Subcutaneous CD20xCD3 T-cell–engaging bispecific monoclonal antibody that bridges CD20 on malignant B cells and CD3 on T cells to redirect cytotoxic T cells and deplete B cells.
Humanized bispecific monoclonal antibody that binds CD20 on B cells and CD3 on T cells to crosslink them, activate cytotoxic T cells, and drive targeted killing and depletion of CD20-expressing malignant B cells.
NO
INDIRECT
Mosunetuzumab binds CD3 on T cells to recruit/activate them against CD20+ B cells; the T cells (CD3ε+) are effectors, not targets, and they kill CD20-expressing cells via perforin/granzyme-mediated cytotoxicity.
Human IgG1 broadly neutralizing monoclonal antibody targeting the HIV-1 Env CD4-binding site; LS modification extends half-life; mediates neutralization and Fc effector functions.
Broadly neutralizing human IgG1 antibody that binds the HIV-1 Env CD4-binding site to block viral attachment and entry, neutralizing circulating virions; Fc region mediates effector functions (e.g., ADCC/ADCP, complement) and contains LS (M428L/N434S) mutation to enhance FcRn binding and extend serum half-life.
NO
INDIRECT
No killing via FcRn. The LS-modified Fc binds FcRn in endosomes to enhance recycling and half-life; cytotoxic functions (neutralization, ADCC/CDC) act against HIV-1 Env on virions/infected cells, not FcRn-expressing cells.
Human IgG1 broadly neutralizing monoclonal antibody targeting the HIV-1 Env CD4-binding site; LS modification extends half-life; mediates neutralization and Fc effector functions.
Broadly neutralizing human IgG1 antibody that binds the HIV-1 Env CD4-binding site to block viral attachment and entry, neutralizing circulating virions; Fc region mediates effector functions (e.g., ADCC/ADCP, complement) and contains LS (M428L/N434S) mutation to enhance FcRn binding and extend serum half-life.
NO
INDIRECT
The antibody’s Fc binds CD16A on NK cells to trigger ADCC against HIV Env–coated/infected cells; CD16A-expressing cells themselves are not targeted or killed.
Autologous, gene-modified T cells engineered to express a bispecific chimeric antigen receptor targeting BCMA (TNFRSF17) and GPRC5D on myeloma cells; CAR engagement triggers CD3ζ/costimulatory signaling to drive T-cell proliferation, cytokine release, and cytotoxic killing, aiming to reduce antigen escape and tumor heterogeneity.
Autologous T cells are engineered to express a bispecific CAR that recognizes BCMA and GPRC5D on myeloma cells. Antigen binding activates CD3ζ and costimulatory signaling, driving T‑cell proliferation, cytokine release, and cytotoxic killing of target cells, with dual targeting intended to limit antigen escape and address tumor heterogeneity.
YES
DIRECT
Bispecific CAR T cells bind BCMA on target cells, triggering CD3ζ/costimulatory signaling and T‑cell activation, leading to perforin/granzyme- and death receptor–mediated killing of BCMA+ cells.
Autologous, gene-modified T cells engineered to express a bispecific chimeric antigen receptor targeting BCMA (TNFRSF17) and GPRC5D on myeloma cells; CAR engagement triggers CD3ζ/costimulatory signaling to drive T-cell proliferation, cytokine release, and cytotoxic killing, aiming to reduce antigen escape and tumor heterogeneity.
Autologous T cells are engineered to express a bispecific CAR that recognizes BCMA and GPRC5D on myeloma cells. Antigen binding activates CD3ζ and costimulatory signaling, driving T‑cell proliferation, cytokine release, and cytotoxic killing of target cells, with dual targeting intended to limit antigen escape and address tumor heterogeneity.
YES
DIRECT
CAR-T cells bind GPRC5D on target cells, activating CD3ζ/costimulatory signaling and degranulation to kill via perforin/granzyme-mediated apoptosis (with additional Fas–FasL/cytokine effects).