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. 2021 Jul 29;21(3):273–283. doi: 10.1007/s40268-021-00357-0

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial 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-nc/4.0/.

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Fig. 6 — Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and host angiotensin-converting enzyme 2 (ACE2) receptor interaction and mechanism of virus entry (left panel). A novel therapeutic peptide 13-amino acid peptide inhibitor (13AApi) blocks the receptor-binding domain (RBD) of the SARS-CoV-2 spike protein from interacting with the host cell surface ACE2 (right panel). The 13AApi is a promising therapeutic candidate to prevent virus entry and infection in the host. The image was created with BioRender