Several antiviral therapies have been identified for human pathogenic CoVs including synthetic inhibitors of neuraminidase, nucleoside analogs, remdesivir, tenofovir disoproxil (TDF), umifenovir (arbidol) and lamivudine (3TC) (Li et al., 2005). Studies involving identification of cellular receptors that facilitate the binding and entry of human associated coronaviruses have been done. Angiotensin I-converting enzyme 2 (ACE2) is a membrane bound aminopeptidase expressed in renal, cardiovascular, vascular and testicular tissue, as well as the small intestine (Donoghue et al., 2000; Hamming et al., 2004; Harmer et al., 2002). It has been shown to be a co-receptor for viral entry of SARS-CoV-2 with increasing evidence that it has a significant role in SARS-CoV-2 pathogenesis. Therefore, targeting the human ACE2 receptor might block the entry and the subsequent pathophysiology of the virus and is one of the premises of the present study (Zhou et al., 2020). SARS-CoV-2 entry into host cells is mediated by transmembrane spike(S) like glycoprotein that causes neutralization of antibodies, facilitates the projection of homotrimers from the viral surface, binds to human ACE2 receptor, and finally mediates membrane fusion and transport (Tortorici & Veesler, 2019). Spike (S) protein initially cleaves itself into two functional subunits (S1 and S2) which remain non-covalently bound to each other in a prefusion conformation. The S1 subunit is responsible for binding to ACE2, whereas S2 subunit has role in viral and host cell membrane fusion (Belouzard et al., 2009; Bosch et al., 2003; Burkard et al., 2014; Kirchdoerfer et al., 2016).