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KMBJN

07/27/21 4:55 PM

#367330 RE: Bad_Timing #367320

Agree with all this:

As you note direct viral disruption has been discussed quite a bit. I think most people here understand that is the primary MoA of interest at the moment. If it also blocks replication, great.



Not sure about the accusations of FUD, but I guess it just goes to show how hard it is to stay objective and dispassionate.

Somebody asked about the MOA of the Japanese drug and our MOA, and I responded that they share the inhibition of the CoV main protease.

https://onlinelibrary.wiley.com/doi/full/10.1002/minf.202000115

According to the docking protocol described above, the following drugs can be listed as potential inhibitors of the SARS-CoV-2 Mpro:
..
Brilacidin (CHEMBL2219413), an investigational drug for the supportive care of mucositis, stomatitis, and head and neck neoplasms (interestingly, Brilacidin is being investigated for direct inhibition of SARS-CoV-2 (press release of April 6th, 2020 (www.ipharminc.com/press-release); Flovagatran (DB05714)



https://investorshub.advfn.com/boards/read_msg.aspx?message_id=165114269

What's the science behind this medicine? Is it the same as B?



So, when someone asks for a comparison of MOA, that is what they get, a discussion of some of the similarities and differences.

There are at least 4 oral antivirals in trials or soon to be. 3 of them inhibit the main protease like brilacidin is predicted to do. 1 blocks viral replication by introducing copying errors during RNA replication.