Open CD19-B Cell Depletion in PAIS-ME/CFS Patients (PIONEER_PAIS) [Berlin, Germany - Study of Inebilizumab]

forestglip

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Official title
Prospective, Randomized, Double-blind, Placebo-controlled Phase 2b Trial Evaluating the Efficacy and Safety of the Anti-CD19 Monoclonal Antibody Inebilizumab Compared With Placebo in Patients With Post-acute Infection Syndromes Fulfilling ME/CFS Criteria (PIONEER)

Brief summary
Post-acute infection syndromes (PAIS) are long-lasting health problems that can develop after an infection. They include post-COVID-19 syndrome and similar illnesses following other infections. Some people with PAIS develop myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a serious and disabling illness that can greatly limit everyday activities. People with ME/CFS may experience severe fatigue, reduced physical and mental function, pain, sleep problems, and problems with the regulation of heart rate and blood pressure. A key feature is post-exertional malaise (PEM), in which symptoms become worse after physical or mental activity. The biological causes of PAIS and ME/CFS are not fully understood, and there is currently no established treatment that targets the underlying disease process.

Research suggests that changes in the immune system may contribute to PAIS and ME/CFS in some patients. In particular, B cells (a type of immune cell) and autoantibodies (antibodies that react with the body's own structures) may play a role. Previous studies of immunoadsorption, a procedure that removes antibodies from the blood, have shown improvements in some patients with ME/CFS. These findings support further investigation of treatments that target B cells in selected patients.

The PIONEER_PAIS study will investigate whether inebilizumab can improve physical function in adults with PAIS who meet the diagnostic criteria for ME/CFS. The study includes a selected group of patients with evidence of autoantibodies and immune activation who previously improved after immunoadsorption but later experienced worsening of their symptoms. Inebilizumab is a monoclonal antibody that targets CD19, a protein found on B cells, and leads to the depletion of these cells.

Participants will be randomly assigned to receive either inebilizumab or placebo (saline solution) as an infusion into a vein. Inebilizumab will be given at a dose of 300 mg on Day 1, Day 15, and Week 24. The study is double-blind, meaning that neither the participants nor the study team assessing them will know which treatment they receive.

The main research question is whether treatment with inebilizumab leads to a greater improvement in physical function (PF) than placebo. PF will be measured using the PF scale of the SF-36 health questionnaire, comparing the change from the start of the study to Month 9 (Week 36).

The study will also examine other aspects of health and daily functioning, including fatigue, post-exertional malaise, pain and headache, disability, symptoms related to the autonomic nervous system, muscle strength and fatigability, heart rate and blood pressure responses during standing, daily step count, and cognitive function. Adverse events will be monitored to assess the safety of the treatment. In addition, the study includes biomarker research focusing on B cells, autoantibodies, and other markers in the blood.

This research aims to explore biological characteristics that may be associated with response to treatment and may help inform future studies of B-cell-targeted treatment in PAIS and ME/CFS.

Inclusion criteria
  • Male/female/diverse adults who are 18-65 years old at time of enrollment
  • Subject is able and willing to give informed consent
  • Signed informed consent prior to initiation of any trial related measure
  • Diagnosis of PAIS as defined by WHO for PCS, wi th other infectious triggers
  • Diagnosis of ME/CFS according to CCC criteria with PEM > 14 hours = PAIS/CFS
  • Detection of autoantibodies (elevated ß2R adrenergic AAB) prior to immunoadsorption or prior to inclusion to PIONEER
  • Pre-treatment with immunoadsorption in the immunoadsorption studies at least 6 months before study inclusion
  • Documented clinical response to immunoadsorption (minimum increase in SF-36 PF of 10 points at week 8) followed by consecutive worsening of symptoms (minimum decrease in SF-36 PF of 10 points for at least 3 months)
  • Evidence of activated pro inflammatory immune cell status
  • Bell score at screening visit: 30-60
  • Normal thyroid function or sufficiently medicated dysfunction
  • For women of childbearing potential (WOCBP):
    1. Confirmed post-menopausal state, defined as amenorrhea for at least 12 months, or
    2. If being of childbearing potential: Negative highly sensitive urine or serum pregnancy test before randomization, and practicing a highly effective birth control method (failure rate of less than 1%)
Intervention
Drug: Inebilizumab
  • The treatment period comprises three intravenous administrations of 300 mg inebilizumab: on Day 1, Day 15, and after 6 months, followed by a 3-months follow-up period. Each infusion will be preceded by a premediaction (methylprednisolone 125 mg, dimetindene maleate 4 mg, and paracetamol 500 mg) to reduce the risk of infusion-related reactions.
  • Other Names:
    • Anti-CD19 monoclonal antibody
Drug: Placebo
  • The treatment period comprises three intravenous placebo administrations: on Day 1, Day 15, and after 6 months, followed by a 3-month follow-up period. To maintain blinding, each placebo infusion is preceded by the same premedication (methylprednisolone 125 mg, dimetindene maleate 4 mg, and paracetamol 500 mg) as the inebilizumab infusion.
  • Other Names:
    • Saline solution (0.9% sodium chloride solution)

