A recent study posted to the bioRxiv preprint server assessed whether niclosamide could be employed in coronavirus disease 2019 (COVID-19) therapy.

Diagram of niclosamides effect on SARS-CoV-2 entry and  spike protein-mediated syncytia formation. 1.) SARS-CoV-2 binds to the ACE2 receptor of the host cell and enters. Niclosamide has been shown to inhibit this entry step in vitro 2.) Viral replication generates many copies of the RNA genome. 3.) Infection results in an increased expression of viral spike (S) protein and host cell TMEM16F at the plasma membrane. 4.) The S protein at the surface on an infected cell binds to the ACE2 receptor of an adjacent uninfected cell. 5.) Spike-dependent syncytia formation is mediated by the calcium-dependent lipid scramblase TMEM16F to generate multinucleated infected cell bodies. Niclosamide, an inhibitor of TMEM16F, has been shown to block spike-dependent syncytia formation.