INNATE IMMUNITY · CROHN’S DISEASE

A different approach
to Crohn’s disease.

Developing Etiostat to address an underlying defect in the body’s first line of defence.

Restoring innate immunity.
Rethinking disease prevention.

Science founded on innate immunityOur goal: prevent recurrence after surgery

01 / OUR APPROACH

Addressing what
may drive disease.

Our research focuses on a potential underlying cause of Crohn’s disease: an impaired innate immune response.

Innate immunity is the body’s first line of defence. Pyrinome’s approach is based on the hypothesis that an inadequate initial response to bacteria in the bowel can contribute to the development and persistence of Crohn’s disease.

Etiostat is being developed to restore this early protective response. This represents a distinct therapeutic strategy: improving innate immune function, compared with conventional approaches that suppress the immune processes associated with established disease.

Our strategy is to correct the innate immune deficiency of Crohn’s disease by activating the pyrin inflammasome locally, in the parts of the bowel affected by the disease.

Conventional approaches

Suppress the immune processes associated with established disease.

Pyrinome’s approach

Restore the early protective innate immune response by activating the pyrin inflammasome locally.

02 / OUR LEAD PROGRAMME

Etiostat

An investigational therapy
with a different starting point.

Designed to support effective innate immunity in the intestine.

Etiostat is Pyrinome’s lead development programme for Crohn’s disease, and the first product of our approach: it is designed to activate the pyrin inflammasome where it is needed, in the diseased bowel.

Our aim is to help the body deal more effectively with the bacterial triggers that may contribute to disease.

The programme brings together research into Crohn’s disease biology with drug discovery and clinical development expertise.

Etiostat is investigational. Its safety and efficacy, including its ability to prevent recurrence, remain to be established in clinical trials.

HOW ETIOSTAT WORKS

Restoring the first line of defence.

In Crohn’s disease, the innate immune response to bacteria that enter the bowel wall is too weak. Too few neutrophils arrive, bacteria persist, and chronic inflammation follows. Etiostat is designed to correct this deficit by activating the pyrin inflammasome.

BOWEL LUMEN BOWEL LINING BOWEL WALL 1 pyrin inflammasome Macrophage Etiostat activates 2 3 IL-1β released BLOOD VESSEL 4 Neutrophils recruited migrate to the bacteria and clear them
Proposed mechanism. Etiostat is designed to activate the pyrin inflammasome in the bowel wall, increasing production of IL-1β, which draws neutrophils from the bloodstream to clear invading bacteria. Etiostat is investigational and this mechanism remains to be confirmed in clinical trials.
  1. 1

    Bacteria cross the bowel lining

    Bacteria from the gut contents enter the bowel wall.

  2. 2

    Etiostat activates the pyrin inflammasome

    It acts within macrophages, the immune cells that first meet the bacteria.

  3. 3

    IL-1β is generated

    This signalling molecule calls for reinforcements.

  4. 4

    Neutrophils are recruited

    They move from the bloodstream to the site and clear the bacteria.

In Crohn’s disease

The innate response is too weak.

Too few neutrophils arrive, bacteria persist and chronic inflammation develops.

With Etiostat

The innate response is restored.

IL-1β is generated and neutrophils are drawn in to clear the bacteria.

03 / THE NEED · CROHN’S DISEASE

A substantial burden.
An unmet need after surgery.

1.3 million

US adults with diagnosed Crohn’s disease

Approximately 0.5% of adults, based on the 2023–2024 National Health Interview Survey.[1]

US$15 billion

Estimated global annual treatment market

A 2026 industry estimate of market revenue. This is not a measure of total healthcare costs or US expenditure.[2]

26%

Require surgery within 10 years

The cumulative risk of first major abdominal surgery after diagnosis in contemporary population-based Crohn’s cohorts.[3]

62%

Severe endoscopic recurrence at 26 weeks

Among high-risk patients receiving placebo after ileocolonic resection in the REPREVIO trial.[4]

13%

Repeat surgery within 10 years

Pooled risk of surgical recurrence after a first ileocolic resection in biologics-era cohorts.[5]

These figures describe different populations and outcomes. Recurrence detected on endoscopy does not necessarily mean symptoms have returned or that another operation is needed.

