Table 2.

Treatments under evaluation for COVID-19 and their mechanisms of action.

	Treatments	Action Mechanisms	Limitations
Antivirals	Remdesivir	Viral replication inhibitor (168)	Bradycardia, liver damage, and gastrointestinal reactions that can contribute to the deterioration of the disease (169).
	Favipiravir	Inhibits viral RNA polymerase (170).	Gastrointestinal disorders, skin lesions, liver, and cardiovascular damage (168, 171).
	Lopinavir-ritonavir	Protease inhibitor believed to interfere with viral fusion with cell membrane (172, 173).	Antiviral activity against SARS-CoV-2 has not been found in clinical studies (174, 175).
	Arbidol	Blocks entry and intracellular traffic in vesicles (176).	Some patients may develop hypersensitivity (176).
Other drugs	Chloroquine and hydroxychloroquine	Immunomodulatory effect. It is inhibiting the entry of SARS-CoV-2 (168, 177–179).	Accumulation in various organs and low elimination rate; and arrhythmia and heart failure (178, 180, 181).
	Melatonin	Inhibits calmodulin (182, 183).	This would only allow reducing the associated clinical symptoms (183).
	Dexamethasone	Reduce the duration of mechanical ventilation and mortality from severe acute respiratory distress syndrome (184).	There are only a palliative treatment (184).
	Plasma Treatment	Neutralizing antibodies against SARS-CoV-2 (185).	Doses dependent on the neutralizing title (186).
	Specific monoclonal antibodies to SARS-CoV-2	Blocks the entry of the virus through ACE2 because they are mainly directed against the S protein (187–190)	Although several mAbs have been evaluated in vitro, in vivo, and there are ten clinical trials ongoing (166, 170, 171, 191)
	Tocilizumab	Non-specific Abs for SARS-CoV-2. This directed against IL-6 receptor, IL-6 is one of the cytokines responsible for the inflammatory state persistent in severe patients (192, 193).	It has been reported only beneficial effects in critically ill patients (82, 193).