Faron Pharmaceuticals Oy (AIM:FARN, OTC:FPHAF) has published research identifying a gene mutation that might explain why some patients with severe respiratory disease respond better than others to treatment with interferon-beta and a steroid.
Analysing data from Traumakine’s phase III INTEREST trial in 2018, Faron said its research showed patients carrying a single nucleotide polymorphism (SNP) in the interferon-alpha/beta receptor (IFNAR2) had a significantly better mortality rate in patients also given steroids.
Traumakine failed to hit its primary endpoint in the INTEREST trial as a treatment for acute respiratory distress syndrome (ARDS) with no increase in survival rates, a result which shocked the company and has since led it to investigate the reasons for the outcome.
In a statement today, it said: “The team's findings suggest that administering glucocorticosteroids to ARDS patients receiving IFN beta-1a therapy is not harmful if they carry the mutation.
“However, in patients without the mutation, glucocorticosteroid use was associated with high levels of interferon-gamma, an indicator of increased inflammation instead of immune suppression, which is associated with poor outcomes in ARDS and COVID-19 patients.”
The polymorphism, SNP rs9984273, is relatively common, said Faron, and carried by approximately 45% of people of African origin, 34% of Caucasians and 10% of Asians.
Faron also explored the impact of the SNP on COVID-19 disease severity and found that carrying the mutation was associated with milder disease and less hospitalisation
Juho Jalkanen, Faron’s chief operating officer and author of the research, said: "Endogenous interferon-beta production is one of the body's main first lines of defence against viral infection and it is widely hypothesized that dosing patients with interferon-based therapies can further strengthen this natural defence if given early enough.
"However, our studies have shown that glucocorticosteroids can block this therapeutic effect and may have a potentially negative impact on patient survival.
"Our research also shows that a relatively common polymorphism, which until now has not been recognized as having any clinical significance, actually plays a critical role in disease states where interferons and glucocorticosteroids have an impact on mortality.
“These findings will support our continued research into the potential of intravenous interferon beta-1a therapy as a future treatment for ARDS and other acute settings of systemic inflammation leading to a capillary leak," he concluded.