Quote:

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"We have a lead compound that we really want to explore, because it does, in fact, interact with a viral protein in the way that we predicted it to interact, so it has a chance of inhibiting viral entry into a host cell," said senior author Dr. Brad Pentelute, a researcher in the Department of Chemistry at MIT.

Coronaviruses, including SARS-CoV-2, have many protein spikes protruding from their viral envelope.

A specific region of SARS-CoV-2's spike protein, known as the receptor binding domain, binds to a receptor called angiotensin-converting enzyme 2 (ACE2). This receptor is found on the surface of many human cells, including those in the lungs.

In hopes of developing drugs that could block viral entry, Dr. Pentelute and colleagues performed computational simulations of the interactions between the ACE2 receptor and the receptor binding domain of SARS-CoV-2's spike protein.

These simulations revealed the location where the receptor binding domain attaches to the ACE2 receptor a stretch of the ACE2 protein that forms a structure called an alpha helix.

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http://www.sci-news.com/othersciences/chemistry/peptide-sars-cov-2-coronavirus-08280.html

https://www.biorxiv.org/content/10.1101/2020.03.19.999318v1.full

Second link is the full text of the paper.

sounds promising

How long does it take to get something like this in a useable format?

Or just use soluble whole ACE2

We have previously provided the first genetic evidence that Angiotensin converting enzyme 2 (ACE2) is the critical receptor for SARS-CoV and that ACE2 protects the lung from injury, providing a molecular explanation for the severe lung failure and death due to SARS-CoV infections. ACE2 has now also been identified as a key receptor for SARS-CoV-2 infections and it has been proposed that inhibiting this interaction might be used in treating patients with COVID- 19. However, it is not known whether human recombinant soluble ACE2 (hrsACE2) blocks growth of SARS-CoV-2. Here we show that clinical grade hrsACE2 reduced SARS-CoV-2 recovery from Vero cells by a factor of 1,000-5,000. An equivalent mouse rsACE2 had no effect. We also show that SARS-CoV-2 can directly infect engineered human blood vessel organoids and human kidney organoids, which can be inhibited by hrsACE2. These data demonstrate that hrsACE2 can significantly block early stages of SARS-CoV-2 infections.

https://www.cell.com/pb-assets/products/coronavirus/CELL_CELL-D-20-00739.pdf

A mere 13 months