My favorite take-aways other than the fantastic Selectivity Index of 426 from the preprint:
“Clearly, an effective COVID-19 therapeutic (or therapeutics in combination) ideally would control both viral load and the corresponding inflammatory damage due to SARS-CoV-2,93 and mitigate bacterial co-infections. Exhibiting three-in-one properties—antiviral, immuno/anti-inflammatory, and antibacterial—brilacidin is being developed for the intravenous treatment of COVID-19 in hospitalized patients and may be able to address different disease parameters within the one therapeutic treatment.”
“Interestingly, the inhibitory potential of brilacidin was best observed at the highest MOIs tested, with inhibition of virus at the lower MOIs (0.01 and 0.001) not showing statistical significance (Figure 3C). The inhibition exerted at the MOIs of 0.1 and 0.05 were extremely comparable to each other.”
“Our experiments in the Vero cell line model demonstrate brilacidin decreases viral load in a robust manner when the virus is pre-incubated with brilacidin (Figure 2D), suggesting brilacidin impacts the virus directly.”
“These findings indicate brilacidin causes significant cell wall stress and additional internal stress due to the accumulation of misfolded proteins. Additional mechanistic studies of brilacidin analogs against Escherichia coli, in comparison to the antibiotic polymyxin B, further support this class of compounds ability to destabilize bacterial membranes.”
“Remdesivir and favipiravir are inhibitors that impact the viral RNA synthesis step of the infectious process. These drugs may help decrease progeny viral genomes in infected cells, but they will not be conducive to inhibiting progressive infection of naïve cells once the progeny virions have been released from infected cells.”
“Furthermore, remdesivir and favipiravir do not possess intrinsic anti-inflammatory activity, unlike brilacidin.”
“Consequently, use of a drug strategy that exhibits intrinsic anti-inflammatory activity will add value to controlling later onset inflammatory damage in COVID-19 patients, potentially occurring beyond the time of active viral multiplication.”
“Experiments conducted in endemic human coronaviruses are ongoing, with additional testing planned in other lethal coronaviruses (MERS-CoV, SARS-CoV), toward assessing the potential of brilacidin as a broad spectrum inhibitor of coronaviruses.”
GO IPIX!
