Table 1.
A Summary of Drugs That Are Being Tested for Treatment of COVID-19 or That Have Been Suggested for Use in this Setting
| Drug Class | Drug Name | Mechanism of Action | References |
|---|---|---|---|
| Monoclonal antibodies | Gimsilumab | Anti-GM-CSF antibody. GM-CSF promotes the proinflammatory response. GM-CSF expression was shown to increase in TH1 cells and monocytes in COVID-19 patients, particularly ICU patients. | Zhou et al., 2020a |
| Sarilumab and Tocilizumab | Anti-IL-6 antibodies. Higher blood concentrations of IL-6 were reported to be predictive of fatal outcome in COVID-19 patients. | Ruan et al., 2020 | |
| IL-1 receptor agonist | Anakinra | Competitively inhibits IL-1 binding to the IL-1 type I receptor. Increased concentrations of IL-1 have been reported in COVID-19 patients. IL-1⍺ and IL-1β have been implicated in playing a role in severe COVID-19. | Giamarellos-Bourboulis et al., 2020, Huang et al., 2020, Ong et al., 2020 |
| Tyrosine kinase inhibitors | Ruxolitinib | JAK1 and JAK2 inhibitor. Inhibits NK cell activity and the production of proinflammatory cytokines. It also impacts DC differentiation, migration, and function, which could suppress antigen-specific T cell responses. | Elli et al., 2019 |
| Baricitinib | JAK1 and JAK2 inhibitor. Identified as a numb-associated kinase (NAK) inhibitor, with high affinity for AAK1. AAK1 is a regulator of clathrin-mediated endocytosis, the pathway utilized by SARS-CoV-2 to enter cells. Could prevent viral entry into cells in addition to its anti-inflammatory activity. | Stebbing et al., 2020 | |
| Fedratinib | JAK2-specific inhibitor. Many of the cytokines found to be elevated in the serum of COVID-19 patients either promote TH17 responses or are produced by TH17 cells. IL-6 and IL-23 activate STAT3, the transcription factor responsible for TH17 differentiation and function, through JAK2. Inhibition of JAK2 could limit the proinflammatory activity of TH17 cells. | Wu and Yang, 2020 | |
| Quinoline | Chloroquine and Hydroxychloroquine | Inhibit replication of other viruses by interfering with virion binding to cellular receptors and increasing endosomal pH during viral entry. These drugs can also inhibit antigen processing and presentation by APCs, prevent TLR signaling, and reduce production of proinflammatory cytokines. | Devaux et al., 2020, Schrezenmeier and Dörner, 2020 |
| Interferon | IFN-β | Binds to the IFNAR complex (IFNAR1/IFNAR2) which is expressed by most cells. Stimulates transcription of ISGs via the JAK/STAT/IRF9 pathway. Interferes with viral replication and dissemination. | Hemann et al., 2017, Sallard et al., 2020 |
| IFN-λ | Binds to the IFNL complex (IFNLR1/IL10R2). Expression of the IFNL complex is limited to epithelial cells and some immune cell subsets, such as neutrophils. Stimulates transcription of ISGs via the JAK/STAT/IRF9 pathway. Interferes with viral replication and dissemination. | Hemann et al., 2017, Prokunina-Olsson et al., 2020 | |
| Vaccine | BCG | An attenuated strain of Mycobacterium bovis. Thought to provide broad protection against respiratory infections through its similarity to viral antigens, antigen-independent activation of adaptive immune cells, and/or long-term activation and reprogramming of innate immune cells. | Redelman-Sidi, 2020 |
| Corticosteroid | Methylprednisolone | Acts on the transcriptional level to inhibit the production and function of proinflammatory mediators. | Zha et al., 2020 |