"I still wonder how brilacidin didn't make the cut."
From the Yale article:
"A multi-institutional study published in Nature (PDF), which screened more than 13,000 existing drugs against two strains of the live SARS-CoV-2 virus, found LAM-002A to be the most effective in combatting the virus, including in lung cells infected with the virus."
From the Accelerated Article Preview:
"9. Towards this end, we profiled a library of known drugs encompassing approximately 12,000 clinical-stage or FDA-approved small molecules. We report the identification of 100 molecules that inhibit viral replication, including 21 known drugs that exhibit dose response relationships."
It should have made the universe of 12,000 unless they specifically elected to exclude it, right?
Could this be where there may have been an issue (and you KNOW how scientifically inept I am so if I'm obviously wrong about this go easy on me)?:
"100 molecules that inhibit viral replication"
I searched the IPIX Covid PRs for "replic...." and found 5, 3 of which discussed plans versus results. Here are the excerpts from the other two that use the term replication:
5/19 PR
"These statistically significant lab results strongly support Brilacidin’s prophylactic treatment potential given the drug’s potent and rapid virucidal activity—a unique ability, different from any other known drug currently in development to treat COVID-19, to inactivate the novel coronavirus prior to host cell entry and subsequent viral replication. A majority of antiviral agents targeting SARS-CoV-2 attempt to inhibit viral replication rather than completely eliminating the virus (virustatic versus virucidal)."
7/20 PR
"In the RBL assay (which included Brilacidin pre-incubated with virus), Brilacidin exhibited approximately 90 percent inhibition against SARS-CoV-2 at a concentration similar to that of Remdesivir™, which again reported 50 percent inhibition of the coronavirus. The Brilacidin inhibition assay was tested in a human lung epithelial cell line, with Remdesivir™ tested in Vero cells. The RBL data also supports Brilacidin showing an ability to inhibit viral entry into cells, a highly desirable mechanism of action as it is the first step in the infection process enabling viruses to be targeted outside the cell, whereas Remdesivir™ impacts viral replication only after the host cell has been infected."
Is there something about the mechanism of action....to inhibit viral entry into cells.....versus the study's criteria of "inhibit viral replication" that could have acted to exclude B from the group of 100?
If that's true, couldn't that be seen as a plus for the use of B to limit entry into the cell and a second drug to inhibit viral replication of the virus that evades that B "shield"?
In which case, missing this cut wouldn't be so bad at all?
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