Should I raise funds for Edinburgh/AfME or Daratumumab Phase 2?

Should I raise funds for Edinburgh/AfME or Daratumumab Phase 2?

  • Edinburgh/AfME

    Votes: 7 30.4%

  • Daratumumab Phase 2

    Votes: 16 69.6%
  • Total voters
    23
V

V.R.T.

Senior Member (Voting Rights)
I am planning to sell off a good amount of my musical instruments and gear, as well as a lot of my books (I have far too many books) and donate the proceeds to ME/CFS research.

I was thinking of donating the proceeds to the AfME/Edinburgh fund, but the daratumumab phase 2 funding situation has got me wondering if maybe its better to raise money for that study right now.

What does everyone think would be the best use of the funds I raise this way? We have been discussing the fact that daratumumab/CD38 is an important piece of the puzzle as well as a possible treatment, but it is just one trial which will succeed or fail, and perhaps it would be better to invest in the longer term, broader scope research of SequenceME and related projects.

On the other hand daratumumab needs much less money and so perhaps my fundraising will make more of a difference there, and SequenceME may well get adequate government funding, we don't know yet. I've already supported both myself when I've been able to. But I'm finding myself torn on what to focus on for this project.

Poll is not binding, its just to get a feel of the general consensus.
 
Utsikt said:
That’s very generous!

I think Dara has a lower chance of receiving public funding because they have already been rejected many places. So I’m sending most of my donations to them, and I’ll swap to SequenceME when Dara is funded.
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Well, I used to absolutely hoard books in my postgrad days and also have a stash of graphic novels that might fetch a little bit of money. They are taking up space at my parents' house currently (which might be why they agreed to help!) I can barely ever read paper books now, which sucks. But I won't sell my favourites!

Ditto with my instruments, I won't be selling my most beloved guitars, but I picked up a hodgepodge of amps, pedals, synths/keyboards and guitars over the years that arent super valuble on their own but could raise a reasonable sum if I sold them all off. Again, I cant use them much at all and they're taking up space at my folks place!

And yeah, that about was where my thinking was too r.e. daratumumab funding.
 
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Daratumumab might genuinely be a lucky break treatment that really works, but then I have thought this for a number of trials that happened on a small scale and the moment they went mid size they fail. Maybe this is the one, my issue is it fits the same pattern we have seen many times. Its a random bumbled across drug that might work that isn't targeting the known cause of the disease because we don't have one. That might shortcut us out of the hard work and it is the best shot of this type I have seen but people have been taken in by these quite a lot since the pandemic kicked off.

On the other hand AFME and Edinburgh (and other places like MEResearch UK) are about starting at the beginning, looking at what can be reliably found different in ME patients and finding biomarkers. Gradually growing up a solid knowledge base to try and dig through the soup of dysfunctions and odd findings to produce targets that have a good chance of being at the core of the disease. This wont be a quick process, honestly I suspect none of us suffering this disease will be treated by this process as its going to take decades, but its also the sure fire well travelled scientific approach and I don't think we have a process that can go faster and better that isn't basically a random walk.

Both approaches have brought advances in diseases, many diseases are treated by random findings, but less nowadays than in the earlier days of medicine. Perhaps the chance of government funding plays into this and then Daratumumab needs it more than Edinburgh which I think will get funded just because the government is under some pressure and doesn't have a clue what else to even do. I am not sure myself what the right thing is, I lean more towards pessimism and hence believing this is it for us but the future can be changed and hence lean to the longer route. But like all hypocrites I would definitely take part in a Daratumumab trial if it was on offer!
 
I think you make some good points. Daratumumab could be our golden ticket but I remember (other spaces) getting hyped for ampligen, temelimab, efgartigimod, BC007 etc. It does look like the most promising of the 'happenstance' based treatments I've seen in the five years I've been paying attention though.
 
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Hi @Joan Crawford
Together with some others I think it likely that ME/CFS is perpetuatd by some form of signalling loop that keeps generating 'danger' signals either within. the immune system, the brain or both.

We don't have any good leads for brain at present, beyond a fishing exercise trying to calm down different transmitters (that haven't already been tried out).

Signalling loops in the immune system could involve rogue antibodies and the B cells/plasma cells that make them (they almost certainly contribute to loops in autoimmune disease). They could involve T cell subpopulation activation and expansion. They could involve macrophage/dendritic cell activation persisting through epigenetic shifts or matrix bound signals like TGF beta.

Rituximab did not have a measurable effect in phase 3 but the argument for killing long lived plasma cells with Daratumumab is valid and would perhaps address the one aspect of an antibody story that we have not so far tested. So it was a rational thing to attempt. Another important factor for me is that Fluge and Mella have proven themselves to be careful and rigorous investigators.

But in addition, the molecular target of daratumumab, CD38, is a cell surface protein of importan cein activation of a range of immune cells and if antibody is not the answer blocking Cd38 is arguably an intelligent way to try to deal with other rogue cells. It may turn out to be the wrong molecule but it is a drug already licensed and known to reasonably safe.

Over and above all of this there are aspects to the data from the pilot dara trial that look to me very much like real biological response signal. One thing is the common shape of the response tracks. They are not all over the place the way they were for rituximab in phase 2. The other thing is that the responders had clearly different NKcell counts. That might be a fluke but you do not often see separation like that without there being a real basis.

Continuing with the genetics with a whole genome study is maybe equally important but I think the chances of that getting government- based or other institutional funding is stronger. The dara trial depends on more speculative ideas and grant giving bodies tend to expect drug companies to pick up trial bills.
 
Jonathan Edwards said:
Hi @Joan Crawford
Together with some others I think it likely that ME/CFS is perpetuatd by some form of signalling loop that keeps generating 'danger' signals either within. the immune system, the brain or both.

We don't have any good leads for brain at present, beyond a fishing exercise trying to calm down different transmitters (that haven't already been tried out).

Signalling loops in the immune system could involve rogue antibodies and the B cells/plasma cells that make them (they almost certainly contribute to loops in autoimmune disease). They could involve T cell subpopulation activation and expansion. They could involve macrophage/dendritic cell activation persisting through epigenetic shifts or matrix bound signals like TGF beta.

Rituximab did not have a measurable effect in phase 3 but the argument for killing long lived plasma cells with Daratumumab is valid and would perhaps address the one aspect of an antibody story that we have not so far tested. So it was a rational thing to attempt. Another important factor for me is that Fluge and Mella have proven themselves to be careful and rigorous investigators.

But in addition, the molecular target of daratumumab, CD38, is a cell surface protein of importan cein activation of a range of immune cells and if antibody is not the answer blocking Cd38 is arguably an intelligent way to try to deal with other rogue cells. It may turn out to be the wrong molecule but it is a drug already licensed and known to reasonably safe.

Over and above all of this there are aspects to the data from the pilot dara trial that look to me very much like real biological response signal. One thing is the common shape of the response tracks. They are not all over the place the way they were for rituximab in phase 2. The other thing is that the responders had clearly different NKcell counts. That might be a fluke but you do not often see separation like that without there being a real basis.

Continuing with the genetics with a whole genome study is maybe equally important but I think the chances of that getting government- based or other institutional funding is stronger. The dara trial depends on more speculative ideas and grant giving bodies tend to expect drug companies to pick up trial bills.
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Thanks for sharing your thoughts @Jonathan Edwards
 
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