Table 4.

Commonly used drugs for the treatment of COVID-19.

Name of Drug	Potential Role in COVID-19	Problems/Issues/Remarks
β-D-N4-hydroxycytidine (NHC) [54]	Ribonucleoside analogue with broad-spectrum antiviral activity (oral route) Effective against Remdesivir-resistant virus, MERS-CoV, SARS-CoV-2, and SARS-CoV in primary HAE cell cultures Reduces virus titres in a dose-dependent manner	Coronavirus may achieve 2-fold resistance after 30 passages [55].
Interferons (IFN-I and III) [56]	Produces innate immune response in human cells and stimulates IFN-stimulated genes (ISGs) through JAK/STAT pathway, affecting viral replication at all stages of its replicative cycle. Early administration can decrease the viral spread and can produce extended-lasting responses without inflammatory side effects.	Virus adapts to IFNs by turning over interferon receptors, leading to a diminished response by helper T cells and NK cells. IFNs can produce flu-like symptoms on their own [57,58].
Chloroquine (CQ), Hydroxychloroquine (HCQ) [56]	Inhibits intracellular replication of viral particles. It prevents the interaction between the virus and its receptor, thus blocking its effect. Both drugs are immunomodulatory and downregulate Toll-like receptors, thus suppressing the cytokine storm.	HCQ is a less toxic derivative of CQ; hence it is favoured in the treatment of COVID-19. Both these drugs produce reactive oxygen species, which can damage host cells.
Azithromycin (AZM) [56,59,60]	Inhibits replication of virus in bronchial cells by decreasing the synthesis of adhesion molecules like ICAM-1. Downregulates cytokine production (IL2, 6, 8), maintains alveolar cell integrity and reduces lung fibrosis Acts synergistically with HCQ in reducing viral load It also prevents bacterial co-infection by Prevotella, which can enhance the pathogenicity of SARS-CoV-2 by internalizing it.	It can cause gastrointestinal upset, nausea, headache, hepatotoxicity, and bacterial resistance. It can prolong QTc interval, ventricular tachycardia, and sudden cardiac arrest by causing intracellular sodium overdose.
Tocilizumab [61,62]	Recombinant humanized anti-IL-6 receptor monoclonal antibody, which is a competitive blocker of membrane-bound and soluble IL-6. Potential role in patients presenting with symptoms associated with cytokine storm.	Compochiaro et al. found no statistically significant survival benefit with a slightly increased propensity towards the development of fungal infections; however, it may reduce the need for ventilatory support in hospitalized COVID-19 patients [63].
Steroids [64,65,66]	Usually administered steroids include methylprednisolone (32 mg/day), dexamethasone (6 mg/day), and hydrocortisone. Dexamethasone is favoured as it causes minimal fluid retention. It may have a role in reducing the tissue injury due to cytokine storm.	Conflicting body of evidence regarding improvement in survival and decreased hospital stay. May be beneficial but should not be given to all the patients. It can lead towards the development of hyperglycaemia, hypernatremia and mucormycosis and aspergillosis. It can reduce the duration of fever but has no overall effect on the duration of hospitalization.
Remdesvir [67,68]	Broad-spectrum antiviral which is an inhibitor of viral RNA-dependent RNA polymerase	Conflicting data on improvement in symptoms with no significant impact on mortality, however, may offer a survival benefit if given early in mild to moderately ill COVID-19 patients.
Vitamins	A high dose of vitamin C can prevent cytokine storm in COVID-19 patients, which reduces lung injury and inflammatory damage.