Trial Report Plasma cell targeting with the anti-CD38 antibody daratumumab in ME/CFS -a clinical pilot study, 2025, Fluge et al

Does the very binary response tell us anything at all? There were no middle responders for example - all reached normal levels or remained at baseline
May also be a consequence of choice of outcome measures.

For example for the placebo-controlled trial the outcome measures seems to be:
Primary: DSQ-SF total score
Secondary: 2 modified DSQ-SF scores, SF-36 Physical Function, steps, Function level, AEs
and then a whole host of exploratory outcome measures (FUNCAP, heart rate and HRV, handgrip strength, NASA lean, workload, PVP,....).
 
What is the link between the measure used and this binary response in this case? It’s either line went up by a big amount or line stayed flat.

No line went up in the midele
 
Last edited:
What is the link between the measure used and this binary response in this case? It’s either line went up by a big amount or line stayed flat.

No line went up in the midele
Insofar that not all of the data of the study might look like that, but then I realised that expect for a few exceptions (like NIRS which might have failed for other reasons and as a consequence is also not part of the larger trial and HRV which is probably anyways not particularly interesting) they are reporting all data.

But I would suggest that at least one or 2 people are looking a bit variable, which should be expected.
 




He is an autoantibody specialist.
 
He agrees with me it’s an LLPC problem. Or he believes AABs are responsible for a lot of unsolved chronic illnesses. So suggested he reach out to FM and they are working on a project using blood samples from the pilot study with the end goal of finding out if it is an AAB problem or not
 
Last edited:
Nice work introducing them @ryanc97 will be interesting to see what they turn up.

Do you know if he/they are also looking at NK cells themselves? We’ve talked before about the idea of memory in the innate immune system as well as the adaptive, there seems to be increasing discussion of memory here and in NK cells.

I think you do get situations in Daratumumab with NK cells killing other NK cells. Now if there is a problem for us with these memory NK cells and you want nice new fresh ones to kill them then boosting numbers of fresh ones makes sense. I can definitely see that being a possibility. And maybe there’s something like differential CD38 expression on different NK cell subtypes to boot. Just speculation but some thoughts that have been floating around my head recently. And an alternative to traditional auto-antibody or ‘exhausted’ NK cell mechanisms.
 
Back
Top Bottom