On May 26, 2020, Innovation Pharma reported receiving data from a leading public health research institute showing Brilacidin inhibits SARS-CoV-2, the novel coronavirus responsible for COVID-19, in a human cell line. Brilacidin, in comparison to vehicle control, exhibited an inhibitory effect on SARS-CoV-2 in a dose-dependent manner-an average 29 percent inhibition at 0.1ug/ml (the lowest concentration) to an 85 percent inhibition at 100ug/ml (the highest concentration).

Brilacidin is one of the few drugs targeting COVID-19 that has been tested in phase 2 human trials for other clinical indications, providing an established safety and efficacy profile.

For the experiment, the SARS-CoV-2 spike pseudotyped luciferase virus was incubated with Brilacidin at different concentrations—from a low of 0.1ug/ml to a high of 100ug/ml—for 1 hour before being added to HEK/293T cells (a human kidney cell line) expressing hACE2 for 2 hours. Then, the infected cells were cultured in media for 3 days before cells were lysed, with the inhibitory effect measured as a function of luciferase activity. Multiple measurements were taken to determine an average efficacy.

The primary investigator characterized the results as promising, especially given inhibitory effects in this particular human cell line are difficult to achieve based on the PHRI’s experience testing other defensins. The researcher also theorizes Brilacidin’s inhibitory effect may be partially due to the drug’s ability to prevent viral entry by blocking the SARS-CoV-2 Spike 1 (S1) Receptor-Binding Domain (RBD) from interacting with the Angiotensin-Converting Enzyme-2 (ACE2) receptor, the method by which the novel coronavirus gains entry into human cells. Additional anti-SARS-CoV-2 testing in human cell lines is underway at both the PHRI and the RBL to further elucidate Brilacidin’s antiviral properties.

Related, the article highlights how defensins/peptides and their synthetic mimics, like Brilacidin, might be able to block the uptake of the novel coronavirus into host cells via the ACE2 receptor given their unique molecular properties. The article further points out that SARS-CoV-2 might be losing the battle in the intestines, in contrast to the lungs, due to defensins (present naturally) exerting a protective effect.