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Updated: May 10, 2026

In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients

In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients

Published on: August 12, 2017

Targeting CD38 in Antibody-Mediated Rejection.

Katharina A Mayer¹, Klemens Budde², Matthias Diebold^1,3

¹Division of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria.

Transplant International : Official Journal of the European Society for Organ Transplantation

|May 30, 2025

Summary

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CD38-targeted therapy, like felzartamab, shows promise in treating late antibody-mediated rejection (AMR) after transplantation by reducing inflammation and NK cells. While effective, its impact on donor-specific antibodies is limited, with ongoing trials exploring prolonged treatment benefits.

Area of Science:

Immunology
Transplantation Medicine
Oncology

Background:

Antibody-mediated rejection (AMR) is a significant obstacle in organ transplantation, with current treatments offering variable success rates.
CD38, a target on plasma cells and NK cells, presents a potential therapeutic avenue for AMR by addressing both antibody production and cellular rejection mechanisms.

Purpose of the Study:

To review recent advancements in CD38-targeted therapies for AMR, focusing on felzartamab's efficacy and safety.
To explore the dual mechanism of CD38 targeting in mitigating AMR pathophysiology.

Main Methods:

Review of clinical data, including phase 2 trial results for felzartamab in late AMR.
Analysis of felzartamab's effects on microvascular inflammation, gene expression, cell-free DNA, NK cell counts, and donor-specific antibodies.

Keywords:

CD38 antibody-mediated rejection kidney transplantation natural killer cells treatment

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Last Updated: May 10, 2026

In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients

In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients

Published on: August 12, 2017

Main Results:

Felzartamab demonstrated safety and efficacy in a phase 2 trial for late AMR, leading to reduced microvascular inflammation and rejection markers.
Treatment correlated with decreased NK cell counts and donor-derived cell-free DNA, but did not significantly impact donor-specific antibodies.
Observed effects on rejection activity were rapid but transient, prompting further investigation into prolonged therapy.

Conclusions:

CD38-targeted therapy, exemplified by felzartamab, offers a promising strategy for managing late AMR, primarily through NK cell depletion.
Further research, including phase 3 trials, is warranted to establish the long-term benefits and expand applications to early AMR or other transplant complications.