Anti-HER2 antibody–drug conjugate (RC48) that binds HER2, is internalized, and releases the microtubule-disrupting payload MMAE; can also induce ADCC.
Anti-HER2 IgG1 antibody–drug conjugate that binds HER2, is internalized, and releases the cytotoxic payload monomethyl auristatin E (MMAE) to inhibit tubulin polymerization, leading to microtubule disruption, G2/M arrest, and apoptosis; the IgG1 Fc can also induce ADCC.
NO
INDIRECT
The ADC targets HER2 on the cell surface; after internalization it releases MMAE, which binds beta‑tubulin (vinca site) to disrupt microtubules and induce G2/M arrest and apoptosis. Beta‑tubulin expression alone does not make cells targets of the drug.
Autologous, gene-modified CAR T-cell therapy; patient T cells engineered to express a chimeric antigen receptor targeting B-lineage antigens (e.g., CD19 and CD22) to induce targeted cytotoxicity.
Autologous T cells are gene-modified to express a chimeric antigen receptor targeting B-lineage antigens (e.g., CD19 and CD22). Antigen binding activates the CAR signaling domains, driving T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B cells.
YES
DIRECT
CAR T cells recognize CD19 on target cells, activate, and kill via perforin/granzyme-mediated cytolysis leading to apoptosis.
Autologous, gene-modified CAR T-cell therapy; patient T cells engineered to express a chimeric antigen receptor targeting B-lineage antigens (e.g., CD19 and CD22) to induce targeted cytotoxicity.
Autologous T cells are gene-modified to express a chimeric antigen receptor targeting B-lineage antigens (e.g., CD19 and CD22). Antigen binding activates the CAR signaling domains, driving T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B cells.
YES
DIRECT
CAR T cells bind CD22 on target cells; CAR signaling activates T-cell cytotoxicity, leading to perforin/granzyme-mediated lysis and apoptosis of CD22+ cells.
Autologous, gene-modified CAR T-cell therapy; patient T cells engineered to express a chimeric antigen receptor targeting B-lineage antigens (e.g., CD19 and CD20) to induce targeted cytotoxicity.
Autologous T cells are gene-modified to express a chimeric antigen receptor recognizing B-lineage antigens (e.g., CD19/CD20). Upon antigen binding, CAR signaling (CD3ζ with costimulatory domains) activates the T cells independently of MHC, inducing proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B cells.
YES
DIRECT
CAR T cells recognize CD19 via the CAR and directly lyse target cells through perforin/granzyme-mediated cytotoxicity (and death-receptor signaling).
Autologous, gene-modified CAR T-cell therapy; patient T cells engineered to express a chimeric antigen receptor targeting B-lineage antigens (e.g., CD19 and CD20) to induce targeted cytotoxicity.
Autologous T cells are gene-modified to express a chimeric antigen receptor recognizing B-lineage antigens (e.g., CD19/CD20). Upon antigen binding, CAR signaling (CD3ζ with costimulatory domains) activates the T cells independently of MHC, inducing proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B cells.
YES
DIRECT
CAR T cells bind CD20 on target cells, activating CAR signaling (CD3z with costimulation) and directly killing CD20+ cells via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).