If you’d like to give a detailed explanation of what the mechanism is and why there is proof beyond doubt please do, I’m all for hearing it.
I’m comfortable that I’m coming at all this from a place of ignorance and lack of experience, and find questions are a good way to learn.
Presumably this balance matters even for a particular cell type, like in the theory here? It’s not just ‘cell with this receptor gets killed’ it’s a probabilistic thing depending upon receptor makeup, how much daratumumab binds and other factors on deciding if a cell is killed?
Separately to...
I’m a bit late to some of the detail of this paper but some questions I had which seem relevant to the current discussion
When is the assumption made that ADCC and NK is important (Daratumumab seems to have other mechanisms of action)? Why is there an assumption of autoantibodies being...
They used SF-36 Physical Function (SF-36 PF) and DePaul Questionnaire-Short Form (DSQ-SF). Is that what you need?
Edit: was just about to post a better link but @Utsikt got there with the relevant text.
Got you. Sorry I’d misunderstood and assumed you meant before study completion and unblinding. My mistake and crossed wires with other posts.
On recruitment, is it that or funding that would be the limiting factor here I wonder? I guess it’s difficult to know for sure.
How? This is in the study design (linked from the english fundraising page)
It’s great there’s so much interest, hope and positivity about this trial. I know it’s hard but we should try to base discussion in what is known about the trial.
Yeah, I think we’ve discussed this before, but getting appropriate basic support in place should be our focus I think. That’s not only badly needed but everything else including trials or treatments depends upon or builds on that.
Yeah I’ve heard that can happen too, but what looks like the...
It looks like length of this study is 72 weeks per person, with staggered involvement (not everyone starting or finishing at the same time) and recruitment open from 06.06.2025 until 01.12.2026. So I wouldn’t expect results until later into 2028 at the earliest.
One of the documents attached to the english fund-raising page talks a lot about the mechanism and goal being reduction of autoantibodies, my understanding was this was not the case and it’s some other mechanism involving B cells/plasma cells, potentially antibodies but more autoimmune adjacent...
That was the misunderstanding I thought it was important to correct, so people reading this don’t jump to conclusions. This all off a bit of a side topic and speculation, we just don’t know the reasons for Fluge and Mella making this patent claim. It may be useful to, but we don’t.
The points...
That isn’t always the case. There are other reasons. You could even patent something and give it away, to ensure nobody else patents it and charges or even withholds it. Not saying that is the case here. Just that we don’t know the reasons. It would be good to of course.
This all sounds really really interesting. Hope you get the funding and look forward to hearing how the experiments go.
The wait should give me some more time to read up so I can understand what any results mean!
Ohhh, I need to go back through some posts then. Quite likely I read something and it lurked somewhere until it made sense with ither things I’ve been reading!
Sure, I will try to post some wild speculations at some point. It’s all vey high level and hand wavey stuff, it’s impossible not to see...
Yes, I was less expecting answers as throwing thoughts and questions out there.
I’m doing a phase of learning things again and the potential possible connections seem… extensive.
If this is the case are we looking at Immature or Transitional B Cells?
https://en.m.wikipedia.org/wiki/Transitional_B_cell
I also read that CD38 can influence intracellular calcium levels. In the linked thread on the paper there was discussion of energy production, but what about implications...
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