Henrik Landgren
Seminars
As interest grows in developing antifibrotics with cross-indication potential, this workshop critically examines whether a true “pan-antifibrotic” is biologically and clinically feasible. Through real-world data, mechanistic comparisons, and forward-looking trial design strategies, we’ll explore what it would take to deliver a truly universal fibrosismodifying
therapy.
This workshop will gather experts to discuss:
- Reviewing trials of known antifibrotic targets (e.g., LOXL2, galectin-3, autotaxin, integrins) and why translation across organs often fails
- Clarifying what pan-antifibrotic really means, is it shared MoA, cross-organ signal, or a generalized fibrosis resolution mechanism?
- How to design development programs (e.g., patient populations, biomarkers, endpoints) to test and support pan-organ antifibrotic claims in Phase 2 and beyond.
As GLP-1 receptor agonists continue to redefine the treatment landscape for metabolic diseases, antifibrotic developers face mounting pressure to demonstrate clinical value beyond metabolic control. This panel explores the evolving expectations for antifibrotic therapies in MASH and beyond, as well as the implications of real-world GLP-1 usage.
Key Questions for Discussion:
- Who are the patients not responding that would benefit from additional therapeutic?
- How do we position these therapeutics to help the most people in the context of the new approvals?
- What does combination therapy look like in the post-GLP-1 world? How must antifibrotics differentiate themselves and prove additive value?
- Do GLP-1s sufficiently address fibrotic burden in MASH patients with moderate-to severe disease (F2–F4), or is there still a clear need for targeted antifibrotics?
- What happens to fibrosis progression in patients who discontinue GLP-1s? Are we underestimating the risk of rebound pathology?
- How can clinical trials be designed to account for the variability in GLP-1 exposure, adherence, and metabolic response in real-world populations?
