ArticleScience advances2022
Optimized ACE2 decoys neutralize antibody-resistant SARS-CoV-2 variants through functional receptor mimicry and treat infection in vivo.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Optimized ACE2-Fc fusion proteins with picomolar neutralization activity against highly evolved SARS-CoV-2 variants.Protein science : a publication of the Protein Society · 2026Article
- Development of ACE2-tropic-betacoronavirus therapeutics for future pandemic preparedness.Nature communications · 2025Article
- Primary cilium and TULP3-dependent ciliary targeting of ACE2 in SARS-CoV-2 tropism.Cell communication and signaling : CCS · 2025Article
- An ACE2-Fc decoy produced in glycoengineered plants neutralizes ancestral and newly emerging SARS-CoV-2 variants and demonstrates therapeutic efficacy in hamsters.Scientific reports · 2025Article
- Broad Neutralization Capacity of an Engineered Thermostable Three-Helix Angiotensin-Converting Enzyme 2 Polypeptide Targeting the Receptor-Binding Domain of SARS-CoV-2.International journal of molecular sciences · 2024Article
- Facilitating and restraining virus infection using cell-attachable soluble viral receptors.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- In Silico Design of miniACE2 Decoys with In Vitro Enhanced Neutralization Activity against SARS-CoV-2, EncompassingInternational journal of molecular sciences · 2024Article
- Modulation of the pharmacokinetics of soluble ACE2 decoy receptors through glycosylation.Molecular therapy. Methods & clinical development · 2024Article
- Variant-proof high affinity ACE2 antagonist limits SARS-CoV-2 replication in upper and lower airways.Nature communications · 2024Article
- SARS-CoV-2 Omicron: Viral Evolution, Immune Evasion, and Alternative Durable Therapeutic Strategies.Viruses · 2024Review
- Machine learning for functional protein design.Nature biotechnology · 2024Review
- Decoy peptides effectively inhibit the binding of SARS-CoV-2 to ACE2 on oral epithelial cells.Heliyon · 2023Article
- Comparison of SARS-CoV-2 entry inhibitors based on ACE2 receptor or engineered Spike-binding peptides.Journal of virology · 2023Article
- Broadly Effective ACE2 Decoy Proteins Protect Mice from Lethal SARS-CoV-2 Infection.Microbiology spectrum · 2023Article
- Bibliometric evaluation of 2020-2022 publications on COVID-19-related cardiovascular disease.Frontiers in cardiovascular medicine · 2022Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
Abstract
As severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) evolves to escape natural antibodies, it also loses sensitivity to therapeutic antibody drugs. By contrast, evolution selects for binding to ACE2, the cell-surface receptor required for SARS-CoV-2 infection. Consistent with this, we find that an ACE2 decoy neutralizes antibody-resistant variants, including Omicron, with no loss in potency. To identify design features necessary for in vivo activity, we compare several enzymatically inactive, Fc effector-silenced ACE2-Fc decoys. Inclusion of the ACE2 collectrin-like domain not only improves affinity for the S protein but also unexpectedly extends serum half-life and is necessary to reduce disease severity and viral titer in Syrian hamsters. Fc effector function is not required. The activity of ACE2 decoy receptors is due, in part, to their ability to trigger an irreversible structural change in the viral S protein. Our studies provide a new understanding of how ACE2 decoys function and support their development as therapeutics to treat ACE2-dependent coronaviruses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.