Autologous gene-modified T cells expressing a chimeric antigen receptor targeting cadherin-17 (CDH17), infused intravenously to mediate targeted cytotoxicity against CDH17-positive tumors after lymphodepletion.
Autologous T cells are engineered to express a chimeric antigen receptor targeting cadherin-17 (CDH17). Upon binding CDH17 on tumor cells, CAR signaling activates T-cell effector functions, leading to proliferation, cytokine release, and targeted cytotoxic killing of CDH17-positive tumors following lymphodepleting conditioning.
Anti-CDH17 CAR-T cells bind CDH17 on target cells, become activated, and kill them via T cell effector mechanisms (perforin/granzyme-mediated apoptosis and death receptor pathways).
Autologous T-cell product expanded ex vivo; provides tumor-reactive lymphocytes that mediate TCR-dependent cytotoxicity as adoptive cell therapy.
Autologous tumor-draining lymph node–derived T cells expanded ex vivo and reinfused to provide tumor-reactive lymphocytes that recognize tumor antigens via native TCRs and kill target cells through perforin/granzyme cytotoxicity and cytokine-mediated immune activation.
Native TCRs on reinfused tumor-reactive T cells recognize the tumor antigen peptide–HLA-DQ complex and kill the presenting cell via perforin/granzyme (and Fas–FasL) cytotoxicity.
CD19-directed CAR-engineered natural killer (NK) cellular immunotherapy; adoptive transfer of CAR+ NK cells to target CD19-positive B-cell malignancies.
Engineered natural killer cells expressing an anti-CD19 chimeric antigen receptor are adoptively transferred to recognize CD19 on malignant B cells and induce targeted cytotoxicity (perforin/granzyme release and cytokine-mediated killing). Lymphodepleting preconditioning (e.g., fludarabine/cyclophosphamide) enhances CAR-NK expansion and persistence.
Anti-CD19 CAR-NK cells bind CD19 on target cells, triggering NK degranulation (perforin/granzyme-mediated lysis) and death receptor/cytokine-dependent apoptosis.
A HER2-targeted antibody–drug conjugate (IgG1 anti-HER2 linked to MMAE) that binds HER2 on tumor cells, is internalized, releases MMAE to inhibit microtubules causing mitotic arrest and apoptosis, and may also trigger ADCC.
HER2-targeted IgG1 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and via a cleavable linker releases MMAE, a microtubule inhibitor, causing mitotic arrest and apoptosis; the IgG1 backbone may also mediate Fc-dependent ADCC.
The ADC binds HER2, is internalized, and the cleavable linker releases MMAE, which disrupts microtubules causing mitotic arrest and apoptosis; the IgG1 Fc can also induce ADCC.
Chimeric IgG1 monoclonal antibody against TNF-α that neutralizes soluble and transmembrane TNF-α, suppressing TNFR1/2→NF-κB signaling, macrophage activation, and Th1/Th17-driven granuloma maintenance.
Chimeric IgG1 monoclonal antibody that binds and neutralizes soluble and transmembrane TNF-alpha, preventing TNFR1/2 engagement and downstream NF-kB signaling, thereby reducing macrophage activation, Th1/Th17-mediated inflammation, and granuloma maintenance.
Infliximab binds transmembrane TNF-α and, via its IgG1 Fc, triggers ADCC and complement-dependent cytotoxicity; tmTNF engagement can also induce reverse-signaling–mediated apoptosis in TNF-expressing cells.