An antibody–drug conjugate consisting of a humanized anti–Trop-2 monoclonal antibody linked to SN-38 (active metabolite of irinotecan). It delivers a topoisomerase I inhibitor to Trop-2–expressing tumor cells, causing DNA damage and apoptosis with a bystander effect.
Humanized anti–Trop-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor). Binds Trop-2 on tumor cells, is internalized, and releases SN-38 after cleavage, stabilizing topoisomerase I–DNA complexes to cause DNA breaks, inhibit replication, and trigger apoptosis; released payload can exert a bystander effect on neighboring cells.
YES
INDIRECT
The ADC binds Trop-2 on tumor cells, is internalized, and releases SN-38, which inhibits DNA topoisomerase I to cause DNA breaks and apoptosis; killing is determined by Trop-2 targeting (with a bystander effect), not by direct recognition of topoisomerase I.
Autologous tumor-infiltrating lymphocyte (TIL) therapy expanded ex vivo; adoptive cellular immunotherapy delivering tumor-reactive T cells to mediate antigen-specific cytotoxicity and effector cytokine secretion.
Autologous tumor-infiltrating lymphocytes are isolated from the patient’s tumor, expanded ex vivo, and reinfused. These non-engineered T cells use their native TCRs to recognize tumor antigens presented by MHC on cancer cells, execute antigen-specific cytotoxicity (perforin/granzyme) and secrete effector cytokines (e.g., IFN-γ, TNF-α), enhancing antitumor immune responses.
YES
DIRECT
Infused autologous TILs use native TCRs to recognize the neoantigen peptide–HLA class I complex on tumor cells and directly kill them via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Autologous tumor-infiltrating lymphocyte (TIL) therapy expanded ex vivo; adoptive cellular immunotherapy delivering tumor-reactive T cells to mediate antigen-specific cytotoxicity and effector cytokine secretion.
Autologous tumor-infiltrating lymphocytes are isolated from the patient’s tumor, expanded ex vivo, and reinfused. These non-engineered T cells use their native TCRs to recognize tumor antigens presented by MHC on cancer cells, execute antigen-specific cytotoxicity (perforin/granzyme) and secrete effector cytokines (e.g., IFN-γ, TNF-α), enhancing antitumor immune responses.
YES
DIRECT
Native TCRs on infused TILs recognize the neoantigen peptide–HLA class II complex and directly kill the presenting tumor cell via perforin/granzyme release and Fas/FasL-mediated apoptosis, with supportive effector cytokines.
Autologous tumor-infiltrating lymphocyte (TIL) therapy expanded ex vivo; adoptive cellular immunotherapy delivering tumor-reactive T cells to mediate antigen-specific cytotoxicity and effector cytokine secretion.
Autologous tumor-infiltrating lymphocytes are isolated from the patient’s tumor, expanded ex vivo, and reinfused. These non-engineered T cells use their native TCRs to recognize tumor antigens presented by MHC on cancer cells, execute antigen-specific cytotoxicity (perforin/granzyme) and secrete effector cytokines (e.g., IFN-γ, TNF-α), enhancing antitumor immune responses.
YES
DIRECT
Autologous TILs recognize tumor‑associated peptide–HLA class I complexes via their native TCRs and directly kill target cells through perforin/granzyme-mediated cytolysis (and death receptor pathways).
Autologous tumor-infiltrating lymphocyte (TIL) therapy expanded ex vivo; adoptive cellular immunotherapy delivering tumor-reactive T cells to mediate antigen-specific cytotoxicity and effector cytokine secretion.
Autologous tumor-infiltrating lymphocytes are isolated from the patient’s tumor, expanded ex vivo, and reinfused. These non-engineered T cells use their native TCRs to recognize tumor antigens presented by MHC on cancer cells, execute antigen-specific cytotoxicity (perforin/granzyme) and secrete effector cytokines (e.g., IFN-γ, TNF-α), enhancing antitumor immune responses.
YES
DIRECT
Autologous TILs recognize HPV E6/E7 peptide–HLA class I via native TCRs and induce tumor cell death via perforin/granzyme-mediated cytolysis (and death receptor pathways).