Single intravenous infusion of haploidentical donor-derived CD3+ T cells (CD4+ and CD8+) enriched for cytomegalovirus- and adenovirus-specificity via antigen stimulation and IFN-γ capture; designed to restore antiviral immunity post-transplant by recognizing viral peptides and killing infected cells.
Allogeneic, haploidentical donor-derived virus-specific T cells (CD4+ and CD8+) enriched by antigen stimulation and IFN-γ capture are adoptively transferred to restore antiviral immunity. Their native TCRs recognize CMV and adenovirus peptides presented by HLA on infected cells, leading to activation, IFN-γ secretion, and cytotoxic killing via perforin/granzyme, thereby clearing infected cells without genetic engineering.
YES
DIRECT
Virus-specific donor T cells recognize adenovirus peptide–HLA complexes via their native TCRs and kill the infected cells through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
An anti-HER2 antibody–drug conjugate (RC48-ADC) consisting of a humanized anti‑HER2 monoclonal antibody linked via a cleavable linker to the microtubule inhibitor monomethyl auristatin E (MMAE); upon HER2 binding and internalization, MMAE is released to disrupt tubulin, causing G2/M arrest and apoptosis, with potential bystander effect.
Humanized anti-HER2 monoclonal antibody linked via a cleavable linker to monomethyl auristatin E (MMAE). After HER2 binding and internalization, the linker is cleaved to release MMAE, which binds tubulin and inhibits microtubule polymerization, causing G2/M cell-cycle arrest and apoptosis; the membrane-permeable payload can produce a bystander effect.
YES
DIRECT
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits tubulin/microtubule polymerization, causing G2/M arrest and apoptosis (with potential bystander killing).
An anti-HER2 antibody–drug conjugate (RC48-ADC) consisting of a humanized anti‑HER2 monoclonal antibody linked via a cleavable linker to the microtubule inhibitor monomethyl auristatin E (MMAE); upon HER2 binding and internalization, MMAE is released to disrupt tubulin, causing G2/M arrest and apoptosis, with potential bystander effect.
Humanized anti-HER2 monoclonal antibody linked via a cleavable linker to monomethyl auristatin E (MMAE). After HER2 binding and internalization, the linker is cleaved to release MMAE, which binds tubulin and inhibits microtubule polymerization, causing G2/M cell-cycle arrest and apoptosis; the membrane-permeable payload can produce a bystander effect.
NO
INDIRECT
Disitamab vedotin targets HER2 on the cell surface; after internalization, MMAE is released and binds beta‑tubulin to disrupt microtubules and induce apoptosis (with a bystander effect). Expression of beta‑tubulin alone does not make cells directly targeted or killed by the drug.
In vivo gene therapy delivered by viral vector to transduce patient immune cells to express an anti-CD19 CAR-like receptor, activating T-cell signaling to kill CD19+ B cells; administered IV or via splenic artery/lymph node.
Viral vector delivered in vivo transduces the patient's T cells to express an anti-CD19 CAR-like receptor. Upon binding CD19 on B cells, the engineered T cells activate CAR signaling, expand, and kill CD19-positive malignant B cells, resulting in on-target B-cell depletion.
YES
DIRECT
Engineered anti-CD19 CAR T cells bind CD19 on B cells and induce cytolysis via perforin/granzyme and apoptosis signaling, depleting CD19+ cells.
An oral, bacteria-based personalized DNA cancer vaccine encoding patient-specific neoantigens; delivers neoantigen DNA to antigen-presenting cells to drive MHC I/II presentation and expand neoantigen-specific CD8+/CD4+ T cells.
An oral, live-attenuated Salmonella (Ty21a) vector delivering plasmid DNA encoding patient-specific tumor neoantigens to antigen-presenting cells in the gut-associated lymphoid tissue, leading to intracellular expression and MHC I/II presentation of the neoantigens and expansion/activation of neoantigen-specific CD8+ and CD4+ T cells for anti-tumor immunity.
YES
INDIRECT
Vaccination expands neoantigen-specific CD8+ T cells that recognize the neoantigen peptide–MHC I on tumor cells and kill them via perforin/granzyme cytolysis and Fas–FasL apoptosis.