Restoring the body's structural foundation.
Elastin degrades irreversibly throughout life — driving disease across the vascular system, lungs, and skin. We're developing first-in-class dual-action therapies that protect and rebuild it.
Elastin drives disease. No drug addresses it.
Elastin is one of the most abundant proteins in the body — the elastic scaffold that lets tissues stretch and recoil. It degrades irreversibly throughout life, driving pathology in multiple organ systems, yet virtually all drug discovery targets cellular mechanisms instead.
Vascular System
Elastin loss directly drives maladaptive cardiac and vessel-wall remodelling — a root mechanism in heart failure, aneurysm, and rare vascular disease.
Lungs
The elastic lamella gives lungs their recoil. Proteolytic fragmentation underlies emphysema and COPD, where elastin is destroyed and never replaced.
Skin
Elastin gives skin its resilience. As it fragments, skin loses recoil and structure — the goal is true elastogenesis, not superficial hydration.
Also implicated: Abdominal Aortic Aneurysm · Cutis Laxa · and other elastin-deficiency conditions.
Synthesised once. Never replaced.
Proteases cleave the elastic fibre
Matrix metalloproteinases (MMPs), serine and cysteine proteases from inflammatory cells fragment the elastic lamella — proteolytic breakdown that accumulates with inflammation and age.
Decades of cumulative structural injury
Oxidative damage, UV radiation, calcification, and mechanical fatigue degrade elastin irreversibly over a lifetime. The by-products of degradation are themselves biochemically active — further driving ageing.
Unlike collagen, elastin has near-zero turnover in adults.
Elastin fibres are laid down in fetal and early postnatal development and barely renewed afterwards. No endogenous regeneration exists — once fibres fragment, structural integrity is permanently lost without therapeutic intervention. That gap is exactly what we set out to close.
A dual-action elastin restoration platform
A systematic, pathway-informed literature search identified candidates targeting the ECM and elastin pathway. Our platform pairs two complementary mechanisms — simultaneously blocking elastin degradation and stimulating new synthesis — for a net gain in functional elastin that outperforms any single agent.
Inhibit elastin degradation
Assets that shield existing elastic fibres from proteolytic and inflammatory breakdown.
Stimulate elastin synthesis
Assets that switch native elastin production back on — depositing new, functional, cross-linked fibres.
One mechanism. Multiple high-value indications.
A single mechanistic validation supports multiple independent commercial opportunities. The dual-action platform addresses elastin deficiency across organ systems — from rare disease to cardiovascular and dermatology.
Williams Syndrome is our beachhead: 100% penetrance, no disease-modifying therapy, and a clear orphan-drug route to accelerated clinical development.
Williams Syndrome & the WISER Consortium
A de-risked, EU-funded, multi-institutional programme to develop a first-in-class therapy for the vascular pathology of Williams Syndrome — caused by deletion of the ELN (elastin) gene, with 100% of patients developing severe cardiovascular disease and no cure available today.
4 partners across 3 countries · 3-year programme · Post-WISER route to IND submission and Phase 1/2 clinical trials via Orphan Drug / Fast Track designation.
Interested in working together?
We partner with researchers, clinicians, and investors advancing elastin biology. Whether it's collaborative research, licensing, or investment — we'd love to hear from you.