Long-acting (LS-engineered) human IgG1 broadly neutralizing monoclonal antibody targeting the HIV-1 Env gp120 CD4-binding site; neutralizes free virions, blocks Env–CD4/coreceptor-mediated entry, and can recruit Fc-mediated effector functions.
LS-engineered human IgG1 broadly neutralizing monoclonal antibody targeting the HIV-1 Env gp120 CD4-binding site; neutralizes free virions and blocks Env–CD4/coreceptor-mediated entry. The Fc domain can recruit effector functions (e.g., ADCC/ADCP) against Env-expressing infected cells, and LS mutations enhance FcRn binding to extend serum half-life.
NO
INDIRECT
The antibody’s Fc binds CD16a on NK cells/macrophages to trigger ADCC/ADCP against HIV Env–expressing infected cells; CD16a-expressing cells are not targeted or killed by the drug.
Long-acting (LS-engineered) human IgG1 broadly neutralizing monoclonal antibody targeting the HIV-1 Env gp120 CD4-binding site; neutralizes free virions, blocks Env–CD4/coreceptor-mediated entry, and can recruit Fc-mediated effector functions.
LS-engineered human IgG1 broadly neutralizing monoclonal antibody targeting the HIV-1 Env gp120 CD4-binding site; neutralizes free virions and blocks Env–CD4/coreceptor-mediated entry. The Fc domain can recruit effector functions (e.g., ADCC/ADCP) against Env-expressing infected cells, and LS mutations enhance FcRn binding to extend serum half-life.
NO
INDIRECT
3BNC117-LS-J binds HIV-1 Env on infected cells; its Fc engages Fcγ receptors (including CD32a) on immune effectors to mediate ADCC/ADCP against Env+ cells. CD32a+ cells are effectors, not targets, and are not killed by the drug.
An influenza virus–vector therapeutic vaccine engineered to present HPV16 E6/E7 oncoprotein antigens to induce HPV-specific cellular immunity (CD8+ and CD4+ T cells). Administered as an initial intracervical dose followed by intramuscular doses, 3 total over 12 weeks.
Influenza viral-vector therapeutic vaccine encoding HPV16 E6/E7 (delNS attenuated). Following administration, host cells express E6/E7, which are presented via MHC I/II to activate HPV16-specific CD8+ cytotoxic and CD4+ helper T cells, leading to immune-mediated elimination of E6/E7-expressing infected or neoplastic cervical cells.
YES
INDIRECT
Vaccination induces HPV16 E6-specific CD8+ T cells that recognize E6 peptides on MHC I of infected/neoplastic cells and kill them via perforin/granzyme-mediated cytolysis (with CD4+ T-cell help).
An influenza virus–vector therapeutic vaccine engineered to present HPV16 E6/E7 oncoprotein antigens to induce HPV-specific cellular immunity (CD8+ and CD4+ T cells). Administered as an initial intracervical dose followed by intramuscular doses, 3 total over 12 weeks.
Influenza viral-vector therapeutic vaccine encoding HPV16 E6/E7 (delNS attenuated). Following administration, host cells express E6/E7, which are presented via MHC I/II to activate HPV16-specific CD8+ cytotoxic and CD4+ helper T cells, leading to immune-mediated elimination of E6/E7-expressing infected or neoplastic cervical cells.
YES
INDIRECT
Therapeutic vaccination induces HPV16 E7–specific CD8+ T cells that recognize E7 peptides on MHC I of tumor/infected cells and kill them via perforin/granzyme (and Fas–FasL) cytotoxicity.
Off-the-shelf, gene-modified T cells from umbilical cord blood expressing chimeric antigen receptors against BCMA (TNFRSF17) and CD19; administered as a single IV infusion to induce T-cell mediated cytotoxicity against malignant plasma and B-lineage cells.
Off‑the‑shelf, umbilical cord blood–derived T cells engineered to express chimeric antigen receptors against BCMA and CD19. Upon binding either antigen on malignant plasma and B‑lineage cells, the CARs trigger T‑cell activation and perforin/granzyme‑mediated cytotoxicity independent of the native TCR, with dual targeting intended to reduce antigen escape.
YES
DIRECT
BCMA-binding CAR on the T cells triggers activation and cytolytic killing of BCMA+ cells via perforin/granzyme release (and death receptor pathways).