Autologous, second-generation chimeric antigen receptor T cells engineered to recognize mesothelin on tumor cells and to secrete an IL-21–anti-PD-1 scFv fusion protein for localized cytokine support and checkpoint blockade, enhancing T-cell activation, proliferation, persistence, and cytotoxicity.
Autologous second-generation CAR T cells engineered to recognize mesothelin on tumor cells; CAR engagement (CD3ζ plus costimulatory signaling) activates T-cell cytotoxicity against mesothelin-positive cells, while secretion of an IL-21–anti-PD-1 scFv provides local IL-21 support and PD-1 checkpoint blockade to boost activation, proliferation, persistence, and resistance to exhaustion in the tumor microenvironment.
NO
INDIRECT
The CAR T cells kill mesothelin-positive tumor cells via T-cell cytotoxicity (perforin/granzyme, Fas/FasL) after CAR engagement. The secreted IL-21–anti-PD-1 scFv binds IL-21R on immune cells to enhance T-cell function but does not target IL-21R-expressing cells for killing.
Autologous gene-modified T lymphocytes expressing a chimeric antigen receptor targeting GPRC5D; binding to GPRC5D on myeloma cells triggers T-cell activation, expansion, and cytotoxic killing. Administered after lymphodepleting chemotherapy in relapsed/refractory multiple myeloma.
Autologous T cells are engineered to express a chimeric antigen receptor that recognizes GPRC5D on myeloma cells. CAR engagement activates T‑cell signaling, leading to expansion and targeted cytotoxicity (perforin/granzyme release and cytokine-mediated killing) of GPRC5D‑positive malignant plasma cells following lymphodepleting chemotherapy.
YES
DIRECT
CAR-T cells bind GPRC5D and directly kill target cells via perforin/granzyme-mediated cytolysis (with cytokine/Fas–FasL apoptosis).
Antibody–drug conjugate (IgG1 anti-BCMA) linked to monomethyl auristatin F (MMAF). It binds BCMA on malignant plasma cells, is internalized, and releases MMAF to inhibit tubulin polymerization and induce apoptosis; Fc-mediated ADCC/ADCP may also contribute.
Afucosylated anti-BCMA IgG1 antibody–drug conjugate linked to monomethyl auristatin F (MMAF). Binds BCMA on malignant plasma cells, is internalized, and releases MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; Fc effector functions (ADCC/ADCP) also contribute.
YES
DIRECT
The anti-BCMA ADC binds BCMA, is internalized, and releases MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; its afucosylated Fc also mediates ADCC/ADCP against BCMA+ cells.
Antibody–drug conjugate (IgG1 anti-BCMA) linked to monomethyl auristatin F (MMAF). It binds BCMA on malignant plasma cells, is internalized, and releases MMAF to inhibit tubulin polymerization and induce apoptosis; Fc-mediated ADCC/ADCP may also contribute.
Afucosylated anti-BCMA IgG1 antibody–drug conjugate linked to monomethyl auristatin F (MMAF). Binds BCMA on malignant plasma cells, is internalized, and releases MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; Fc effector functions (ADCC/ADCP) also contribute.
NO
INDIRECT
The ADC binds BCMA (not tubulin), is internalized, and releases MMAF, which inhibits beta‑tubulin polymerization to cause G2/M arrest and apoptosis; Fc-mediated ADCC/ADCP may also contribute.
A subcutaneous, full-length humanized bispecific IgG1 antibody (T-cell–redirecting biologic) that binds CD20 on B cells and CD3 on T cells, bringing T cells into contact with malignant B cells to trigger TCR/CD3 activation, immune synapse formation, cytokine release, and perforin/granzyme-mediated cytotoxicity; depletes CD20+ B cells. Step-up dosing: 5 mg C1D1; 45 mg C1D8 and C1D15; then 45 mg on Day 1 of Cycles 2–8 (21-day cycles).
Humanized bispecific IgG1 antibody that binds CD20 on B cells and CD3 on T cells to physically redirect and activate T cells against CD20+ malignant B cells, inducing immune synapse formation, cytokine release, and perforin/granzyme-mediated cytotoxicity leading to B-cell depletion.
YES
DIRECT
T-cell redirection to CD20+ cells via CD3 engagement forms an immune synapse, leading to perforin/granzyme-mediated killing of the target B cells.