Fig. 1.
Inhibition of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) entry, replication, and endocytosis. Angiotensin type I receptor (AT1R) upregulates ADAM metallopeptidase domain 17 (ADAM17), that potentiates the shredding of angiotensin, converting enzyme 2 (ACE2) through ADAM17. Soluble ACE2 prevents the binding of SARS-CoV-2 with transmembrane bound ACE2. This could reduce the viral spread. Lopinavir and remdesivir inhibit RNA-dependent RNA polymerase (RdRp) and coronavirus main proteinase (3CLpro). Arbidol inhibits the interaction between ACE2 of host and S protein membrane of SARS-CoV-2. Chloroquine and hydroxychloroquine inhibit entry, replication, and endocytosis of SARS-CoV-2. Camostat inhibits transmembrane serine protease 2 (TMPRSS2), which is important for the SARS-CoV-2 infection. TMPRSS2 is the host protein, and activates the spike proteins (S-protein) of SARS-CoV-2 by priming.