Patient-derived T cells genetically engineered to express a chimeric antigen receptor targeting CD19 on B-lineage cells; HLA-independent antigen binding triggers CD3ζ/co-stimulatory signaling to activate T cells, leading to proliferation, cytokine secretion, and perforin/granzyme-mediated killing of malignant B cells (with expected on-target B-cell aplasia).
Autologous T cells engineered to express a CD19-specific chimeric antigen receptor; HLA-independent binding to CD19 triggers CD3zeta and co-stimulatory signaling, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated lysis of CD19-positive malignant B cells, with expected on-target B-cell aplasia.
CAR-T cells bind CD19 on target cells, triggering CD3zeta/co-stimulatory signaling and T-cell cytotoxicity (perforin/granzyme release and death-receptor pathways) that lyse CD19-positive cells.
A beta- and gamma-emitting radionuclide used as a radiopharmaceutical label; when conjugated to NY108, it enables SPECT imaging of biodistribution and delivers targeted beta radiation to PSMA-expressing tumor cells.
Lutetium-177, a beta- and gamma-emitting radionuclide, is chelated to the anti-PSMA monoclonal antibody NY108. After binding PSMA on tumor cells and being internalized, it delivers short-range beta radiation that induces DNA damage and tumor cell death, while gamma emissions enable SPECT imaging of biodistribution.
An anti-PSMA antibody chelated to 177Lu binds PSMA and is internalized, delivering short-range beta radiation that induces DNA damage (e.g., double-strand breaks) and kills the PSMA-expressing cells.
Autologous peripheral blood mononuclear cells (primarily T cells) activated ex vivo with IL-2 and OKT3 and coated with OKT3 and elotuzumab to generate bispecific antibody–armed T cells targeting SLAMF7+ multiple myeloma.
Autologous PBMCs (primarily T cells) are activated ex vivo with IL-2/OKT3 and coated with OKT3 (anti‑CD3) plus elotuzumab (anti‑SLAMF7), creating bispecific antibody–armed T cells that bridge CD3 on T cells to SLAMF7 on myeloma cells, forming an immune synapse and redirecting T‑cell cytotoxicity against SLAMF7+ multiple myeloma.
Bispecific antibody–armed autologous T cells are bridged to SLAMF7 on target cells via elotuzumab and to CD3 on T cells via OKT3, forming an immune synapse and inducing T‑cell cytotoxicity (perforin/granzyme-mediated lysis) of SLAMF7+ cells.
Humanized monoclonal antibody targeting SLAMF7/CS1, used to arm T cells by binding SLAMF7 on myeloma cells to facilitate immune synapse formation.
Humanized IgG1 monoclonal antibody targeting SLAMF7/CS1. By binding SLAMF7 on multiple myeloma cells and engaging Fcγ receptors on NK cells, it triggers antibody-dependent cellular cytotoxicity (ADCC) and can co-activate NK cells via SLAMF7 signaling, leading to immune-mediated killing of SLAMF7+ myeloma cells.
Elotuzumab binds SLAMF7 on myeloma cells and its Fc engages Fcγ receptors on NK cells to trigger ADCC, while also co-activating NK cells via SLAMF7 signaling, leading to lysis of SLAMF7+ cells.
HER2-directed antibody–drug conjugate: a humanized anti‑HER2 IgG1 linked to monomethyl auristatin E (MMAE). Binds HER2 on tumor cells, internalizes, and releases MMAE to disrupt microtubules, causing mitotic arrest/apoptosis; may also mediate ADCC and bystander killing.
HER2-targeted antibody-drug conjugate: a humanized anti-HER2 IgG1 linked to the microtubule toxin MMAE. After binding HER2 and internalization, it releases MMAE to inhibit microtubule polymerization, causing mitotic arrest and apoptosis; may also mediate ADCC and bystander killing.
The ADC binds HER2, is internalized, and releases MMAE intracellularly to inhibit microtubules, causing mitotic arrest and apoptosis; it may also trigger ADCC and bystander killing.