IndraLab

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Hydroxychloroquine glycosylates ACE2. 32 / 32
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"Among these, chloroquine and hydroxychloroquine interfere with Ca release from acidic EL (and with the terminal glycosylation of ACE2), thus impairing virus-receptor endocytosis in SARS-CoV-2 infection (10, 11, 169)."
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"In-vitro studies showed that CQ and HCQ cause glycosylation of ACE2 receptor making cells to be refractory to SARS-COV-2 infection 8."
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"HCQ has shown a potential broad-spectrum antiviral activity [17,18] with one or more from the following mechanism of action:•HCQ could interfere with the glycosylation of the angiotensin-converting enzyme 2 (ACE2) receptor, preventing the virus from binding to its target cells."
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"Another, well-known antimalarial agent, hydroxychloroquine was also proven to inhibit the replication of SARS-CoV by impeding the glycosylation of ACE2 (Vincent et al., 2005)."
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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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"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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"Chloroquine and hydroxychloroquine could inhibit the glycosylation of ACE2 receptors, changing its structure and therefore blocking the binding of S protein to it [2,32,39]."
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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."
| DOI
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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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"Finally, it cannot be excluded that the treatment taken by the patients might modify the ability of the virus to bind to the ACE2 since hydroxychloroquine -was suggested to mediate a deficit in the glycosylation of ACE2 (65, 66) ."
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"Hydroxychloroquine can prevent viral attachment and entry into host cells by impairing glycosylation of ACE2, thus disrupting the interaction between S protein and ACE2."
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"The potential use of CQ and HCQ in COVID-19 was initiated by in vitro studies, in which both CQ and HCQ were found to inhibit the fusion of SARS-CoV-2 and the host cell membranes, inhibit the glycosylation of the cellular ACE2 receptor (the binding site of SARS-CoV-2), and block the transport of SARS-CoV-2 from early endosomes to endolysosomes [3] [4] [5]."
| DOI
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"Chloroquine and hydroxychloroquine could inhibit the glycosylation of ACE2 receptors, changing its structure and therefore blocking the binding of S protein to it [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"Chloroquine and hydroxychloroquine reduce the glycosylation of the ACE2 receptor and the viral penetration into the cell, due to the alcalisation of endocytic compartments -- when not glycosylated, they will have lower affinity towards the viral spike proteins, which probably impedes the virus -- receptor binding, resulting in the inhibition of the infection development [55]."
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"Similarly, antimalarials, such as hydroxychloroquine and chloroquine, which may glycosylate ACE2, have demonstrated no benefit in patients infected with SARS-CoV-2 in randomized, controlled studies 37."
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"Also, previous studies have shown that HCQ interferes with the glycosylation of ACE-2, the receptor of SARS-CoV-2, and inhibits viral fusion into cells2,3."
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"In addition, both CQ and HCQ interfere with the glycosylation of ACE2, impairing binding of the viral spike proteins to host cell surface receptors [267], [268]."
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"CQ and HCQ inhibit viral entry by impairing terminal glycosylation of ACE2, which may reduce enzyme activity, elevating Ang II concentration and favoring the pressor axis."
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"Hydroxychloroquine has been found to interfere with the glycosylation of ACE2 resulting in the prevention of virus binding [60, 61]."
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"Hydroxychloroquine can increase the endosomal pH, inhibit the toll-like receptor activity and interfere with the terminal glycosylation of ACE-2 [33]."
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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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"Also, postprandial glucose levels were normal during the hypoglycemic period.HCQ is an antimalarial drug with immunomodulatory effects and widely used for rheumatic diseases.Also, previous studies have shown that HCQ interferes with the glycosylation of ACE-2, the receptor of SARS-CoV-2, and inhibits viral fusion into cells 2,3 ."
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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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"Mechanistically, hydroxychloroquine inhibits SARS-CoV-2 virus uptake into cells by inhibiting angiotensin converting enzyme 2 glycosylation."
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"2, 3 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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"Hydroxychloroquine is believed to increase the endosomal pH needed for virus-cell fusion, interfere with glycosylation of the ACE2 receptor, and modulate the immune response [12]."
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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 [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
| PMC
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"In addition to its immunomodulant and anti-inflammatory effects, hydroxychloroquine can interfere with the glycosylation of SARS-CoV-2 spike proteins and ACE2 receptors, blocking, in in vitro experimental models, viral entry [26], so that its empiric prophylactic use among patients and healthcare workers at high risk of infection has been recently advocated by the Indian Council of Medical Research (https://icmr.nic.in/content/covid-19)."
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"Chloroquine and hydroxychloroquine cause alkalinisation of the intracellular phagolysosome and thus cause underglycosylation of ACE2 receptors required for cellular entry of COVID-19, which prevents virion fusion and uncoating [60, 61] ."
| PMC
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"In addition, hydroxychloroquine interferes with the terminal glycosylation of ACE2, interfering with virus binding [123] ."
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"Chloroquine and hydroxychloroquine reduce the endosomal pH, prevent virus-cell fusion, and interfere with glycosylation of ACE2 receptors."
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"Among these, chloroquine and hydroxychloroquine interfere with Ca2+ release from acidic EL (and with the terminal glycosylation of ACE2), thus impairing virus-receptor endocytosis in SARS-CoV-2 infection (10, 11, 169)."
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