The team showed that some drugs that targeted the proteins involved in SARS-CoV-2 viral entry significantly reduced levels of infection. These included DX600 — an ACE2 peptide antagonist which is a molecule that specifically targets ACE2 and inhibits the activity of peptides that play a role in allowing the virus to break into the cell.
DX600 was around seven times more effective at preventing infection compared to the antibody, though the researchers say this may be because it was used in higher concentrations. The drug did not affect the number of heart cells, implying that it would be unlikely to be toxic.
“The spike protein is like a key that fits into the ‘lock’ on the surface of the cells — the ACE2 receptor — allowing it entry. DX600 acts like gum, jamming the lock’s mechanism, making it much more difficult for the key to turn and unlock the cell door,” said Professor Anthony Davenport from the Department of Medicine and a fellow at St Catharine’s College, Cambridge.
He added that further research is needed on this drug, “but it could provide us with a new treatment to help reduce harm to the heart in patients recently infected with the virus, particularly those who already have underlying heart conditions or who have not been vaccinated.” It may also “help reduce the symptoms of long Covid”.