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A Randomized Study on Pemphigus Treatment With Humanized CD38 Antibody CM313.
Pemphigus is characterized by the presence of IgG antibodies that lead to the loss of keratinocyte adhesion, resulting in blister formation. The etiology of pemphigus antibodies is multifactorial, involving immune dysregulation, genetic predisposition, and potential viral triggers. CD38, a multifunctional transmembrane glycoprotein, plays a crucial role in B-cell maturation and function. CM313, a novel humanized monoclonal antibody targeting CD38, has shown promise in clinical trials for autoimmune diseases, including refractory/relapsed multiple myeloma (RRMM), systemic lupus erythematosus (SLE), and immune thrombocytopenia (ITP). By binding to CD38 on B cells, CM313 modulates B-cell activation, proliferation, and differentiation, potentially reducing the production of autoantibodies, such as those against desmogleins 1/3 in pemphigus. Preclinical studies have demonstrated that CM313 effectively inhibits CD38 enzymatic activity through antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and Fc-mediated apoptosis. The long-term modulation of B-cell-mediated immune responses by CM313, through the depletion of both short-lived and long-lived plasma cells, suggests a novel therapeutic strategy for pemphigus by targeting the production of pathogenic autoantibodies.
Details
| Lead sponsor | Chao Ji |
|---|---|
| Phase | PHASE1, PHASE2 |
| Status | NOT_YET_RECRUITING |
| Enrolment | 100 |
| Start date | Wed Oct 01 2025 00:00:00 GMT+0000 (Coordinated Universal Time) |
| Completion | Sun Nov 01 2026 00:00:00 GMT+0000 (Coordinated Universal Time) |
Conditions
- Pemphigus Disease
- Pemphigus Vulgaris (PV)
Interventions
- CM313 (SC)
- Glucocorticoids