Paracetamol overdose is a leading cause of acute liver injury in the United Kingdom, and no therapy currently exists to reverse the damage or reliably prevent progression to liver failure.
Indication |
Paracetamol-induced acute liver injury, with potential expansion to other drug-induced liver injury and fibrosis or cirrhosis. |
Technology |
Extracellular vesicles derived from alternatively activated macrophages (AAM-EVs), preclinical stage, validated in vitro and in vivo. |
IP Status |
Priority patent application filed 4 June 2026. |
Seeking |
Licensing partner for the development of an EV-based therapeutic. Contact Dr Philippe Potey, Technology Transfer Executive, Edinburgh Innovations: Philippe.Potey@ei.ed.ac.uk |
Licensing Opportunity
Although N-acetylcysteine is an effective antidote when given early, no therapy currently reverses established liver injury or halts progression to acute liver failure. In severe cases, the only life-saving option is liver transplantation, which is limited by donor availability and carries significant morbidity.
Edinburgh Innovations is seeking a licensing partner to develop AAM-EVs, an off-the-shelf extracellular vesicle therapy that addresses this gap. The technology is designed to be rapid to deploy and scalable, including for late-presenting patients and in settings where complex cell therapies are difficult to administer.
Extracellular vesicle therapy overview
AAM-EVs are extracellular vesicles derived from alternatively activated macrophages (AAMs). They carry bioactive cargo, including proteins and small RNAs, that can reprogramme immune responses and promote tissue repair without the need to administer live cells.
In preclinical studies, AAM-EVs replicate the therapeutic benefits of parent AAM cell therapy in paracetamol-induced acute liver injury. Effects observed include:
AAM-EVs were isolated using a GMP-compatible workflow (ultrafiltration and size exclusion chromatography), supporting a credible path towards clinical-grade manufacture.
Preclinical evidence in acute liver injury
AAM-EVs are validated in vitro, where they are taken up by naive macrophages and drive an anti-inflammatory, pro-repair phenotype with increased phagocytosis. In vivo, in a mouse model of paracetamol-induced acute liver injury, intravenous AAM-EVs reduce hepatic necrosis and neutrophil infiltration and increase hepatocellular regeneration. Therapeutic benefit is observed at doses below the EV yield from an equivalent AAM cell therapy dose. The technology has potential for expansion into other drug-induced liver injury and broader indications such as fibrosis or cirrhosis.
IP and licensing status
A priority patent application was filed on 4 June 2026. Edinburgh Innovations is offering a licensing opportunity for development of an EV-based therapeutic for acute liver injury and prevention of acute liver failure.
Benefits
Compared with macrophage cell therapy and other regenerative approaches, AAM-EVs offer:
Quote: TEC1104899
