Table 2.
Common drugs prescribed for the treatment of COVID-19
Name of the drug | Type of drugs | Mechanism of action | Clinical trial outcomes | Remarks | References |
---|---|---|---|---|---|
Umifenovir | Antiviral | Inhibits viral replication | Reduce the viral load to zero during clinical trials | It has been determined that umifenovir is ineffective in some variants of SARS-CoV-2 in patients | [180, 181] |
Favipiravir | Antiviral | It effectively prevents RNA-dependent RNA polymerase from becoming active | The primary outcome was the effect of favipiravir on reducing the time to viral clearance within 15 days of starting the treatment compared to the placebo group | Demonstrated effectiveness against several SARS-CoV-2 variants including delta and omicron | [182–185] |
Remdesivir | Antiviral | It is a nucleoside analog and inhibits the RNA-dependent RNA polymerase (RdRp) | Clinical state differed statistically significantly after a 5-day regimen of remdesivir | In numerous in vitro studies, Omicron, Delta, and other new SARS-CoV-2 variants were discovered | [62, 186, 187] |
Ribavirin | Antiviral | By attaching to the nucleotide-binding site of the enzyme, inhibits viral mRNA polymerase | Ribavirin was supposed to be effective in curing coronavirus illness due to its broad-spectrum suppression of RNA viruses | Variants that are both susceptible to and resistant to ribavirin have been discovered in increasing numbers | [188–190] |
Ivermectin | Anti-parasitic | The intracellular key transport is the ivermectin acts by inhibiting host importin alpha/beta-1 nuclear transport proteins | Except in clinical trials, the Panel advises against using ivermectin to treat COVID-19 | Regardless of the strain or variant of concern, alpha, beta, gamma, delta, or omicron, ivermectin demonstrated a rather homogenous in vitro action against SARS-CoV-2 | [191] |
Camostat | Serine protease inhibitor | Suppress SARS-CoV-2 invasion in lung cells by inhibiting the virus-activating host cell protease TMPRSS2 | According to a pilot finding in clinical trials, camostat may also be useful in treating the most severe COVID-19 instances accompanied by organ dysfunction | It blocks several serine proteases linked to the SARS-CoV and SARS-CoV-2 viruses | [192, 193] |
Nafamostat | Proteolytic inhibitor | Nafamostat inhibits MERS-CoV infection by blocking TMPRSS2 activity, which prevents membrane fusion between both the virus and human cells | The antiviral efficacy of nafamostat suggests that it has the potential to be an effective COVID-19 therapy option | This drug is effective against SARS-CoV-2 and MERS-Cov | [194] |
Famotidine | Histamin blocker | Competitive histidine H-receptor antagonist | Decrease of inflammation within the body and reported earlier alleviation of symptoms | This drug is effective against SARS-CoV-2 | [195] |
Molnupiravir | Monoclonal antibody (mAbs) | It is a unique nucleoside analog with wide antiviral efficacy against SARS-CoV and SARS-CoV-2. Molnupiravir prevents the replication of many viruses | Based on clinical trial data, it appears that molnupiravir operates as a mutagenizing agent that induces an "error catastrophe" during viral replication | It has been demonstrated that molnupiravir works well against SARS-CoV-2 variants other than the Omicron type | [196, 197] |
Babtelovimab | Monoclonal antibody (mAbs) | A recombinant neutralizing human IgG1 monoclonal antibody called bamlanivimab binds to the receptor-binding region of the SARS-CoV-2 spike protein and stops the spike protein from attaching to the human ACE2 | In comparison to the placebo, bamlanivimab plus etesevima lowered the rate of hospitalization and deaths attributable to Covid-19 and hastened the reduction in SARS-CoV-2 viral load | All COVID-19 variations of interest, including BA.2, the strain that is currently dominant in the United States, are responsive to bebtelovimab | [198, 199] |
Casirivimab | Monoclonal antibody (mAbs) | The clinical therapy of coronavirus disease is proposed to use neutralizing antibodies in COVID-19 | Various variants of the SARS-CoV-2 spike protein's many epitopes are targeted by antibodies | It shows a better response against SARS-COV -2 | [200–202] |
Sotrovimab | Monoclonal antibody (mAbs) | This antibody binds to an epitope on the SARS-CoV-2 spike protein receptor-binding domain (RBD), where it blocks an unidentified process that happens after viral attachment but before the fusing of the viral and host cell membranes | It is still unknown how immunization affects the safety and efficacy of sotrovimab | It shows a better response against SARS-COV -2, but 20-fold less effective against omicron variant | [203–205] |
Tixagevimab | Monoclonal antibody (mAbs) | It consists of a mixture of two human monoclonal antibodies, tixagevimab (AZD8895) and cilgavimab (AZD1061), both of which are directed against the surface spike protein of SARS-CoV-2 | It maintained antiviral activity and reduces hospitalizations by more than 50% in non-hospitalized individuals | Without any obvious safety issues, AZD7442 was effective in preventing Covid-19 with a single dose | [192, 206, 207] |
AT-527 | Antiviral | It act as an Guanosine Nucleotide analog | Undergoing clinical trial for efficacy in COVID-19 | It has been shown to be effective against Hepatitis C virus and can play role in SARS-CoV-2 | [50] |
Niclosamide | Antihelmint drug | It decreases the replication of virus by inhibiting S- phase kinase associated protein activity | Undergoing clinical trial for efficacy in COVID-19 | It inhibits COVID-19 infection and decrease cytokine stroms in COVID-19 patients | [50] |
Dexamethasone | Corticosteroids drug | Suppress Immune System | Found to be effective in COVID-19 patients | Improve recovery, prevent cytokine stroms in COVID-19 patients, decrease inflammmtion and fluid retention in lungs | [50] |
Artesunate | Antimalarial | It decreases the replication of viruses | Found to be effective in COVID-19 patients | It’s a combination of two drug such as Artesunate and pyronaridine and shows a broad spectrum of antimalarial activity | [50] |