COVID-19, the disease caused by the SARS-CoV-2 virus, is a respiratory disease that is easily transmitted. While most people infected with the virus develop no or only mild symptoms, a certain percentage develops much more severe symptoms, leading to prolonged hospitalization, long-term morbidity and frequently death.
Such critically ill COVID-19 patients, which are hospitalized and invasively mechanically ventilated, are dealing with a severely dysregulated immune system as a response to the viral infection, which can be characterized as a virally induced sepsis. Severe systemic inflammation and thrombosis in addition to respiratory symptoms and severe tissue damage, causing acute respiratory distress syndrome (ARDS) and potentially multi-organ failure are hallmarks of this severe manifestation of the disease. Patients show abnormalities in the coagulation system and elevated levels of proinflammatory cytokines as well as an infiltration of macrophages and neutrophils in the lung.
Widespread complement activation in lungs and kidneys of critically ill COVID-19 patients has been observed. The terminal complement protein C5a has been implicated in the pathology of COVID-19 in two ways; first, as an attractor and activator of neutrophils, leading to subsequent tissue damage and secondly as an activator of the coagulation system via its action on endothelial cells and neutrophils. Thus, C5a has a central role in the development of ARDS and vascular thrombosis (blood clots in the veins) in critically ill COVID-19 patients.
In April 2023, Gohibic (vilobelimab) received an emergency use authorization (EUA) from the US FDA. For more information please visit www.gohibic.com.
The development of vilobelimab for the treatment of critically ill, invasively mechanically ventilated COVID-19 patients was partly funded by a grant from the German Ministry of Education and Research and the German Ministry of Health (grant number 16LW00113).
