An intrathecal, autologous dendritic cell (DC1) vaccine loaded with HER2 and HER3 peptides to present tumor antigens and prime/activate tumor-specific T cells (Th1/CTL) within the cerebrospinal fluid for immune-mediated killing of cancer cells in leptomeningeal disease from TNBC or HER2+ breast cancer.
Autologous DC1 dendritic cells pulsed with HER2/HER3 peptides are administered intrathecally to present these antigens via MHC to T cells in the CSF, inducing Th1 polarization and priming/activating tumor‑specific CD4+ and CD8+ cytotoxic T cells to recognize and kill HER2/HER3‑expressing leptomeningeal tumor cells.
YES
INDIRECT
The DC1 vaccine presents HER3 peptides to T cells, priming HER3-specific CD8+ CTLs that recognize HER3 peptide–MHC on tumor cells and kill them via perforin/granzyme and Fas–FasL pathways.
HER2-targeted antibody-drug conjugate that binds HER2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload causing DNA damage and tumor cell death (potential bystander effect).
Anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and via a cleavable linker releases a camptothecin-derived topoisomerase I inhibitor, stabilizing topo I–DNA complexes and causing DNA breaks, replication arrest, and apoptosis; potential bystander killing of adjacent cells.
YES
DIRECT
The anti-HER2 ADC binds HER2, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that traps topo I–DNA complexes, causing DNA breaks, replication arrest, and apoptosis (with possible bystander killing).
HER2-targeted antibody-drug conjugate that binds HER2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload causing DNA damage and tumor cell death (potential bystander effect).
Anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and via a cleavable linker releases a camptothecin-derived topoisomerase I inhibitor, stabilizing topo I–DNA complexes and causing DNA breaks, replication arrest, and apoptosis; potential bystander killing of adjacent cells.
YES
INDIRECT
SHR-A1811 binds HER2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that stabilizes topo I–DNA complexes, causing DNA breaks, replication arrest, and apoptosis; payload can diffuse for bystander killing.
A therapeutic mRNA vaccine encoding hepatitis B virus (HBV) antigens, administered intramuscularly with dose escalation (starting at 20 µg), weekly for 4 doses followed by a 1‑month booster. The mRNA is taken up by antigen-presenting cells (especially dendritic cells), translated into HBV antigens, and presented via MHC I/II to prime HBV-specific CD8+ and CD4+ T-cell responses (and potentially antibody responses) aimed at eliminating HBV antigen–expressing hepatocellular carcinoma cells.
Encapsulated mRNA encoding HBV antigens is taken up by antigen-presenting cells, translated into HBV proteins, and presented via MHC I and II to induce HBV-specific CD8+ and CD4+ T-cell responses (and antibodies), promoting immune-mediated elimination of HBV antigen-expressing hepatocellular carcinoma cells.
YES
INDIRECT
The mRNA vaccine primes HBV-specific CD8+ T cells that recognize HBV peptides on MHC I of target cells and kill them via perforin/granzyme; vaccine-induced antibodies may also mediate ADCC/complement.
Etentamig (ABBV-383; TNB-383B) is an intravenous bispecific T-cell–redirecting antibody that binds BCMA on plasma cells and CD3 on T cells to activate cytotoxic T cells and eliminate BCMA+ plasma cells, reducing amyloidogenic light chains.
Bispecific IgG4 antibody that binds BCMA on plasma cells and CD3 on T cells, creating an immune synapse that activates and redirects cytotoxic T cells to kill BCMA-expressing cells, thereby reducing amyloidogenic light-chain production (with low CD3 activation to limit cytokine release).
NO
INDIRECT
Etentamig engages CD3 to activate T cells, which then kill BCMA+ plasma cells; CD3+ T cells themselves are not targeted for killing.