.00
NAFLD & NASH from the Patient Perspective – What Are Our Next Steps?

Synopsis

  • Presenting the work of the European Liver Patients Association (ELPA)
  • Outlining what can be learnt from HCV patient advocacy and policy successes
  • Transferring good practice from HCV, HCC to NASH/NAFLD
  • Overcoming basic problems for patients in NAFLD/NASH
  • Where and how we move the field forward?

Achieving Metabolic & Hepatic Effects for the Treatment of NASH

09.30
The Therapeutic Potential of Inhibitors of Steatosis for the Treatment of NASH

Synopsis

  • Demonstrating the work of the Pfizer Internal Medicine Research Unit to treat NASH by targeting the root cause of the disease, the accumulation of hepatic lipids
  • Presenting the scientific rationale for targeting Diacylglycerol Transferase 2 (DGAT2) to ameliorate steatosis will be discussed
  • Sharing results of DGAT2 inhibition in preclinical models of NASH will presented

10.00
Morning Break & Networking

Case Studies of Emerging Candidates (Continued)

11.00 Targeting the Wnt Pathway

  • Proving liver fibrosis is the most important histological feature that is associated with long term outcomes of NASH patients
  • Targeting the Wnt signaling pathway could potentially provide an important therapeutic intervention for liver fibrosis

Weilin Xie
Senior Principal Scientist
Celgene

11.30 Rationale for the Use of Bile Acid Modulators for the Treatment of NASH

  • Demonstrating preclinical data of bile acid modulators
  • Reviewing literature and presenting an argument for the use of bile acid modulators against NASH

Patrick Horn
Chief Medical Officer
Albireo Pharma

12.00 Targeting Alpha V Integrins for Liver Fibrosis

  • Anti-fibrotic treatment represents an unmet medical need for patients with fibrosis diseases, such as NASH, kidney fibrosis, and IPF
  • Alpha V integrins are membrane proteins that bind to latencyassociated peptide (LAP) of TGF-β as its principal ligands and activate mature TGF-β to lead to fibrogenesis
  • Morphic Therapeutic is leading the development of a new generation of oral drugs to target alpha V integrins for fibrotic disorders

Min Lu
Director, Head of Fibrosis
Morphic Therapeutics

The Relationship of NASH in the Context of Wider Liver & Cardiovascular Disease

11.00 Combating NASH as a Metabolic, Non-Communicable Disease with Significant Global Burden

  • Investigating strategies for target discovery
  • Evaluating options for precision medicine

Maria-Chiara Magnone
Vice President, Metabolic Complications
Janssen Research & Development

11.30 Understanding Hepatocellular Carcinoma as an Extension of NASH: The Cirrhosis-HCC Connection, Practical Implications for Preclinical & Clinical Drug Testing

  • Investigating cellular and molecular mechanism of fibrosis-HCC crosstalk
  • Analyzing caveats of current practices of preclinical anti-fibrotic drug testing – short duration, mild disease, reliance on surrogate endpoints instead of clinically-relevant long-term outcomes
  • Strategizing overcoming these caveats, and how to move towards using clinically-relevant end-points in preclinical drug evaluation in practice

Yury Popov
Assistant Professor of Medicine
Harvard Medical School

12.00 The Endocrinologist Perspective: Profiling NASH in the Context of Metabolic Syndrome

  • The systemic and heterogenous nature of NAFLD and its relationship to type 2 diabetes and cardiovascular disease
  • Common mechanistic underpinnings

Manu Chakravarthy
Senior Vice President & Chief Medical Officer
Axcella Health

Safety & Efficacy Within the Clinic

11.00 How to Develop a Differentiated FXR Agonist that Avoids the Side Effects of 1st Generation FXR Drugs

  • Reviewing the NASH clinical “icebreaker” as the FXR agonist OCA
  • How to avoid OCA showing HDL lowering and pruritus
  • Explaining how the 2nd generation FXR agonist GS-9674 differs from OCA to avoid these liabilitie

Claus Kremoser
Chief Executive Officer
Phenex Pharamceuticals

11.30 The Polypharmacological Anti-NASH Effects of Namodenoson are Mediated via De-Regulation of the Wnt/bcatenin Pathway

  • Namodenoson is a small molecule agonist at the A3 adenosine receptor with excellent safety profile tested in >200 patients
  • Definitive molecular mechanism of action including de-regulation of Wnt/b-catenin
  • Current Phase 2 in NAFLD/NASH patients is on going

Pnina Fishman
Chief Executive Officer
CanFite BioPharma

12.00 Targeting Galectins in NASH Fibrosis

  • Galectins have an potential role in the pathogenesis of fibrosis across multiple organs
  • Galectin-3 is now being targeted clinically for the treatment of NASH
  • The talk will focus on the challenges of targeting fibrosis in NASH, generally, and the evidence for Gal-3

Richard Marshall
Chief Medical Officer
Galecto Biotech

12.30
Lunch & Networking

Reviewing Clinical Advances of NASH Therapeutics in Phase 2 & Phase 3 Clinical Trials

13.30
Showcasing the Clinical Development of MGL3196

  • Rebecca Taub Chief Medical Officer, Executive Vice President Research & Development , Madrigal Pharmaceuticals

Synopsis

  • Reviewing Madrigal’s clinical development of MGL3196
  • Advancing understanding surrounding thyroid hormone receptor beta agonist reducing lipotoxicity in the NASH liver
  • Critically analysing MGL-3196 as the first truly beta selective THR-beta agonist

14.00
Afternoon Break & Networking

15.00
Aramchol Phase 2b Results & Phase 3 Outlook

Synopsis

  • NASH develops through an interplay of several cell types in the liver which exist in varying abundances, although the precise nature of these interactions remains unknown
  • Single Cell Sequencing (SCS) advances the sequencing capabilities of RNAseq by providing quantifiable RNA transcript reads on a single-cell basis
  • By applying SCS technology to NASH and healthy liver samples, an understanding of cellspecific biology can be achieved as it relates to the pathological features of NASH

15.30
An Update of Elafibranor & Use as the Backbone for Combinations

  • Dean Hum Senior Executive Vice President & Chief Scientific Officer , Genfit

Synopsis

  • Overview of Elafibranor including disease model data
  • Presenting data from combination program to identify synergistic mechanisms of action with Elafibranor

16.00
Chairs’ Closing Remarks