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. 2021 Jul 8;11:128. doi: 10.1186/s13578-021-00638-w

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — The mechanism of action of GL25E in inhibiting SARS-CoV-2 infection. The binding of GL25E to S1 subunit (a) and RBD (b) as measured by ELISA. The effect of mannose on the binding of GL25E to S1 subunit (c) and RBD (d). The effect of GL25E on the binding of S1 subunit (e) and RBD (f) to ACE2. The effect of GL25E (g) and GRFT (h) on 6-HB formation. The inhibition of GL25E on SARS-CoV-2 S-mediated cell–cell fusion (i). Each sample was tested in triplicate and the data were presented as means ± SD. Significant difference between two groups was analyzed using the unpaired two-tailed Student’s -t test. **P < 0.01; ***P < 0.001; ****P < 0.0001