Anti-HER2 antibody–drug conjugate delivering the microtubule inhibitor DM1 to HER2-expressing cells.
Trastuzumab (anti‑HER2 mAb) conjugated to DM1, a maytansinoid microtubule inhibitor. After binding HER2 on tumor cells, the complex is internalized and DM1 is released intracellularly to disrupt microtubules, causing cell-cycle arrest and apoptosis; trastuzumab also inhibits HER2 signaling and can mediate ADCC.
YES
DIRECT
Binds HER2, is internalized, and releases the DM1 payload inside the cell to disrupt microtubules, causing mitotic arrest and apoptosis; Fc can also mediate ADCC.
Anti-HER2 antibody–drug conjugate delivering the microtubule inhibitor DM1 to HER2-expressing cells.
Trastuzumab (anti‑HER2 mAb) conjugated to DM1, a maytansinoid microtubule inhibitor. After binding HER2 on tumor cells, the complex is internalized and DM1 is released intracellularly to disrupt microtubules, causing cell-cycle arrest and apoptosis; trastuzumab also inhibits HER2 signaling and can mediate ADCC.
NO
INDIRECT
T-DM1 targets HER2 on the cell surface; after internalization it releases DM1, which binds beta-tubulin to disrupt microtubules and cause mitotic arrest/apoptosis. Beta-tubulin is the intracellular payload target, not the recognized antigen.
Cell-based cancer vaccine in which a patient's own dendritic cells are loaded with patient-specific neoantigen peptides to present via MHC I/II and prime/expand CD8+ cytotoxic and CD4+ helper T-cell responses.
Autologous dendritic cells are loaded ex vivo with patient-specific neoantigen peptides and reinfused to present these antigens via MHC I/II with costimulatory signals, thereby priming and expanding tumor-specific CD8+ cytotoxic and CD4+ helper T cells to mount durable antitumor immune responses.
YES
INDIRECT
The DC vaccine primes and expands neoantigen-specific CD8+ T cells, which recognize the same neoantigen–MHC complexes on tumor cells and kill them via perforin/granzyme release and Fas–FasL–mediated apoptosis.
Cell-based cancer vaccine in which a patient's own dendritic cells are loaded with patient-specific neoantigen peptides to present via MHC I/II and prime/expand CD8+ cytotoxic and CD4+ helper T-cell responses.
Autologous dendritic cells are loaded ex vivo with patient-specific neoantigen peptides and reinfused to present these antigens via MHC I/II with costimulatory signals, thereby priming and expanding tumor-specific CD8+ cytotoxic and CD4+ helper T cells to mount durable antitumor immune responses.
NO
INDIRECT
The vaccine primes neoantigen-specific CD8+ T cells, which then recognize tumor cells presenting the neoantigen peptide on HLA-A and kill them via perforin/granzyme (and Fas–FasL) pathways; HLA-A expression alone is not targeted.
Cell-based cancer vaccine in which a patient's own dendritic cells are loaded with patient-specific neoantigen peptides to present via MHC I/II and prime/expand CD8+ cytotoxic and CD4+ helper T-cell responses.
Autologous dendritic cells are loaded ex vivo with patient-specific neoantigen peptides and reinfused to present these antigens via MHC I/II with costimulatory signals, thereby priming and expanding tumor-specific CD8+ cytotoxic and CD4+ helper T cells to mount durable antitumor immune responses.
NO
INDIRECT
The vaccine primes neoantigen-specific CD8+ T cells that kill cells presenting the specific neoantigen peptide on HLA class I (e.g., HLA-B) via TCR recognition and perforin/granzyme or Fas–FasL pathways; HLA-B expression alone is not targeted.