PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33821268-6 2021 The mechanism of the protease inhibitors nafamostat and camostat extend beyond inhibition of TMPRSS2 to coagulation-induced spike cleavage. nafamostat 41-51 surface glycoprotein Severe acute respiratory syndrome coronavirus 2 124-129 32532094-3 2020 Here we established a quantitative fusion assay dependent on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) S protein, angiotensin I converting enzyme 2 (ACE2) and TMPRSS2, and found that nafamostat mesylate potently inhibited the fusion while camostat mesylate was about 10-fold less active. nafamostat 202-221 surface glycoprotein Severe acute respiratory syndrome coronavirus 2 110-111 32532094-6 2020 Together, our study shows that nafamostat mesylate potently inhibits SARS-CoV-2 S protein-mediated fusion in a cell fusion assay system and also inhibits SARS-CoV-2 infection in vitro in a cell-type-dependent manner. nafamostat 31-50 surface glycoprotein Severe acute respiratory syndrome coronavirus 2 69-70 34541574-2 2021 Here, we evaluate nafamostat mesylate, a potent broad-spectrum serine protease inhibitor that blocks host protease activation of the viral spike protein. nafamostat 18-37 surface glycoprotein Severe acute respiratory syndrome coronavirus 2 139-144 35294338-7 2022 The mechanism of the protease inhibitors nafamostat and camostat may extend beyond inhibition of TMPRSS2 to coagulation-induced spike cleavage. nafamostat 41-51 surface glycoprotein Severe acute respiratory syndrome coronavirus 2 128-133