Can Targeting Plasma Cells Finally Control Refractory TTP? – RPTH Journal
RPTH Journal shared a post on LinkedIn about a recent article by Roman Schimmer et al:
“Can targeting plasma cells finally control refractory TTP?
Relapsed/refractory immune TTP (iTTP) remains one of the toughest challenges, even with plasma exchange, steroids, rituximab, and caplacizumab.
So what if we go one step deeper?
Target the plasma cells producing anti–ADAMTS13 antibodies.
A new RPTH study evaluates daratumumab (anti-CD38) in r/r iTTP — with long-term follow-up.
Here’s the key signal:
- Rapid ADAMTS13 recovery in 7/8 treatment episodes (~88%)
- Complete remission achieved within ~1–3 weeks
- Durable responses (median ~32 months)
Why this works biologically:
Rituximab targets CD20 (B cells), but plasma cells persist and continue autoantibody production
Daratumumab targets CD38 on plasma cells
Directly suppresses pathogenic anti–ADAMTS13 antibodies.
This is not just immunosuppression, it’s precision targeting of the disease-driving cell population.
But there’s nuance:
- Relapse still occurred in most patients longterm
- Retreatment can be effective
- Safety profile was favorable (mainly mild infusion reactions)
Big questions for the field:
- Should daratumumab move earlier in the treatment algorithm?
- Who are the ideal candidates (rituximab failure vs early use)?
- Do we need maintenance strategies to sustain ADAMTS13 recovery?”
Title: Daratumumab for relapsed refractory immune thrombotic thrombocytopenic purpura: initial response and long-term follow-up
Authors: Roman Schimmer, Jana van den Berg, Marissa Schraner, Alice Trinchero, Andreas Holbro, Johanna A. Kremer Hovinga, Jan-Dirk Studt
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