2. Academic Validation
  3. The first case of COVID-19 treated with the complement C3 inhibitor AMY-101

The first case of COVID-19 treated with the complement C3 inhibitor AMY-101

  • Clin Immunol. 2020 Jun;215:108450. doi: 10.1016/j.clim.2020.108450.
Sara Mastaglio 1,  Annalisa Ruggeri 1,  Antonio M Risitano 2,  Piera Angelillo 1,  Despina Yancopoulou 3,  Dimitrios C Mastellos 4,  Markus Huber-Lang 5,  Simona Piemontese 1,  Andrea Assanelli 1,  Cecilia Garlanda 6,  John D Lambris 7,  Fabio Ciceri 8
Affiliations

Affiliations

  • 1 Hematology and Bone Marrow Transplantation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.
  • 2 Department of Clinical Medicine and Surgery, Federico II University of Naples, Naples, Italy.
  • 3 Amyndas Pharmaceuticals, Glyfada, Greece.
  • 4 National Center for Scientific Research 'Demokritos', Aghia Paraskevi, Athens, Greece.
  • 5 Institute of Experimental Trauma-Immunology, University Hospital of Ulm, Ulm, Germany.
  • 6 IRCCS Humanitas Clinical and Research Center, Milan, Italy; Humanitas University, Milan, Italy.
  • 7 Department of Pathology & Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: [email protected].
  • 8 Hematology and Bone Marrow Transplantation Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy; University Vita Salute San Raffaele, Milan, Italy. Electronic address: [email protected].
PMID: 32360516 DOI: 10.1016/j.clim.2020.108450
Abstract

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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