Table 1.

Summed up the current SARS-CoV-2 treatment options.

Drugs	Pharmacological Mechanism	Therapeutic Utility	Cons	Summary of Evidence	References
VIRUS TARGETING ANTIVIRAL (VTA)
Remdesivir (Nucleotide analog)	Inhibit viral replication via interacting with RNA-dependent PNA Polymerase (RdRp)	SARS-CoV; Middle East respiratory syndrome-CoV (MERS-CoV); Influenza; and Ebola	There is no proof of safety or efficacy. Adverse effects like renal failure and increased liver enzymes	Remdesivir effectiveness was demonstrated in a study with 53 individuals infected with SARS-CoV-2, according to Gilead Sciences. The findings revealed a lower death rate in severe instances.	[33,34]
Ribavirin (Ribonucleic analog)	Interferes with DNA and RNA viral replication and suppresses natural guanosine synthesis by direct action on enzyme inosine monophosphate dehydrogenase.	SARS; MERS; Respiratory syncytial virus (RSV) infection; and Hepatitis C	Adverse effects like hematologic toxicity, high risk of anemia, and teratogenic effect in pregnant women.	Ribavirin is primarily used in combination with Ritonavir/Lopinavir and IFN-β.	[35]
Favipiravir (Viral RNA-dependent RNA polymerase inhibitor)	It prevents viral growth by inhibiting RNA polymerase activity.	Ebola; Influenza A	Efficacy is yet unknown. Adverse effects like hyperuricemia, increased liver enzymes, diarrhea, decreased neutrophil count, and teratogenicity.	According to a recent study, favipiravir suppressed COVID-19 development and favored viral clearance.	[34,36]
Ritonavir/ Lopinavir (Protease inhibitor)	Inhibition of the viral PL-pro or Mpro (3CL-pro)	HIV type 1	Adverse effects like hepatotoxicity, pancreatitis, cardiac conduction abnormalities, increase the risk of cardiac arrhythmia.	In a clinical study with 199 individuals, lopinavir did not show therapeutic improvement.	[37]
VIRUS-HOST INTERACTION
Chloroquine and Hydroxychloroquine (Anti-malarial)	Both chloroquine and hydroxychloroquine block glycosylation of ACE2 receptor chains in SARS-CoV-2, reducing ligand binding and preventing the viral S protein from mediating cell entrance.	Chloroquine-Malaria; SARS-CoV; and extra-intestinal amoebiasis Hydroxychloroquine-Malaria; lupus erythematosus	Long-term use of chloroquine and hydroxychloroquine increasing the risk of retinal damage, hypoglycemia, and cardiac arrhythmias.	A recent investigation with 96,032 patients looked at the effectiveness of chloroquine or hydroxychloroquine, which is frequently administered in combination with a second-generation macrolide. The study found that chloroquine is linked to a greater incidence of ventricular arrhythmias.	[37,38]
Umifenovir (Fusion inhibitors)	Umifenovir prevents viral genes from entering the nucleus by impeding the interaction between ACE2/S protein and the fusion of the viral lipid envelope with the host cell membrane.	SARS-CoV-2; Influenza A and B	Common side effects like increased liver enzymes, gastrointestinal intolerance, and allergic reactions.	Umifenovir monotherapy was shown to be more effective than ritonavir/lopinavir in lowering viral load in COVID-19 patients.	[39,40]
Camostat Mesylate (Transmembrane protease, serine 2 inhibitors)	SARS-CoV-2 invasion into host cells is prevented by inhibiting TMPRSS2-mediated glycoprotein activation.	Chronic pancreatitis	Adverse effects like gastrointestinal intolerance, itching, skin rashes, and increased liver enzymes.	Camostat mesylate significantly inhibited the entrance of MERS-CoV, SARS-CoV, and SARS-CoV-2 into the lung cell line Calu-3, resulting in cytotoxic consequences. Furthermore, in cell line investigations, camostat mesylate therapy decreased SARS-CoV-2 infection.	[41]
HOST-TARGETING ANTI-VIRAL
Convalescent plasma	Direct viral neutralization and immune system control molecules (cytokine storm, Th1/Th17 ratio, complement activation, etc.). Immunomodulation of a hypercoagulable condition.	SARS-CoV; MERS-CoV; H1N1; Spanish influenza A; and Sepsis	Expensive. The effects of passive vaccination are generally short-lived.	After receiving a convalescent plasma infusion, five patients with severe COVID-19 showed considerable clinical improvement. Using convalescent plasma therapies, 10 patients with COVID-19 were also cured in another clinical research.	[42]
Corticosteroids (Steroid hormones)	The interaction with glucocorticoid steroid (GR) receptors in the cell cytoplasm neutralizes pro-inflammatory cytokines, preventing inflammation.	Inflammation	Increase the risk of secondary infection	There is some benefit in the early stages of infection, and its effectiveness in the treatment of COVID-19 is still being debated by the World Health Organization.	[43]
Sarilumab (Recombinant humanized mAb, IL-6 antagonist)	Interaction with the IL-6 receptor inhibits IL-6 signaling.	Cytokine release syndrome; Rheumatoid arthritis	Still, there is not enough evidence to suggest sarilumab for COVID-19 therapy.	The use of sarilumab is under investigation.	[44]
Tocilizumab (Recombinant humanized mAb, IL-6 antagonist)	Interaction with the IL-6 receptor reduces inflammatory responses and protects against immunological dysregulation caused by inflammation.	Cytokine release syndrome; Rheumatoid arthritis	Expensive. Adverse effects like hepatotoxicity, gastrointestinal perforations, hypertension, and hypersensitivity reactions,	The research found that after a few doses of administration, C-reactive protein levels in 15 individuals with COVID-19 decreased, improving their medical state.	[45]