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Updated: May 16, 2026

Murine Model of CD40-activation of B cells
12:24

Murine Model of CD40-activation of B cells

Published on: March 5, 2010

Modulating CD38 enzymatic activity during antibody-based immunotherapy in multiple myeloma: a basic science

Alberto L Horenstein1,2,3, Kristine A Frerichs4,5, Angelo C Faini6

  • 1Laboratory of Immunogenetics, Department of Medical Sciences, Turin, Italy.

Frontiers in Immunology
|May 15, 2026
PubMed
Summary
This summary is machine-generated.

Multiple myeloma treatments targeting CD38 antibodies still face resistance. Adenosine production persists in the bone marrow, suggesting combination therapies could improve outcomes.

Keywords:
CD38adenosinedaratumumabimmunosuppressionimmunotherapyinosineisatuximabmultiple myeloma

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In Vitro Methods for Comparing Target Binding and CDC Induction Between Therapeutic Antibodies: Applications in Biosimilarity Analysis
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In Vitro Methods for Comparing Target Binding and CDC Induction Between Therapeutic Antibodies: Applications in Biosimilarity Analysis

Published on: May 4, 2017

Area of Science:

  • Immunology
  • Oncology
  • Biochemistry

Background:

  • Multiple myeloma (MM) bone marrow is immunosuppressive.
  • CD38 degrades NAD+, fueling adenosine (ADO) production via the CD38/CD203a/CD73 pathway.
  • CD38-targeting antibodies (daratumumab, isatuximab) face resistance.

Purpose of the Study:

  • Investigate CD38 enzymatic functions.
  • Assess in vitro effects of daratumumab (DARA) and isatuximab (ISA) on CD38-mediated NAD+ degradation in MM cells.
  • Analyze in vivo dynamics of ADO and inosine (INO) in MM patients receiving DARA.

Main Methods:

  • In vitro enzymatic assays using MM cells.
  • In vivo pharmacokinetic analysis of ADO and INO in patient plasma.
  • Measurement of NAD+ degradation products.

Main Results:

  • DARA and ISA promoted NAD+ degradation in vitro.
  • In vivo, bone marrow ADO remained high during DARA therapy, while inosine increased, reducing the bone marrow-peripheral blood gradient.
  • Sustained adenosinergic metabolism was observed, potentially due to reduced CD38 expression and adenosine deaminase activity.

Conclusions:

  • Adenosinergic immunosuppression persists in the bone marrow despite CD38-targeted therapy.
  • Sustained ADO may promote immune evasion and therapeutic resistance in MM.
  • Combining CD38 antibodies with adenosinergic signaling inhibitors may enhance antitumor immunity and clinical outcomes.