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
  • 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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