A subcutaneous therapeutic vaccine/APC-based immunotherapy naturally loaded with EBV antigens that enhances antigen presentation, activates dendritic cells, and primes EBV-specific CD4+ and CD8+ T cells to mount cytotoxic responses against EBV-positive tumor cells.
Autologous APC/dendritic cell–based therapeutic vaccine naturally loaded with EBV antigens that enhances antigen presentation (MHC I/II), activates dendritic cells, and primes EBV‑specific CD4+ and CD8+ T cells to mount cytotoxic responses against EBV‑positive tumor cells.
YES
INDIRECT
Vaccine-primed EBV-specific CD8+ T cells recognize EBV peptide–HLA class I on tumor cells and kill them via cytotoxic T-cell mechanisms (perforin/granzyme, Fas–FasL).
A subcutaneous therapeutic vaccine/APC-based immunotherapy naturally loaded with EBV antigens that enhances antigen presentation, activates dendritic cells, and primes EBV-specific CD4+ and CD8+ T cells to mount cytotoxic responses against EBV-positive tumor cells.
Autologous APC/dendritic cell–based therapeutic vaccine naturally loaded with EBV antigens that enhances antigen presentation (MHC I/II), activates dendritic cells, and primes EBV‑specific CD4+ and CD8+ T cells to mount cytotoxic responses against EBV‑positive tumor cells.
YES
INDIRECT
The vaccine activates dendritic cells and primes EBV-specific T cells. CD4+ T cells recognizing EBV peptides on MHC II (and the CD8+ CTLs they help) kill EBV-positive, MHC II–expressing cells via perforin/granzyme and/or Fas–FasL apoptosis; the drug itself does not directly kill cells.
Intravenous bispecific T-cell engager antibody that binds CD123 on AML blasts/leukemia stem cells and CD3 on T cells to redirect cytotoxic killing; priming doses used to mitigate cytokine release syndrome.
Fc-modified bispecific antibody that binds CD123 (IL-3Rα) on AML blasts/leukemia stem cells and CD3 on T cells, crosslinking tumor cells with T cells to activate and expand cytotoxic T lymphocytes and drive perforin/granzyme-mediated lysis of CD123+ cells; Fc domain extends half-life and step-up dosing is used to mitigate cytokine release syndrome.
YES
DIRECT
The bispecific antibody links CD123 on target cells to CD3 on T cells, activating T cells to mediate perforin/granzyme-dependent cytolysis of CD123+ cells.
Intravenous bispecific T-cell engager antibody that binds CD123 on AML blasts/leukemia stem cells and CD3 on T cells to redirect cytotoxic killing; priming doses used to mitigate cytokine release syndrome.
Fc-modified bispecific antibody that binds CD123 (IL-3Rα) on AML blasts/leukemia stem cells and CD3 on T cells, crosslinking tumor cells with T cells to activate and expand cytotoxic T lymphocytes and drive perforin/granzyme-mediated lysis of CD123+ cells; Fc domain extends half-life and step-up dosing is used to mitigate cytokine release syndrome.
NO
INDIRECT
APVO436 binds CD3 on T cells to activate and redirect them to kill CD123+ tumor cells via perforin/granzyme; CD3+ T cells themselves are not targeted for lysis.
Oral small-molecule BCL-2 inhibitor that restores mitochondrial apoptosis in AML cells.
Selective oral BH3 mimetic that inhibits BCL-2 by binding its hydrophobic groove, neutralizing its anti-apoptotic function and restoring mitochondrial apoptosis (via BAX/BAK activation) in tumor cells; spares BCL-XL.
YES
DIRECT
Venetoclax directly binds and inhibits BCL-2, freeing proapoptotic signaling to activate BAX/BAK, trigger mitochondrial outer membrane permeabilization, cytochrome c release, caspase activation, and apoptotic death of BCL-2–dependent cells.