Primary outcome measure
  • Improvement in Physical Function (PF) as measured by the Short Form 36 Health Survey Questionnaire (SF-36) comparing Inebilizumabwith placebo
    • 9 months (36 weeks) after first IMP administration

Enrollment (Estimated)
38

Study Completion (Estimated)
2029-03-01

Registration
https://clinicaltrials.gov/study/NCT07724834
 
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I rewatched the Berlin conference talk about this CD19 trial yesterday and the 3 case studies they showed looked quite interesting.

If it wasn't for the weight of evidence being against an autoantibody pathology and the failure of ritux and immunoabsoption I would be a bit hopeful for this.

Randomly wondered watching it - is there any way this drug could be working other than antibodies, similar to how dara might be doing something through other effects of anti cd38?
 
I wonder if this will just pick a set of super Placebo responders in the case immunoabsorption does not work after all.

Then you will have a large effect in the Placebo group, potentially cloaking any real but small effect of the drug.
That is a very good point. Although the effect in the three case studies looked large so if (a very big if) it is real this might be less of a problem.
 
38 is a strange number. Why not 40?
It is probably just about enough to pick up a major effect.
I would say money reasons.
The National Clinical Study Group Phase 2 is NOT part of the National Decade against postinfectious diseases (yet, hopefully), the 8 million € come from a Bundestag decision back in 2024.
They have to do 3 trials with these 8 million, 1 being LDA, 1 being the PIONEER study- and Inebilizumab is not cheap.
I remember Carmen Scheibenbogen saying a while ago, that Amgen didn’t even want to give them Inebilizumab for their study, which big companies like Amgen normally do for studies. So they have to pay the treatment as well for the participants -if that hasn’t changed since she made that remark.
 
That is a very good point. Although the effect in the three case studies looked large so if (a very big if) it is real this might be less of a problem.
That would only be true if those three were not already immunoabsorption responders (or 'responders').

IIRC, during the conference it was mentioned that those three responded to absorption twice.
 
The study includes a selected group of patients with evidence of autoantibodies and immune activation who previously improved after immunoadsorption but later experienced worsening of their symptoms.
Has that study been published?

IIRC the results were presented at the conference in spring. Does anyone remember if they said anything about comorbidities?

Charité being such a large and renowned hospital probably gets more patients with rare and not-so-rare-but-not-really-common diseases, some of which might be hard to diagnose, than an average hospital (or referred from another hospital to Charité due to their expertise and treatment options). So I'm wondering if the group consisted of pwME/CFS for whom they really couldn't find an alternative diagnosis that would explain the symptoms or if it looked like ME/CFS but other possibilities hadn't been fully explored and patients possibly had comorbidities other than the usual POTS, MCAS,...
 
Has that study been published?

IIRC the results were presented at the conference in spring. Does anyone remember if they said anything about comorbidities?

Charité being such a large and renowned hospital probably gets more patients with rare and not-so-rare-but-not-really-common diseases, some of which might be hard to diagnose, than an average hospital (or referred from another hospital to Charité due to their expertise and treatment options). So I'm wondering if the group consisted of pwME/CFS for whom they really couldn't find an alternative diagnosis that would explain the symptoms or if it looked like ME/CFS but other possibilities hadn't been fully explored and patients possibly had comorbidities other than the usual POTS, MCAS,...
Tbh that's what I am asking myself with all of those people who seem to react extremely positive to immunadsorption or other treatment of autoimmunity.

Given that this isn't all placebo, how likely is it that those people actually have a neglected or rarely correctly diagnosed but already known autoimmune illness like e.g. seronegative sjögrens syndrom? I am pretty sure this is at least possibly but I can't estimate how likely it is.

I took Sjögrens as an example because I know someone personally who was diagnosed as "Long Covid", ME was suspected despite sjögrens symptoms because she had no sjögrens specific Aabs but after pushing for it a lip biopsy was positive for sjögrens. Most Drs who aren't specialists don't seem to know that seronegative sjögrens exist and lip biopsies certainly aren't a standard procedure in immunological assessment. It's even possible to have no sjögrens Aab, no ANA and still have this illness.

Knowing this and that afaik people with Sjögrens seem to often react positive to b-cell depletion like e.g. Rituximab I started to wonder how many of those people with seronegative sjögrens or other known but hard to diagnose autoimmune-conditions are among the people in those, by Scheibenbogen et al. postulated, autoimmunity "ME-subgroups"...
 
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