Chris Heminway, Exec-Chair at Time To ACT, explains why now is the right time for the Group to IPO. Watch the video here.
Ditto, thank you WEDme, awesome piece of work.
Yes I think that Paul and Eleanor are the only ones who read it properly - and as one expects, find weaknesses in the study (there are always weaknesses).
The others are just repeating the findings in the abstract - they haven't read it. You can always tell because they are 100% supportive and review is short and worthless.
Sorry - it was their reply to my enquiry - they are drafting the formal letter at present ...
Hi - I received the notification from HL on the open offer this morning.
Andrew Hill, a senior visiting research fellow at the University of Liverpool’s department of pharmacology, said a trial as large as Solidarity “would be expected to show a survival benefit [for the drug, if one existed].”
Earlier this month, the EU signed an agreement with Gilead to supply up to 500,000 treatment courses of the drug for European countries — including the UK — with an option to increase orders further.
Gilead has priced remdesivir at $2,340 per five-day course. Some public health experts have said the cost is too high for a drug that has not been proven to reduce the likelihood of death.
Final analysis of the US NIH study of 1,062 patients released last week in The New England Journal of Medicine, showed a decrease in hospital stays of about five days, from 15 to 10, but no significant mortality benefit for remdesivir.
The Covid-19 treatment remdesivir has no substantial effect on a patient’s chances of survival, a clinical trial by the World Health Organization has found, delivering a significant blow to hopes of identifying existing medicines to treat the disease.
Results from the WHO’s highly anticipated Solidarity trial, which studied the effects of remdesivir and three other potential drug regimens in 11,266 hospitalised patients, found that none of the treatments “substantially affected mortality” or reduced the need to ventilate patients, according to a copy of the study seen by the Financial Times.
“These remdesivir, hydroxychloroquine, lopinavir and interferon regimens appeared to have little effect on in-hospital mortality,” the study found.
The results of the WHO trial also showed that the drugs had little effect on how long patients stayed in hospital. However, WHO researchers said the study was primarily designed to assess impact on in-hospital mortality. The study has not yet been peer-reviewed.
Remdesivir was one of a series of drugs used to treat US President Donald Trump after he tested positive for Covid-19. It was developed by US drugmaker Gilead Sciences, initially as a potential medicine to treat Ebola.
Remdesivir received partial approval for use in the US and EU after a trial by the US National Institutes of Health in April showed that it cut the time to recover from Covid-19 from 15 days to 11. In July Gilead released further data suggesting the treatment may reduce the likelihood of death, but that finding had not been confirmed in a randomised controlled trial — the gold standard for drug approval.
We are aware that initial data from the World Health Organization’s (WHO) Solidarity trial has been made public prior to publication in a peer-reviewed journal,” Gilead said in response to a request for comment. “The emerging data appear inconsistent with more robust evidence from multiple randomised, controlled studies validating the clinical benefit of [remdesivir]."
The WHO declined to comment, saying the results of the study were not yet public.
The WHO’s findings mean that the only drug proven to increase Covid-19 survival rates is dexamethasone, a cheap steroid that can be taken orally and is widely available around the world. The WHO has recommended the use of steroids for patients with severe cases of Covid-19.
The Solidarity trial is one of the biggest ongoing studies of Covid-19 treatments. Drugs can be added or removed from the trial at any time. The results for the four drugs in the study seen by the FT cover the period from March to the beginning of October.
The remdesivir arm of the trial involved 2,750 patients. Participants received the treatment for 10 days, with 200mg delivered on the first day and 100mg for the subsequent days.
Andrew Hill, a senior visiting research fellow at the University of Liverpool’s department of pharmacology, said a trial as large as Solidarity “would be expected to
PMJH - Sadly it wouldn't matter - even if they said intravenous the subtleties of this would be lost and most wouldn't know the difference between oral, inhaled, topical or up your ar*e. It's like shock horror, crumbling a nurofen on your head didn't cure that headache.
I am beginning to think may on here will have read more about this field than many advisors would dare admit!
Sparkle - They have an abundance of interferons though apparently.
PS whatever happens this has been a welcome relief while I watch University life disintegrate.
Yes slide decks are ripe for snippets getting left on there - a footnote, a date, a presentation to .gov :)
re: FT article - not sure what study this is yet or which interferon regimen, type, administration or cohort they are talking about.
Agree Woodstock - and the social unrest that ensues.
Mr Trump's physician Sean Conley said in a statement earlier on Friday that the president had "as a precautionary measure received an 8g dose of Regeneron's polyclonal antibody ****tail", which is administered to help reduce virus levels and speed recovery.
He is over 100 Kg - so that is in the region of 6-8 mg per Kg. That is quite a lot right?
Nice work pmjh. Just about to watch the Oxford University Hospitals live stream.
Sorry DPunter, I must have missed that in the flurry of 'noise'. The difference now to even just 10 years ago is the ability to 'keep up' with a virus and to sequence these strains for peanuts in cash terms. It is the first time we have been presented with this challenge BUT been able to keep up with Mother Nature. Scientifically I would say we are in good shape. What we are lacking is leadership and mechanisms to respond rapidly.
Be careful to read the article and the caveats at the end about the *two* patients in Ecuador and the association with additional mutations in this gene and pathogenicity - and loss of too many stop codons in this region actually reduces it pathogenicity. What they are saying is SARS-COV-2 encodes a tiny little peptide of 22 amino acids that can interfere with IFN response. Must read more ... and anyone on here can read the free to read PDF and get a crash course in immunology and molecular biosciences ;)
Hi Shrek - no I don't think this one has, good spot. This is VERY interesting, have not read it yet but seems this could be pointing to the missing link as to why SARS-COV-2 might efficiently suppress the interferon response.
Published in a good journal.
Good spot!
Welcome! There is a lot of good discussion on this board and we would certainly welcome any views from the frontline. Not to mention admiration that frontline staff like yourselves are doing at the present time.
I posted a response and essentially urged them to look at this company and act fast.
I keep thinking about RM's words. He says it is a small dataset but a good dataset. He says he has been in talks with the people that matter. If they thought the data wasn't robust, or as robust as it can possibly be with this sample, the guy would not be able to seriously get in front of a camera and say it is good without losing all credibility. So I read this as Pharma agree this is good and therefore Pharma and/or other parties are very very interested.
apologies I did realise this had been posted already...