A patient-specific therapeutic cancer vaccine composed of mutated peptide epitopes derived from the patient’s tumor (selected by exome/RNA sequencing and HLA typing). Administered subcutaneously, the peptides are taken up by antigen-presenting cells and presented on HLA class I/II to prime and boost neoantigen-specific CD8+ cytotoxic and CD4+ helper T-cell responses for tumor-specific killing and immune memory.
Patient-specific mutated peptide epitopes from the tumor are administered subcutaneously and taken up by antigen‑presenting cells. The peptides are presented on HLA class I and II to prime and expand neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, driving tumor-specific recognition and killing and establishing immunologic memory.
NO
INDIRECT
The vaccine primes T cells against patient-specific neoantigen peptides; cytotoxic T cells kill cells presenting those neoantigen peptides on HLA (mainly class I) via perforin/granzyme. HLA-DRA (MHC II) itself is not a target, so cells expressing HLA-DRA are not killed for expressing it.
A patient-specific therapeutic cancer vaccine composed of mutated peptide epitopes derived from the patient’s tumor (selected by exome/RNA sequencing and HLA typing). Administered subcutaneously, the peptides are taken up by antigen-presenting cells and presented on HLA class I/II to prime and boost neoantigen-specific CD8+ cytotoxic and CD4+ helper T-cell responses for tumor-specific killing and immune memory.
Patient-specific mutated peptide epitopes from the tumor are administered subcutaneously and taken up by antigen‑presenting cells. The peptides are presented on HLA class I and II to prime and expand neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, driving tumor-specific recognition and killing and establishing immunologic memory.
NO
INDIRECT
The vaccine primes neoantigen-specific T cells; CD8+ T cells kill tumor cells presenting neoantigen peptides on HLA class I, with CD4+ help via HLA-DRB1 on APCs. HLA-DRB1-expressing cells are not directly targeted or killed.
A patient-specific therapeutic cancer vaccine composed of mutated peptide epitopes derived from the patient’s tumor (selected by exome/RNA sequencing and HLA typing). Administered subcutaneously, the peptides are taken up by antigen-presenting cells and presented on HLA class I/II to prime and boost neoantigen-specific CD8+ cytotoxic and CD4+ helper T-cell responses for tumor-specific killing and immune memory.
Patient-specific mutated peptide epitopes from the tumor are administered subcutaneously and taken up by antigen‑presenting cells. The peptides are presented on HLA class I and II to prime and expand neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, driving tumor-specific recognition and killing and establishing immunologic memory.
NO
INDIRECT
The vaccine primes TCRαβ+ T cells via APC-presented neoantigen peptides; the activated T cells then kill tumor cells displaying those neoantigens. TCRαβ-expressing cells themselves are not targeted or killed by the drug.
An autologous CAR T‑cell therapy made from a patient’s T cells engineered ex vivo to express a chimeric antigen receptor recognizing a glioblastoma-associated surface antigen. Upon antigen engagement, CAR signaling activates the T cells, leading to cytokine release and perforin/granzyme-mediated cytotoxicity to lyse tumor cells. Dosed as multiple infusions (starting around 5×10^4 CAR+ T cells) with safety/PK-guided escalation.
Autologous T cells engineered ex vivo to express a CAR that recognizes a glioblastoma-associated surface antigen. Upon antigen engagement, CAR signaling activates the T cells, inducing cytokine release, expansion, and perforin/granzyme-mediated cytotoxic lysis of the tumor cells.
NO
INDIRECT
CAR T cells kill only cells expressing the CAR-recognized glioblastoma antigen via perforin/granzyme after CAR engagement; this unknown target is not established as that antigen.
HER2-directed antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and delivers a cytotoxic payload.
Trastuzumab-based HER2-directed ADC (trastuzumab rezetecan) that binds HER2 on tumor cells, is internalized, and upon linker cleavage releases a camptothecin-derived topoisomerase I inhibitor, inducing DNA breaks, apoptosis, and growth inhibition in HER2-expressing tumors.
YES
DIRECT
HER2-binding ADC is internalized into HER2+ cells; linker cleavage releases a camptothecin-derived topoisomerase I inhibitor that causes DNA breaks, leading to apoptosis and growth inhibition.