Original Agenda
We are actively working with our speakers to confirm their availability for the virtual event. Initial response from our speakers has been very positive, and we are optimistic we will have the new programs ready to share here soon.

Cambridge Healthtech Institute’s 2nd Annual

Targeting Fibrosis

Developing Medical Therapies for Fibrotic Diseases

September 17 - 18, 2020

CHI’s 2nd Annual Targeting Fibrosis conference will follow the model of last year’s successful launch by covering a mix of drug discovery successes and development challenges in the field of fibrosis. Presentations will focus on new molecular entities being targeted by small molecules, biologics, or newer modalities that show potential for reducing organ fibrosis. Most of the compounds with clinical success are in the lung, so much of the conference will focus on that organ. However, fibrosis of the kidney, skin, and other organs may also be covered to assess common scarring mechanisms and molecular pathways. Liver fibrosis will mostly be covered in the preceding NASH conference at this Discovery on Target event. We hope you can join us to share progress and discuss future directions in the field of fibrosis, an area whose disease burden is steadily increasing as the population of elderly, and thus, chronic disease and inflammation, rises.

Thursday, September 17

11:20 am Conference Registration for Part B Programs


12:20 pm Event Chairperson's Opening Remarks
An-Dinh Nguyen, Team Lead, Discovery on Target 2020, Cambridge Healthtech Institute
12:30 Plenary Keynote Introduction (Sponsorship Opportunity Available)

Tackling Undruggable Oncoproteins: Lessons from the VHL Tumor Suppressor Protein

William G. Kaelin, Jr., MD, Professor and Investigator, Howard Hughes Medical Institute, Oncology, Dana-Farber Cancer Institute

VHL tumor suppressor protein (pVHL) inactivation is common in kidney cancer and upregulates the HIF2 transcription factor. PT2977/MK-6482 is an allosteric HIF2 inhibitor now in Phase 3 testing. Thalidomide-like drugs (IMiDs) bind to cereblon which, like pVHL, is the substrate-binding unit of a ubiquitin ligase. IMiDs redirect cereblon to destroy the myeloma oncoproteins, IKZF1 and IKZF3. We have developed new assays for identifying drugs that can destabilize oncoproteins of interest.


De-Risking Early Drug Discovery

Panel Moderator:
Nadeem Sarwar, PhD, Founder & President, Eisai Center for Genetics Guided Dementia Discovery, Eisai, Inc.
  • Data Sciences
  • ​Novel Chemical Modalities
  • Investment and Partnering Models
  • COVID-19 Progress as Examples of Successful Partnerships
Anthony A. Philippakis, PhD, Chief Data Officer, Data Sciences & Data Engineering, Broad Institute; Venture Partner, GV
Andrew Plump, MD, PhD, President, Research & Development, Takeda Pharmaceuticals, Inc.
2:00 Close of Plenary Keynote Program
2:00 Dessert Break in the Exhibit Hall with Poster Viewing


2:45 Organizer's Welcome Remarks

Cambridge Healthtech Institute

2:50 Chairperson's Remarks

Cory M. Hogaboam, PhD, Professor, Medicine, Cedars-Sinai Medical Center


Small-Molecule Inhibitors Targeting Nox4 for the Treatment of Lung Fibrosis

Louise Hecker, PhD, Assistant Professor, Medicine, University of Arizona

Cell-Specific Roles of Integrin Alpha V in Inflammation and Fibrosis

Kevin Hart, PhD, Principal Scientist, Inflammation, Pfizer Inc.

Integrin-alpha V serves as a master driver of fibroproliferative diseases in multiple organs. We investigated roles for integrin-alpha V interactions on fibroblasts and cholangiocytes and defined novel roles for cell-specific expression of ITGAV in the regulation of inflammatory responses and in driving microenvironmental fibrogenesis.

John O'Neill, CSO, Xylyx Bio, Inc.

Xylyx IN MATRICOTM Fibrosis Assay Platform is a standardized fibrosis model that recapitulates the fibrosis disease environment using intact human fibrotic ECM, as well as patient-specific clinical data corresponding to the human tissue ECM substrates, enabling compound testing assays in diseased human ECM.

4:10 Sponsored Presentation (Opportunity Available)
4:25 Refreshment Break in the Exhibit Hall with Poster Viewing



ROCK Updates and New Fibrosis Targets

Masha Poyurovsky, PhD, Vice President, Discovery Biology, Kadmon Corporation

Molecular mechanisms linking changes in the mechanical environment during injury, repair, and fibrosis to cellular activation, regulate transient and persistent alterations that contribute to fibrosis. Kadmon will present data on two regulators of these mechanisms. ROCK, an intracellular regulator, integrating mechanical stress, biochemical signals, and activation of transcription of fibrotic ECM and CCN1, a matricellular protein, strongly induced at the sites on injury and fibrosis.


