compstatin and Atrial-Fibrillation

Acute respiratory distress syndrome (ARDS) is a devastating clinical manifestation of COVID-19 pneumonia and is mainly based on an immune-driven pathology. Mounting evidence suggests that COVID-19 is fueled by a maladaptive host inflammatory response that involves excessive activation of innate immune pathways. While a "cytokine storm" involving IL-6 and other cytokines has been documented, complement C3 activation has been implicated as an initial effector mechanism that exacerbates lung injury in preclinical models of SARS-CoV infection. C3-targeted intervention may provide broader therapeutic control of complement-mediated inflammatory damage in COVID-19 patients. Herein, we report the clinical course of a patient with severe ARDS due to COVID-19 pneumonia who was safely and successfully treated with the compstatin-based complement C3 inhibitor AMY-101.

Topics: Aged; Antiviral Agents; Atrial Fibrillation; Betacoronavirus; Complement Activation; Complement C3; Complement Inactivating Agents; Coronavirus Infections; COVID-19; Humans; Hypercholesterolemia; Hypertension; Lung; Male; Pandemics; Peptides, Cyclic; Pneumonia, Viral; SARS-CoV-2; Treatment Outcome