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.