Traumakine® is based on a patent-protected use of intra-venous interferon beta to prevent leakage of vascular beds in acute respiratory distress syndrome (ARDS) and other hypoxic organ injuries. The active pharmaceutical ingredient in Traumakine® is recombinant human IFN beta-1a.
Mechanism of action
The mechanism behind Traumakine®’s action was invented by scientists at Turku University from 1995 to 2003. Through extensive research and ex-vivo studies, it was identified that a molecule called CD73 is an essential entity needed to maintain endothelial barrier function. CD73 is an ectoenzyme capable of breaking down extracellular AMP to produce locally active adenosine. Adenosine maintains the endothelial barrier and downregulates inflammation escalation, preventing both early vascular leakage and escalation of inflammation, which are the two early patho-physiological events leading to ARDS.
One of the key findings that led to the development of Traumakine®, was a discovery that interferon beta-1a could enhance CD73 expression and therefore could be used to treat a range of vascular leakage conditions including ARDS. Traumakine® works by enhancing lung CD73 expression and increasing production of anti-inflammatory adenosine such that vascular leaking and escalation of inflammation are reduced.
The sub-cutaneous and intra-muscular use of recombinant human IFN beta-1a is an approved treatment for patients with relapsing remitting MS and the safety profile of recombinant human IFN beta-1a in such patients is well characterised.