Human IgG1 monoclonal antibody targeting CD38; depletes CD38+ immune cells (plasma cells, B cells, T cells, dendritic cells, macrophages) via ADCC, CDC, ADCP, and apoptosis to reduce pathogenic auto/alloantibody production.
Human IgG1 monoclonal antibody targeting CD38 that depletes CD38-expressing cells (plasma cells, selected B/T cells, myeloid and tumor cells) by inducing antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, antibody-dependent cellular phagocytosis, and apoptosis, thereby reducing pathogenic antibody production.
YES
DIRECT
Daratumumab binds CD38 on target cells; its Fc domain recruits immune effectors to induce ADCC (NK cells), CDC (complement), ADCP (macrophages), and can trigger apoptosis of CD38+ cells.
A bispecific T-cell engager (BiTE) antibody construct that binds CD19 on B-ALL cells and CD3 on T cells to redirect cytotoxic T cells to kill CD19+ leukemic cells; administered IV in conditioning.
A bispecific anti-CD19/anti-CD3 antibody (BiTE) that simultaneously binds CD19 on B cells and CD3 on T cells, bringing them into proximity to activate T cells and mediate cytotoxic killing of CD19-positive leukemic cells.
YES
DIRECT
Blinatumomab bridges CD19 on target cells to CD3 on T cells, activating T cells to kill CD19+ cells via perforin/granzyme-mediated cytotoxicity (immunologic synapse formation).
A bispecific T-cell engager (BiTE) antibody construct that binds CD19 on B-ALL cells and CD3 on T cells to redirect cytotoxic T cells to kill CD19+ leukemic cells; administered IV in conditioning.
A bispecific anti-CD19/anti-CD3 antibody (BiTE) that simultaneously binds CD19 on B cells and CD3 on T cells, bringing them into proximity to activate T cells and mediate cytotoxic killing of CD19-positive leukemic cells.
NO
INDIRECT
Blinatumomab binds CD3 on T cells to activate/redirect them; the activated T cells kill CD19+ target cells, not the CD3-expressing T cells.
Autologous, genetically modified T lymphocytes engineered to express a chimeric antigen receptor targeting a B-cell surface antigen; CAR signaling (CD3ζ with costimulatory domains) activates T cells to proliferate, release cytokines, and kill malignant B cells.
Autologous T lymphocytes are genetically engineered to express a chimeric antigen receptor that binds a B‑cell surface antigen. Antigen engagement triggers CAR signaling (CD3ζ with costimulatory domains), activating the T cells to expand, release cytokines, and kill malignant B cells via cytotoxic mechanisms (e.g., perforin/granzyme‑mediated apoptosis).
YES
DIRECT
CAR binding to the B‑cell surface antigen activates the engineered T cells, which kill target cells via perforin/granzyme-mediated apoptosis (and death-receptor pathways).
An anti-HER2 antibody–drug conjugate (RC48-ADC) that binds HER2, is internalized, and releases the microtubule inhibitor MMAE to induce cell cycle arrest and apoptosis; can also mediate ADCC and bystander killing.
Anti‑HER2 (ERBB2) antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE via a cleavable linker, leading to microtubule disruption, G2/M cell‑cycle arrest, and apoptosis; also can induce ADCC and bystander killing.
YES
DIRECT
The ADC binds HER2, is internalized, and releases MMAE via a cleavable linker; MMAE disrupts microtubules, causing G2/M arrest and apoptosis. It can also induce ADCC and bystander killing.