COVID-19 is caused by a type of coronavirus called 'severe acute respiratory syndrome coronavirus 2' (SARS-CoV-2). The World Health Organization (WHO) declared a Public Health Emergency of International Concern on 30 January 2020 and a pandemic on 11 March 2020 [1],[2]. COVID-19 is more contagious than the common flu and causes more severe complications in some people [3]. These complications often take the form of Acute Respiratory Distress Syndrome (ARDS) and multiple organ failure in the later stages of the illness or even during recovery [4],[5].
One of the causes of these life-threatening complications, and subsequently the severity of the disease overall, is a physiological reaction of the innate immune system. Excessive amounts of pro-inflammatory molecules (cytokines) are released — the so-called "cytokine storm’’ [6],[7]. If therapeutics are able to prevent the overreaction of our immune system, then fewer patients would need immediate hospitalization, reducing the mortality rate caused by COVID-19 and freeing up much-needed hospital capacity to treat other illnesses. Yet we know of few medications that can act as a preventive mechanism for such a response. One such drug is the monoclonal antibody called bamlanivimab (single dose of 700 mg via IV infusion over 60 minutes), which the FDA approved for use as an early treatment of mild-to-moderate COVID-19. The clinical evidence so far suggests that it reduces COVID-19-related hospitalization or emergency room visits in patients at high risk within 28 days after treatment compared to a placebo [8].
