Based on animal models, FX06 has considerable therapeutic potential for all diseases and pathological conditions associated with increased vascular permeability (Gröger et al. 2009 PLoS ONE, Bergt et al. 2016 Crit Care Med). FX06 binds to vascular endothelial (VE)-cadherin, preventing the transmigration of leukocytes. With the recent global pandemic, the importance of understanding and addressing vascular leakage has become even more critical. Cytokines released during COVID-19 promote the disintegration of adherence junctions in the endothelial cell layer, the recruitment, and the transendothelial migration (TEM) of peripheral blood mononuclear cells (PBMCs).
For clinicians, the team found that FX06 can alter the protein expression pattern of endothelial cells after stimulation with COVID-19-triggered cytokines. The cocktail of COVID-19-induced cytokines alters the expression of 456 proteins in endothelial cells. Compared to this hyper-inflammatory state, 25 proteins are up- and 31 are down-regulated upon FX06 treatment, including Angiopoetin-related protein 4, which is known to reduce vascular leakage. But it’s not just scientists and clinicians who can benefit from these new findings.
The team also emphasises the importance of health-economic modelling in making market access and reimbursement decisions for therapies like FX06. Health-economic evaluation for FX06 involves comparing the relative value for money of FX06 to existing alternatives. Clinical data from the IXION trial and supplementary evidence will be used to estimate the cost-effectiveness of FX06. Additionally, a hospital-level budget impact analysis will assess the financial consequences of adopting FX06 in clinical practice. A special thanks to the teams from University College Dublin and University Medical Center Groningen for their contributions to this research. By sharing this knowledge and contributing to advancing medical research, we can help bring innovative therapies like FX06 to those who need it most.
