To demonstrate the usefulness of the method for immunotherapy applications, we investigated the interaction of primary multiple myeloma cells with the therapeutic monoclonal antibodies daratumumab and isatuximab and a polyclonal anti-CD38 antibody. Our approach might lay the foundation for improved personalized diagnostics and treatment with therapeutic antibodies.
2 days ago
Journal
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PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • CD69 (CD69 Molecule)
P3, N=662, Active, not recruiting, University of Heidelberg Medical Center | Trial completion date: Mar 2027 --> Jun 2028 | Trial primary completion date: May 2025 --> Jun 2028
3 days ago
Trial completion date • Trial primary completion date
By synergizing real-world pharmacovigilance with transcriptomic data, this study delineates novel clinical AE signals and mechanistic insights linking CD38-driven immunometabolic dysregulation to isatuximab toxicity. These findings underscore the imperative for vigilant monitoring and tailored therapeutic strategies to mitigate risks of immune dysfunction, informing both clinical practice and future biomarker-driven interventions.
Treatment regimens comprised lenalidomide (n = 36) or thalidomide (n = 15) with daratumumab, and pomalidomide (n = 2) with isatuximab. Most patients (n = 38) received frontline therapy, and all were given thromboprophylaxis according to guidelines, mainly aspirin (73%)...Given the limited number of patients and thrombotic events, and the cytokine data available for only two VTE cases, these associations should be regarded as exploratory and interpreted with caution. Overall, these exploratory findings warrant validation in larger, independent cohorts and may help generate hypotheses on how inflammatory signatures influence thrombotic risk and prophylaxis efficacy in MM patients receiving IMiD/anti-CD38-based regimens.
The effects of IMiDs (pomalidomide, lenalidomide) on CD38 expression and isatuximab-induced apoptosis, either alone or in combination with IMiDs, were also examined. Additionally, both antibodies effectively inhibited MM cell migration and significantly reduced cell adhesion. Their non-competitive binding and shared impact on cell dynamics suggest opportunities for optimizing treatment strategies through combinatorial or sequential approaches in MM therapy.