Ructurally, SARS-CoV-2, an enveloped positive-sense single stranded RNA (+ssRNA) virus belonging for the b genus on the Coronaviridae family, has four most important ALDH2 Inhibitor Accession structural proteins including the tiny envelope (E) glycoprotein, membrane (M) protein, nucleocapsid (N) protein, and spike (S) glycoprotein, as well as three accessory proteins involve: papain-like protease (PLpro) and 3Chemotrypsin-like protease (3CLpro, also called the principle protease-Mpro), that are accountable for cleavage of viral polypeptide into functional units; and RNA-dependent RNA polymerase (RdRp), that is essential for viral replication and transcription [4,5]. The virus penetrates the host cell by means of the binding of its S-protein with the angiotensin converting enzyme II (ACE-2) receptor, which can be identified in virtually all human organs in varying degrees [6]. As a result, it is actually recommended that the disruption from the interaction amongst ACE-2 and SARS-CoV-S protein is actually a potential therapeutic target for treating COVID-19. Normally, S protein, PLpro, 3CLpro, RdRp and ACE-2 will be the most attractive targets for the improvement of new drugs against COVID-19 [7]. The clinicalY. PashaeiJournal of Clinical Neuroscience 88 (2021) 163features of COVID-19 are varied, ranging from an asymptomatic or mild symptom state (prevalent cold-type) to acute respiratory distress syndrome (ARDS), sepsis and septic shock, multiple organ dysfunction, and, finally, death. Also, the SARS-CoV-2 infection mediates hyper-inflammation and dysregulated immunity major to CS. The management on the illness includes preventive and therapeutic methods as well as the treatment of CS. CS is definitely an exaggerated or aberrant host immune response to viral infection, which is regarded to become one of the principle causes of ARDS in COVID-19. ARDS is usually a potentially life-threatening situation leading to severe pulmonary edema, respiratory failure and arterial hypoxemia refractory to oxygen therapy [8,9]. The severity of COVID-19 depends largely on the immunity and the release of inflammatory mediators such as cytokines and chemokines for example interleukin (IL)-2, IL-6, IL-7, IL-1b, tumor necrosis factor-alpha (TNF-a), monocyte chemoattractant protein-1 (MCP1; also referred to as CCL2 [CCchemokine ligand 2]), macrophage inflammatory protein-1 alpha (MIP-1a; also referred to as CCL3), ferritin, C-reactive protein (CRP), and D-dimers [10]. One example is, Del Valle et al. [11] located that high serum IL-6 and TNF-a levels at presentation had been robust predictors of RSK4 Purity & Documentation disease severity and survival. In addition they proposed that serum IL-6 and TNF-a levels ought to be regarded in the management and treatment of sufferers with COVID-19 to stratify potential clinical trials, guide resource allocation and inform therapeutic possibilities. COVID-19 crisis poses a severe threat to global public health and an effective and inexpensive therapeutic tactic could present a essential implies of overcoming this crisis [12]. Unfortunately, till now, no productive vaccine or drug for the prevention (prophylaxis) or treatment of this contagious disease has been established. Though remdesivir, a broad spectrum anti-viral drug, an RdRp inhibitor, advanced into human clinical trials to treat COVID-19, it truly is still not readily available for most from the patients [13]. Because of the urgency from the situation, drug repurposing (i.e. testing the efficacy of existing drugs utilised previously to treat other diseases), as a faster and less costly pathway, is often a basic purpose so that you can identify doable efficient therapeutic optio.