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.
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.
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).
An intravenously administered biparatopic anti-5T4 (TPBG) antibody-drug conjugate that binds two epitopes on 5T4 to enhance binding/internalization and delivers an intracellular cytotoxic payload to kill 5T4-expressing tumor cells.
JK06 is a biparatopic anti‑5T4 (TPBG) antibody–drug conjugate that binds two distinct epitopes on 5T4 to enhance binding and internalization, then releases an intracellular cytotoxic payload to kill 5T4‑expressing tumor cells.
Anti-5T4 antibody-drug conjugate binds 5T4, is internalized, and releases an intracellular cytotoxic payload that kills 5T4-expressing cells.
Intravenous antibody–drug conjugate (ado-trastuzumab emtansine, T-DM1) linking trastuzumab to the maytansinoid DM1 via a non-cleavable linker; binds HER2, inhibits signaling, mediates ADCC, and delivers DM1 to disrupt microtubules causing mitotic arrest and apoptosis, including activity in brain metastases.
HER2-targeted monoclonal antibody (trastuzumab) linked via a non-cleavable linker to the maytansinoid DM1. Binds HER2 to inhibit signaling and mediate ADCC; after internalization, DM1 binds tubulin to disrupt microtubules, causing mitotic arrest and apoptosis in HER2-overexpressing tumor cells.
Binds HER2, is internalized, and releases the DM1 payload that disrupts microtubules causing mitotic arrest and apoptosis; Fc engagement can also mediate ADCC against HER2-positive cells.
Oral small-molecule, highly selective HER2 (ERBB2) tyrosine kinase inhibitor with CNS penetration that suppresses downstream PI3K/AKT and MAPK signaling in HER2-driven tumors.
Highly selective HER2 (ERBB2) tyrosine kinase inhibitor that blocks HER2 autophosphorylation and downstream PI3K/AKT and MAPK signaling, inhibiting proliferation and promoting death of HER2-driven tumor cells; has CNS penetration.
Inhibits HER2 kinase activity, blocking autophosphorylation and downstream PI3K/AKT and MAPK signaling, leading to growth arrest and apoptosis of HER2-dependent tumor cells.