IndraLab

Statements


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"There are many ongoing clinical trials which may provide more information on this issue.At the beginning of COVID-19 pandemic, scientists discovered in in-vitro studies that Chloroquine (CQ) and Hydroxychloroquine (HCQ) can inhibit glycosylation of ACE2 receptors [77] and block SARS-CoV-2 transfer from primary endosomes to intracellular lysosomes, thus potentially preventing the release of viral genome [78]."

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"XREF_BIBR Hydroxychloroquine is found to reduce the entry of coronavirus into a cell through interference with the terminal glycosylation of the angiotensin converting enzyme 2 (ACE2) receptor, which inhibits viral replication."

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"Hydroxychloroquine is also shown to inhibit the terminal glycosylation of the ACE2 receptor, which in turn inhibits SARS-CoV-2 entry, infection, and disease progression [XREF_BIBR]."

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"However, recent studies indicate that Hydroxychloroquine may also reduce glycosylation of ACE2, therefore inhibiting virus/ACE2 interaction (Devaux et al., 2020)."

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"In addition to endosomal pH increase mentioned above, HCQ is also said to inhibit terminal glycosylation of ACE2 receptor, which is considered to be the target of SARS-CoV and SARS-CoV-2 cell entry."
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"Hydroxychloroquine (HCQ) inhibits terminal glycosylation of ACE2 receptor, which may reduce the efficiency of its interaction with SARS-CoV spike protein."
| PMC

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"In vitro data suggest that hydroxychloroquine can reduce glycosylation of the ACE2 receptor and also can lower blood glucose concentrations, both which could be possible mechanisms of antiviral activity."

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"XREF_BIBR, XREF_BIBR Hydroxychloroquine is thought to impair the terminal glycosylation of the angiotensin-converting-enzyme 2 (ACE2) receptor, which is the binding site for the envelope spike glycoprotein and has been shown to inhibit endolysosome function."

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"However, Hydroxychloroquine increase in human organelles raises their pH, thereby inhibiting antigen processing, preventing the alpha and beta chains of the major histocompatibility complex (MHC) class II from dimerizing, inhibiting antigen presentation of the cell, and reducing the inflammatory response.10 Hydroxychloroquine prevents terminal glycosylation of ACE2, the receptor that SARS-CoV and SARS-CoV-2 target for cell pass."

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"Hydroxychloroquine blocks sialic acid receptors at the upper respiratory pathway and prevents the glycosylation of the angiotensin converting enzyme 2 (ACE2) receptor [116,117,118,119]."

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"Chloroquine and hydroxychloroquine may reduce glycosylation of the ACE2 receptor which prevents the virus binding to and entering the new cells."

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"HCQ impairs the 69 terminal glycosylation of ACE2 and thereby inhibits cell binding and consequently entry of the virus 70 into the cell [13-15]."
| DOI

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"HCQ and CQ have been reported to reduce the glycosylation of ACE2 in host cells, which is essential for its activity [ 57–59 ]."

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"HCQ impairs the terminal glycosylation of ACE2 and thereby inhibits cell-binding and entry of the virus into the cell [14–16]."

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"It is believed that hydroxychloroquine (HCQ) and chloroquine (CQ) impede viral terminal glycosylation of ACE2; however, they do not alter ACE2 in mammalian cells; therefore, they might theoretically be used to treat neo-crown pneumonia [268]."

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"In vitro studies have shown that HCQ can inhibit viral entry, replication and glycosylation of the viral surface receptor angiotensin-converting enzyme 2 by increasing the pH of intracellular endosomes (100,101)."

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"Implications of HCQ Mediated Inhibition of ACE-2 Glycosylation in People with Hypertension and Obesity."

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"The antimalarial drugs chloroquine phosphate (CQ) and hydroxychloroquine (HCQ) impair in vitro the terminal glycosylation of ACE2 without significant change of cell-surface ACE2 and, therefore, might be potent inhibitors of SARS-CoV-2 infections."
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"The antimalarial drugs chloroquine phosphate (CQ) and hydroxychloroquine (HCQ) impair in vitro the terminal glycosylation of ACE2 without significant change of cell-surface ACE2 and, therefore, might be potent inhibitors of SARS-CoV-2 infections."
| PMC

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"The antimalarial drugs CQ and HCQ impair the terminal glycosylation of ACE2 without significant change of cell-surface."

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"The terminal glycosylation of ACE2 is inhibited by hydroxychloroquine, prevents the interaction of ACE2 with SARS-CoV-2 “spike” protein, and hence inhibits the entry of the virus."

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"Hydroxychloroquine inhibits glycosylation of angiotensin converting enzyme-2 (ACE2), a cell surface receptor thought to facilitate entry of SARS-nCoV-2 into cells [XREF_BIBR, XREF_BIBR]."

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"By contrast, hydroxychloroquine, which inhibits viral entry by increasing endosomal pH and affecting terminal glycosylation of the ACE2 receptor (19) , is predicted by the model to be less likely to be effective since drugs that act on viral entry would require exceptionally high suppression to achieve appreciable effects on viral production."
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"In fact, HCQ might prevent the glycosylation of ACE2."

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"HCQ was reported to inhibit the viral infection by glycosylating the ACE2 receptor of SARS-CoV-1 and increases the endosomal pH, rendering the membrane fusion [XREF_BIBR, XREF_BIBR]."
| PMC

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"It has been posited that the antimalaric drugs chloroquine and hydroxychloroquine reduce glycosylation of ACE2, thus preventing SARS-CoV-2 from binding to host cells."
| PMC

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"Chloroquine and hydroxychloroquine (CQ/HCQ) are thought to alter endosomal pH and reduce glycosylation of the ACE2 receptor, thus preventing viral entry [60,61]."

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"HCQ inhibits terminal glycosylation of ACE2 receptor, the main portal of entry for SARS-CoV and SARS-CoV-2."