The Remdesivir Riddle
The drug was knowingly deployed in a way that prevented it from being effective. Why?
Alexandros Marinos
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.
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:
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.
This explains the absolutely terrible reputation the drug has. The WHO recommends against its usage due to bad results in the trials it organized, and overall the evidence of its effectiveness apear to be extremely weak.
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.
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.
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?
The plot thickens, as it turns out the FDA knew the treatment timing made no sense.
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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