Anti-CD47 monoclonal antibody immunotherapy that blocks the CD47–SIRPα "don’t‑eat‑me" signal to promote macrophage-mediated phagocytosis and innate antitumor immunity.
Anti-CD47 monoclonal antibody that blocks the CD47–SIRPα inhibitory ('don’t‑eat‑me') signal on tumor cells, enabling macrophage-mediated phagocytosis (ADCP) and enhancing innate antitumor immunity, with potential downstream priming of adaptive responses.
YES
DIRECT
Blocks the CD47–SIRPα ‘don’t‑eat‑me’ signal and opsonizes CD47+ cells; macrophages engage the antibody Fc via Fcγ receptors and directly phagocytose/kill the target cells (ADCP).
Anti-HER2 antibody–drug conjugate that delivers the microtubule inhibitor MMAE to HER2-expressing tumor cells, causing mitotic arrest and apoptosis.
Disitamab vedotin is an anti‑HER2 monoclonal antibody linked via a cleavable linker to the microtubule inhibitor MMAE. Upon binding HER2 on tumor cells, the ADC is internalized and the linker is proteolytically cleaved in lysosomes to release MMAE, which disrupts tubulin polymerization, causing G2/M mitotic arrest and apoptosis; the membrane‑permeable payload can mediate bystander killing, with potential additional Fc‑mediated effector activity.
YES
DIRECT
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE in lysosomes; MMAE disrupts microtubules, causing G2/M arrest and apoptosis. The membrane-permeable payload can also cause bystander killing; Fc functions may add ADCC.
Anti-HER2 antibody–drug conjugate that delivers the microtubule inhibitor MMAE to HER2-expressing tumor cells, causing mitotic arrest and apoptosis.
Disitamab vedotin is an anti‑HER2 monoclonal antibody linked via a cleavable linker to the microtubule inhibitor MMAE. Upon binding HER2 on tumor cells, the ADC is internalized and the linker is proteolytically cleaved in lysosomes to release MMAE, which disrupts tubulin polymerization, causing G2/M mitotic arrest and apoptosis; the membrane‑permeable payload can mediate bystander killing, with potential additional Fc‑mediated effector activity.
NO
INDIRECT
Disitamab vedotin targets HER2, not beta-tubulin. After HER2-mediated internalization, MMAE is released and inhibits tubulin polymerization, causing G2/M arrest and apoptosis; bystander killing can occur.
Autologous gene-engineered T cells modified ex vivo to express a chimeric antigen receptor targeting CD147, enabling antigen-specific activation and cytotoxic killing of CD147-positive malignant T cells in relapsed/refractory T-cell non-Hodgkin’s lymphoma; administered in a dose-escalation range of 0.1–2.0×10^6 CAR T cells/kg.
Autologous T cells engineered ex vivo to express a chimeric antigen receptor targeting CD147; CAR binding to CD147 activates T cells via CD3ζ and costimulatory signaling, driving antigen-specific cytotoxic killing of CD147-positive malignant T cells.
YES
DIRECT
CD147-targeted CAR T cells recognize CD147 on tumor cells and, upon CAR activation (CD3ζ/costimulatory signaling), kill CD147+ cells via perforin/granzyme-mediated cytolysis and death receptor pathways.
An autologous monocyte-derived dendritic cell vaccine pulsed with Epstein–Barr virus (EBV)-associated antigens. The ex vivo–generated dendritic cells present EBV antigens via MHC I/II to prime and expand EBV-specific CD8+ cytotoxic and CD4+ helper T cells, enhancing IFN-γ production and perforin/granzyme-mediated killing of EBV-positive lymphoma cells.
Autologous monocyte-derived dendritic cells pulsed with EBV antigens present peptides via MHC I/II to prime and expand EBV-specific CD8+ cytotoxic and CD4+ helper T cells, enhancing IFN-gamma production and perforin/granzyme-mediated killing of EBV-positive lymphoma cells.
YES
INDIRECT
Dendritic cell vaccine primes/expands EBV (including LMP1)-specific CD8+ T cells, which recognize LMP1-derived peptides on MHC I of EBV-positive cells and kill them via perforin/granzyme-mediated cytotoxicity.