BC007 - what are your thoughts?

[Dude]

In any case, it remains exciting. Should this person be "cured" or improved by BC, that will definitely raise even more questions about the testing methodology. In some social media posts ive read, people have received positive and negative findings over time. This again raises the question, of whether these fluctuate or if there is another problem? Was there any Statement why they used functional tests in Erlangen?

 

[Osaca]

In any case, it remains exciting. Should this person be "cured" or improved by BC, that will definitely raise even more questions about the testing methodology. In some social media posts ive read, people have received positive and negative findings over time. This again raises the question, of whether these fluctuate or if there is another problem? Was there any Statement why they used functional tests in Erlangen?

Hohberger likely doesn't have all the say in that matter and simply agreed to using the biossay by BC (of course bioassay+other methods is always far more preferable, especially since the biossay is itself very problematic). Sometimes antibodies can also fluctuate a bit over time, especially those we are talking about here which are present in HC in virtually the same amount as in people with LC & ME/CFS. However, in all the diseases where faabs are known to play a role such fluctuations are completely irrelevant and ELISA is sufficient to establish said disease (positive and negative findings don't mean anything if these ab's don't play a role and if positivity can't be associated to disease status, because then the word "positive" is anyways meaningless and wrong). So far the evidence unfortunately points in the direction that GPCR-AABs might not play a central role in LC & ME/CFS, but luckily there's now some studies to prove or disprove that and properly examine it.

One should be very careful about hoping to conclude anything from patient reports in blinded trials, before results have been announced and patients have been unblinded. If anything should be learned from the Rituximab trials and the CBT/GET non-sense then the fact that placebo-effects and regression to the mean are very real effects in ME/CFS and especially in LC. Basic mathematics already tells us that for someone reporting improvements in such a trial the probability is far higher that is has nothing to do with the actual drug that is given than it being correlated to the drug. That is one of the reasons why we need well-conducted placebo-controlled RCTs.

 

[Murph]

I feel conflicted about bc007.

On the one hand I think autoantibodies to gpcr receptors are an extremely plausible mechanism. And I benefit from beta blockers and alpha activators, both of which suggest a problem around g-protein coupled receptors.

The failure of alpha-, beta- and muscarinic receptors would go a long way to explaining vascular problems in the disease: these are all involved in vascular homeostasis (i.e. keeping your blood vessels nice and tight) .

Post-infection autoimmunity is very safe ground too, (although it does get a bit shakier if you have to use weird novel tests to find the autonatobodies.) So the study proceeds on what I consider highly plausible terms.

However a few tiny doubts have crept in about Scheibenbogen . When the study came out that found her favoured Cell Trend test didn't replicate, I didn't see her respond to that. She just kept pressing. Her recent ivig papers are pretty small. I feel like she's one of these tenured senior academics who is dead set on a particular theory. And we need those people because they do a lot of work. But we can't assume confident = right.

What's more I suspect bc007 is getting pushed because it's novel and patentable rather than because it has a great track record in other diseases. To me it seems like a longshot. But look, at least they're trying something. I will be the first to pay $20,000 a year to take it if it works!