From the article (bold added):

Remdesivir is a broad-spectrum anti-viral that early on in the pandemic was touted as our first victory in the fight against COVID-19. Ever since, however, the drug has remained controversial, and different public health institutions have wildly varying approach to whether, and how, it should be used.

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The first thing to know about antivirals in treating COVID-19 is that they are best given early. Both Paxlovid and Molnupiravir insist that treatment should start as soon as possible, and definitely no later than 5 days after onset of symptoms.

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However, something strange happened with remdesivir. Until recently, the treatment guidelines insisted that it only be used for severe COVID-19 patients, which in practice meant 7 or 8 days after the onset of symptoms...

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In other words, remdesivir is being given after the viral replication phase has wound down, at a time where the patient is in a far worse state, and there is little or no help it can provide.

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You might be surprised to hear that about 20% of Gilead’s 2021 revenue came from sales of remdesivir, which enjoyed USD 5.6 billion in sales. As far as they are concerned, remdesivir is a runaway success.

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In fact, the US government goes as far as to pay hospitals to use it, with a bonus in the tens of thousands of dollars per patient that uses it, called the “New Treatments Add-On Payment”. No wonder US hospitals spent over USD 1 billion on remdesivir last year, more than on any other drug.

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So we are faced with the riddle of remdesivir: why is a drug that costs more than $2000 per treatment, which is associated with kidney failure, being given at a time that reason, and research, tells us it can’t have much of an effect?...

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The Emergency Use Authorization (EUA) of remdesivir, released via a Freedom of Information Act (FOIA) request contains an incredibly troubling paragraph:

Clinical Virology remains concerned about the disconnect regarding this drugs mechanism of action and the timing of treatment administration. Remdesivir is an analog of adenosine triphosphate that inhibits viral RNA synthesis, and as such, the drug would most likely work early in the infection cycle when SARS-CoV-2 replication is occurring at a high level. Most patients who are hospitalized with COVID-19 are entering the hospital during the second week of infection when viral loads are in decline and the underlying disease is associated with severe lung pathology driven by a hyperactive immune response and cytokine release syndrome. It is not clear that remdesivir will have much of an impact on viral replication this late into the infection cycle.

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In other words, exactly what we’ve documented in this article so far.

The story of the approval of remdesivir back in April/May 2020 is a head scratcher, given the evidence we had on hand. Many good pieces tell the story, and “The Strange Story Of Remdesivir, A Covid Drug That Doesn’t Work” is a good summary.

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At this point, one is forced to speculate. The forced early approval, as well as the odd placement of remdesivir on the treatment schedule left a gap in early treatment options that is just now beginning to be filled.

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Was there a deliberate decision for the greater good that early treatment must be held back until as many as possible are vaccinated and/or the main vaccines receive full authorization? This will sound conspiratorial, but how else can we explain that remdesivir continues to be provided to this day on highly controversial data, and yet fluvoxamine, an off-patent early treatment drug for which the evidence is mounting, cannot get past “inconclusive”, as far as the NIH is concerned.