Anti-CD30 antibody–drug conjugate that delivers monomethyl auristatin E (MMAE); binds CD30, internalizes, releases MMAE to inhibit microtubule polymerization and induce apoptosis.
Anti-CD30 IgG1 antibody–drug conjugate that binds CD30 on tumor cells, is internalized, and releases monomethyl auristatin E (MMAE) via proteolytic cleavage; MMAE binds tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis (with some Fc-mediated ADCC).
Anti-CD30 antibody–drug conjugate binds CD30, is internalized, and releases MMAE intracellularly, inhibiting microtubule polymerization to cause G2/M arrest and apoptosis (with some Fc-mediated ADCC).
FDA-approved autologous anti-CD19 CAR T-cell therapy with 4-1BB costimulation; patient T cells are engineered to express a CAR recognizing CD19, leading to T-cell activation, cytotoxicity, cytokine release, clearance of malignant B cells, and B-cell aplasia.
Autologous T cells are genetically engineered to express an anti‑CD19 chimeric antigen receptor with 4‑1BB costimulation, enabling recognition of CD19 on B-lineage cells and triggering T‑cell activation, proliferation, cytokine release, and cytotoxic killing of malignant B cells, resulting in clearance of CD19+ disease and B‑cell aplasia.
Anti-CD19 CAR T cells recognize CD19 on target B cells and directly induce cytotoxicity via perforin/granzyme-mediated apoptosis and Fas–FasL signaling, with cytokine release contributing.
Investigational autologous anti-CD22 CAR T-cell therapy infused 28–42 days after tisagenlecleucel; engineered T cells target CD22 to eliminate residual or antigen-shifted B-ALL via CAR-mediated T-cell activation and cytotoxicity.
Autologous T cells engineered to express a chimeric antigen receptor targeting CD22 on B-lineage cells. Upon CD22 binding, the CAR (CD3z with costimulation) activates the T cell, driving expansion, cytokine release, and perforin/granzyme-mediated cytotoxicity to eliminate CD22-positive malignant B cells, including residual or antigen-shifted blasts after CD19-directed therapy.
Anti-CD22 CAR T cells bind CD22, become activated via CAR signaling, and kill target cells through perforin/granzyme-mediated cytolysis and death-receptor (e.g., Fas/FasL) apoptosis.
Injectable bispecific T‑cell–engaging antibody that binds GPRC5D on myeloma plasma cells and CD3 on T cells to activate TCR/CD3 signaling and redirect cytotoxic T cells to kill GPRC5D-positive malignant plasma cells.
Bispecific T-cell–engaging antibody that binds GPRC5D on myeloma cells and CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, and redirect cytotoxic T cells to kill GPRC5D-positive malignant plasma cells via perforin/granzyme release.
Bispecific T‑cell engager binds GPRC5D on target cells and CD3 on T cells, forming an immune synapse that activates T cells to release perforin and granzymes, killing GPRC5D-positive cells.
Autologous BCMA-directed CAR T-cell therapy; patient T cells are engineered with a 4-1BB/CD3ζ chimeric antigen receptor targeting BCMA (TNFRSF17) to activate T cells and mediate cytotoxic killing of myeloma cells.
Autologous T cells engineered to express a BCMA-targeted CAR with 4-1BB costimulatory and CD3ζ signaling domains; upon binding BCMA on malignant plasma cells, the CAR T cells activate, proliferate, and mediate cytotoxic killing of myeloma cells.
BCMA-directed CAR T cells bind BCMA on target cells, activate via CD3ζ/4-1BB signaling, and kill through perforin/granzyme-mediated cytolysis and apoptosis pathways.