Postoperative prevention remains incompletely served by current therapy.

Existing treatments reduce recurrence, but protection is incomplete. In REPREVIO, severe endoscopic recurrence occurred in 23% of patients receiving vedolizumab, compared with 62% receiving placebo, at 26 weeks.[4] Pyrinome’s goal is to investigate a different approach through restoration of effective innate immunity.

Sources and definitions
  1. CDC/NCHS, 2026: US adults, NHIS 2023–2024. Self-reported ever-diagnosed Crohn’s disease; 1,257,000 adults, rounded to approximately 1.3 million. This is US adult prevalence, not global prevalence.
  2. Grand View Research, Crohn’s Disease Therapeutics Market, updated July 2026. US$15.0 billion global market estimate for 2026. The publisher includes surgical and non-surgical segments. This is an industry estimate, not an audited total for all care.
  3. Tsai et al., Clinical Gastroenterology and Hepatology, 2021. Meta-analysis: 26.2% risk of first major abdominal surgery at 10 years in patients diagnosed after 2000.
  4. D’Haens et al., REPREVIO, Lancet Gastroenterology & Hepatology, 2025. Patients with one or more recurrence risk factors after ileocolonic resection. Severe endoscopic recurrence (modified Rutgeerts score ≥i2b) at week 26: 23/37 (62.2%) with placebo and 10/43 (23.3%) with vedolizumab.
  5. Haanappel et al., Inflammatory Bowel Diseases, 2026. Meta-analysis of surgical recurrence following primary ileocolic resection: 5.7% at 5 years and 13.0% at 10 years in post-2000 cohorts. These are not lifetime reoperation rates.

04 / OUR THERAPEUTIC FOCUS

After surgery.
Before recurrence.

Our goal is to prevent Crohn’s disease from returning after surgical treatment.

We aim to evaluate whether restoring effective innate immunity can help protect the bowel after surgery and reduce the risk of recurrent disease.

This focus reflects our wider ambition: to address an underlying disease mechanism and change the long-term course of Crohn’s disease.

05 / OUR TEAM

Experience across science
and therapeutic development.

Pyrinome brings together expertise in innate immunity, Crohn’s disease, drug discovery and clinical development.

Professor Anthony Segal

Professor Anthony Segal

MD, PhD, FRS, FMedSci

CEO & Scientific Founder

Emeritus Professor of Medicine at UCL. A gastroenterologist, immunologist and biochemist whose research has helped shape understanding of innate immunity in Crohn’s disease.

Professor Malcolm Weir

Professor Malcolm Weir

Drug Discovery Director

Biochemist and biotechnology entrepreneur. Former CEO of Inpharmatica and co-founder and former CEO of Heptares, with extensive experience in drug discovery and early development.

Jeremy Stakol

Jeremy Stakol

Chairman

Early-stage investor supporting Pyrinome’s financial strategy, corporate planning and business development as the company advances its therapeutic programme.

Dr Tim Tasker

Dr Tim Tasker

Clinical Development

Physician and executive with more than 30 years of clinical development experience across pharmaceutical and biotechnology companies, including GSK, Evotec and Heptares.

Sir Philip Cohen

Sir Philip Cohen

FRS, FMedSci

Biochemistry Advisor

Authority on protein phosphorylation and cell signalling, bringing deep expertise in the biochemical pathways that regulate innate immune function.

Professor Arthur Kaser

Professor Arthur Kaser

FMedSci

IBD Biology Advisor

Professor at the University of Cambridge and an expert in inflammatory bowel disease, mucosal immunology and the biological mechanisms of intestinal disease.