Remdesivir

Potently blocked virus infection at low-micromolar concentration

the most effective antiviral

drug which can construct a covalent bond with Cys145 inside binding site SARS-CoV-2 main protease

optimal combination therapy against SARS-CoV-2 was comprised of remdesivir, ritonavir, and lopinavir

remdesivir treatment led to a statistically significantly 29% reduction of death from COVID-19

reference drug control

Remdesivir was superior to placebo in shortening the time to recovery in adults hospitalized with Covid-19 and evidence of lower respiratory tract infection. However, given high mortality despite the use of remdesivir, it is clear that treatment with an antiviral drug alone is not likely to be sufficient.

 most effective for medium-risk patients

synergistic effect in combination with riboprine or 10-deazaaminopterin

significantly increased the discharge rate and decreased the occurence of serious adverse events and mortality

synergistic effect in combination with nitazoxanide, but antagonistic effect in combination with camostat mesilate, NCGC00411883-01 or hydroxychloroquine sulfate

better in combination with omeprazole

lower IC50 value in Calu-3 cells than VERO E6 cells

better in combination with simeprevir

Patients in the 5-day course of remdesivir treatment had statistically significant difference in clinical status compared to the control. The clinical importance of this observation is uncertain, however. No statistically significant difference was observed for secondary endpoints or in the 10-day course of remdesivir treatment versus control group. Sample size: 193 (10-day course) + 191 (5-day course) + 200 control. Dosage: 200 mg IV on day 1, 100 mg on days 2+. Endpoints: (assessed on the 11th day): Clinical scaling status distribution (primary). Adverse effects, clinical improvement (multiple classes) (secondary).

Manifests additive antiviral effect in combination with GC376 in vitro.

Significant decrease in mortality rate among patients under mechanical ventilation. Sample size: 25 + 26 control. Dosage: 200 mg IV on day 1, 100 mg daily on days 2-10.

Predicted to inhibit the SARS-CoV-2 RNA-dependent RNA polymerase.

Observed antiviral efficacy in both upper and lower respiratory tract in an in vitro model basted on cultured human airway epithelial cells.

Clinical improvement and negative PCR result in a patient previously not responding to lopinavir/ritonavir, chloroquine, and favipiravir therapies. Dosage: 200 mg IV on day 1, 100 mg on days 2-10.

remdesivir (200 mg loading dose on day 1, followed by 100 mg daily for up to 9 additional days) was superior to placebo in shortening the time to recovery in adults who were hospitalized with Covid-19 and had evidence of lower respiratory tract infection

Besides its primary action on RNA-dependent RNA polymerase, remdesivir disrupts viral RNA complementary strand synthesis (if high dNTP pools prevent remdesivir-induced polymerisation termination) in vitro.

Remdesivir is a potent SARS-CoV-2 inhibitor in human pluripotent stem cells-derived cardiomyocytes in vitro (60-fold lower EC50 than in Vero E6 cells). It does exhibit potential cardiotoxicity effects in these cells in concentrations similar to estimated plasma concentrations, however.

Predicted to inhibit the SARS-CoV-2 RNA-dependent RNA polymerase.

The remdesivir triphosphate metabolite is incorporated into the nascent SARS-CoV-2 RNA, which leads to delayed chain termination in vitro.

Inhibits SARS-CoV-2 in vitro. It could be cytotoxic in low-micromolar range, however.

In combination with chloroquine. Predicted to inhibit the SARS-CoV-2 3C-like protease.

Reduces viral load in cell culture and kidney organoids, especially (at low doses) in combination with

Successful clinical outcome in majority of children with COVID-19. One death occurred, but the patient received treatment late after symptoms onset. Sample size: 8. Dosage: 200 mg on day 1 and 100 mg on days 2 to 10 (body weight ≥40 kg); 5 mg/kg on day 1 and 2.5 mg on days 2 to 10 (body weight <40 kg).

Significantly increased rates of extubation and hospital discharge. The observed decrease in mortality was only numerical, however. Early administration was observed to be beneficial.

Predicted to bind both the SARS-CoV-2 RNA-dependent RNA polymerase and 3C-like protease.

RTP incorporation into nascent RNA by SARS-CoV-2 RNA-dependent RNA polymerase is more efficient than that of ATP.

At 0.5 μM concentration, if combined with 10 μM

Remdesivir was computationally modelled to inhibit SARS-CoV-2 RNA-dependent RNA polymerase (RdRpol) activity by delayed RNA chain termination and also destabilization of the RdRpol complex. In contrast to some other nucleotide analogues, it was predicted to base-pair with the complementary stand.

