Protocol Evaluating the Efficacy of Remdesivir for Long COVID Following a Confirmed COVID-19 Infection. (ERASE-LC), 2023, Mark Faghy, University of Derby, UK

https://clinicaltrials.gov/study/NCT05911906?cond=Long COVID&intr=Remdesivir&rank=2

Adding this link to LC trial on Remdesivir. At least 3 people have queried if intention or desire is to add on a MECFS trial and Mark Faghy has been brief but very affirmative. Also included a comment by Christoph Strock highlighting WeandMecfs interest in assistance.
Chia used Remdesivir?
Strain in charge but not sure how motivated he is for MECFS?
 
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"The University of Derby is leading the £1.2m study that involves about 100 people who have lived with the condition for more than two years".

"Patients eligible to take part in the trial will undergo a series of tests before and after they are given remdesivir, including exercise tolerability, to monitor any improvements".

I think waiting 2 years for pwLC is a good thing. I don't think monitoring symptoms such as PEM would be accurate if they tested sooner in the illness.
 
From the protocol

Study Overview
Brief Summary
One in ten people following a COVID-19 infection develop ongoing symptoms which can last for months and even years. These symptoms affect people in different ways and have been demonstrated to broadly impact physical, mental and cognitive health. Currently, there are no treatments available to address the issues that patients experience but anti-viral medications have been suggested as being potentially effective. This pilot study will test how effective an existing anti-viral medication (Remdesivir) is at reducing the impact of Long COVID in patients.

Intervention / Treatment
  • Drug: Remdesivir
Other Study ID Numbers
  • UoD/ERASE-LC/23
Study Start (Estimated)
2024-01-01
Primary Completion (Estimated)
2025-01-01
Study Completion (Estimated)
2025-10-01
Enrollment (Estimated)
98

Study Type
Interventional
Phase
Phase 1
Design Details
Primary Purpose : Basic Science
Allocation : Randomized
Interventional Model : Parallel Assignment
Interventional Model Description:
Two groups within the model.

One will receive remdesivir, the other group will not. Allocation to the treatment group to be randomised.

Masking : None (Open Label)
Masking Description: Open label.
 
So it's a phase 1 trial with 98 participants in 2 groups. One group gets the drug, the other group gets nothing, so it's an open label trial.

I'm curious why they wouldn't go straight to a double blind placebo controlled trial.
Edit: I guess because they are using it to test feasiblity and safety as well as efficacy, so they need to know unblinded whether the drug is safe for this patient group.
 
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Outcome measures:
Primary outcomes:
Quality of life, functional status, and post-exertional symptoms.
Using questionniares: Health-related quality of life (EQ-5D-5L), & Symptom Burden Questionnaire for Long COVID.
At 53 days.
Also feasibility and safety data.

Secondary outcomes:
A long list of questionnaires and tests.
 
I see no good reason for a trial of this size not to be placebo controlled. I think making matched placebos can be expensive but in view of the total cost it is hard to seat being an impossibility.

With those outcome measures it looks a bit of a dead duck.
 
Jonathan Edwards said:
With those outcome measures it looks a bit of a dead duck.
Click to expand...
I didn't list all the secondary outcome measures:

Observe changes in exercise tolerance and reduced post-exertional symptom exacerbation following incremental exercise
Modified De Paul Symptom Questionnaire-Post Exertional Malaise (DSQ-PEM), symptom Burden Questionnaire for Long COVID
53 days

Functional Status
Post COVID Functional Status Scale,
Impact on daily life subscale of the Symptom Burden Questionnaire for Long COVID
4 weeks

Explore whole-body FDG uptake using PET/CT methods in patients with Long COVID.
The standardised uptake volume (SUV) and Ki of 18FDG uptake observed during PET/CT scans.
53 days

