"In other words, Brilacidin is NOT a compound that would fail in a clinical setting due to it causing phospholipidosis because it has already been through multiple clinical trials and has NOT failed."
I do wish people would actually read my post and the associated article and try to understand them rather than construct a straw man of their own choosing and then rather pointlessly beat it to death.
Again, I'm not suggesting brilacidin causes phospholipidosis in the clinical setting - quite the opposite.
The point is that if the anti-coronavirus success of brilacidin in vitro is due to an in vitro phospholipidosis effect - and it plausibly could be as anyone who has read Dr. DeGrado's papers on MoA will realise - then as it doesn't seem to cause phospholipidosis in the doses used, it's unlikely to work as an anti-viral in humans.
The fcat that it appears to have worked in Phase II studies as an anti-bacterial, anti-modulatory or anti-inflammation agent is not relevant to its action as an antiviral.
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