Chloroquine (Antimalarial) |
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In vitro activity against SARS-CoV-2 and may have immunomodulating properties.
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Inhibition of viral enzymes or processes such as viral DNA and RNA polymerase, viral protein glycosylation, virus assembly, new virus particle transport, and virus release.
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ACE2 cellular receptor inhibition, acidification at the surface of the cell membrane inhibiting fusion of the virus, and immunomodulation of cytokine release.
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Risk of cardiac arrhythmias (e.g., QT prolongation)
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Risk of retinal damage, especially with long term use
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Caution in patients with G6PD deficiency
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Caution in diabetics
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Significant drug interactions
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In vitro and limited clinical data suggest potential benefit. |
Hydroxychloroquine (Antimalarial) |
Same as above |
Same as above |
Same as above
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Lopinavir; Ritonavir (HIV Protease Inhibitor) |
Lopinavir and ritonavir may bind to Mpro, a key enzyme for coronavirus replication. This may suppress coronavirus activity. |
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Risk of cardiac arrhythmias (e.g., QT prolongation)
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Caution in patients with hepatic disease or hepatitis
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Significant drug interactions
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Role in the treatment of COVID-19 is unclear. Preclinical data suggested potential benefit; however, more recent data has failed to confirm. |
Remdesivir (Investigational Nucleoside Analogue) |
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Act as a broad-spectrum antiviral with in vitro activity against coronaviruses.
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Acts as an inhibitor of RNA-dependent RNA polymerases (RdRps).
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Remdesivir-TP competes with adenosine-triphosphate for incorporation into nascent viral RNA chains.
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Once incorporated into the viral RNA at position i, RDV-TP terminates RNA synthesis at position i + 3.
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Because RDV-TP does not cause immediate chain termination (i.e., 3 additional nucleotides are incorporated after RDV-TP), the drug appears to evade proofreading by viral exoribonuclease (an enzyme thought to excise nucleotide analog inhibitors).
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Investigational and available only through expanded access and study protocols; several large clinical trials are underway. |
Azithromycin (Macrolide Antibacterial) |
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It may prevent bacterial superinfection, and macrolides may have immunomodulatory properties to work as adjunct therapy.
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It may have immunomodulatory properties in pulmonary inflammatory disorders.
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They may downregulate inflammatory responses and reduce the excessive cytokine production associated with respiratory viral infections; however, their direct effects on viral clearance are uncertain.
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Immunomodulatory mechanisms may include reducing chemotaxis of neutrophils (PMNs) to the lungs by inhibiting cytokines (i.e., IL-8), inhibition of mucus hypersecretion, decreased production of reactive oxygen species, accelerating neutrophil apoptosis, and blocking the activation of nuclear transcription factors.
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Used in some protocols based on theoretical mechanism and limited preliminary data as adjunct therapy. |
Tocilizumab (Interleukin-6 (IL-6) Receptor-Inhibiting Monoclonal Antibody) |
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Cytokine release syndrome may be a component of severe disease in COVID-19 patients.
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Inhibits IL-6-mediated signaling by competitively binding to both soluble and membrane-bound IL-6 receptors. IL-6 is a proinflammatory cytokine that is involved in diverse physiological processes such as T-cell activation, immunoglobulin secretion induction, hepatic acute-phase protein synthesis initiation, and hematopoietic precursor cell proliferation and differentiation stimulation. IL-6 is produced by various cell types, including T- and B-cells, lymphocytes, monocytes, and fibroblasts.
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Immunomodulating agent used in some protocols based on theoretical mechanism and limited preliminary data as adjunct therapy. |
COVID-19 convalescent plasma (Plasma collected from persons who have recovered from COVID-19 that may contain antibodies to CoV-19) |
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Investigational use is being studied. |
Corticosteroid therapy |
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Not recommended for viral pneumonia; however, use may be considered for patients with refractory shock or acute respiratory distress syndrome. |