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.
YES
DIRECT
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).
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.
NO
INDIRECT
The ADC targets Trop-2 on the cell surface, is internalized, and releases SN-38, which inhibits topoisomerase I to cause DNA damage and apoptosis. Topoisomerase I is the intracellular payload target, not the antigen used for selective cell killing.
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.
YES
DIRECT
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.
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.
YES
DIRECT
TILs recognize tumor antigen peptide–HLA-B complexes via their native TCR and directly kill target cells through immunologic synapse formation and perforin/granzyme-mediated apoptosis (with possible Fas–FasL engagement).
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.
YES
DIRECT
Adoptively transferred TILs recognize tumor antigen peptide–HLA-C complexes via their native TCRs and directly kill the presenting cells through cytotoxic T-cell mechanisms (perforin/granzyme and Fas–FasL).