To infect healthy cells, the SARS-CoV-2 coronavirus responsible for the COVID-19 pandemic relies on the spike proteins on its surface, which bind to specific receptors in the body like keys in locks. But the VE607 molecule discovered in 2004 in the fight against SARS could perhaps impede the mechanism. At least that’s what Andrés Finzi, professor in the Department of Microbiology, Infectious Diseases and Immunology at Université de Montréal and researcher at the CHUM Research Centre, is aiming to demonstrate.

He and his collaborators have confirmed, in silico and in vitro, that VE607 can inhibit SARS-CoV-2 and its close cousin without affecting the viability of the host cells. Based on these results, the experts focused their attention on the four specific configurations of the SARS-CoV-2 key to see if the molecule could lock them out. Good news: it can. That means VE607 is indeed effective against all the coronavirus variants of concern. In vivo studies in mice showed that VE607 reduces the viral load of SARS-CoV-2 in the lungs by almost 40 times.

The molecule is therefore promising in the context of the COVID-19 pandemic and has the added advantage of being able to attack different mechanisms of action than other antiviral treatments such as Paxlovid or remdesivir. It may also represent an interesting alternative to monoclonal antibody infusions and prove effective against several coronaviruses. Still, a lot of work lies ahead—including research to determine whether the molecule is safe to administer in humans—before VE607 is approved as a treatment. With the pandemic still upon us, the project is moving very quicky.