Anti-CD20 monoclonal antibody intended to deplete CD20-positive B cells and lessen autoimmune-mediated platelet destruction.
Anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, reducing autoantibody production and immune-mediated platelet destruction.
YES
DIRECT
Anti-CD20 antibody binds CD20 on B cells and induces killing via Fc-mediated ADCC, complement-dependent cytotoxicity, and direct apoptotic signaling, depleting CD20+ cells.
Autologous, gene-modified anti-CD19 CAR T-cell therapy (axi-cel) that expresses a CD19-specific CAR with CD28 costimulatory and CD3ζ signaling domains to recognize and kill CD19+ B cells.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor with CD28 costimulatory and CD3 zeta signaling domains. Upon binding CD19 on B cells, the CAR T cells activate, expand, release cytotoxic granules and cytokines, and kill CD19+ malignant (and normal) B cells.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on B cells, activate, and kill via T-cell cytotoxic pathways (perforin/granzyme-mediated lysis and apoptosis, +/- Fas-FasL).
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 CD8+ T cells that recognize tumor neoantigen peptides presented on HLA class I (e.g., HLA-A) and kill those cells via perforin/granzyme; HLA-A itself is not the cytotoxic target.
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 CD8+ T cells that recognize tumor neoantigen peptides presented on HLA class I (e.g., HLA‑B) and kill those tumor cells via CTL-mediated lysis (perforin/granzyme, Fas/FasL). HLA‑B expression alone is not the cytotoxic target.
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 CD8+ T cells that recognize tumor cells presenting the mutated peptide in HLA class I (possibly HLA-C) and kill them via perforin/granzyme (and Fas–FasL) pathways; HLA-C alone is not the cytotoxic target.