Camostat mesylate may hold promise against COVID-19

Last Updated: 2020-03-17

By David Douglas

NEW YORK (Reuters Health) - German researchers say a drug used against chronic pancreatitis could block entry of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into human host cells and thereby possibly prevent coronavirus disease 2019 (COVID-19).

"We found that camostat mesylate, a drug approved for human use in Japan, inhibits SARS-CoV-2 infection of lung cells in cell culture," Dr. Stefan Poehlmann of Leibniz Institute for Primate Research, in Goettingen, told Reuters Health by email. "We also know that the compound blocks SARS-CoV infection in a rodent model. Therefore, we feel that the suitability of camostat mesylate for treatment of COVID-19 should be evaluated within clinical trials."

SARS-CoV first emerged in China in 2002, Dr. Poehlmann and colleagues note in Cell. In a series of studies, they determined that SARS-CoV-2 uses the SARS-CoV receptor angiotensin-converting enzyme 2 (ACE2) for entry and the cellular serine protease TMPRSS2 for viral spike (S) protein priming.

"At present," they write, "it is unknown whether the sequence similarities between SARS-CoV-2 and SARS-CoV translate into similar biological properties."

They add, "In light of the potentially increased transmissibility of SARS-CoV-2 relative to SARS-CoV, one may speculate that the new virus might exploit cellular attachment-promoting factors with higher efficiency than SARS-CoV to ensure robust infection of ACE2+ cells in the upper respiratory tract."

To help interrupt this process, a potential candidate is the clinically proven serine-protease inhibitor camostat mesylate, which is active against TMPRSS2 and thus S protein priming.

This suggests, say the researchers, that "that antibody responses raised against SARS-CoV could at least partially protect against SARS-CoV-2 infection."

"Our results reveal important commonalities between SARS-CoV-2 and SARS-CoV infection and identify a potential target for antiviral intervention," the team concludes.

The research had no commercial funding, and the authors report no conflicts of interest.

SOURCE: https://bit.ly/38ROBdb Cell, online March 5, 2020.