Autologous tumor-infiltrating lymphocyte (TIL) product expanded ex vivo from a patient’s resected tumor and reinfused to mediate TCR-dependent antitumor cytotoxicity.
Autologous TILs expanded ex vivo are reinfused to recognize patient-specific tumor antigens via their native TCRs (MHC-restricted) and exert cytotoxic killing of tumor cells, supported by cytokine release; typically given after lymphodepletion with IL-2 support to enhance engraftment and activity.
YES
DIRECT
TCR recognition of tumor-associated peptides presented on HLA class II by CD4+ TILs triggers cytotoxic degranulation (perforin/granzymes) and death-receptor pathways, leading to lysis of the presenting cell.
An antibody–drug conjugate (Aidixi, RC48) consisting of a humanized anti‑HER2 IgG1 linked via a cleavable linker to the microtubule toxin MMAE; binds HER2, internalizes, releases MMAE to disrupt microtubules, causing mitotic arrest and apoptosis, with potential bystander effect.
Disitamab vedotin is a humanized anti-HER2 IgG1 antibody–drug conjugate linked via a cleavable linker to MMAE. It binds HER2 on tumor cells, is internalized, and releases MMAE intracellularly to inhibit microtubule polymerization, inducing G2/M arrest and apoptosis, with a potential bystander effect on neighboring HER2-low cells.
YES
DIRECT
ADC binds HER2 on target cells, is internalized, and releases MMAE intracellularly to inhibit microtubule polymerization, causing G2/M arrest and apoptosis (with possible bystander effect).
An antibody–drug conjugate (Aidixi, RC48) consisting of a humanized anti‑HER2 IgG1 linked via a cleavable linker to the microtubule toxin MMAE; binds HER2, internalizes, releases MMAE to disrupt microtubules, causing mitotic arrest and apoptosis, with potential bystander effect.
Disitamab vedotin is a humanized anti-HER2 IgG1 antibody–drug conjugate linked via a cleavable linker to MMAE. It binds HER2 on tumor cells, is internalized, and releases MMAE intracellularly to inhibit microtubule polymerization, inducing G2/M arrest and apoptosis, with a potential bystander effect on neighboring HER2-low cells.
NO
INDIRECT
The ADC binds HER2 on tumor cells, is internalized, and releases MMAE, which binds the vinca site on β‑tubulin to block microtubule polymerization, causing G2/M arrest and apoptosis. β‑tubulin is the intracellular payload target, not the ADC’s binding antigen; cells are killed only after HER2-mediated uptake (with possible bystander effect).
An antibody–drug conjugate consisting of a humanized anti-CD22 monoclonal antibody linked to the cytotoxic agent calicheamicin; it binds CD22 on B-lineage lymphoblasts, is internalized, and releases calicheamicin to induce DNA double-strand breaks and apoptosis.
Humanized anti-CD22 monoclonal antibody linked to calicheamicin; binds CD22 on B-cell lymphoblasts, is internalized, and releases calicheamicin that binds the DNA minor groove, causing double-strand breaks and apoptosis.
YES
DIRECT
ADC binds CD22, is internalized, and releases calicheamicin that binds DNA and induces double‑strand breaks, triggering apoptosis of CD22+ cells.
An antibody–drug conjugate consisting of a humanized anti-CD22 monoclonal antibody linked to the cytotoxic agent calicheamicin; it binds CD22 on B-lineage lymphoblasts, is internalized, and releases calicheamicin to induce DNA double-strand breaks and apoptosis.
Humanized anti-CD22 monoclonal antibody linked to calicheamicin; binds CD22 on B-cell lymphoblasts, is internalized, and releases calicheamicin that binds the DNA minor groove, causing double-strand breaks and apoptosis.
NO
INDIRECT
The ADC binds CD22 on B cells, is internalized, and releases calicheamicin, which binds the DNA minor groove to cause double-strand breaks and apoptosis. DNA (minor groove) is the payload’s intracellular binding site, not the targeting antigen.