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Posted On: 07/31/2021 2:15:58 PM
Post# of 72440
My responses to sunscatter on the same topic…
sunspotter said, “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.l
My response…. This statement is false. I have not seen anything in Dr. DeGrado’s papers that says that Brilacidin is “unlikely to work as an anti-viral in humans.” If you know different, please quote the appropriate passages and provide a cite so that the rest of us can see that you did not make it up.
sunspotter said, “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.”
My response… It’s not relevant? That makes no sense. The phospholipidosis occurs in the cells, not the bacteria or the virus. The dosage for the ABSSSI trial is comparable to the dosage for the current Covid trial so why would the human cells react differently? Phospholipidosis has not, is not, and will not be an issue for the current Covid trial.
sunspotter said, “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.l
My response…. This statement is false. I have not seen anything in Dr. DeGrado’s papers that says that Brilacidin is “unlikely to work as an anti-viral in humans.” If you know different, please quote the appropriate passages and provide a cite so that the rest of us can see that you did not make it up.
sunspotter said, “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.”
My response… It’s not relevant? That makes no sense. The phospholipidosis occurs in the cells, not the bacteria or the virus. The dosage for the ABSSSI trial is comparable to the dosage for the current Covid trial so why would the human cells react differently? Phospholipidosis has not, is not, and will not be an issue for the current Covid trial.
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