An antibody–drug conjugate composed of a humanized anti-HER2 monoclonal antibody (trastuzumab) linked via a cleavable linker to a membrane-permeable topoisomerase I inhibitor payload (DXd). It binds HER2, mediates ADCC, is internalized, and releases DXd to inhibit topoisomerase I, leading to DNA damage and apoptosis with a bystander effect.
A HER2-targeting monoclonal antibody (trastuzumab) linked via a cleavable linker to a membrane-permeable topoisomerase I inhibitor payload (DXd). After HER2 binding and internalization, the linker is cleaved and DXd is released to inhibit topoisomerase I, causing DNA damage, cell-cycle arrest, and apoptosis; Fc-mediated ADCC and a bystander killing effect also contribute.
The ADC binds HER2, is internalized, and releases the topoisomerase I inhibitor DXd, causing DNA damage and apoptosis; Fc-mediated ADCC and a bystander effect also contribute.
CD20-targeted monoclonal antibody (375 mg/m2 ×2) that depletes CD20+ B cells via ADCC, CDC, and apoptosis to limit new donor-specific anti-HLA antibody production.
Rituximab is a CD20-targeted monoclonal IgG1 that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, thereby reducing formation of donor-specific anti-HLA antibodies.
Anti-CD20 antibody binds CD20 on B cells and induces killing via Fc-mediated ADCC, complement-dependent cytotoxicity, and direct apoptosis signaling, depleting CD20+ cells.
Gene-modified natural killer (NK) cells engineered to express an NKG2D-based chimeric antigen receptor (CAR) that recognizes NKG2D ligands (MICA, MICB, ULBP family) on tumor cells, activating NK cytotoxicity for treatment of relapsed/refractory multiple myeloma.
Gene‑modified NK cells expressing an NKG2D‑based CAR recognize stress‑induced NKG2D ligands (MICA, MICB, ULBP family) on tumor cells. CAR signaling activates NK cytotoxic functions, inducing degranulation (perforin/granzyme), cytokine‑mediated killing, and apoptosis of malignant cells, targeting relapsed/refractory multiple myeloma.
NKG2D-CAR NK cells recognize ULBP6 on target cells, activating NK cytotoxicity and causing direct lysis via perforin/granzyme release and apoptosis-inducing signals.
Autologous, gene-edited tumor-infiltrating lymphocyte (TIL) therapy with SOCS1 inactivation to enhance JAK-STAT signaling, boosting T-cell activation, proliferation, persistence, and cytotoxicity against tumor antigens.
Autologous TILs engineered with CRISPR-Cas9 to inactivate SOCS1, removing negative regulation of cytokine/JAK-STAT signaling and thereby enhancing T-cell activation, proliferation, persistence, and cytotoxic killing of tumor cells.
Autologous SOCS1-inactivated TILs recognize the patient-specific neoantigen–HLA complex via their endogenous TCR and directly kill target cells through perforin/granzyme-mediated cytolysis and death-receptor pathways (e.g., Fas–FasL), with enhanced activity from boosted JAK-STAT signaling.
Autologous, gene-edited tumor-infiltrating lymphocyte (TIL) therapy with SOCS1 inactivation to enhance JAK-STAT signaling, boosting T-cell activation, proliferation, persistence, and cytotoxicity against tumor antigens.
Autologous TILs engineered with CRISPR-Cas9 to inactivate SOCS1, removing negative regulation of cytokine/JAK-STAT signaling and thereby enhancing T-cell activation, proliferation, persistence, and cytotoxic killing of tumor cells.
Autologous SOCS1-knockout TILs recognize the tumor-associated peptide–HLA complex via their native TCRs and directly lyse target cells through cytotoxic T-cell mechanisms (perforin/granzyme and Fas–FasL apoptosis), with enhanced activity from SOCS1 inactivation.