ArticleJournal of advanced pharmaceutical technology & research
Preventive treatment of coronavirus disease-2019 virus using coronavirus disease-2019-receptor-binding domain 1C aptamer by suppress the expression of angiotensin-converting enzyme 2 receptor.
Article in Journal of advanced pharmaceutical technology & research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 1 citations in OpenAlex.
- Autophagy in emerging and highly concerned severe zoonotic infectious diseases.Frontiers in immunology · 2026Review
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Authors and funding
3 authors at 1 institution in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
The cause of the worldwide coronavirus disease-2019 (COVID-19) pandemic is the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). It is known to employ the same entry portal as SARS-CoV, which is the type 1 transmembrane angiotensin-converting enzyme 2 (ACE2) receptor. The receptor-binding domain (RBD) is located on the spike S-protein's S1 subunit of the spike glycoprotein. The most important and effective therapy method is inhibiting the interaction between the ACE2 receptor and the S-spike RBD. An aptamer is a small, single-chain oligonucleotide that binds strongly to the target molecule. Recently, a CoV-2-RBD-1C aptamer-based system with a 51-base hairpin structure was discovered to have substantial binding affinity against the SARS-CoV-2RBD with similar binding sites at ACE. In the current study, we will study the aptamer's effect as a SARS-CoV-2 spike blocker and inhibit its ACE2 receptors' binding by studying the toxicity of aptamer for this cell line by calcein assay and the inhibition test of CoV-2-RBD-1C aptamers on spike RBD-ACE2 binding. The results show the half-maximum inhibitory concentration of CoV-2-RBD-1C aptamer is 0.08188 μM. The inhibition effect of CoV-2-RBD-1C aptamer on spike RBD-ACE2 binding was determined at half-maximal effective concentration of 0.5 μM concentration. The percentage of spike-ACE2 binding inhibition in A549-hACE2 cells in the D614G variant after 30 s was 77%. This percentage is higher than D614 and N501Y and equals 55% and 65%, respectively, at 0.15 μM of CoV-2-RBD-1C aptamer. The CoV-2-RBD-1C aptamer prevents virus entrance through spike inhibition, which results in a 90% reduction in spike D614 virus transduction at 1.28 μM. In conclusion, the CoV-2-RBD-1C aptamer might be an effective treatment against COVID-19 infection because it directly affects the virus by blocking the S-spike of SARS-CoV-2 and preventing ACE2 receptor binding.
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