Conventional approaches
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.
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.
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.
- 1
Bacteria cross the bowel lining
Bacteria from the gut contents enter the bowel wall.
- 2
Etiostat activates the pyrin inflammasome
It acts within macrophages, the immune cells that first meet the bacteria.
- 3
IL-1β is generated
This signalling molecule calls for reinforcements.
- 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.
US adults with diagnosed Crohn’s disease
Approximately 0.5% of adults, based on the 2023–2024 National Health Interview Survey.[1]
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]
Require surgery within 10 years
The cumulative risk of first major abdominal surgery after diagnosis in contemporary population-based Crohn’s cohorts.[3]
Severe endoscopic recurrence at 26 weeks
Among high-risk patients receiving placebo after ileocolonic resection in the REPREVIO trial.[4]
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
- 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.
- 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.
- 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.
- 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.
- 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
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
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
Chairman
Early-stage investor supporting Pyrinome’s financial strategy, corporate planning and business development as the company advances its therapeutic programme.

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
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
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.