Traumakine Program description

The Traumakine program focuses on the development of a first pharmacological treatment for acute respiratory distress syndrome (ARDS) and is supported by a grant from the 7th Framework Programme for Research and Technological Development of the Cooperation Work Programme: Health-2012. The Traumakine consortium consists of the European Commission as a granting Agency, Faron Pharmaceuticals as a Coordinator, and three other participating Partners of the Traumakine program (University College London Hospital (UCLH), University of Torino and University of Turku).

The key activity of the Traumakine-program is a phase III clinical study aiming at the European marketing authorization of FP-1201-lyo treatment of ARDS, which also has an orphan designation from the European Commission (EU/3/07/505). The previously performed clinical study with FP-1201 has indicated significant decrease in mortality of the acute lung injury (ALI)/ARDS patients with good safety profile. The phase III trial will be a pan-European study conducted by more than 100 hospitals with significant intensive care units (ICU) around Europe.

About ARDS and FP-1201-lyo (lyophilized human recombinant interferon-beta 1a)

ARDS is a serious clinical disorder, which follow a variety of severe direct and indirect lung insults. In serious life threatening situations such as infection leading to sepsis or trauma causing massive tissue injury, an escalation of the systemic inflammatory response leads to multiple organ failure including ARDS. In the case of ARDS, the predominant pathophysiological event is increased vascular leakage, which has been shown to be due to the lack of adenosine, an end product of AMP degradation by 5’-nucleotidase (CD73). Adenosine acts to enhance endothelial barrier function via adenosine receptor activation. Therefore, any biological substance, which acts to increase adenosine level, will reduce vascular leakage and be of benefit in ARDS patients. Such substances are type I interferons, and especially the interferon-beta (IFN-beta). IFN-beta has been shown to up-regulate 5’-nucleotidase (also known as a CD73 molecule and expressed abundantly by normal endothelial cells) and prevent ALI in animal models (Kiss et al. (2007) Eur. J. Immunol. 37:3334). IFN-beta is therefore a potential treatment for ALI/ARDS.

The Traumakine mechanism of action is shown in a video on the front page. The medical need for an effective and safe treatment of ARDS is high, since this condition is life threatening with 35-45 % mortality rate (Rubenfeld et al. (2005) N Engl J Med 353, 1685) (Phua et al. (2009) Am J Respir Crit Care Med 179, 220) and affects close to 175.000 patients in Europe alone. Currently no approved pharmacological treatment of ARDS by the regulatory authorities in Europe is available.