Autologous, gene-modified CAR T cells engineered to express an anti-CD30 chimeric antigen receptor and CCR4 to enhance trafficking to the Hodgkin lymphoma microenvironment; CAR engagement of CD30 triggers T-cell activation and cytotoxicity.
Autologous T cells are gene-modified to express an anti‑CD30 chimeric antigen receptor and the chemokine receptor CCR4. CAR binding to CD30 on malignant cells triggers T‑cell activation, cytokine release, proliferation, and targeted cytotoxicity, while CCR4 enhances trafficking to the Hodgkin lymphoma microenvironment via CCL17/CCL22 gradients.
NO
INDIRECT
CCL22 engages CCR4 on the CAR T cells to enhance trafficking; killing occurs only when the CAR binds CD30 on target cells (perforin/granzyme cytolysis), not via CCL22.
An anti-HER2 antibody–drug conjugate (Enhertu) composed of humanized IgG1 trastuzumab linked to a topoisomerase I inhibitor payload (DXd). It binds HER2 on tumor cells, is internalized, and releases DXd to inhibit topoisomerase I, causing DNA damage and bystander killing; it also retains trastuzumab functions such as ADCC and HER2 signaling blockade.
Humanized anti-HER2 monoclonal antibody (trastuzumab) linked to a topoisomerase I inhibitor (DXd). Binds HER2 on tumor cells, is internalized, and releases DXd to inhibit topoisomerase I, causing DNA damage, replication arrest, and apoptosis with a bystander-killing effect; retains trastuzumab functions including HER2 signaling blockade and antibody-dependent cell-mediated cytotoxicity (ADCC).
NO
INDIRECT
Trastuzumab deruxtecan binds HER2, is internalized, and releases DXd that inhibits topoisomerase I to cause DNA damage and apoptosis (with bystander killing and ADCC). Topoisomerase I itself is not the binding target that determines cell killing.
Patient-derived TIL product consisting of >=5 x 10^9 autologous ex vivo-expanded T cells administered intravenously to mediate antigen-specific tumor cytotoxicity.
Autologous ex vivo‑expanded tumor-infiltrating T cells that recognize patient-specific tumor antigens via native TCRs and kill tumor cells through cytotoxic effector functions (perforin/granzyme and cytokines); conditioning/IL-2 support engraftment and persistence.
YES
DIRECT
TILs recognize the patient-specific peptide–HLA complex via native TCRs and directly kill target cells through cytotoxic effector functions (perforin/granzyme-mediated apoptosis; also Fas–FasL and inflammatory cytokines).
Patient-derived TIL product consisting of >=5 x 10^9 autologous ex vivo-expanded T cells administered intravenously to mediate antigen-specific tumor cytotoxicity.
Autologous ex vivo‑expanded tumor-infiltrating T cells that recognize patient-specific tumor antigens via native TCRs and kill tumor cells through cytotoxic effector functions (perforin/granzyme and cytokines); conditioning/IL-2 support engraftment and persistence.
YES
DIRECT
Native TCRs on infused TILs recognize the tumor-associated peptide–HLA complex and directly kill the presenting cell via perforin/granzyme release and Fas–FasL–mediated apoptosis.
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement activation, and apoptosis to reduce platelet/HLA alloantibody-producing cells.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, thereby reducing alloantibody-producing B cells (anti-platelet/HLA).
YES
DIRECT
Rituximab binds CD20 on B cells and triggers Fc-dependent ADCC by NK/macrophages, complement-dependent cytotoxicity (C1q/MAC), and can induce apoptosis via CD20 crosslinking.