Anti-CD30 antibody-drug conjugate linked to MMAE; binds CD30 on malignant T cells, is internalized, releases MMAE to disrupt microtubules causing G2/M arrest and apoptosis.
Anti-CD30 monoclonal antibody linked via a protease-cleavable valine-citrulline linker to the cytotoxic payload MMAE. After binding CD30 and internalization by CD30-positive tumor cells, MMAE is released intracellularly and inhibits tubulin polymerization, disrupting microtubules, causing G2/M arrest and apoptosis.
NO
INDIRECT
Brentuximab vedotin targets CD30 on cells, is internalized, and releases MMAE, which binds beta-tubulin to disrupt microtubules and induce G2/M arrest and apoptosis. Beta-tubulin is the intracellular payload target, not the selective targeting antigen.
Humanized anti-HER2 monoclonal antibody that blocks HER2 signaling and mediates ADCC.
Humanized monoclonal antibody against HER2 (ERBB2) that binds the receptor’s extracellular domain, blocks HER2 signaling and receptor dimerization, and mediates antibody-dependent cell-mediated cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
YES
DIRECT
Trastuzumab binds HER2 on tumor cells and its Fc engages immune effectors (e.g., NK cells) via Fcγ receptors to trigger ADCC; it can also activate complement (CDC) and inhibit HER2 signaling, promoting apoptosis.
An antibody–drug conjugate targeting Trop-2 that delivers the topoisomerase I inhibitor SN-38 to tumor cells, causing DNA damage and tumor cell death with a bystander effect.
Humanized anti-Trop-2 antibody (hRS7) delivers the topoisomerase I inhibitor SN-38 to Trop-2–expressing tumor cells. After binding and internalization, linker cleavage releases SN-38, which stabilizes topoisomerase I-DNA covalent complexes, causing DNA breaks, replication arrest, and apoptosis; released payload can also produce a bystander cytotoxic effect.
YES
DIRECT
Anti-TROP2 ADC binds and is internalized; linker cleavage releases SN-38 (topoisomerase I inhibitor) in TROP2+ cells, causing DNA damage, replication arrest, and apoptosis; released payload can also cause bystander killing.
A personalized cancer vaccine composed of patient-specific tumor neoantigens administered subcutaneously to load antigen-presenting cells (primarily dendritic cells), enhance MHC I/II presentation, and expand tumor-specific CD8+ cytotoxic and CD4+ helper T cells to eliminate residual micrometastatic disease and establish immune memory in post-resection stage IIIA lung adenocarcinoma.
Personalized neoantigen peptide vaccine given subcutaneously to be taken up by antigen‑presenting cells (mainly dendritic cells), enhancing MHC I/II presentation and priming/expanding neoantigen‑specific CD8+ cytotoxic and CD4+ helper T cells to eradicate residual tumor cells and establish durable immune memory.
NO
INDIRECT
The vaccine primes neoantigen-specific CD8+ T cells that kill cells presenting the neoantigen peptide on MHC class I (e.g., HLA-A/B/C) via perforin/granzyme or Fas–FasL; HLA-C itself is not the cytotoxic target.
Autologous dendritic cell (cellular) vaccine loaded with the circular RNA–encoded cryptic peptide CircFAM53B-219aa; HLA-A*02:01–restricted; primes antigen-specific CD8+ T cells via MHC-I presentation against tumors with high CircFAM53B expression.
Autologous dendritic cells loaded with the circular RNA–encoded cryptic peptide CircFAM53B-219aa (HLA-A*02:01–restricted) present the antigen via MHC class I to prime antigen-specific CD8+ T cells, promoting cytotoxic T-cell responses against tumors with high CircFAM53B expression.
YES
INDIRECT
DC vaccine primes antigen-specific CD8+ T cells that recognize HLA-A*02:01-presented CircFAM53B-219aa peptide on tumor cells and kill them via perforin/granzyme-mediated apoptosis.