Inhibition of Dimeric Calpains Results in Reduction of Lung and Liver Fibrosis

Maria E. Fuentes, PhD, Executive Vice President, Research, Blade Therapeutics

Calpains are non-lysosomal, calcium-activated cysteine proteases that play multiple roles in a wide range of cell types. A subgroup of this calpain family, dimeric calpains (CAPN1, 2 and 9), have been shown to play a role in fibrotic disease models. Blade Therapeutics has developed selective calpain inhibitors that are active at inhibiting collagen production in in vitro systems and they reduce lung and liver fibrosis in vivo.


Caveolin, a New IPF Target

Brian Windsor, PhD, CEO, Lung Therapeutics
6:30 Dinner Short Course Registration (Premium Package or separate registration required)
7:00 Dinner Short Courses 10-12 (see Short Courses page for details)
9:30 Close of Day

Friday, September 18

7:00 am Registration
7:30 Interactive Breakfast Breakout Discussion Groups
Grab a cup of coffee and join a breakout discussion group. These are informal, moderated discussions with brainstorming and interactive problem solving, allowing participants from diverse backgrounds to exchange ideas and experiences and develop future collaborations around a focused topic. Visit the conference website for discussion topics and moderators.
8:30 Transition to Sessions


8:40 Chairperson's Remarks

John O’Neill, CSO, Xylyx Bio, Inc.


Targeting Integrins for Lung and Other Organ Fibrosis

Scott M. Turner, PhD, Vice President, Translational Sciences, Pliant Therapeutics

Characterization of IDL-2965, a Clinical-Stage Integrin Antagonist for the Treatment of IPF

Karl J. Kossen, PhD, Senior Vice President, Translational Science, Indalo Therapeutics

Targeting Autotaxin for Treating Idiopathic Pulmonary Fibrosis (IPF)

Gwanghee Lee, PhD, Senior Vice President, Translational Research, Bridge Biotherapeutics Inc.
10:15 Coffee Break in the Exhibit Hall with Poster Viewing and Poster Competition Winner Announced



Translational Pharmacology of TD139, an Inhaled Small-Molecule Galectin-3 Inhibitor for the Treatment of IPF

Rob Slack, PhD, Director of Pharmacology, Galecto, Inc.

Galectin-3 is a ß-galactoside-binding lectin highly expressed in fibrotic tissue of diverse etiologies and has been shown to play a key role in organ fibrosis. Galecto, Inc. has developed a number of high-affinity and selective galectin-3 inhibitors currently undergoing clinical investigation in fibrotic diseases of the lung and liver. This talk will focus on the translational pharmacology of these galectin-3 inhibitors and their potential as anti-fibrotic therapies.


Clinical Compounds for and against NOX4 for Targeting Fibrosis

Elias Papatheodorou, Chief Business Officer, GenkyoTex SA
11:55 Sponsored Presentation (Opportunity Available)
12:25 Session Break
12:35 Luncheon Presentation (Sponsorship Opportunity Available) or Enjoy Lunch on Your Own
1:05 Refreshment Break in the Exhibit Hall with Poster Viewing


1:50 Chairperson's Remarks

Vanessa M. Morales-Tirado, PhD, Principal Research Scientist I, Translational Immunology, AbbVie Bioresearch Center


Translational Trends in Fibrosis Drug Discovery

Carolyn Cuff, PhD, Lead, Translational Immunology & Discovery R&D, AbbVie

Humanized IPF Mouse Models

Cory M. Hogaboam, PhD, Professor, Medicine, Cedars-Sinai Medical Center

Initiated by the intravenous injection of cells from IPF lung biopsy or explants into SCID mouse strains, IPF cells promote persistent, non-resolving, lung remodeling in SCID mice, unlike cells from normal lung samples. Potential advantages and pitfalls of human-specific targeting approaches in a humanized SCID model of pulmonary fibrosis will also be addressed. 


From Genes to Mechanisms to Medicines: The Arc of Discovery for Fibrotic Diseases

Anna Greka, MD, PhD, Associate Professor of Medicine, BWH/Harvard Medical School/Broad Institute
3:25 Talk Title to be Announced
Ji Zhang, PhD, Scientist, Cardiorenal Metabolic & Ophthalmologic Drug Discovery, Merck Research Labs
3:55 Close of Conference

Please click here to return to the agenda for Targeting NASH

Choose 2 Short Courses and 2 Conferences/Training Seminars
Sept. 15 Short Course: SC1: Immunology Basics: Focusing on Autoimmunity and Cancer
Sept. 16-17 Conference: Targeting NASH
Sept. 17 Dinner Short Course: SC12: DNA-Encoded Libraries
Sept. 17-18 Conference: Targeting Fibrosis