An autologous CD19-directed chimeric antigen receptor (CAR) T-cell therapy given as a single IV infusion; patient T cells are engineered to express a CAR targeting CD19 to mediate cytotoxic killing and cytokine-driven clearance of malignant B cells, with expected on-target B-cell aplasia.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor targeting CD19. Upon infusion, CAR engagement of CD19 on malignant and normal B cells activates CD3ζ and costimulatory signaling, driving T-cell expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CD19+ cells, resulting in on-target B-cell aplasia.
CD19 CAR-T cells bind CD19 on targets, trigger CD3ζ/costimulatory signaling, form an immune synapse, and kill via perforin/granzyme release (and death-receptor pathways), lysing CD19+ cells.
Autologous gene-modified T lymphocytes engineered to express chimeric antigen receptors that recognize tumor antigens independently of MHC, leading to potent T-cell activation and antitumor activity; associated with cytokine release syndrome and potential cardiotoxic effects.
Autologous T lymphocytes are genetically engineered to express chimeric antigen receptors (scFv-based receptors with CD3ζ and costimulatory domains such as CD28 or 4-1BB) that bind tumor-associated surface antigens independently of MHC. Antigen engagement triggers potent T-cell activation, expansion, and cytotoxic killing of target cells via perforin/granzyme and cytokine release, which can cause cytokine release syndrome and potential cardiotoxic effects.
CAR T cells recognize the tumor-associated surface antigen and directly kill antigen-positive cells via T-cell effector functions (perforin/granzyme-mediated apoptosis and death-receptor signaling) after CAR activation.
HER3-directed antibody–drug conjugate targeting ERBB3; internalization after receptor binding with subsequent release of a cytotoxic payload to kill HER3-expressing tumor cells.
HER3 (ERBB3)-targeted IgG1 ADC that binds HER3 on tumor cells, undergoes internalization and cleavable-linker processing to release a topoisomerase I inhibitor payload, stabilizing Topo I–DNA complexes and inducing DNA breaks, replication arrest, and apoptosis in HER3-expressing cells.
ADC binds HER3 on target cells, is internalized, and releases a topoisomerase I inhibitor via a cleavable linker, causing DNA damage/replication arrest and apoptosis in HER3-expressing cells.
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.
The anti‑CD30 ADC binds CD30, is internalized, and its linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis in CD30‑positive cells.
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).
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).