Gene-modified natural killer cells engineered to express a chimeric antigen receptor targeting CLL-1 (CLEC12A) for treatment of relapsed/refractory AML; upon CAR engagement of CLL-1, NK cytotoxic mechanisms (perforin/granzyme, cytokines) kill AML blasts and leukemia stem/progenitor cells.
Gene‑modified natural killer cells expressing a CAR that recognizes CLL‑1 (CLEC12A) on AML blasts and leukemia stem/progenitor cells; CAR engagement activates NK cell signaling leading to degranulation and cytotoxic killing via perforin/granzyme and cytokine secretion, with relative sparing of normal hematopoietic stem cells.
CAR-engineered NK cells bind CLEC12A (CLL-1) and, upon CAR engagement, directly kill target cells via NK degranulation with perforin/granzyme-mediated apoptosis and cytotoxic cytokine release.
HER2-directed antibody–drug conjugate consisting of an anti-HER2 monoclonal antibody linked to the microtubule inhibitor MMAE; binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing mitotic arrest and apoptosis; may also induce ADCC and immunogenic cell death.
HER2-directed antibody–drug conjugate in which an anti-HER2 monoclonal antibody delivers the microtubule inhibitor MMAE to HER2-expressing tumor cells. After binding and internalization, MMAE is released to inhibit tubulin polymerization, causing mitotic arrest and apoptosis; the antibody component may also mediate ADCC and promote immunogenic cell death.
The HER2-targeted ADC binds HER2, is internalized, and releases MMAE that inhibits tubulin polymerization, causing mitotic arrest and apoptosis; the antibody Fc can also mediate ADCC.
Autologous CAR T-cell therapy engineered to target CS1 (SLAMF7/CD319) on multiple myeloma cells to induce T-cell–mediated cytotoxicity.
Autologous T cells are engineered to express a chimeric antigen receptor that binds CS1 (SLAMF7/CD319) on multiple myeloma cells, initiating antigen-dependent T-cell activation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CS1-positive malignant plasma cells.
CAR T cells recognize SLAMF7 on target cells, become activated, and kill via perforin/granzyme–mediated cytotoxicity (and related T cell effector pathways).
Subcutaneous CD3-directed T-cell engager bispecific antibody that binds CD3 on T cells and a B-cell tumor antigen to redirect cytotoxic T cells against malignant B cells.
Fully human effector-silent IgG1 trispecific antibody that binds CD79b and/or CD20 on B cells and CD3 on T cells, creating an immune synapse that activates and redirects cytotoxic T lymphocytes to lyse malignant B cells via TCR/CD3 signaling and perforin/granzyme-mediated killing.
The trispecific T-cell–engaging antibody binds CD79b on B cells and CD3 on T cells, forming an immune synapse that activates CTLs to kill the CD79b+ cells via perforin/granzyme-mediated cytotoxicity.
Subcutaneous CD3-directed T-cell engager bispecific antibody that binds CD3 on T cells and a B-cell tumor antigen to redirect cytotoxic T cells against malignant B cells.
Fully human effector-silent IgG1 trispecific antibody that binds CD79b and/or CD20 on B cells and CD3 on T cells, creating an immune synapse that activates and redirects cytotoxic T lymphocytes to lyse malignant B cells via TCR/CD3 signaling and perforin/granzyme-mediated killing.
Trispecific T‑cell engager binds CD20 on B cells and CD3 on T cells, forming an immune synapse that activates T cells to kill CD20+ cells via TCR/CD3 signaling and perforin/granzyme-mediated cytolysis.