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Understanding the details of cellular and molecular basis of the virus\u2013host cell interaction is essential for developing variant\u2010independent therapeutic options. The internalization of SARS\u2010CoV\u20102, into lung epithelial cells, is mediated by endocytosis, especially clathrin\u2010mediated endocytosis (CME). Although vaccination is the gold standard strategy against viral infection, selective inhibition of endocytic proteins, complexes, and associated adaptor proteins may present a variant\u2010independent therapeutic strategy. Although clathrin and\/or dynamins are the most important proteins involved in CME, other endocytic mechanisms are clathrin and\/or dynamin independent and rely on other proteins. Moreover, endocytosis implicates some subcellular structures, like plasma membrane, actin and lysosomes. Also, physiological conditions, such as pH and ion concentrations, represent an additional factor that mediates these events. Accordingly, endocytosis related proteins are potential targets for small molecules that inhibit endocytosis\u2010mediated viral entry. This review summarizes the potential of using small molecules, targeting key proteins, participating in clathrin\u2010dependent and \u2010independent endocytosis, as variant\u2010independent antiviral drugs against SARS\u2010CoV\u20102 infection. The review takes two approaches. The first outlines the potential role of endocytic inhibitors in preventing endocytosis\u2010mediated viral entry and its mechanism of action, whereas in the second computational analysis was implemented to investigate the selectivity of common inhibitors against endocytic proteins in SARS\u2010CoV\u20102 endocytosis. The analysis revealed that remdesivir, methyl\u2010\u03b2\u2010cyclodextrin, rottlerin, and Bis\u2010T can effectively inhibit clathrin, HMG\u2010CoA reductase, actin, and dynamin I GTPase and are more potent in inhibiting SARS\u2010CoV\u20102 than chloroquine. 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