The Severe Acute Respiratory Syndrome (SARS) Coronavirus 2 (SARS-CoV-2) that leads to the Coronavirus disease (COVID-19) is an extremely potent virus. It has been frequently demonstrated to attach to the Angiotensin Converting Enzyme II (ACE2) , which is critical to the control of blood flow and immune responses; ACE2 is present in endothelial cells, arterial smooth muscle cells, and many other organs, but most abundant in humans epithelia of the lung and small intestine, providing easier routes of entry for SARS-CoV . Similar to SARS-CoV , the interaction between the SARS-CoV-2 and the ACE2 exists at the point where the viral spike binds to the edge of the ACE2 receptor; unlike the human-adapted Middle Eastern Respiratory Syndrome Coronavirus (MERS-CoV) spike protein that binds to human dipeptidyl peptidase-4 (DPP4) but not ACE2 [24], SARS-CoV-2 does not also bind to DPP4 and seems to only bind to most other animal ACE2 except mouse ACE2 . Based on several prior decades of clinical precedent in broad-spectrum antiviral treatment of malaria, HIV, and other viral infections through immunomodulation using chloroquine, hydroxychloroquine, and their various salts , several clinical trials are presently under development or running, such as trials of lopinavir/ritonavir or hydroxychloroquine [2] ; however, twenty-three clinical trials as of March 10, 2020 from the Chinese Clinical Trial Register were found to be taking place in China to assess the use of chloroquine or hydroxychloroquine in the treatment of COVID-19 link between the concentration of chloroquine, the resulting increase of the endosomal pH, and interference with the glycosylation of cellular receptors of SARS-CoV . However, the actual binding of these drugs to domains of the SARS-CoV-2 spike protein -ACE2 complex to inhibit the spread of the virus has not been studied sufficiently.