Based on computational assessment and in vitro validation, remdesivir therapy combined with

When used in a hamster model in combination with

The drug was significantly associated with 2-point improvement on an ordinal scale at days 21 and 28. The treated patients experienced fewer adverse effects compared to the

Combined with

There was a clinical and laboratory improvement observed after remdesivir treatment in a pregnant (3rd trimester) 39-year-old women suffering from rheumatoid arthritis and Sjögren's syndrome diagnosed with COVID-19 pneumonia. Dosage: 200 mg IV on day 1; 100 mg daily on days 2-5.

The drug inhibited infection by SARS-CoV-2 isolates in a human epithelial cell line with sub-micromolar EC50s, which were similar or slightly higher than those of PF-00835231.

Up to 4 remdesivir monophosphates (RMPs) were observed to be incorporated into the nascent RNA chain, with the fourth being incorporated significantly slower. The fourth RMP was observed not to translocate from the active site of SARS-CoV-2 RNA-dependent RNA polymerase (RdRp), possibly due to steric inhibition between the first RMP and RdRp.

Inhibited SARS-CoV-2 infection in Caco-2 cells in a dose-dependent manner with an EC50 of 0.3 μM and 0.4 μM in two different assays. At 6.25 μM the compound reduced SARS-CoV-2 RNA loads in Caco-2 cells by ca. 3 orders of magnitude.

Predicted to bind SARS-CoV-2 Membrane protein.

Predicted to target the host furin protease.

Inhibited SARS-CoV-2 replication in Huh7.5 cells, Calu-3 cells, primary normal human bronchial epithelial cells, or iPSC-derived AT2 cells.

Inhibited SARS-CoV-2 RNA-dependent RNA polymerase in a cell-based assay with an EC50 of 0.67 μM.

Attenuated SARS-Cov-2 replication in Calu-3 cells.

Inhibited SARS-CoV-2 RNA-dependent RNA polymerase in an enzyme assay and also in a cell-based assay with an EC50 of 0.67 μM. 

The compound retains its anti-SARS-CoV-2 activity in vitro against strains Alpha, Beta, Gamma, and Omicron. 

The treatment in combination with baricitinib was effective in blocking cytokine storm in a 35 years old (otherwise healthy) COVID-19 patient. Fast pulmonary and retarded CNS recovery was observed afterwards. Sample size: 1. Dosage: 200 mg IV on day one, 100 mg on days 2 to 5. 

Combined with baricitinib and dexamethasone, the treatment mostly led to a favourable clinical outcome. Sample size: 45. Dosage: 200 mg on day 1; 100 mg daily on days 2–5 or until hospital discharge. Main outcome: Hospitalization length, shock presence, and thrombosis occurrence.

The previous baricitinib treatment did not improve patient’s clinical status. It was improved following tocilizumab administration. The improvement was only partial/temporal and further recovery was observed only after remdesivir administration. Sample size: 1. Dosage: 200 mg loading dose; then 100 mg daily for 9 days. 

The combination of baricitinib, remdesivir and dexamethasone seemed to generally lead to improved survival in hospitalized COVID-19 patients. Sample size: 85 yes + 15 no. 

The combination of baricitinib, remdesivir and dexamethasone seemed to generally lead to positive clinical outcomes in the treatment of severe COVID-19 patients. There was no control group, however. Sample size: 44. Dosage: 200 mg on day 1; 100 mg on days 2 to 5 or 2 to 10. 

Administration of anakinra and remdesivir led to radiological and clinical improvement in a severe COVID-19 patient. Sample size: 1. Dosage: A 200 mg loading dose, then 100 mg daily for 7 days. 

A paediatric patient with severe COVID-19, requiring extracorporeal membrane oxygenation, was successfully treated using methylprednisolone, anakinra, and remdesivir. Sample size: 1. Dosage: 200 mg on day 1, 100 mg daily on days 2–5. 

In a juvenile patient experiencing severe immunodeficiency after hematopoietic stem cell transplantation and COVID-19, decrease in viral load, expansion of CD3 lymphocytes and clinical/radiological improvement were observed after treatment with CD45RO+ memory T cells, remdesivir, and regdanvimab. Sample size: 1. Dosage: Two courses of treatment, before and after stem cell transplantation. 200 mg loading dose, 100 mg IV daily for 10 days. 

The compound did not display significant inter-variant difference in its in vitro anti-SARS-CoV-2 activity – it was active. 

Treatment (remdesivir with monoclonal antibodies - casirivimab in combination with imdevimab) was effective in a lung transplant recipient. Sample size: 1. Dosage: 200 mg remdesivir for 5 days from postoperative day 2.   

The use of monoclonal antibodies and off-label remdesivir in COVID-19 patients with depleted B cells and prolonged infection proved to be effective and well-tolerated. Sample size: 3. Dosage: A single dose of 1,200 mg casirivimab and imdevimab IV and a 5-day course of remdesivir 200 mg IV, then 100 mg daily.