Figure 1:PCR detection value of virus in patients infected with ”2019-ncov” after hospitalization

In fact, remdesivir was originally used to cure Ebola, which end up in failure in the Phase 3 clinical trials. Before the outbreak of the COVID-19, only no more than 5 articles were confirmed the drug treatment for coronavirus [12, 14, 15], such as MERS-CoV, SARS-CoV , etc. In this few studies, we found that remdesivir is used to cure the coronavirus by early treatment or prophylactic outside the body or inside the animal. The relationship between the viral titer and time of the remdesivir was studied [12], the author observed maximal inhibition when remdesivir was added between 2 h preinfection and 2 h postinfection. These results indicate that even if remdesivir really has been successfully used in the treatment of COVID-19 in the end, it is best used to cure the coronavirus by early treatment or prophylactic. So, we can infer from these basic studies that remdesivir is not a magic bullet for COVID-19.
With the progress of the COVID-19 epidemic, two clinical trials results on remdesivir had been published. Patients with severe COVID-19 by compassionate use of remdesivir showed that the clinical improvement was observed in 36 of 53 patients (68%) [16]. Unfortunately, this study lack ongoing randomized, placebo-controlled trials of remdesivir therapy. On 29 April, the Phase 3 clinical of remdesivir run in China announced that it had found no benefits from remdesivir when compared with a placebo in severe COVID-19 patients [17]. There are still many scholars believe that remdesivir is the antiviral hope against SARS-CoV-2 [18, 19]. In light of the current findings we need to look at this drug objectively and rationally.
Furthermore, from pharmaceutical perspective we objectively explore the therapeutic effects of the remdesivir. Studies showed that in primary human lung epithelial cell cultures, the drug half-maximum effective concentration (EC50) is 0.07 µM for SARS-CoV and MERS-CoV, which is 10 times lower than that of COVID-19 [5]. This data indicates that the inhibitory effect of remdesivir on COVID-19 is lower than that of SARS and MERS. Besides, remdesivir inhibits Ebola replication in multiple relevant human cell types with EC50 values of 0.06 to 0.14 μM [20]. The current remdesivir administration is based on the Phase 3 clinical trial of Ebola, which may need to be re-explored since there is a tenfold difference in EC50 between them. Unfortunately, we were unable to find the blood concentration data of remdesivir in humans. The above results suggest that we should treat the drug remdesivir cautiously and objectively, and remdesivir is not a magic bullet for COVID-19 from pharmaceutical perspective, at least for now.
Although, due to the large scale outbreak of the COVID-19, people were easy to panic and could not correctly understand these knowledge. With the focus on therapeutic efficacy, more and more clinical data of remdesivir will be available in the foreseeable future with urgent need. Accordingly, a clearer understanding of the clinical pharmacology and significance of remdesivir will break through the clouds to see the sky in the ongoing pandemic. In the meantime, we must look at any drug objectively and rationally, and remdesivir may not be a magic bullet for COVID-19.