HER2-directed antibody-drug conjugate composed of trastuzumab linked to a topoisomerase I inhibitor (deruxtecan); binds HER2, inhibits HER2 signaling and mediates ADCC, then internalizes to release a topo-I payload that induces DNA damage with a potential bystander effect.
HER2-directed antibody-drug conjugate composed of trastuzumab linked to a topoisomerase I inhibitor (deruxtecan). Trastuzumab binds HER2 to inhibit signaling and mediate ADCC, then the complex is internalized and the payload is released to inhibit topoisomerase I, causing DNA damage and cell death, with potential bystander effect.
YES
DIRECT
The HER2-binding ADC is internalized and releases deruxtecan (topoisomerase I inhibitor), causing DNA damage and apoptosis in HER2+ cells; Fc can also mediate ADCC, with potential bystander killing from the membrane-permeable payload.
HER2-directed antibody-drug conjugate composed of trastuzumab linked to a topoisomerase I inhibitor (deruxtecan); binds HER2, inhibits HER2 signaling and mediates ADCC, then internalizes to release a topo-I payload that induces DNA damage with a potential bystander effect.
HER2-directed antibody-drug conjugate composed of trastuzumab linked to a topoisomerase I inhibitor (deruxtecan). Trastuzumab binds HER2 to inhibit signaling and mediate ADCC, then the complex is internalized and the payload is released to inhibit topoisomerase I, causing DNA damage and cell death, with potential bystander effect.
NO
INDIRECT
T-DXd binds HER2 (not topoisomerase I); after HER2-mediated internalization, the deruxtecan payload inhibits topoisomerase I causing DNA damage and cell death, with possible bystander killing.
Humanized IgG1 anti-HER2 monoclonal antibody that blocks ERBB2/HER2 signaling and mediates ADCC against HER2-amplified tumor cells.
Humanized IgG1 anti-HER2 monoclonal antibody that binds ERBB2/HER2 on tumor cells, inhibits HER2 receptor activation and downstream PI3K/AKT/MAPK signaling, and engages Fc receptors to mediate antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing cells.
YES
DIRECT
Trastuzumab binds HER2 and recruits Fc receptor-bearing immune cells to kill HER2+ cells via ADCC (with possible CDC); HER2 signaling blockade can also promote apoptosis.
CRISPR-edited, healthy-donor T cells engineered with an anti-CD19 STAR receptor inserted at the TRAC locus and knockouts of TRAC, HLA-A/B, CIITA, and PD-1 to target CD19+ B cells while reducing rejection and GvHD.
Allogeneic CRISPR-edited donor T cells engineered with an anti‑CD19 STAR receptor inserted at the TRAC locus redirect TCR–CD3 signaling to recognize and kill CD19+ B cells independent of MHC. Knockout of TRAC removes the endogenous TCR to reduce GvHD; HLA‑A/B and CIITA knockouts lower allorecognition and host rejection by minimizing MHC I/II expression; and PD‑1 knockout enhances resistance to checkpoint-mediated inhibition, improving antitumor activity against CD19+ malignancies.
YES
DIRECT
Engineered allogeneic T cells expressing an anti-CD19 STAR receptor bind CD19 and, via redirected TCR–CD3 signaling, directly kill target cells through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis), MHC-independent.
Personalized cellular immunotherapy using patient-derived tumor-resident T cells (primarily CD8+ and CD4+) expanded ex vivo and reinfused as a single IV infusion (e.g., 2.0×10^7 cells/kg) to recognize tumor/neoantigens via TCR–MHC interactions and mediate cytotoxicity through perforin/granzyme and cytokine release.
Autologous tumor-resident T cells (CD8+/CD4+) expanded ex vivo and reinfused; they recognize patient-specific tumor/neoantigens via native TCR–MHC I/II interactions and mediate cytotoxicity through perforin/granzyme release and cytokine secretion (e.g., IFN-γ, TNF-α), enhancing antitumor immunity within the tumor microenvironment.
YES
DIRECT
Patient-derived TILs recognize MAGE-A1 peptide epitopes presented on MHC via their native TCRs and kill target cells through perforin/granzyme-mediated cytolysis (and Fas–FasL/cytokine-mediated apoptosis).