• Baseimmune unveils a new multi-pathway immunotherapy strategy, applying its computational protein design platform to develop next-generation therapies for fibrosis.
• Fibrosis is driven by complex and redundant biological pathways, limiting the effectiveness of single-target approaches.
• Baseimmune uses advanced computational protein design to target multiple pro-fibrotic pathways simultaneously.
• Initially focused on IPF, where approved single-target therapies only slow lung function decline.
• Fibrosis pipeline advancing toward proof-of-concept efficacy readouts in 2026 and 2027.
• Assembled world-class Scientific Advisory Board: John Cijiang He, Scott L. Friedman, Toby Maher, Paul Noble, and Joel Rurik.

Baseimmune, a biotechnology company leveraging computational protein design to create next-generation immunotherapies, today unveiled its new fibrosis-focused pipeline, beginning with IPF.

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Kevin Walton, Baseimmune CEO

IPF is a progressive and life-threatening condition marked by aberrant wound healing, dysregulated tissue repair, and persistent activation of pro-fibrotic fibroblasts. Despite decades of research, approved therapies only slow lung function decline and do not halt or reverse progression. The complex and redundant biology underlying fibrosis is widely believed to contribute to the limited effectiveness of single-target approaches.

“Fibrosis is a biologically complex, organ-specific disease process that has consistently challenged single-target drug development,” said Kevin Walton, US-based Chief Executive Officer at Baseimmune. “IPF in particular represents an area where patients have few options and biology has repeatedly outpaced traditional drug development. Over the past several months, we’ve been expanding our computational design engine to meet exactly this kind of complexity. Our approach is built for multi-pathway immune biology from the outset, designing proteins that influence interconnected signalling networks, not isolated components.”

“IPF is driven by redundant and interconnected biological circuits that sustain fibrotic progression,” said Dr. Joshua Blight, Co-founder and Chief Scientific Officer of Baseimmune. “Dysregulation across these pathways locks tissue into a self-reinforcing pro-fibrotic state. Our strategy is to engineer antigens that harness the body’s immune system to interrupt and reset these networks by engaging multiple pathways simultaneously, restoring balance with the goal of halting, and potentially reversing, disease progression.”

Baseimmune’s fibrosis strategy focuses on multi-pathway immune modulation, enabled by the company’s proprietary antigen-design platform. By integrating advanced computational design with emerging delivery modalities, the company aims to address the compensatory immune and stromal mechanisms that drive fibrosis progression. The company is advancing its IPF program through preclinical development, with key proof-of-concept efficacy readouts expected in 2026 and 2027.

To support this expansion, Baseimmune has established a Scientific Advisory Board (SAB) composed of leading experts in fibrosis biology and clinical science across lung, liver, kidney, and heart. The SAB is advising on target strategy, program design, and early translational planning.

The SAB comprises:

• John Cijiang He, MD: Professor of Medicine and Chief of the Division of Nephrology, Icahn School of Medicine at Mount Sinai; recognised leader in renal fibrosis, chronic kidney disease, and translational nephrology.
• Scott L. Friedman, MD: Professor of Medicine and Director of the Institute for Liver Research at the Icahn School of Medicine at Mount Sinai and Dean for Collaborative Research and Partnerships; recognised leader in hepatic fibrosis, stellate cell biology, and anti-fibrotic drug development.
• Toby Maher, MD: Professor of Medicine and Director of Interstitial Lung Disease at the Keck School of Medicine of USC; recognised expert in idiopathic pulmonary fibrosis and interstitial lung disease clinical research.
• Paul Noble, MD: Former Chair of Medicine at Cedars-Sinai Medical Center; recognised leader in pulmonary fibrosis biology and translational ILD research, elected to the National Academy of Medicine in 2025.
• Joel Rurik, PhD: Biotech entrepreneur; formerly of University of Pennsylvania and Karolinska Institutet; recognised for pioneering in vivo cellular immunotherapy approaches for fibrotic disease. Early work provided scientific proof-of-concept for approaches now being developed by companies such as Capstan Therapeutics (acquired by AbbVie).

“We’re excited to support Baseimmune as it brings a fundamentally new design approach to address the challenge of treating fibrosis,” said Toby Maher, Professor of Medicine and Director of Interstitial Lung Disease, Member of Baseimmune’s SAB. “Targeting the interconnected and compensatory pathways that drive fibrotic disease is essential if we’re going to make meaningful therapeutic progress. Baseimmune’s multi-pathway framework represents a promising and innovative step in that direction.”

“Baseimmune’s approach aligns with where the field needs to go,” said Scott Friedman, Director of the Institute for Liver Research at the Icahn School of Medicine at Mount Sinai, Member of Baseimmune’s SAB. “Fibrosis is sustained by redundant biological circuits, and overcoming that redundancy requires new thinking and new modalities. The platform that Baseimmune is building has real potential to change the trajectory of fibrotic disease.”

About Baseimmune

Baseimmune is a biotechnology company developing next-generation immunotherapies using advanced computational protein design. The company’s platform integrates multi-pathway antigen design, structural modelling, and experimental screening to create therapeutics engineered for complex, chronic disease biology. Based in London, Baseimmune is focused on fibrosis, where traditional single-pathway approaches have struggled to deliver durable impact.

For more information, visit www.baseimmune.co.uk

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IPF in particular represents an area where patients have few options and biology has repeatedly outpaced traditional drug development.