Autologous adoptive T-cell therapy expanded from tumor-associated lymph nodes; tumor-reactive T cells that recognize tumor antigens via TCRs and mediate cytotoxicity.
Autologous T cells expanded from tumor-associated lymph nodes that retain native TCRs specific for tumor antigens. After infusion, they recognize peptide–MHC on tumor cells via their endogenous TCRs and mediate antitumor activity through cytotoxic granule release and cytokine secretion.
TAL-T cells recognize the tumor peptide–HLA class II complex via their endogenous TCRs and directly lyse the presenting cell through perforin/granzyme-mediated cytotoxicity (and Fas–FasL).
Autologous glypican-3 (GPC3)–targeted chimeric antigen receptor T-cell therapy. Patient T cells are engineered to express a CAR recognizing GPC3 on tumor cells; engagement activates CD3ζ with costimulatory signaling to drive T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of GPC3-positive hepatocellular carcinoma.
Autologous T cells engineered to express a chimeric antigen receptor targeting glypican-3 (GPC3). Antigen engagement activates CD3ζ and costimulatory signaling, driving T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of GPC3-positive tumor cells (e.g., hepatocellular carcinoma).
GPC3-targeted CAR-T cells recognize GPC3 on tumor cells, activating T cells to kill via perforin/granzyme-mediated cytolysis/apoptosis.
A fully human anti-CD20 monoclonal antibody (B-cell–depleting immunotherapy) administered subcutaneously; binds CD20 on B lymphocytes and induces complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, resulting in sustained depletion of circulating CD20+ B cells. Also marketed as Kesimpta.
Ofatumumab is a fully human IgG1 monoclonal antibody that binds the CD20 antigen on B lymphocytes, inducing complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and apoptosis, leading to sustained depletion of circulating CD20+ B cells while sparing stem cells and plasma cells.
Binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC; can also induce apoptosis, leading to lysis/depletion of CD20+ cells.
A humanized anti-CEACAM5 antibody-drug conjugate that binds CEACAM5 on tumor cells, is internalized, and releases the camptothecin-class topoisomerase I inhibitor payload (tocentecan), causing DNA damage and tumor cell death.
Humanized anti-CEACAM5 antibody-drug conjugate that binds CEACAM5 on tumor cells, is internalized, and releases the camptothecin-class topoisomerase I inhibitor tocentecan, causing DNA damage and tumor cell death.
ADC binds CEACAM5 on tumor cells, is internalized, and releases the topoisomerase I inhibitor tocentecan, causing DNA damage and apoptotic cell death.
An anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule toxin MMAE to disrupt microtubules and induce apoptosis; can also trigger antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti‑HER2 monoclonal antibody conjugated to the microtubule toxin MMAE. Upon binding HER2 on tumor cells, the complex is internalized and the linker is cleaved to release MMAE, which inhibits tubulin polymerization leading to G2/M arrest and apoptosis; the antibody Fc can also mediate ADCC.
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE to disrupt microtubules, causing G2/M arrest and apoptosis; its Fc can also trigger ADCC against HER2+ cells.