Anti-CD30 antibody–drug conjugate linked to MMAE; binds CD30 on Hodgkin Reed–Sternberg cells, internalizes, releases microtubule poison causing G2/M arrest and apoptosis.
Chimeric anti‑CD30 monoclonal antibody linked to the microtubule inhibitor MMAE via a protease‑cleavable valine‑citrulline linker; after binding CD30 on tumor cells and internalization, the linker is cleaved to release MMAE, which binds tubulin and blocks microtubule polymerization, causing G2/M arrest and apoptosis with selectivity for CD30‑positive cells.
NO
INDIRECT
The ADC binds CD30 and is internalized; the linker is cleaved to release MMAE, which binds beta‑tubulin (vinca site) to block microtubule polymerization, causing G2/M arrest and apoptosis. Beta‑tubulin expression alone does not direct the drug to kill the cell.
Autologous gene-engineered T cells expressing an HLA-A*02:01–restricted TCR targeting the HPV16 E7 peptide; adoptive cellular gene therapy.
Autologous T cells are genetically engineered to express an HLA-A*02:01–restricted T-cell receptor specific for the HPV16 E7 peptide. After infusion, these TCR-T cells recognize E7 peptide presented on tumor MHC class I, become activated, expand, and kill antigen-positive cancer cells via cytotoxic effector mechanisms (perforin/granzyme and cytokine-mediated responses).
YES
DIRECT
TCR-engineered T cells recognize the HPV16 E7 peptide presented by HLA-A*02:01 on tumor MHC I and kill target-positive cells via perforin/granzyme-mediated cytolysis (and Fas/FasL, cytokine-driven apoptosis).
Autologous gene-engineered T cells expressing an HLA-A*02:01–restricted TCR targeting the HPV16 E7 peptide; adoptive cellular gene therapy.
Autologous T cells are genetically engineered to express an HLA-A*02:01–restricted T-cell receptor specific for the HPV16 E7 peptide. After infusion, these TCR-T cells recognize E7 peptide presented on tumor MHC class I, become activated, expand, and kill antigen-positive cancer cells via cytotoxic effector mechanisms (perforin/granzyme and cytokine-mediated responses).
NO
INDIRECT
E7 TCR-T cells require recognition of the HPV16 E7 peptide presented by HLA-A*02:01; HLA-A*02:01 alone is not sufficient. When the E7 peptide–HLA-A*02:01 complex is present, T cells kill via perforin/granzyme-mediated cytolysis and cytokine-induced apoptosis.
Autologous BCMA-directed chimeric antigen receptor (CAR) T-cell therapy in which a patient’s T cells are engineered to express a CAR targeting BCMA, enabling depletion of BCMA-positive plasmablasts/plasma cells to reduce autoantibody production in systemic lupus erythematosus.
Autologous CD8+ T cells are transiently engineered via mRNA to express a CAR targeting BCMA, enabling antigen-specific recognition and cytotoxic elimination of BCMA-positive plasmablasts/plasma cells, thereby depleting autoantibody-producing cells and reducing pathogenic humoral immunity in SLE.
YES
DIRECT
CAR-engineered CD8+ T cells bind BCMA on target cells, form an immunologic synapse, and induce cytolysis primarily via perforin/granzyme-mediated apoptosis (and potentially Fas–FasL).
Anti-HER2 antibody–drug conjugate (RC48) that delivers MMAE; binds HER2, internalizes, and releases MMAE to disrupt microtubules and kill tumor cells.
Anti-HER2 monoclonal antibody–drug conjugate that binds HER2, is internalized, and releases the microtubule inhibitor MMAE via a cleavable linker, inhibiting tubulin polymerization to induce G2/M arrest and apoptosis in HER2-expressing tumor cells.
YES
DIRECT
ADC binds HER2, is internalized, and releases MMAE intracellularly to inhibit tubulin polymerization, causing G2/M arrest and apoptosis of HER2-expressing cells.