Autologous T cells genetically engineered ex vivo to express a tumor‑specific T‑cell receptor, enabling antigen-specific recognition and cytotoxicity after adoptive transfer; designed for persistent gene expression.
Autologous T cells are genetically engineered ex vivo to express a tumor-specific T-cell receptor, enabling HLA-restricted recognition of peptide–MHC on tumor cells and TCR-mediated activation that drives cytotoxic killing (perforin/granzyme) and cytokine release; integrated viral vectors support durable TCR expression after adoptive transfer.
YES
DIRECT
Engineered TCR-T cells recognize the tumor antigen peptide–HLA class I complex and, upon TCR engagement, directly kill target cells via perforin/granzyme-mediated cytolysis and death receptor pathways.
A monoclonal antibody immunotherapy targeting MICA/MICB on tumor cells to enhance NKG2D-mediated immune recognition, reduce shedding of soluble MICA/MICB, and engage Fcγ receptors to promote ADCC/ADCP in relapsed/refractory multiple myeloma.
CLN-619 is a human IgG1 monoclonal antibody that binds the alpha3 domain of MICA/MICB on tumor cells, preventing their proteolytic shedding and reducing soluble MICA/MICB. This preserves and enhances NKG2D-mediated recognition by NK cells and cytotoxic T cells, activating antitumor immunity. Its Fc domain engages Fcγ receptors to promote antibody-dependent cell-mediated cytotoxicity and phagocytosis (ADCC/ADCP).
YES
DIRECT
CLN-619 binds MICA on tumor cells and opsonizes them; its Fc engages Fcγ receptors on NK cells/macrophages to trigger ADCC/ADCP. By blocking MICA shedding, it also enhances NKG2D-dependent killing by NK and cytotoxic T cells.
A monoclonal antibody immunotherapy targeting MICA/MICB on tumor cells to enhance NKG2D-mediated immune recognition, reduce shedding of soluble MICA/MICB, and engage Fcγ receptors to promote ADCC/ADCP in relapsed/refractory multiple myeloma.
CLN-619 is a human IgG1 monoclonal antibody that binds the alpha3 domain of MICA/MICB on tumor cells, preventing their proteolytic shedding and reducing soluble MICA/MICB. This preserves and enhances NKG2D-mediated recognition by NK cells and cytotoxic T cells, activating antitumor immunity. Its Fc domain engages Fcγ receptors to promote antibody-dependent cell-mediated cytotoxicity and phagocytosis (ADCC/ADCP).
YES
DIRECT
CLN-619 binds MICB on tumor cells and engages Fcγ receptors on effector cells to drive ADCC/ADCP; it also prevents MICB shedding, enhancing NKG2D-mediated NK/CTL cytotoxicity against the target-expressing cells.
TROP2-targeted antibody–drug conjugate delivering a topoisomerase I inhibitor payload to TROP2-expressing tumor cells.
TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I–inhibiting payload, causing DNA damage and apoptotic cell death (with potential bystander effect).
YES
DIRECT
ADC binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload that causes DNA damage and apoptotic cell death (with possible bystander effect).
TROP2-targeted antibody–drug conjugate delivering a topoisomerase I inhibitor payload to TROP2-expressing tumor cells.
TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I–inhibiting payload, causing DNA damage and apoptotic cell death (with potential bystander effect).
NO
INDIRECT
SKB264 binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I–inhibiting payload that causes DNA damage and apoptosis. Cytotoxicity is driven by TROP2-targeted delivery (with possible bystander effect), while DNA topoisomerase I is the intracellular enzymatic target of the payload, not the targeting antigen.