Unmeet Need
In major surgery and trauma, tPA levels rise dramatically as part of the body’s stress response. This surge in tPA activity drives pathological fibrinolysis, the breakdown of protective blood clots, at exactly the moment patients are most vulnerable to haemorrhage. Uncontrolled bleeding is the leading preventable cause of death in cardiac surgery and major trauma, and existing anti-fibrinolytic agents do not address the tPA mechanism directly or selectively.
Current standard-of-care agents such as tranexamic acid act on the fibrinolytic pathway broadly, with limitations in both efficacy and safety. No approved biologic therapy specifically targeting human tPA exists anywhere in the world.
Key Figures
Bleeding accounts for approximately 40% of preventable deaths in major trauma
Major cardiac surgery procedures number more than 800,000 annually across the US, EU and China, with haemorrhage a primary driver of mortality and extended ICU stays
Blood product transfusion in surgical bleeding costs healthcare systems billions annually
How EmstoPA Works
EmstoPA is a humanised monoclonal antibody fragment that binds with high affinity and specificity to human tPA in the presence of fibrin, blocking its catalytic activity and preventing the tPA-driven fibrinolytic cascade that leads to haemorrhage.
The mechanism delivers three core advantages:
Targeted efficacy
EmstoPA neutralises tPA directly at the site of its elevated activity in surgery and trauma, rather than acting on downstream pathway components.
Superior safety profile
EmstoPA does not block uPA, the plasminogen activator involved in maintenance of the vascular lining and wound healing. This selectivity is expected to produce a significantly better thrombosis safety profile compared to current anti-fibrinolytics that inhibit both tPA and uPA pathways. This is a meaningful clinical differentiation from current standard of care.
Validated in preclinical and human ex vivo translational models
EmstoPA has demonstrated significant reduction in tPA-induced bleeding in validated preclinical studies, and causes concentration-dependent inhibition of human plasma clot lysis, supporting progression to IND.
Target Indications
Cardiac Surgery (Primary Indication)
Major cardiac procedures including coronary artery bypass grafting, valve replacement and ECMO for pulmonary failure are associated with marked elevation of tPA and significant perioperative bleeding risk. EmstoPA’s targeted mechanism addresses this specifically, offering the potential to reduce haemorrhage, transfusion requirements and associated mortality.
Major Trauma (Primary Indication)
Traumatic injury triggers a systemic rise in tPA as part of the acute stress and hypoperfusion response. This contributes substantially to the coagulopathy and uncontrolled bleeding that accounts for a large proportion of preventable trauma deaths. EmstoPA offers the first specific biologic intervention at the source of this mechanism.
Thrombolysis-Induced Haemorrhage
EmstoPA may also serve as an antidote for haemorrhagic complications arising from therapeutic thrombolysis in clinical settings where high-dose tPA, tenecteplase or reteplase is administered as a treatment. This represents a further addressable population and is being evaluated as part of the development programme.
Regulatory Position
EmstoPA is in preclinical development and has received formal Scientific Advice from both the US Food and Drug Administration and the UK Medicines and Healthcare products Regulatory Agency, with both bodies endorsing an accelerated development pathway. The programme is recommended for the UK ILAP Accelerated Access Programme.
Intellectual Property
| Patent / IP Item | Status |
|---|---|
| US murine patent | Granted — exclusive rights held |
| Humanised EmstoPA patent filed | 2019 |
| Chinese humanised patent | Granted 6 June 2025 |
| US humanised patent | Granted 2 December 2025 |
| EU humanised patent | Allowed — grant pending first half 2026 |
| IP exclusivity | To 2039 |
| Further patents | Manufacture and formulation patents planned |