Researchers gave mice infected with the COVID‑19 virus a synthetic peptide called hexarelin, which can bind to a cell‑surface protein (CD36) that helps drive the harmful inflammation seen in severe disease. In the mouse model, hexarelin changed the behavior of lung immune cells, lowering the flood of inflammatory signals that can cause breathing failure. The work is still early‑stage and done only in animals, so it isn’t a ready‑to‑use treatment for people yet.

The scientific and medical community faced an unprecedented global health hazard that led to nearly 7 million deaths attributable to the rapid spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In spite of the development of efficient vaccines against SARS-CoV-2, many people remain at risk of developing severe symptoms as the virus continues to spread without beneficial patient therapy. The hyper-inflammatory response to SARS-CoV-2 infection progressing to acute respiratory distress syndrome remains an unmet medical need for improving patient care. The viral infection stimulates alveolar macrophages to adopt an inflammatory phenotype regulated, at least in part, by the cluster of differentiation 36 receptor (CD36) to produce unrestrained inflammatory cytokine secretions. We suggest herein that the modulation of the macrophage response using the synthetic CD36 ligand hexarelin offers potential as therapy for halting respiratory failure in SARS-CoV-2-infected patients.