Table 1.
The main treatments that have been administered to COVID-19 patients.
| Treatments | Mechanisms of Action | Type of Study | Main Results | Ref. |
|---|---|---|---|---|
| Remdesivir | A monophosphoramidate prodrug of an adenosine analogue that inhibits viral RNA polymerases | (a) Clinical trial (b) Compassionate use |
(a) No association with statistically significant clinical benefits. (b) Clinical improvement in 36 of 53 patients (68%). |
(a) [1] (b) [2] |
| Lopinavir/Ritonavir | A co-formulation of two structurally related protease-inhibitors as antiretroviral agents (HIV type 1 aspartate protease inhibitors) | Clinical trial | No significant benefit from the treatment compared to standard care. | [3] |
| Favipiravir plus IFN-α | Inhibits the RNA-dependent RNA polymerase (RdRp) of RNA viruses | Open label control study | Attenuated disease progression and improved viral clearance. | [4] |
| Ivermectin | A synthetic derivative of a macrocyclic lactone antiparasitic agent. Inhibits the nuclear import of host and viral proteins | In-vitro antiviral activity against SARS-CoV-2 | Compared to the DMSO-treated control, a 93% reduction in viral RNA and a 99.9% in cell-associated viral RNA. | [5] |
| Hydroxychloroquine and Chloroquine | Both drugs accumulate in lysosomes, leading to elevated intra-vesicular pH that prevents endosome trafficking and viral fusion. They also interfere with the glycosylation of ACE-2 receptors, which prevents their binding by SARS-CoV-2 and thus infection. | (a) Prospective randomized trial (b) A pilot observational study (c) Discontinued by WHO |
(a) No significant difference between patients with hydroxychloroquine + conventional treatment and those with the conventional treatment alone. (b) Clinical improvement in all participating patients receiving co-administration of hydroxychloroquine with azithromycin. |
(a) [6] (b) [7] (c) [8] |
| Interferon (IFN)-α | A broad-spectrum antiviral agent | Clinical trials in process | IFN-β1a and IFN-α2b are currently being evaluated as potential candidates for the treatment of patients with COVID-19. | [9] |
| Arbidol/lopinavir/ritonavir | By inhibiting the virus-mediated fusion with the target membrane, arbidol blocks virus entry into the target cells | (a) Retrospective cohort study (b) Cohort of 50 patients in two groups: lopinavir/ritonavir regimen (34 cases) and arbidol alone (16 cases) |
(a) A significant increase in the conversion rate from positive to negative results for the coronavirus test on days 7 and 14 for patients receiving arbidol plus lopinavir/ritonavir versus monotherapy with lopinavir/ritonavir. (b) After 14 days of treatment, there was no viral load for the arbidol-treated group, but a 44.1% viral load for the lopinavir/ritonavir-treated group. |
(a) [10] (b) [11] |
| Tocilizumab | A humanized anti-interleukin-6-receptor (IL-6R) monoclonal antibody that inhibits IL-6 | (a) Retrospective observational study (b) Cohort of 100 patients (c) Retrospective study |
(a) No attenuation of the disease in critically ill patients after a single dose of tocilizumab. (b) A rapid and sustained positive response to tocilizumab treatment. (c) Alleviation of the clinical symptoms and avoidance of severe COVID-19 with tocilizumab treatments. |
(a) [12] (b) [13] (c) [14] |
| Convalescent plasma therapy |
Appears to exhibit a neutralizing antibody response directed against the viral S protein. The antibodies block SARS-CoV-ACE2 entry. |
(a) Evaluation of 6 COVID-19 patients (b) Case series analysis of 5 critically ill patients (c) Open-label, multi-center, randomized clinical trial |
(a) Effective in alleviating patient symptoms and ameliorating radiological injuries. (b) Improved clinical status of patients. (c) No statistically significant improvement in the clinical condition of patients. |
(a) [15] (b) [16] (c) [17] |
| Corticosteroids | Anti-inflammatory effects are due to a negative regulatory mechanism (transrepression). | Cohort of 41 patients | Suppressed lung inflammation in 21% of patients. | [18] |
| Prezcobix | HIV protease inhibitor | Under clinical trials | The primary endpoints included symptom improvement and virus nucleic acid turning negative, but the optimal endpoint has not been determined. | [19] |
| Oseltamivir | Neuraminidase inhibitor. | (a) COVID-19 patients (75) (b) Non-severe and severe COVID-19 patients (393) |
(a) Recovery rate: 31%; Mortality rate: 11%. (b) No significant improvement in the clinical condition of patients. |
(a) [20] (b) [21] |