CD123-targeted immunotoxin (IL-3 fused to truncated diphtheria toxin) that binds IL-3Rα (CD123), is internalized, ADP-ribosylates EF-2 to block protein synthesis and induce apoptosis.
Recombinant IL-3–diphtheria toxin immunotoxin that binds CD123 (IL-3Rα) on target cells, is internalized, and the diphtheria toxin catalytic domain ADP-ribosylates elongation factor-2 (EF-2), blocking protein synthesis and inducing apoptotic cell death.
NO
INDIRECT
Tagraxofusp binds CD123 on the cell surface, is internalized, and its diphtheria toxin moiety ADP-ribosylates EF-2 to block protein synthesis and induce apoptosis. EF-2 is not the targeting antigen; its inhibition is a downstream intracellular effect in CD123+ cells.
Autologous adoptive T-cell therapy derived from tumor-draining lymph node T cells, ex vivo activated and expanded with patient-specific neoantigen proteins, then infused intravenously to provide polyclonal, neoantigen-specific T-cell immunity against colorectal cancer.
Autologous T cells from tumor‑draining lymph nodes are activated and expanded ex vivo with patient‑specific neoantigen proteins to enrich polyclonal, neoantigen‑specific TCRs. Following lymphodepletion, the infused cells recognize neoantigen peptides presented on MHC I/II on tumor cells and mediate cytotoxic killing (perforin/granzyme) and cytokine‑driven immune responses, boosting tumor‑specific immunity and overcoming tolerance in colorectal cancer.
YES
DIRECT
Neoantigen-specific TCRs recognize the mutant peptide–HLA class I complex on tumor cells, activating cytotoxic T cells to kill via perforin/granzyme-mediated apoptosis (± Fas–FasL), with supportive cytokine effects.
Autologous, gene-modified CAR T-cell therapy in which a patient’s T cells are transduced to express a CD19-directed KIR-based chimeric antigen receptor; upon binding CD19 on malignant B cells, the KIR-derived signaling domain activates the T cell to mediate cytokine release and cytotoxic killing of CD19+ cells.
Autologous T cells are genetically modified to express a CD19-directed KIR-based chimeric antigen receptor; binding to CD19 on malignant B cells triggers KIR-derived signaling that activates the T cells, inducing cytokine release and cytotoxic killing of CD19+ cells.
YES
DIRECT
CAR T cells expressing a CD19-directed KIR-based receptor bind CD19 and are activated to kill CD19+ cells via perforin/granzyme-mediated cytolysis (and Fas/FasL), with cytokine release.
Autologous adoptive T-cell therapy derived from tumor-draining lymph node T cells, ex vivo activated and expanded with patient-specific neoantigen proteins, then infused intravenously to provide polyclonal, neoantigen-specific T-cell immunity against colorectal cancer.
Autologous T cells from tumor‑draining lymph nodes are activated and expanded ex vivo with patient‑specific neoantigen proteins to enrich polyclonal, neoantigen‑specific TCRs. Following lymphodepletion, the infused cells recognize neoantigen peptides presented on MHC I/II on tumor cells and mediate cytotoxic killing (perforin/granzyme) and cytokine‑driven immune responses, boosting tumor‑specific immunity and overcoming tolerance in colorectal cancer.
YES
DIRECT
TCR recognition of the personalized neoantigen peptide–HLA class II complex on tumor cells activates infused neoantigen-specific T cells, which kill targets via perforin/granzyme release (and potentially Fas–FasL).
Anti-HER2 antibody–drug conjugate delivering a topoisomerase I inhibitor payload to induce DNA damage.
Anti-HER2 antibody–drug conjugate (trastuzumab linked to the topoisomerase I inhibitor deruxtecan). After HER2 binding and internalization, deruxtecan is released to inhibit topoisomerase I, inducing DNA damage, replication arrest, and apoptosis; also elicits ADCC and a bystander killing effect.
YES
DIRECT
HER2-targeted ADC binds HER2 and is internalized; the deruxtecan payload (topoisomerase I inhibitor) is released intracellularly, causing DNA damage and apoptosis; can also trigger ADCC and a bystander effect.