Antibody–drug conjugate targeting TROP-2; an anti–TROP-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor) that delivers cytotoxic payload to TROP-2–expressing tumor cells causing DNA damage and cell death.
Anti–TROP-2 monoclonal antibody (hRS7) conjugated to SN-38 (topoisomerase I inhibitor). The antibody binds TROP-2 on tumor cells, is internalized, and the linker is cleaved to release SN-38, which stabilizes topoisomerase I–DNA complexes, causing DNA breaks, inhibition of DNA replication, and apoptosis.
NO
INDIRECT
The ADC binds TROP-2 (not topoisomerase I); after internalization it releases SN-38, which inhibits topoisomerase I to cause DNA damage and apoptosis. Topoisomerase I expression alone is not selectively targeted.
Microbial-derived therapeutic peptide cancer vaccine containing two peptides that mimic CD8+ T-cell epitopes from tumor-associated antigens plus a CD4+ helper peptide (UCP2), emulsified with Montanide; primes/expands TAA-specific cytotoxic CD8+ T cells with CD4+ T-cell help; HLA-A2–restricted.
Off-the-shelf microbiome-derived peptide cancer vaccine containing two onco-mimic peptides homologous to tumor-associated antigens plus a CD4 helper peptide (UCP2), adjuvanted with Montanide. After uptake by dendritic cells, peptides are presented (HLA-A2 restricted) to T cells, priming and expanding TAA-specific cytotoxic CD8+ T cells with CD4+ Th1 help, leading to CTL-mediated killing of TAA-expressing tumor cells.
YES
INDIRECT
Peptide vaccine is taken up by dendritic cells and presented on HLA-A2, priming/expanding TAA-specific CD8+ T cells (with CD4 Th1 help). Activated CTLs then recognize HLA-A2–restricted TAA peptides on tumor cells and kill them via perforin/granzyme-mediated cytotoxicity.
Microbial-derived therapeutic peptide cancer vaccine containing two peptides that mimic CD8+ T-cell epitopes from tumor-associated antigens plus a CD4+ helper peptide (UCP2), emulsified with Montanide; primes/expands TAA-specific cytotoxic CD8+ T cells with CD4+ T-cell help; HLA-A2–restricted.
Off-the-shelf microbiome-derived peptide cancer vaccine containing two onco-mimic peptides homologous to tumor-associated antigens plus a CD4 helper peptide (UCP2), adjuvanted with Montanide. After uptake by dendritic cells, peptides are presented (HLA-A2 restricted) to T cells, priming and expanding TAA-specific cytotoxic CD8+ T cells with CD4+ Th1 help, leading to CTL-mediated killing of TAA-expressing tumor cells.
NO
INDIRECT
UCP2 is a CD4 helper epitope that activates Th1 cells to support priming/expansion of CD8+ T cells. CTLs then kill tumor cells expressing the TAA targets from the onco‑mimic peptides, not cells expressing UCP2.
Microbial-derived therapeutic peptide cancer vaccine containing two peptides that mimic CD8+ T-cell epitopes from tumor-associated antigens plus a CD4+ helper peptide (UCP2), emulsified with Montanide; primes/expands TAA-specific cytotoxic CD8+ T cells with CD4+ T-cell help; HLA-A2–restricted.
Off-the-shelf microbiome-derived peptide cancer vaccine containing two onco-mimic peptides homologous to tumor-associated antigens plus a CD4 helper peptide (UCP2), adjuvanted with Montanide. After uptake by dendritic cells, peptides are presented (HLA-A2 restricted) to T cells, priming and expanding TAA-specific cytotoxic CD8+ T cells with CD4+ Th1 help, leading to CTL-mediated killing of TAA-expressing tumor cells.
NO
INDIRECT
Peptide vaccine induces TAA-specific CD8+ T cells (with Th1 help); CTLs recognize TAA peptides presented on HLA-A2 on tumor cells and kill via perforin/granzyme. HLA-A2 itself is only the restriction element, not the cytotoxic target.
Autologous, gene-modified cellular therapy (CD19-directed CAR-T; relma-cel, JWCAR029) made from the patient’s T cells; administered as a single fixed dose of 1×10^8 CAR+ T cells to target and kill CD19+ B-cell lymphoma cells; expected on-target effect includes B-cell aplasia.
Autologous T cells genetically modified to express a CD19-directed chimeric antigen receptor; after infusion, the CAR binds CD19 on B cells, activating and expanding the T cells to release cytotoxic mediators and kill CD19+ lymphoma cells, with on-target B-cell aplasia.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target B cells, become activated, and directly kill them via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).