Day One

• Examining the evolution of antifibrotic drug development over the past decade, including scientific advances, regulatory progress, and persistent challenges
• Discussing lessons learned from clinical successes & failures that can inform future development strategies
• Envisioning the next decade: breakthrough opportunities in fibrosis resolution, precision medicine, and cross-indication therapeutic development

• Single-cell mapping across hundreds of human donors nominates surface targets that mark pathogenic fibroblasts in IPF and fibrotic liver
• Cell-depleting biologics directed against these targets (ARDA-101, ARDA-204) eliminate pathogenic fibroblasts and cut collagen production in human IPF lung and fibrotic liver tissue, with rapid, target-dependent depletion in vivo.
• Close target-effector cell distance and low pathogenic-cell burden in fibrosis enable efficient tissue-level killing with a wide therapeutic window.

• Design principles for targeted delivery approaches
• Leveraging fibroblast-selective targeting to concentrate drug exposure in target cells/tissue
• Balancing the complexity of targeted delivery with the therapeutic benefit & competitive differentiation

This informal session provides the perfect opportunity to connect with the industry frontrunners and key opinion leaders focusing on fibrosis across the Lung, Liver, Kidney, Cardiac, Gastrointestinal and Scleroderma Landscapes. Establish meaningful connections to build upon for the rest of the conference and gain exclusive first-hand insights into the latest research and developments driving progression across the cross-fibrosis disease field.

• Integrating single-cell and spatial datasets across lung, liver, kidney, joint, gut, skin, and other fibrotic tissues 
• Identifying conserved macrophage states that persist across organs to distinguish truly pan-fibrotic mechanisms from tissue-specific biology 
• Using cross-tissue atlases to prioritize targets, select the most relevant disease indications, and match mechanisms with fit-for-purpose translational models

• AT2 receptor agonism restores the protective arm of the renin–angiotensin system, promoting epithelial resilience and repair following alveolar injury – an early pathogenic event that can contribute to inflammation, metabolic dysfunction, vascular remodelling, and fibrosis
• Positioning the AT2 receptor as an upstream modulatory node at the intersection of fibrotic remodelling: where diverse pathological insults converge on shared profibrotic pathways, while disease-specific biology defines therapeutic opportunity and indication boundaries
• Translational evidence for AT2 receptor agonism in fibrotic disease in preclinical and early clinical studies

• Evaluating the rationale for artificial intelligence (AI)-enabled pan-fibrotic development approaches
• Discussing failures and successes of human-in-the-loop AI to prioritize cross-organ fibrosis drug targets and patient-relevant wet lab target validation at scale

• Examining the epithelial-fibroblast mechanistic interplay underlying PDE4 inhibitor efficacy in lung, skin, & gut fibrosis
• Assessing the translational pathway from preclinical models to clinical development & understanding efficacy benchmarks
• Identifying opportunities for pleiotropic anti-inflammatory & antifibrotic mechanisms in other progressive fibrosing diseases

• Determining when preclinical evidence is sufficiently robust to justify expanding an antifibrotic program into additional fibrotic indications rather than remaining disease-specific
• Identifying the biological, translational, regulatory, and commercial factors that should guide indication prioritization, including shared mechanisms, biomarker availability, clinical endpoints, and unmet need 
• Exploring whether future antifibrotic programs should be intentionally designed as multi-indication assets from discovery or whether expansion should remain a staged, indication-by-indication strategy

Immerse yourself in an engaging session in a relaxed atmosphere that encourages meaningful 

conversations and discussions. Explore a range of exciting poster presentations and showcase 

your own research and developments in the antifibrotics therapeutics space. Don’t miss out on the 

chance to connect, learn, and present. Get ready to be impressed!

• Understanding how senescent cells perpetuate pro-fibrotic signaling & prevent resolution even after initial injury removal
• Evaluating senolytic & senostatic approaches to eliminate or reprogram senescent cell populations in fibrotic tissues
• Assessing early clinical evidence for senescence-targeted therapies in promoting fibrosis regression across multiple organs

• Understanding how matrix stiffness and mechanical signaling create self-sustaining fibrotic pathways across organs, independent of the initiating injury or inflammation
• Identifying and validating druggable nodes across the mechanotransduction pathway, from focal-adhesion mechanosensors to downstream transcriptional effectors
• Applying emerging discovery platforms and translational models to develop selective mechanobiology-targeted therapies that disrupt fibrotic tissue while preserving normal homeostasis and repair