Monoclonal antibodies linked to cytotoxic payloads that deliver intracellular chemotherapy to antigen-expressing lymphoma cells.
Tumor-targeting monoclonal antibodies linked to a cytotoxic payload bind an antigen on lymphoma cells, internalize, and release the payload intracellularly to damage DNA or microtubules and induce apoptosis, enabling antigen-directed chemotherapy with potential bystander effects.
YES
DIRECT
An anti-CD22 ADC binds CD22, is internalized, and releases a cytotoxic payload that damages DNA or microtubules, triggering apoptosis (with possible bystander effect).
An antibody–drug conjugate targeting Nectin-4 (PVRL4). The monoclonal antibody binds Nectin-4 on tumor cells, is internalized, and releases an intracellular cytotoxic payload to kill the cancer cell; Fc-mediated effector functions may also contribute. Evaluated in advanced solid tumors including urothelial cancer, triple-negative breast cancer, and cervical cancer.
Monoclonal antibody targets Nectin-4 (PVRL4) on tumor cells, is internalized, and releases a tubulin-inhibiting cytotoxic payload (AP052), leading to inhibition of microtubule polymerization, G2/M arrest, and apoptosis in Nectin-4–expressing cells; Fc-mediated effector functions may also contribute.
YES
DIRECT
ADC binds Nectin-4 on tumor cells, is internalized, and releases a tubulin-inhibiting payload (AP052) that disrupts microtubules, causing G2/M arrest and apoptosis; Fc-mediated effector functions (e.g., ADCC/CDC) may also contribute.
An antibody–drug conjugate targeting Nectin-4 (PVRL4). The monoclonal antibody binds Nectin-4 on tumor cells, is internalized, and releases an intracellular cytotoxic payload to kill the cancer cell; Fc-mediated effector functions may also contribute. Evaluated in advanced solid tumors including urothelial cancer, triple-negative breast cancer, and cervical cancer.
Monoclonal antibody targets Nectin-4 (PVRL4) on tumor cells, is internalized, and releases a tubulin-inhibiting cytotoxic payload (AP052), leading to inhibition of microtubule polymerization, G2/M arrest, and apoptosis in Nectin-4–expressing cells; Fc-mediated effector functions may also contribute.
NO
INDIRECT
The ADC targets Nectin-4 on tumor cells, is internalized, and releases a tubulin inhibitor (AP052) that blocks microtubule polymerization, leading to G2/M arrest and apoptosis; Fc effector functions may contribute. Tubulin expression alone does not make cells targets for the drug.
Investigational tetra-specific (multispecific) antibody biologic given by weekly IV infusion for relapsed/refractory B-cell malignancies (CLL/SLL and other NHL); designed to bind multiple antigens to enhance immune-mediated killing and reduce antigen escape.
Tetra-specific T‑cell–engaging antibody that binds ROR1 on tumor cells and CD3 on T cells to redirect cytotoxic T lymphocytes, while simultaneously blocking PD-L1 to relieve PD-1–mediated inhibition and agonizing 4-1BB to provide costimulation. The combined actions enhance T-cell activation and CTL-mediated lysis of ROR1+ malignant B cells and help mitigate antigen escape.
YES
DIRECT
T-cell redirected cytotoxicity: the tetra-specific engager binds ROR1 on tumor cells and CD3 on T cells, provides 4-1BB costimulation and blocks PD-L1, activating CTLs to kill ROR1+ cells via perforin/granzyme-mediated lysis.
Investigational tetra-specific (multispecific) antibody biologic given by weekly IV infusion for relapsed/refractory B-cell malignancies (CLL/SLL and other NHL); designed to bind multiple antigens to enhance immune-mediated killing and reduce antigen escape.
Tetra-specific T‑cell–engaging antibody that binds ROR1 on tumor cells and CD3 on T cells to redirect cytotoxic T lymphocytes, while simultaneously blocking PD-L1 to relieve PD-1–mediated inhibition and agonizing 4-1BB to provide costimulation. The combined actions enhance T-cell activation and CTL-mediated lysis of ROR1+ malignant B cells and help mitigate antigen escape.
NO
INDIRECT
The drug binds CD3 on T cells to recruit and activate them; these T cells are then redirected to kill ROR1+ tumor cells (enhanced by PD-L1 blockade and 4-1BB costimulation) via perforin/granzyme-mediated cytolysis. CD3+ T cells themselves are not the targets of killing.