An HPV-16–targeted therapeutic mRNA vaccine delivered intramuscularly that encodes HPV-16 antigens to drive intracellular antigen expression, dendritic cell activation, MHC I/II presentation, and robust HPV-16–specific CD8+ and CD4+ T-cell immunity to eliminate HPV-16–infected dysplastic and cancer cells.
Intramuscular mRNA delivery encoding HPV-16 antigens leads to in situ antigen expression in host antigen-presenting cells, dendritic cell activation, and MHC I/II presentation, inducing robust HPV-16–specific CD8+ cytotoxic and CD4+ helper T-cell responses that eliminate HPV-16–infected dysplastic and cancer cells.
YES
INDIRECT
The mRNA vaccine induces HPV16-specific CD8+ T cells that recognize E7-derived peptides on MHC I of infected/cancer cells and kill them via perforin/granzyme-mediated apoptosis (with CD4+ T-cell help).
A HER2-targeted antibody–drug conjugate composed of a humanized anti-HER2 monoclonal antibody linked via an enzyme-cleavable linker to a topoisomerase I inhibitor payload; upon HER2 binding and internalization, linker cleavage releases the payload to inhibit topoisomerase I, causing DNA damage and tumor cell death.
Humanized anti-HER2 monoclonal antibody linked via an enzyme-cleavable linker to a topoisomerase I inhibitor. After binding HER2 on tumor cells and internalization, the linker is cleaved to release the payload, which inhibits topoisomerase I, inducing DNA damage and tumor cell death with HER2-targeted delivery.
YES
DIRECT
The ADC binds HER2 on target cells, is internalized, and releases a topoisomerase I inhibitor that causes DNA damage, leading to apoptosis and cell death.
A HER2-targeted antibody–drug conjugate composed of a humanized anti-HER2 monoclonal antibody linked via an enzyme-cleavable linker to a topoisomerase I inhibitor payload; upon HER2 binding and internalization, linker cleavage releases the payload to inhibit topoisomerase I, causing DNA damage and tumor cell death.
Humanized anti-HER2 monoclonal antibody linked via an enzyme-cleavable linker to a topoisomerase I inhibitor. After binding HER2 on tumor cells and internalization, the linker is cleaved to release the payload, which inhibits topoisomerase I, inducing DNA damage and tumor cell death with HER2-targeted delivery.
NO
INDIRECT
The ADC targets HER2, is internalized, and releases a topoisomerase I–inhibiting payload that causes DNA damage and kills HER2-positive cells; topoisomerase I is only the intracellular enzymatic target of the payload, not the cytotoxic targeting antigen.
Autologous CD19-directed chimeric antigen receptor (CAR) T-cell therapy in which a patient’s T cells are engineered ex vivo to express an anti-CD19 CAR; upon infusion, the cells deplete CD19+ B cells and plasmablasts to suppress autoreactive B-cell activity and autoantibody production in SLE/lupus nephritis.
Autologous T cells are engineered ex vivo to express an anti‑CD19 chimeric antigen receptor. After infusion, CAR engagement with CD19 on B cells and plasmablasts activates the T cells to kill CD19+ B‑lineage cells, leading to profound B‑cell depletion and suppression of autoreactive B‑cell activity and autoantibody production in SLE/lupus nephritis.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on B-lineage cells and kill them via T-cell effector mechanisms (perforin/granzyme-mediated apoptosis and Fas–FasL).
Humanized anti-EpCAM monoclonal antibody administered by weekly IV infusion (0.1–15 mg/kg) in dose escalation for advanced solid tumors; binds EpCAM on tumor cells to inhibit EpCAM-mediated adhesion/signaling and engage Fc-dependent immune cytotoxicity (e.g., ADCC/CDC).
Humanized monoclonal antibody that binds EpCAM (CD326) on tumor cells, blocks EpCAM-mediated adhesion/signaling, and triggers Fc-dependent immune effector functions (ADCC/CDC) to kill EpCAM-positive cancer cells.
YES
DIRECT
Anti-EpCAM mAb binds EpCAM on tumor cells and engages immune effectors via its Fc to mediate ADCC and complement activation (CDC), leading to lysis of EpCAM-positive cells.