An antibody–drug conjugate (ADC) targeting CLDN18.2; after binding to CLDN18.2 on tumor cells it is internalized and releases a topoisomerase I–inhibiting cytotoxic payload, inducing DNA damage and cell death with a potential bystander effect.
Monoclonal antibody targeting CLDN18.2 linked to a topoisomerase I inhibitor; upon binding CLDN18.2 on tumor cells the ADC is internalized and releases the payload, inhibiting topoisomerase I to induce DNA damage and tumor cell death, with potential bystander effect.
The anti-CLDN18.2 ADC binds CLDN18.2 on target cells, is internalized, and releases a topoisomerase I–inhibitor payload that induces DNA damage and apoptosis, with potential bystander killing.
Allogeneic, cord blood–derived NK cell therapy engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific T-cell receptor plus IL-15 to enhance activation, proliferation, and persistence; mediates tumor killing via the introduced TCR and native NK cytotoxicity.
Allogeneic cord blood–derived NK cells engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific TCR plus IL-15. The introduced TCR enables recognition of NY-ESO-1 peptide–HLA complexes on tumor cells, while IL-15 enhances activation, proliferation, and persistence. Tumor killing occurs via TCR-driven cytotoxicity and native NK effector functions (perforin/granzyme, activating receptors such as NKG2D).
Engineered NK cells bearing an HLA-A*02:01–restricted NY-ESO-1–specific TCR recognize the NY-ESO-1 peptide–HLA complex on target cells and directly induce cytolysis via TCR-triggered perforin/granzyme (and death-receptor) pathways, with IL-15 enhancing activity and persistence.
Allogeneic, cord blood–derived NK cell therapy engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific T-cell receptor plus IL-15 to enhance activation, proliferation, and persistence; mediates tumor killing via the introduced TCR and native NK cytotoxicity.
Allogeneic cord blood–derived NK cells engineered to express an HLA-A*02:01–restricted NY-ESO-1–specific TCR plus IL-15. The introduced TCR enables recognition of NY-ESO-1 peptide–HLA complexes on tumor cells, while IL-15 enhances activation, proliferation, and persistence. Tumor killing occurs via TCR-driven cytotoxicity and native NK effector functions (perforin/granzyme, activating receptors such as NKG2D).
Engineered NK cells expressing an HLA-A*02:01–restricted NY-ESO-1–specific TCR bind the NY-ESO-1 peptide–HLA-A*02:01 complex on target cells and induce cytolysis via perforin/granzyme release (with IL-15 enhancing activity).
An antibody–drug conjugate comprising a humanized anti–Trop-2 monoclonal antibody linked to SN-38 (the active metabolite of irinotecan), a topoisomerase I inhibitor. After binding Trop-2 on tumor cells, it is internalized and releases SN-38 to inhibit Topo I, causing DNA damage and apoptosis, with potential bystander effect.
Humanized anti–Trop-2 monoclonal antibody linked to SN-38. After binding Trop-2 on tumor cells and internalization, the linker is cleaved to release SN-38, which inhibits topoisomerase I, stabilizes Topo I–DNA complexes, induces DNA damage and apoptosis, and can produce a bystander cytotoxic effect.
The anti–Trop-2 antibody–drug conjugate binds Trop-2, is internalized, and releases SN-38, a topoisomerase I inhibitor that stabilizes Topo I–DNA complexes, causing DNA damage and apoptosis (with possible bystander effect).
Autologous adoptive cell therapy comprising patient-derived tumor-reactive T cells isolated from bladder tumors, expanded ex vivo with IL-2 and anti-CD3 stimulation, and administered intravesically to treat high-grade non-muscle-invasive urothelial carcinoma.
Autologous tumor-infiltrating lymphocytes (TIL) are isolated from the patient’s bladder tumor, activated and expanded ex vivo with IL-2 and anti-CD3, then administered intravesically. These non-engineered T cells recognize tumor antigens via their native TCRs and mediate cytotoxicity (perforin/granzyme) and cytokine release (e.g., IFN-γ), increasing local anti-tumor immunity within the bladder.
TIL recognize tumor antigen peptide–HLA-A complexes via their native TCRs and directly kill target cells through perforin/granzyme release and Fas–FasL signaling.