Table 2.
Class of drugs | Drugs | Mechanism of action | References | |
---|---|---|---|---|
Antivirals | Remdesivir | Inhibitor of RNA-dependent RNA polymerase and, hence, compete for viral ATP, which results in inhibition of viral replication | Young et al., 2021 | |
Lopinavir/ritonavir | Inhibitor of 3-chymotrypsin-like protease (3CLpro) and inhibit viral replication | Cao et al., 2020 | ||
Ivermectin | Blocker importin α/β receptor and, hence, inhibit the transmission of viral protein into the nucleus of host cell | Caly et al., 2020 | ||
Ribavirin | Potent inhibitor of viral RNA synthesis | Iqubal et al., 2021b | ||
Favipiravir | Inhibitor of RNA-dependent RNA polymerase and, hence, compete for viral ATP, which results in inhibition of viral replication | Iqubal et al., 2021b | ||
Umifenovir | Affects the S protein activity and, hence, inhibit its fusion with the host cell | Iqubal et al., 2021b | ||
Immunomodulators |
Corticosteroids
|
Effectively mitigate the pro-inflammatory signaling pathways, stimulate the anti-inflammatory pathways, inhibit COX as well as NF-kB-mediated hyperinflammation, and, hence, reduce the cytokine storm | Hamilton et al., 2021 | |
IFN β-1a | Potentiate the interferon and assist in viral clearance | Davoudi-Monfared et al., 2020 | ||
IL-6R-antagonists
|
Inhibit IL-6-mediated hyperinflammation and cytokine storm | Michot et al., 2020; Gordon et al., 2021 | ||
IL-1R antagonists
Anakinra | ||||
TNF-α inhibitors
Adalimumab |
Inhibit TNF-α-mediated hyperinflammation and control cytokine storm | Iqubal et al., 2021a | ||
Bruton’s tyrosine kinase inhibitors
|
Potent inhibitor of TLR-4 activation and, therefore, mitigate the cytokine storm and inflammatory pathway | Roschewski et al., 2020 | ||
JAK inhibitors
|
Inhibit JAK and activate STAT pathway, leading to inhibition of cytokine production and maturation. Additionally, these drugs inhibit the viral endocytosis via interacting with ACE2 |
Stebbing et al., 2020 | ||
Calcineurin inhibitors
* Cyclosporine * Tacrolimus |
Reduced the production of T-lymphocytes via tumbling the expression of IL-2 receptor and production of IL-2. Inhibit the viral replication |
Cavagna et al., 2020 | ||
Complement inhibitors | Eculizumab | Inhibit the production of inflammatory C5a and C5b-9 | Laurence et al., 2020 | |
Kinin–kallikrein pathway inhibitors | Lanadelumab | Inhibitor of kallikrein and hence offers relief from ARDS | Lipcsey et al., 2021 | |
Icatibant | Antagonist of bradykinin receptor type 2 and thus, inhibit hyperinflammation | |||
Serine protease inhibitors |
C1 esterase inhibitor
|
Inhibit the coagulation and ARDS via interacting with FXIIa and kallikrein | Urwyler et al., 2020 | |
Antimalarials | Hydroxychloroquine | Inhibit the viral entry, replication, cytokine production and coagulation | Mitjà et al., 2021 | |
Chloroquine | ||||
Blood-derived products | Convalescent plasma | Maintain and stimulate the physiological defense against viral infection | Iqubal et al., 2021c | |
Hyperimmune immunoglobulin | ||||
Bamlanivimab | Anti-spike neutralizing IgG1 monoclonal antibody that interferes with the function of viral spike proteins | Gottlieb et al., 2021 | ||
REGN-COV2
|
Cocktail of two anti-spike neutralizing antibodies that that interfere the function of viral spike proteins | Tardif et al., 2021 | ||
Miscellaneous | Colchicine | Reduce hyperinflammation | Tardif et al., 2021 | |
Vitamin D | Maintain the immune function (innate and adaptive immune system). Reduce oxidative stress, inflammation and scavenge free radicals. |
Giannini et al., 2021 | ||
Azithromycin | Assist in viral clearance and inhibit viral replication. | Oldenburg and Doan, 2020 | ||
Sirolimus | Inhibit T-cell differentiation via inhibiting mTOR pathway and, hence, reduces cytokine storm and ARDS. | Omarjee et al., 2020 | ||
Bevacizumab | Inhibition of IL-6 and hence reduces the severity of cytokine storm and ARDS | Pang et al., 2021 |
COVID-19, coronavirus disease 2019; ARDS, acute respiratory distress syndrome.