Treating genetic disease at the source.

Correcting genetic disease
at the causal root.

We map the mechanisms behind genetic disease and design gene-level corrections.

5 High-leverage targets in the lead programme

10,000+ Known monogenic disease conditions

4 Scientific advisors, each a university professor

Open research on Zenodo

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Featured Preprint

Causal-circuit analysis of ileal Crohn's disease

Scored topology of the disease pathway, ranked candidates for gene-level correction, and prespecified falsification tests for each directed edge.

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Lead Programme

Ileal Crohn's Disease

Existing therapies suppress inflammation downstream of the genes that cause the disease. We target the source: a small set of high-leverage candidates where a single gene-level correction could change the disease course.

No approved gene therapy exists for inflammatory bowel disease. Current treatments manage symptoms in a market worth tens of billions, but none correct the underlying genetic cause. The same computational approach that identifies correction targets in Crohn's applies to over 10,000 other monogenic conditions, each an underserved niche, collectively an enormous addressable market.

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~3.6M Patients in the US and Europe

Age 15–35 Typical age at diagnosis

~24% Don't respond to first-line biologics

28% Maintain biologic response at 5 years

48% Need major surgery within 10 years

0 Approved gene therapies

Why Now

Computational Tools Have Arrived

AI and large-scale genomic databases now let a small team do what once required a pharmaceutical R&D division. We use these tools to map disease architecture computationally, compressing years of target identification into months.

A Long Tail of Unmet Need

Over 10,000 monogenic diseases affect tens of millions of patients worldwide. Most are too small individually to attract conventional drug development. A computational-first approach that reuses the same methodology across diseases changes the unit economics entirely.

Precision Editing, Minimal Risk

Modern gene editing can correct point mutations, insertions, and deletions with minimal risk of miscut or unintended mutation. Single-variant correction is now feasible at clinical scale. The tool matches the precision the biology demands.

Methodology