Autologous CD19-directed CAR T-cell therapy (Breyanzi) composed of defined CD4+ and CD8+ T cells engineered to express an anti-CD19 CAR, targeting and killing CD19+ B cells.
Autologous CD4+ and CD8+ T cells are engineered with a lentiviral vector to express an anti‑CD19 chimeric antigen receptor containing 4‑1BB costimulatory and CD3ζ signaling domains. Upon binding CD19 on B cells, the CAR activates T‑cell effector functions, leading to proliferation, cytokine release, and targeted lysis of CD19+ malignant B cells. A truncated EGFR tag enables in vivo tracking and potential elimination of the modified cells.
YES
DIRECT
Anti-CD19 CAR T cells recognize CD19 on B cells, become activated (4-1BB/CD3zeta signaling), and kill targets via T-cell cytotoxicity (perforin/granzyme and Fas-FasL).
Bispecific T‑cell engager (BiTE) antibody that binds CD3 on T cells and CD19 on target cells to activate T‑cell cytotoxicity, including against CF33‑CD19–tagged tumors.
Bispecific CD3xCD19 T-cell engager (BiTE) that links T cells to CD19-expressing target cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme) to kill CD19+ cells; in this trial, redirects T cells to CF33-CD19-tagged tumors.
YES
DIRECT
Blinatumomab bridges CD3 on T cells to CD19 on target cells, forming an immune synapse; engaged T cells kill CD19+ cells via perforin/granzyme-mediated cytotoxicity (apoptosis/lysis).
Bispecific T‑cell engager (BiTE) antibody that binds CD3 on T cells and CD19 on target cells to activate T‑cell cytotoxicity, including against CF33‑CD19–tagged tumors.
Bispecific CD3xCD19 T-cell engager (BiTE) that links T cells to CD19-expressing target cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme) to kill CD19+ cells; in this trial, redirects T cells to CF33-CD19-tagged tumors.
NO
INDIRECT
Blinatumomab binds CD3ε on T cells to activate them and redirect killing toward CD19+ cells; T cells mediate perforin/granzyme cytotoxicity against CD19+ targets, not CD3+ cells.
A humanized anti-CD20 monoclonal antibody (biologic) administered by IV infusion that depletes CD20+ B cells via ADCC, CDC, and apoptosis; used to reduce B-cell–mediated immune activity in multiple sclerosis.
Humanized anti-CD20 monoclonal antibody that binds CD20 on pre-B to mature B cells and depletes them via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis, reducing B cell–mediated immune activity (e.g., antigen presentation and proinflammatory cytokine signaling) in multiple sclerosis.
YES
DIRECT
Ocrelizumab binds CD20 on B cells and depletes them via Fc-mediated ADCC, complement-dependent cytotoxicity, and induction of apoptosis.
Biologic antibodies intended to bind glioblastoma-specific cell-surface antigens to block oncogenic/survival receptor signaling and recruit immune effector functions such as ADCC and CDC.
Unconjugated monoclonal antibodies that bind glioblastoma-restricted cell-surface antigens to block oncogenic/survival receptor signaling and trigger Fc-mediated immune effector functions (ADCC and CDC) to eliminate tumor cells.
YES
DIRECT
Unconjugated mAbs bind glioblastoma-specific surface antigens and, via their Fc regions, recruit immune effectors to kill target cells through NK cell–mediated ADCC and complement-dependent cytotoxicity (CDC).