Abstract
Successful development of a chemoprophylaxis against SARS-CoV-2 could provide a tool for infection prevention implementable alongside vaccination programmes. Camostat and nafamostat are serine protease inhibitors that inhibit SARS-CoV-2 viral entry in vitro but have not been characterised for chemoprophylaxis in animal models. Clinically, nafamostat is limited to intravenous delivery and while camostat is orally available, both drugs have extremely short plasma half-lives. This study sought to determine whether intranasal dosing at 5 mg/kg twice daily was able to prevent airborne transmission of SARS-CoV-2 from infected to uninfected Syrian golden hamsters. SARS-CoV-2 viral RNA was above the limits of quantification in both saline- and camostat-treated hamsters 5 days after cohabitation with a SARS-CoV-2 inoculated hamster. However, intranasal nafamostat-treated hamsters remained RNA negative for the full 7 days of cohabitation. Changes in body weight over the course of the experiment were supportive of a lack of clinical symptomology in nafamostat-treated but not saline- or camostat-treated animals. These data are strongly supportive of the utility of intranasally delivered nafamostat for prevention of SARS-CoV-2 infection and further studies are underway to confirm absence of pulmonary infection and pathological changes.
Competing Interest Statement
AO and SR are Directors of Tandem Nano Ltd and co-inventors of patents relating to drug delivery. AO has received research funding from ViiV, Merck, Janssen and consultancy from Gilead, ViiV and Merck not related to the current paper. SR has received research funding from ViiV and AstraZenecaand consultancy from Gilead not related to the current paper. JPS has received research funding from ENA respiratory, and consultancy from Byotrol Technologies, not related to current paper. No other conflicts are declared by the authors.
Footnotes
Conflicts of interest statement AO and SR are Directors of Tandem Nano Ltd and co-inventors of patents relating to drug delivery. AO has received research funding from ViiV, Merck, Janssen and consultancy from Gilead, ViiV and Merck not related to the current paper. SR has received research funding from ViiV and AstraZenecaand consultancy from Gilead not related to the current paper. JPS has received research funding from ENA respiratory, and consultancy from Byotrol Technologies, not related to current paper. No other conflicts are declared by the authors.
Funding The current work was funded by Unitaid as part of a COVID-19 supplement to project LONGEVITY. AO acknowledges research funding from EPSRC (EP/R024804/1; EP/S012265/1), NIH (R01AI134091; R24AI118397), and European Commission (761104). SR acknowledges research funding from EPSRC (EP/R024804/1; EP/S012265/1) and NIH (R01AI134091). JPS acknowledges funding from MRC (MR/W005611/1, MR/R010145/1), BBSRC (BB/R00904X/1; BB/R018863/1; BB/N022505/1) and Innovate UK (TS/V012967/1).