I have some sitting on my desk for use in case of emergency too!

https://www.nytimes.com/2020/04/30/health/coronavirus-antiviral-drugs.html

Clorpromazine?, whats next Qualudes ?

Yeah f**k Gilead the ass-holes
been disseminating the sof/dac stuff & indomethacin info
targeted mostly medical ppl,
im just scared now, essential/expendable worker. thankfully not much face time,
when i hit ICU they’ll put me on a trolley in the hallway,”just wait over here” too many comorbidities, too old etc,

Oral sofosbuvir delivers the phosphorylated nucleotide to the liver with great efficacy. It is possible that the nucleoside is released into circulation, and gets phosphorylated in lung AT2 cells. In that case, it might work, assuming sars co v polymerase is sensitive.

Study suggests that ( mild) enteric symptoms may be marker for severity
https://www.medrxiv.org/content/10.1101/2020.04.23.20076935v1

Not that that’s a bad thing at all if it works.

Sadly it does not.

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31022-9/fulltext

Interpretation
In this study of adult patients admitted to hospital for severe COVID-19, remdesivir was not associated with statistically significant clinical benefits.

Worse, the NIH did an emergency review and emergency press release because they knew this study was coming out.

Ignoring the Anthony Fauci backed, non-peer reviewed, non-published, interim analysis from NIH from 2 days ago https://www.niaid.nih.gov/news-events/nih-clinical-trial-shows-remdesivir-accelerates-recovery-advanced-covid-19 or not ignoring that and noting that report states:

Results also suggested a survival benefit, with a mortality rate of 8.0% for the group receiving remdesivir versus 11.6% for the placebo group (p=0.059) is far more accurately worded:

Results FAILED TO DEMONSTRATE ANY STATISTICALLY SIGNIFICANT survival benefit, with a mortality rate of 8.0% for the group receiving remdesivir versus 11.6% for the placebo group (p=0.059)
(despite being n=>1000…

IF remdesivir delivers any benefit whatsoever it is, at best, in the ballpark of the benefit of ribavirin which, when added to Sofosbuvir and an NS5A is ~ 1% extra SVR12 ie so small you can barely measure it.

In short, remdesivir

• is not a potent NUC,
• it is not even close to a potent NUC and
• even at n > 1000 it has failed to demonstrate any significant benefit.

Compared to a real NUC like sofosbuvir it is complete and utter rubbish, leaving aside the issues that it is IV only and exists only at experimental scale.

Here is a reasonably thorough analysis of the remdesivir trials (credit Dr Andrew Hill)

There are 5 main randomised trials of remdesvir. We need all the results from these 5 clinical trials to be combined. Then we could interpret the overall outcomes in a meaningful way.

When the World Health Organisation review a drug, they always run a systematic review and meta-analysis of all available data.

A: Chinese trial of remdesivir versus placebo showed no benefits (Lancet publication), n=237

1. There is no effect of remdesivir on coronavirus viral load levels – they are the same as the control arm. With 237 patients, this trial show easily have enough statistical power to detect an effect on viral load.

2. Remdesivir was stopped early for adverse events in 12% of patients, versus four (5%) who stopped placebo early.

3. Mortality was 14% for remdesivir versus 13% for placebo.

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31022-9/fulltext

B: Gilead’s trial in severe infection seem to suggest that 5 days of treatment is better than 10 days. What does this tell us about how well the drug works? Why should less treatment show trends for better outcomes?

1. Clinical recovery: 65% for 5 days, 54% for 10 days of treatment

2. Mortality: 8% for 5 days, 11% for 10 days

3. Adverse events leading to discontinuation: 5% for 5 days, 10% for 10 days

https://www.gilead.com/news-and-press/press-room/press-releases/2020/4/gilead-announces-results-from-phase-3-trial-of-investigational-antiviral-remdesivir-in-patients-with-severe-covid-19

C: NIH trial. Why was the clinical endpoint and sample size changed in the middle of the trial? n=1063, unpublished interim analysis.

This study, announced by Anthony Fauci, shows a slightly lower mortality for remdesivir (8.0%) versus placebo (11.6%), but this is not statistically significant. Remember that in the comparison of 5 versus 10 days of remdesivir, we also had 8% mortality for 5 days of remdesivir, versus 11% for 10 days of treatment. How do we interpret these two non-significant trends in the two trials?

Combined with the Chinese survival data, any difference in survival between remdesivir and placebo will be small and not statistically significant.

https://www.nih.gov/news-events/news-releases/nih-clinical-trial-shows-remdesivir-accelerates-recovery-advanced-covid-19

D: Missing data from the second Chinese trial.

This study of 308 patients was suspended for poor recruitment, but no results are available for the people who were actually recruited before April 15th. The website mentions 308 patients. What results are available? When will they be published?

https://clinicaltrials.gov/ct2/show/NCT04252664?cond=remdesivir&draw=2&rank=4

E: Main Gilead trial of remdesivir for people with moderate coronavirus infection (n=1600).

This trial is still ongoing, with results not yet available. We should see these results by the end of May.

https://clinicaltrials.gov/ct2/show/NCT04292730?cond=remdesivir&draw=2&rank=7

Even if remdesivir does show overall efficacy, there is the question of drug supplies. Will there be enough drug to treat everyone in need? Also the daily IV infusions of remdesivir will be a large burden on healthcare services.

Hi fitz,

I had the exact same response, although mine was more like “WTAF, if this is good I’d hate to think what bad looks like”

Indomethacin has a positive impact on COVID-19 symptoms

Doctors in New York have been using indomethacin in the treatment of the symptoms of COVID-19 for some time and now have experience of using the drug in more than 60 patients.
Three primary care physicians, Dr Jonathan Leibowitz, Dr Robert Rothstein and Dr Aline Benjamin, have shared their insights and experiences.

Dr Leibowitz explained how the first patient was one of his own colleagues, Dr Aline Benjamin, another primary care physician in New York, who was suffering from COVID-19. After one dose of indomethacin, by the next morning her cough was “a million times better”, according to Dr Benjamin

Indomethacin is useful in the management of respiratory symptoms – relieving the pain on taking a deep breath and the incessant (and exhausting) coughing. The effect is evident after only one or two doses of 25-50mg. About 90% of patients respond to indomethacin treatment.

The feedback from patients has been very positive. “I have received many messages of thanks through my patient portal – we didn’t get that with hydroxychloroquine!” says Dr Leibowitz.

The beneficial effect appears to be specific to indomethacin rather than being a class effect with non-steroidal anti-inflammatory drugs (NSAIDs). Ibuprofen did not appear to have a beneficial effect on the cough.

Dr Leibowitz said, “If we had used indomethacin earlier, many patients would not have gone to the emergency room – and infected perhaps 100 other people in the process”.