CD20×CD3 bispecific IgG T‑cell engager used with step‑up dosing to redirect T cells to kill CD20+ B cells; also given as post–CAR‑T maintenance.
CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells to crosslink them, activate T cells, and induce perforin/granzyme-mediated cytotoxic killing of CD20-positive B cells (step-up dosing used to mitigate CRS).
YES
DIRECT
CD20×CD3 bispecific crosslinks CD20 on B cells with CD3 on T cells, activating T cells to deliver perforin/granzyme-mediated cytotoxic killing of CD20+ cells.
CD20×CD3 bispecific IgG T‑cell engager used with step‑up dosing to redirect T cells to kill CD20+ B cells; also given as post–CAR‑T maintenance.
CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells to crosslink them, activate T cells, and induce perforin/granzyme-mediated cytotoxic killing of CD20-positive B cells (step-up dosing used to mitigate CRS).
NO
INDIRECT
Glofitamab engages CD3 on T cells to activate them and crosslink to CD20 on B cells; the activated T cells kill CD20+ cells via perforin/granzyme, not the CD3+ T cells.
Glycoengineered type II anti‑CD20 monoclonal antibody used for B‑cell depletion/bridging and to mitigate cytokine release syndrome.
Glycoengineered humanized anti‑CD20 IgG1 that binds CD20 on B cells and, via enhanced FcγRIIIa engagement from afucosylated Fc glycans, drives potent antibody‑dependent cellular cytotoxicity and phagocytosis, while its type II binding induces direct, caspase‑independent cell death, resulting in efficient B‑cell depletion.
YES
DIRECT
Anti-CD20 mAb binds CD20 on B cells; its afucosylated Fc engages Fc-gamma RIIIa to drive strong ADCC by NK cells and ADCP by macrophages, and type II binding triggers direct, caspase-independent cell death (with minimal complement involvement).
Patient‑derived T cells engineered to express a CD19‑directed chimeric antigen receptor; adoptive cellular therapy administered after lymphodepletion.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor that binds CD19 on B cells. Upon CD19 engagement, the CAR’s activation (CD3ζ) and co‑stimulatory domains (e.g., CD28 or 4‑1BB) trigger T‑cell activation, proliferation, cytokine release, and cytotoxic killing (perforin/granzyme) of CD19+ malignant and normal B cells after lymphodepleting chemotherapy enhances expansion.
YES
DIRECT
CAR on infused T cells binds CD19 on target cells, triggering CD3ζ/co‑stimulatory signaling that activates the T cells to kill CD19+ cells via perforin/granzyme and death‑receptor–mediated apoptosis.
An antibody–drug conjugate immunotherapy consisting of a humanized anti-CD22 IgG4 monoclonal antibody linked to the cytotoxic agent calicheamicin; it binds CD22 on B-lineage blasts, is internalized, and releases calicheamicin to induce DNA double-strand breaks leading to apoptosis.
Humanized anti-CD22 monoclonal antibody targets CD22 on B-lineage cells, is internalized, and releases the cytotoxic payload calicheamicin, which binds the DNA minor groove to induce double-strand breaks and apoptosis.
YES
DIRECT
Antibody-drug conjugate binds CD22, is internalized, and releases calicheamicin, which induces DNA double-strand breaks leading to apoptosis.