Ok so here’s the news report (I couldn’t find a paper) showing Remdesivir improves time to recovery in #COVID19https://www.niaid.nih.gov/news-events/nih-clinical-trial-shows-remdesivir-accelerates-recovery-advanced-covid-19 …
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And here’s the Lancet study from China showing no mortality benefit from remdesivir:https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31022-9/fulltext?utm_campaign=tlcoronavirus20&utm_source=twitter&utm_medium=social …
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You’ll notice the NIH study...also doesn’t show a statistically significant mortality benefit for remdesivir!!
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As
@MarkHoofnagle pointed out, remdesivir is supposed to work via viral replication inhibition; it prevents RNA viruses from copying their genetic material.1 reply 0 retweets 12 likesShow this thread -
This means a trial on advanced
#COVID19 patients was never gonna tell us jack shit. Viral load in this disease peaks around the onset of symptoms!!3 replies 0 retweets 22 likesShow this thread -
If your drug works by killing virus or blocking it from replicating, you’ve got to test it on *brand new* cases!
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(Mea culpa; I could have known this trial was gonna suck before the results came out, based on trial design, but I didn’t check.)
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Look; this means *mechanism is bullshit*. An antiviral that “works” but doesn’t decrease viral load? Sure, I guess, it can have a different mechanism, but given how often this happens, should we really be framing drugs as having “known” MOAs at all?
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Replying to @s_r_constantin
I was/am also puzzled by the viral load data but i think it’s worth entertaining the possibility that viral RNA as measured in the respiratory tract may not be the best measure for these patients. In the rhesus macaque remdesivir study, the effect on swab results was also null...
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would blood samples be better? I thought the respiratory tract was where the virus was most common?
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