No.
Nvcov2 uses a ligand similar to ace2 such that the virus binds to that instead of cellular ace2.
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The Company determined, based on molecular modeling screening that it had in its chemicals library ligands that could bind to SARS-CoV S1 spike protein at the same position where the S1 binds to the human receptor ACE2. It is a reasonable expectation that these relatively broad-spectrum ligands would also be able to bind the S1 spike protein of the SARS-CoV-2 coronavirus in the same fashion. Since then, the Company has generated several nanoviricides based on these ligands and has tested them in its own BSL2 virology lab facility against known available human pathogen coronaviruses, including those that use ACE2 as the cellular receptor, with success.
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They are counting on S1 binding to chosen nvcov2 ligand similar to ace2.
However, they always used to claim that if virus mutates such that S1 escapes binding to nvcov2 ace2 mimic ligand and thus that nvcov2 no longer neutralizes virus, then that vitus could no longer infect any cells very well. But how can this be the case if they claim nvcov2 also blocks a virus with different s1 spike that binds to APN at the same time it blocks ACE2 binding?
Juat trying to understand how can blocking be broad when before they said ligands were very specific to only one receptor?
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We strive hard to develop virus-binding small chemical ligands mimic the cognate cellular receptor of the virus, using rational design and molecular modeling strategies and our internal, accumulated expertise. This is the receptor to which a virus binds to gain entry into the human cell. Some viruses use more than one, different, receptors. The nanoviricide® platform technology allows use of different ligands on the same nanoviricide drug to be able to attack such difficult viruses.
It would be very difficult for a virus to become resistant to a nanoviricide that mimics the virus’ cellular receptor. This is because, no matter how much a virus mutates or changes, its binding to the cellular receptor does not change. If the virus does not bind to the nanoviricide efficiently, it would likely have lost its ability to bind to the cellular receptor efficiently as well, resulting in an attenuated version with limited pathogenicity.
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