- 비알코올성 지방간염(NASH)과 섬유증:중개연구와 전략 -

비알코올성 지방간염(NASH)과 섬유증을 테마로 한 이 컨퍼런스 프로그램에서는 간질환과 섬유증 영역에 참여하고 있는 Drug Discovery 연구자가 이 분야의 임상 연구와 전임상 연구의 최신 동향을 소개하며, 의약품 개발 가속화로 연결되는 중개연구를 위한 툴 및 접근에 대한 견해를 제시합니다.

Final Agenda

Recommended All Access Package:

11월 27일: 장기 칩과 미소 생리 시스템

11월 27일 Dinner Course: 쇼트코스 1:Drug Discovery 연구자를 위한 면역학 기초 강좌, 파트 1:면역계 개요

11월 28-29일: 비알코올성 지방간염(NASH)과 섬유증:중개연구와 전략

11월 29-30일: 인공 유도 다능성줄기세포(iPS 세포)

11월 29일 Dinner Course: 쇼트코스 4:Drug Discovery 연구자를 위한 면역학 기초 강좌, 파트 2:암면역과 자가면역

11월 28일(수)

7:00 Registration and Morning Coffee

현재 개발중인 NASH용 화합물

8:20 Welcome Remarks

Anjani Shah, PhD, Conference Director, Cambridge Healthtech Institute

8:25 Chairperson’s Remarks

Bryan C. Fuchs, PhD, Assistant Professor of Surgery, Harvard Medical School

8:30 Development of Dual PPAR Agonist and IVD in NASH

Dean W. Hum, PhD, CSO, 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. Additionally, GENFIT is developing a blood-based in vitro diagnostic to identify NASH patients who are at risk of disease progression and should be considered for therapeutic intervention - a key unmet clinical need.

9:00 Galectin 3 Inhibitor for Cirrhosis

Peter Traber, MD, CEO, Galectin Therapeutics

9:30 Presentation to be Announced

9:45 Sponsored Presentation (Opportunity Available)

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

현재 개발중인 NASH용 화합물(계속)

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.

11:15 KEYNOTE PRESENTATION: Targeting GLP-1 for NASH

Karin 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 Sponsored Presentation (Opportunity Available)

12:15 Luncheon Presentation (Sponsorship Opportunity Available) or Enjoy Lunch on Your Own

12:45 Session Break

중개연구 단계의 NASH 치료제 개발 프로젝트

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

Claus 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.

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

16:45 New NASH-Related Targets

Thomas F. Baumert, MD, Professor of Medicine, INSERM and University of Strasbourg

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

Gabriel 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

11월 29일(목)

8:00 Registration and Morning Coffee

NASH와 섬유증의 중개연구 툴

8:25 Chairperson’s Remarks

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


8:30 KEYNOTE PRESENTATION: Biomarkers to Assess the Impact of Therapeutics on Patients with Liver Fibrosis

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

9:00 Molecular MR Imaging to Monitor Fibrosis in NASH

Bryan C. Fuchs, PhD, Assistant Professor of Surgery, Harvard Medical School

There are a number of anti-fibrotic therapies entering clinical trials in NASH patients, but a major obstacle to their development is the lack of sensitive and noninvasive tools for assessing fibrogenesis. Here, we discuss our preclinical work to develop molecular imaging of collagen as a biomarker that could not only be used to select patients for clinical trials but also provide an early assessment of treatment efficacy.

9:30 Sponsored Presentation (Opportunity Available)

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

NASH와 섬유증의 중개연구 툴(계속)

10:45 NASH and Fibrosis Serum Biomarkers

Saurabh Gupta, PhD, Associate Director, Translational Medicine Group, Takeda

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

James 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 Talk Title to be Announced

Detlef Schuppan, MD, PhD, Director, Institute of Translational Immunology, University of Mainz

12:15 Brief Session Break

12:20 Bridging Luncheon Presentation (Sponsorship Opportunity Available) or Enjoy Lunch on Your Own

12:50 Close of Conference

* 주최측 사정에 따라 사전 예고없이 프로그램이 변경될 수 있습니다.

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