Physical & Physiological function:
Impact on daily life subscale of the Symptom Burden Questionnaire for Long COVID, & DSQ-PEM.
Fatigue Assessment Scale (FAS), Medical Research Council (MRC)
Dyspnoea Scale.
Maximum inspiratory and expiratory mouth pressure, lung function, blood pressure, oxygen saturation, breathing rate, and resting heart rate, rate of perceived exertion and oxygen saturation.
53 days

Functional Status
Post-COVID Functional Status Scale,
6-minute walk test and timed up and go.
53 days

Cognitive Function
Perceived Deficit Questionnaire (PDQ-5) and Montreal Cognitive Assessment 'Blind' version (MoCA-Blind)
53 days

Biochemical/inflammatory markers
Full blood count, eGFR, LFTs, CRP, d-dimers, IL6, IL16, IL18, PCT, IFN-Y, TNF-A, VEGF-D, CRP, HLA-DP, and Vitamin D.
4 weeks

Emotional Status
Generalised Anxiety Disorder (GAD-7)
53 days

________________________

I agree it should be double blind placebo controlled.

Also the outcome measures are done at only 53 days (7 weeks and 4 days)
For a condition that is long lasting and fluctuating, that seems far too short. Surely they need a 6 month and 12 month follow up.
 
Cornwall13 said:
Regardless of trial design, is the rational behind the use of Remdesivir in long covid a valid one?
Click to expand...

I doubt it. Persistent viral antigen may explain a subset of LC but probably a minority. There is some evidence [1, 2] to suggest this might be the case so anti-spike MAbs are worth trialling. Though one problem is trying to select who might benefit, as persistent antigen may be quite common if you look and is found in those without LC symptoms.

I don't think we've seen good evidence of replication-competent SARS-CoV-2 reservoirs, so inhibiting RNA polymerase seems unlikely to be useful.

(I'd be looking much more intently at the role of latent viruses and targeting those mechanisms.)
 
SNT Gatchaman said:
I doubt it. Persistent viral antigen may explain a subset of LC but probably a minority. There is some evidence [1, 2] to suggest this might be the case so anti-spike MAbs are worth trialling. Though one problem is trying to select who might benefit, as persistent antigen may be quite common if you look and is found in those without LC symptoms.

I don't think we've seen good evidence of replication-competent SARS-CoV-2 reservoirs, so inhibiting RNA polymerase seems unlikely to be useful.

(I'd be looking much more intently at the role of latent viruses and targeting those mechanisms.)
Click to expand...

I can completely understand why many researchers are currently focusing more on going after a persistent SARS-COV-2 virus rather than something like EBV.

First of all there are actually mAbs for SARS-COV-2 as well as many different antivirals, with different mAbs and antivirals being in development. With that PET tagging the virus suddenly becomes an option as well. From a naive pharmaceutical perspective it should also be easier to deal with persistent COVID-19 rather than some Herpesvirus whose possible mechanisms we don’t understand.

There’s far more knowledge on the possible and tangible opportunities for the EBV connection in MS and yet no-one has any idea why 99% of the people have no problems after an EBV infection and what the relationship between EBV and MS could look like. So going down a similar EBV route that has been tried in ME/CFS, probably doesn’t seem too useful to most LC researchers. Companies like Atara Bio, probably will only start working or supplying their means to study EBV’s role in LC once there is more knowledge or biomarkers of the disease. Cooperation with pharmaceutical companies is close to impossible for Long-Covid researchers, cooperation with those that have an EBV related therapeutic is even harder.

Finally, for funding purposes it’s often a lot easier to apply for a grant that says “we’re doing something new based on a new virus and new evidence” rather than saying “we’ll be doing something that was sort of done before without substantially more evidence being present, but now we’ll do it properly”.

I expect to see more latent virus research either if there are more positive results in MS research, once the viral persistence research has yielded more answers, positive or negative, or if the current latent virus research in LC yields breakthrough results (which I’m very sceptical about given the lack of research). From what I can tell it’s not really “either or” but rather “let’s try the simpler and more tangible solution first”.
 
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From TwitterX a timeline of what this team has been doing and people involved.
Posting for info and still feel a little dubious but can’t place it.
 

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