An investigational CD3 T‑cell engager bispecific antibody (protein immunotherapy) that binds CD3 on T cells and a B‑cell tumor antigen to redirect and activate cytotoxic T cells against malignant B cells in relapsed/refractory B‑cell NHL; administered at fixed subcutaneous dosing in combination with JNJ‑80948543.
A bispecific antibody that binds CD3 on T cells and CD22 on malignant B cells, crosslinking T cells to target cells to form an immune synapse, activate and redirect cytotoxic T-lymphocyte activity, and induce lysis of CD22-expressing B-cell lymphoma cells.
YES
DIRECT
The bispecific antibody bridges CD3 on T cells to CD22 on target B cells, forming an immune synapse and triggering T‑cell–mediated cytolysis (perforin/granzyme-induced apoptosis) of CD22+ cells.
An investigational CD3 T‑cell engager bispecific antibody (protein immunotherapy) that binds CD3 on T cells and a B‑cell tumor antigen to redirect and activate cytotoxic T cells against malignant B cells in relapsed/refractory B‑cell NHL; administered at fixed subcutaneous dosing in combination with JNJ‑80948543.
A bispecific antibody that binds CD3 on T cells and CD22 on malignant B cells, crosslinking T cells to target cells to form an immune synapse, activate and redirect cytotoxic T-lymphocyte activity, and induce lysis of CD22-expressing B-cell lymphoma cells.
NO
INDIRECT
The bispecific binds CD3E on T cells to activate and redirect them to kill CD22-positive B cells; CD3E-expressing T cells are not the lytic target.
Anti-HER2 IgG1 monoclonal antibody that binds the HER2 extracellular domain IV, inhibiting receptor phosphorylation and downstream PI3K/AKT and MAPK signaling (extracellular blockade).
Fc-engineered humanized IgG1 monoclonal antibody that binds the HER2 extracellular domain IV, blocking HER2-mediated receptor phosphorylation and downstream PI3K/AKT and MAPK signaling, and engaging immune effector functions to induce ADCC against HER2-overexpressing tumor cells.
YES
DIRECT
Binds HER2 on tumor cells and engages Fcγ receptor–bearing immune cells to mediate ADCC, causing lysis/apoptosis of HER2+ cells (with additional growth inhibition via signaling blockade).
Autologous, fully human anti-CD19 CAR T-cell therapy; patient T cells are engineered to express a chimeric antigen receptor targeting CD19 to deplete CD19+ B-lineage cells and reset humoral immunity in refractory dermatomyositis.
Autologous T cells engineered with an anti-CD19 CAR (CD28 costimulatory and CD3ζ signaling domains) recognize CD19 and, upon engagement, become activated to kill CD19+ B-lineage cells (B cells and plasmablasts), depleting autoantibody-producing cells and resetting humoral immunity.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells, become activated, and kill them via T-cell cytotoxicity (perforin/granzyme-mediated apoptosis, and Fas-FasL pathways).
An anti–PD-L1 IgG1 monoclonal antibody (checkpoint inhibitor) that blocks PD-1/PD-L1 signaling to restore cytotoxic T-cell activity and can mediate ADCC. Brand name: Bavencio.
Avelumab is an IgG1 anti–PD-L1 monoclonal antibody that blocks PD-1/PD-L1 checkpoint signaling to restore cytotoxic T-cell activity and can also mediate antibody-dependent cellular cytotoxicity (ADCC) against PD-L1–expressing tumor cells.
YES
DIRECT
Avelumab binds PD-L1 and its IgG1 Fc engages Fc-gamma receptors on NK cells to trigger ADCC (and possibly ADCP), directly killing PD-L1–expressing cells; it also restores T-cell killing via PD-1/PD-L1 blockade.