Teclistamab for ME/CFS

If, after careful consideration taking your cost function into account, you believe the expected value of a risky treatment like this is higher than doing nothing, that still doesn't mean you should do it. Your choices aren't just "risky treatment" and "do nothing." There are many other treatments with much lower risk. Given that the evidence for this one is all based on anecdotes and speculation, why not go for a less risky one instead?

For example, some people report remarkably large effects from very safe things like the kitchen spice cumin (not even a special type or amount -- just the amount you might find in curry). This probably won't work for most people, but neither will these speculative high-risk treatments. Why not try all of the low-risk options first?
 
ryanc97 said:
But you can always try and mitigate the side effects or risks with supps, diets, etc.
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But the implausibility of that is almost comical. Even if it were a serious proposition, how could we know the risks?

Some of these agents are too new for long term effects to have become clear. It's possible some of them are more likely than others to cause serious consequences—immediate reactions, cancers, other long term diseases—but it could easily take a decade for that to begin to work through in large enough numbers of people that scientists can start to understand the risks.
 
ryanc97 said:
But the main thing is, for me at least, if I see some positive evidence coming out of Habet's crazy Teclistamab trials, ethics aside, I will interpret it as more evidence that supports the underlying theory of Daratumumab, as BCMAs are another receptor on the surface of LLPCs and target it.

If it fails, then it would make the underlying theory less valid. So just need to wait for him to do this thing.
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I think your cost function might not be taking into account that it's not Fluge and Mella you're talking about, but a person, who by his own accounts has absolutley no idea of what he is doing and has extremely likely caused suffering and possibly death, without anything to show for it.

That won't be helpful when someone develops neutropenia but the mister talks about spike proteins detoxing and mast cells activating.

Happy to see how things with Fluge and Mella will turn out and what leads they'll continue pursuing.
 
I think I read in this thread that Teclistamab risk (especially CRS is probabaly not that related to dosage.
I think Gemini also claimed this.

I found a paper discussion step Up dosing for Tecil, but No study that looked at risk dosage relationship.

Has anybody a paper or reasoning for this topic ?
 
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I have been suffering from ME-CFS since 2019 and am now being treated by Dr. Habets. I could start treatment with Teclistamab next week, but I'm unsure whether I should do so. The suffering caused by the disease is severe, and if there is a chance of reducing the symptoms even slightly, I would take the risk. Perhaps there are others who already have experience with this therapy?


*Among other things, my beta2 adrenergic receptor antibodies (B2AR-AK) as well as eosinophil cationic protein and
anti-pertussis toxin (IgG, CLI) are extremely elevated.
 
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Welcome!
Somealone said:
The suffering caused by the disease is severe, and if there is a chance of reducing the symptoms even slightly, I would take the risk.
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What if the risk is getting permanently worse? There is no bottom for how bad ME/CFS can get, how much it can take from you.

I’m personally risk averse, but as someone who’s bedridden but have been even worse for just a few months, there is nothing I would do that would risk me going back to that place.
 
Somealone said:
I have been suffering from ME-CFS since 2019 and am now being treated by Dr. Habets. I could start treatment with Teclistamab next week, but I'm unsure whether I should do so. The suffering caused by the disease is severe, and if there is a chance of reducing the symptoms even slightly, I would take the risk. Perhaps there are others who already have experience with this therapy?


*Among other things, my beta2 adrenergic receptor antibodies (B2AR-AK) as well as eosinophil cationic protein and
anti-pertussis toxin (IgG, CLI) are extremely elevated.
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Have you asked him how the other patients are doing?

My concern is the dosage he is giving is too low. But I really hope this works.

If it does it will let us hone in on wherever it is really CD38 related vs pure plasma cell related.
 
Sometimes I think “low dose” approaches might be justified, especially if there is suspicion that “big pharma” might be trying to maximize dosages for profit. But I have no idea here.
 
Jaybee00 said:
Does this make any sense @Jonathan Edwards
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No, it is complete nonsense.

The things we can be sure of are that people with ME/CFS don't have much more in the way of GPCR antibodies than normal people and that treating with ritux makes the ones they have go down without any improvement.

And I cannot see what it has to do with cytokine release anyway. The autoantibodies have nothing to do with that.

If I had ME/CFS I would keep well clear of any doctor making statements like that.
 
I might add that if the benefit from daratumumab comes from blocking CD38 on other cells then teclistamab is likely to be much less potent and more likely to produce unwanted effects. It makes use of bispecific Fab segments that link to T cells as well as CD38.
 
@Jaybee00 was citing me and I was trying to cite what I heard from the doctor so that might not be accurate. It was not that CRS is due to GPCR antibodies but rather that he observes the correlation between ME/CFS / GPCR levels and severity of the reaction (so normal doses are too toxic for ME/CFS patients). It might be similar to what prof. Mella mentioned in CycloME presentation: where they also seen toxicity tougher than in oncology patients.
 
Teclistamab was also suggested by my Dr. recently and I'm now in the same boat of patients trying to weigh the potentially serious consequences of this treatment.

I'm less concerned about the immediate adverse side effects (Cytokine Release Syndrome etc.) than about the long term effects of this level of immunosuppresion. Of course there's the drastically increased risk of infection in the months until B-cell maturation, but what has me worried the most is the unknown potential of developing auto immune diseases down the line as a result of the treatment. Someone please correct me if I'm wrong, but as I understand it, the level of LLPS depletion caused by Teclistamab is like fire clearing an ecosystem and seeing which species turn out to dominate this new environment.

I know these are different medications, but given the lack of data for Teclistamab, I've been looking at known long term effects of other immune reset drugs like Alemtuzumab (a B-cell depleter). A large part of patients being treated with this drug develop Graves disease or one several other auto immune diseases down the line. I've seen similar things for other drugs that completely reset the immune system as well. It seems that it's not at all uncommon for a new type of potentially detrimental immune system reaction becoming dominant if you wipe out your immune system's "learned balance".

Does anyone know more about this - specifically how it applies to Teclistamab - and can weigh in on this?
Am I overblowing this aspect of immunosuppression or is this a valid concern?
 
Weltverloren said:
Someone please correct me if I'm wrong, but as I understand it, the level of LLPS depletion caused by Teclistamab is like fire clearing an ecosystem and seeing which species turn out to dominate this new environment.
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I don't think there is any analogy. B cell clones (i.e. plasma cell producing clones) do not compete with each other for survival in any relevant sense.
Weltverloren said:
A large part of patients being treated with this drug develop Graves disease or one several other auto immune diseases down the line.
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Weltverloren said:
Does anyone know more about this - specifically how it applies to Teclistamab - and can weigh in on this?
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You may not be aware that I introduced B cell depletion therapy for autoimmune disease in the 1990s. I have treated over 200 patients myself and none developed any new autoimmune disease. Graves disease does occur occasionally, mostly in the context of treating lymphoma where other major immunosuppressives are used in addition. I do not know about Teclistamab specifically though.

My general thought about using teclistamab is that it is not a sensible idea to try something like that when we have so little evidence for it being relevant. Perhaps the more important issue is that if you have a drug like this in the wrong dose you may become immune to it and lose the opportunity of benefit later.

Inasmuch as we have any relevant evidence that I would take note of it is for daratumumab and that may not be acting by killing plasma cells at all. So Tecli might be completely irrelevant.
 
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