Selected article for: "complement activation and inflammatory response"
Author: Mastaglio, Sara; Ruggeri, Annalisa; Risitano, Antonio M.; Angelillo, Piera; Yancopoulou, Despina; Mastellos, Dimitrios C.; Huber-Lang, Markus; Piemontese, Simona; Assanelli, Andrea; Garlanda, Cecilia; Lambris, John D.; Ciceri, Fabio
Title: The first case of COVID-19 treated with the complement C3 inhibitor AMY-101
  • Cord-id: m0omw4xf
  • Document date: 2020_4_29
    • ID: m0omw4xf
    Snippet: 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 in
    Document: 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.

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