Table 1.

Monoclonal antibodies studied in COVID-19

Drug class	Molecule	Mechanism of action
Immunomodulators	Tocilizumab	Inhibits both the membrane interleukin-6 receptors (mIL-6R) and soluble interleukin receptors (sIL-6R), thereby preventing IL-6R activation and hyper-interleukin-6 (IL-6) formation which is known to play a central role in cytokine storm [22]
	Sarilumab
	Itolizumab	Binds to domain 1 of cluster of differentiation 6 (CD6), a receptor present on effector T cells which blocks co-stimulation pathway leading to the inhibition of proliferation of naive T cells as well as proinflammatory cytokines such as interleukin-17A (IL-17A), tumor necrosis factor-alpha (TNF-α), IL-6, interferon-gamma (IFN-γ), and interleukin-2 (IL-2) [23]
	Siltuximab	Binds to IL-6, resulting in the inhibition of IL-6R activation and hyper IL-6 formation [22]
	Infliximab	Binds to TNF-α and supresses hyper immune response [24]
	Lenzilumab	Directly binds granulocyte-macrophage colony-stimulating factor (GM-CSF), blocks intracellular signaling and reduces hyperinflammation [25]
	Emapalumab	Acts by blocking the binding of IFNγ to cell surface receptors and activation of inflammatory signals [26]
	Canakinumab	Specifically inhibits interleukin-1 beta (IL-1β), a pro-inflammatory cytokine that mediates immune responses during infection and inflammation [27]
	Anakinra	Interleukin-1 (IL-1) receptor antagonist that inhibits the activity of the proinflammatory cytokine IL-1, specifically interleukin-1 alpha (IL-1α) and IL-1β [28]
	Adalimumab	Binds to TNF-α and prevents subsequent release of inflammatory cytokines [22]
	Bevacizumab	Binds to vascular endothelial growth factor (VEGF) to inhibit pulmonary edema caused by VEGF overexpression [22]
	Meplazumab	Binds to cluster of differentiation 147 (CD147) on the host cells which is used by the S protein of SARS-CoV-2 for gaining entry [29], [30]
nMAbs	Bamlanivimab plus Etesevimab	Binds to the receptor-binding domain (RBD) of the S protein and blocks its attachment to the human ACE-2 receptors [31]
	Sotrovimab	Targets an epitope in the RBD of the S protein that is conserved between SARS-CoV and SARS-CoV-2 [31]
	Tixagevimab plus Cilgavimab	Binds to the nonoverlapping epitopes of the S protein RBD of SARS-CoV-2 [31]
	Bebtelovimab	Binds to the S protein of SARS-CoV-2 [31]
	Casirivimab plus Imdevimab	Binds to the nonoverlapping epitopes of the S protein RBD of SARS-CoV-2 [16]
	Regdanvimab	Binds to the RBD of the S protein of SARS-CoV-2 to block the interactions with the host ACE-2 receptors [32]

According to latest NIH COVID-19 treatment guidelines, Bamlanivimab plus Etesevimab or Casirivimab plus Imdevimab is recommended in outpatients with mild-to-moderate COVID-19 who are at high risk for disease progression [6].