Retapamulin for COVID-19

c19early.org

COVID-19 Treatment Clinical Evidence

COVID-19 involves the interplay of 400+ viral and host proteins and factors, providing many therapeutic targets. c19early analyzes 6,000+ studies for 210+ treatments—over 17 million hours of research. Only three high-profit early treatments are approved in the US. In reality, many treatments reduce risk, with 25 low-cost treatments approved across 163 countries.

Naso/oropharyngeal treatment Effective Treatment directly to the primary source of initial infection.
Healthy lifestyles Protective Exercise, sunlight, a healthy diet, and good sleep all reduce risk.
Immune support Effective Vitamins A, C, D, and zinc show reduced risk, as with other viruses.
Thermotherapy Effective Methods for increasing internal body temperature, enhancing immune system function.
Systemic agents Effective Many systemic agents reduce risk, and may be required when infection progresses.
High-profit systemic agents Conditional Effective, but with greater access and cost barriers.
Monoclonal antibodies Limited Utility Effective but rarely used—high cost, variant dependence, IV/SC admin.
Acetaminophen Harmful Increased risk of severe outcomes and mortality.
Remdesivir Harmful Increased mortality with longer followup. Increased kidney and liver injury, cardiac disorders.

Retapamulin may be beneficial for COVID-19 according to the studies below. COVID-19 involves the interplay of 400+ viral and host proteins and factors providing many therapeutic targets. Scientists have proposed 11,000+ potential treatments. c19early.org analyzes 210+ treatments. We have not reviewed Retapamulin in detail.

Studies suggesting benefit with Retapamulin

Gupta et al., Protein structure-based in-silico approaches to drug discovery: Guide to COVID-19 therapeutics, Molecular Aspects of Medicine, doi:10.1016/j.mam.2022.101151

Bello et al., Innovative, rapid, high-throughput method for drug repurposing in a pandemic—A case study of SARS-CoV-2 and COVID-19, Frontiers in Pharmacology, doi:10.3389/fphar.2023.1130828

Several efforts to repurpose drugs for COVID-19 treatment have largely either failed to identify a suitable agent or agents identified did not translate to clinical use. Reasons that have been suggested to explain the failures include use of inappropriate doses, that are not clinically achievable, in the screening experiments, and the use of inappropriate pre-clinical laboratory surrogates to predict efficacy. In this study, we used an innovative algorithm, that incorporates dissemination and implementation considerations, to identify potential drugs for COVID-19 using iterative computational and wet laboratory methods. The drugs were screened at doses that are known to be achievable in humans. Furthermore, inhibition of viral induced cytopathic effect (CPE) was used as the laboratory surrogate to predict efficacy. Erythromycin, pyridoxine, folic acid and retapamulin were found to inhibit SARS-CoV-2 induced CPE in Vero cells at concentrations that are clinically achievable. Additional studies may be required to further characterize the inhibitions of CPE and the possible mechanisms.

Bello et al., Erythromycin, Retapamulin, Pyridoxine, Folic acid and Ivermectin dose dependently inhibit cytopathic effect, Papain-like Protease and M^PROof SARS-CoV-2, bioRxiv, doi:10.1101/2022.12.28.522082

AbstractWe previously showed that Erythromycin, Retapamulin, Pyridoxine, Folic acid and Ivermectin inhibit SARS-COV-2 induced cytopathic effect (CPE) in Vero cells. In this study and using validated quantitative neutral red assay, we show that the inhibition of CPE is concentration dependent with Inhibitory Concentration-50(IC50) of 3.27 μM, 4.23 μM, 9.29 μM, 3.19 μM and 84.31 μM respectively. Furthermore, Erythromycin, Retapamulin, Pyridoxine, Folic acid and Ivermectin dose dependently inhibit SARS-CoV-2 Papain-like Protease with IC50of 0.94 μM, 0.88 μM, 1.14 μM, 1.07 μM, 1.51 μM respectively and the main protease(MPRO) with IC50of 1.35 μM, 1.25 μM, 7.36 μM, 1.15 μM and 2.44 μM respectively. The IC50for all the drugs, except ivermectin, are at the clinically achievable plasma concentration in human, which supports a possible role for the drugs in the management of COVID-19. The lack of inhibition of CPE by Ivermectin at clinical concentrations could be part of the explanation for its lack of effectiveness in clinical trials.