Weiterer CD38-Antikörper bei Immunthrombozytopenie offenbar wirksam – News – Deutsches Ärzteblatt

New clinical evidence reported by Deutsches Ärzteblatt indicates that a CD38-targeting antibody is effective in treating patients with immune thrombocytopenia (ITP), particularly those who have failed to respond to conventional therapies. This therapeutic approach focuses on depleting the plasma cells responsible for producing the autoantibodies that destroy platelets in the bloodstream.

Immune thrombocytopenia is an autoimmune disorder where the immune system mistakenly identifies platelets as foreign entities. This leads to a significant drop in platelet counts, which increases the risk of spontaneous bruising, mucosal bleeding and in severe cases, life-threatening internal hemorrhages.

For many patients, the condition is chronic and refractory, meaning it does not respond to first-line treatments such as corticosteroids or intravenous immunoglobulin (IVIg). The introduction of CD38-targeted therapy represents a shift toward addressing the root source of the autoantibodies rather than simply suppressing the general immune response.

The Mechanism of CD38 Targeting

The effectiveness of this treatment lies in the specific biological role of the CD38 protein. CD38 is a transmembrane glycoprotein expressed on the surface of various immune cells, including B cells, T cells, and most notably, plasma cells.

Plasma cells are the final stage of B-cell differentiation and act as the primary factories for antibody production. In patients with ITP, these plasma cells produce the specific anti-platelet antibodies that mark platelets for destruction by the spleen.

While previous treatments like rituximab target the CD20 protein, they are often ineffective against established ITP because CD20 is not expressed on mature plasma cells. By targeting CD38 instead, the antibody can directly eliminate the long-lived plasma cells that continue to secrete harmful antibodies even after B cells have been depleted.

The antibody binds to the CD38 protein, triggering the destruction of the plasma cell through several mechanisms, including antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity.

Clinical Application and Patient Outcomes

The report highlights that patients who previously showed no improvement with standard immunosuppressants experienced a significant rise in platelet counts following the administration of the CD38 antibody. The primary clinical goal in ITP management is typically to reach a platelet threshold that prevents spontaneous bleeding, often cited as above 30,000 per microliter of blood.

Observations suggest that the depletion of CD38-positive cells leads to a measurable decrease in the concentration of circulating anti-platelet antibodies. This reduction allows the bone marrow’s natural production of platelets to outweigh the rate of destruction, thereby stabilizing the patient’s condition.

Medical professionals note that this strategy is particularly relevant for patients who are dependent on high-dose steroids, which carry severe long-term side effects including osteoporosis, diabetes, and hypertension.

Comparing CD38 and CD20 Therapies

The distinction between CD38 and CD20 targeting is central to the advancement of ITP treatment. The following points clarify the difference in their medical application:

• CD20 antibodies target precursor B cells, preventing the creation of new plasma cells but leaving existing antibody-producing cells intact.
• CD38 antibodies target the mature plasma cells themselves, removing the existing source of autoantibodies.
• Many patients who are rituximab-refractory respond to CD38 inhibitors because their disease is driven by mature plasma cells rather than active B-cell proliferation.

Limitations and Future Research

Despite the promising results, researchers emphasize that CD38 antibodies are not without risks. Because CD38 is expressed on other immune cells, there is a potential for broader immunosuppression, which may increase the patient’s susceptibility to certain infections.

the long-term durability of the response remains a subject of investigation. It is not yet fully clear how long the plasma cell depletion lasts or whether the autoantibodies will eventually return, requiring subsequent dosing cycles.

Future studies are expected to focus on optimizing the dosage to balance efficacy with the risk of infection. Clinical trials will also likely investigate whether combining CD38 antibodies with other therapies can lead to complete remission of the disease.

As of May 8, 2026, the use of these antibodies in ITP is largely seen as a targeted intervention for severe or refractory cases rather than a first-line therapy for all patients.