Related Experiment Video
Updated: Apr 25, 2026
07:15
Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
1.1K
Prospective Cohort Study of Felzartamab in Rituximab-Resistant Primary Membranous Nephropathy
Matias Trillini1, Federica Casiraghi1, Alessia Gennarini2
1Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy.
Kidney International Reports
|April 24, 2026
Summary
Felzartamab, an anti-CD38 antibody, was safe but ineffective for treating membranous nephropathy (MN) and nephrotic syndrome (NS) resistant to rituximab. It failed to deplete the specific B cells responsible for the disease.
Area of Science:
- Nephrology
- Immunology
- Clinical Trials
Background:
- Primary membranous nephropathy (MN) with nephrotic syndrome (NS) often shows resistance to rituximab treatment.
- Alternative therapies are needed for patients unresponsive to current treatments.
Purpose of the Study:
- To evaluate the efficacy and safety of felzartamab, a human IgG1 monoclonal anti-CD38 antibody, in patients with MN and rituximab-resistant NS.
Main Methods:
- A prospective, single-arm, open-label trial involving 10 adult patients with MN and rituximab-resistant NS.
- Patients received a 5-month, 9-dose course of felzartamab (16 mg/kg).
- Clinical and laboratory parameters were monitored for 24 months, with 24-hour proteinuria as the primary outcome at 12 months.
Main Results:
- Felzartamab treatment did not significantly reduce 24-hour proteinuria or albuminuria at 12 months compared to baseline.
- While felzartamab decreased certain immune cells (NK, transitional B cells), it did not deplete CD20-expressing memory B cells or plasma cells.
- Anti-phospholipase A2 receptor (PLA2R) antibodies showed transient decreases but were not depleted; overall immunoglobulin levels also decreased transiently.
Conclusions:
- A single course of felzartamab was safe and well-tolerated in patients with MN and rituximab-resistant NS.
- The treatment was ineffective, likely due to the inability to persistently deplete CD38-expressing B cells that produce nephritogenic autoantibodies.
