ArticleScientific reports2025
Anti-CD19/CD20 bispecific antibody with dual Fc domains mediates enhanced effector functions and durable depletion of memory B cells in vivo.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent clinical studies suggest that more potent B cell depleting therapies and targeting more than one B cell antigen may result in improved clinical responses in autoimmune diseases and hematological malignancies. Here we describe an anti-CD19/CD20 bispecific antibody, HB2198, generated using GEM-DIMER™ technology. HB2198 incorporates Fab domains from rituximab and humanized FMC63 (huFMC63) for bivalent binding of both CD19 and CD20 and comprises two enhanced Fc domains to enable powerful effector functions via bivalent binding of Fcγ receptors (FcγR). Enhanced bivalent binding of HB2198 to FcγR was confirmed in vitro. HB2198 demonstrated robust depletion of human B cells that exceeded the levels observed with comparator anti-CD19 or anti-CD20 IgG1 antibodies in vitro. The mechanism of action of HB2198 included enhanced antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), as well as complement-dependent cytotoxicity (CDC) and direct cell killing activity. In cynomolgus monkeys, HB2198 administration resulted in > 99% depletion of circulating B cells within 1-3 days and mediated a durable shift in proportions of naïve and memory B cells in vivo. These data support the conclusion that HB2198 may provide an improved treatment option when potent and broad depletion of both CD19
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