Autologous T cells genetically engineered to express a chimeric antigen receptor targeting CD19 on B cells, incorporating CD3ζ signaling with a costimulatory domain (e.g., CD28 or 4-1BB) to activate, expand, and mediate cytotoxic killing of malignant B cells.
Autologous T cells are engineered to express a chimeric antigen receptor with an anti‑CD19 binding domain linked to CD3ζ signaling and a costimulatory domain (e.g., CD28 or 4‑1BB). Binding to CD19 on B cells triggers MHC‑independent T‑cell activation, proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxicity, leading to elimination of CD19+ malignant B cells and on‑target B‑cell aplasia.
YES
DIRECT
CAR T cells bind CD19 on target cells, triggering MHC-independent T-cell activation and perforin/granzyme (and Fas–FasL) cytotoxicity, leading to apoptosis/lysis of CD19+ cells.
An anti-HER2 antibody–drug conjugate that binds HER2 (ERBB2), is internalized, and releases the microtubule inhibitor MMAE to induce mitotic arrest and apoptosis.
Anti-HER2 monoclonal antibody linked to MMAE. Binds HER2 (ERBB2) on tumor cells, is internalized, and releases the microtubule inhibitor MMAE intracellularly, causing mitotic arrest and apoptosis.
YES
DIRECT
Antibody-drug conjugate binds HER2 on target cells, is internalized, and releases MMAE intracellularly, disrupting microtubules to cause mitotic arrest and apoptosis.
Anti-HER2 (ERBB2) IgG1 monoclonal antibody that binds HER2 on tumor cells to inhibit signaling and enable ADCC.
Humanized IgG1 monoclonal antibody targeting HER2/ERBB2; binds the receptor on tumor cells to inhibit HER2 signaling and dimerization, reduce proliferative/survival pathways, and engage Fc-mediated antibody-dependent cell-mediated cytotoxicity (ADCC).
YES
DIRECT
Trastuzumab binds HER2 on target cells and its Fc engages Fcγ receptor–bearing effectors (e.g., NK cells) to trigger ADCC, killing HER2+ cells; signaling blockade can also promote apoptosis.
An intravenous antibody–drug conjugate (ADC) consisting of a monoclonal antibody that binds a tumor-associated cell-surface antigen, is internalized, and releases a cytotoxic small-molecule payload inside the cancer cell, leading to cell death with a potential bystander effect; being evaluated in a first-in-human Phase 1 study for advanced solid tumors including hepatocellular carcinoma.
A monoclonal antibody-drug conjugate that binds DLK-1 on tumor cells, is internalized, and via a cleavable linker releases the MMAE payload; MMAE inhibits tubulin polymerization, inducing G2/M arrest and apoptosis, with potential bystander killing of adjacent tumor cells.
YES
DIRECT
ADC binds DLK1 on the cell surface, is internalized, and a cleavable linker releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis; released payload may also cause bystander killing of neighboring cells.
An intravenous antibody–drug conjugate (ADC) consisting of a monoclonal antibody that binds a tumor-associated cell-surface antigen, is internalized, and releases a cytotoxic small-molecule payload inside the cancer cell, leading to cell death with a potential bystander effect; being evaluated in a first-in-human Phase 1 study for advanced solid tumors including hepatocellular carcinoma.
A monoclonal antibody-drug conjugate that binds DLK-1 on tumor cells, is internalized, and via a cleavable linker releases the MMAE payload; MMAE inhibits tubulin polymerization, inducing G2/M arrest and apoptosis, with potential bystander killing of adjacent tumor cells.
NO
INDIRECT
The ADC targets DLK-1 for binding and internalization; released MMAE then inhibits tubulin polymerization to cause G2/M arrest and apoptosis, with possible bystander killing of nearby cells.