An anti-HER2 antibody-drug conjugate (ADC) carrying the microtubule inhibitor MMAE. It binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit microtubule polymerization, causing mitotic arrest and apoptosis; the antibody component may also trigger Fc-mediated ADCC.
HER2-targeted IgG1 antibody-drug conjugate delivering the microtubule inhibitor MMAE. After binding HER2 and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the antibody Fc may also mediate ADCC.
The ADC binds HER2, is internalized, and releases MMAE that inhibits microtubule polymerization, causing G2/M arrest and apoptosis; Fc engagement may also mediate ADCC.
Humanized anti-HER2 monoclonal antibody that blocks HER2 signaling/dimerization and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized monoclonal antibody to HER2 (ERBB2) that binds the extracellular domain, blocks receptor dimerization/signaling to inhibit PI3K/AKT and MAPK pathways, and mediates antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 and opsonizes target cells, engaging Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate ADCC; may also activate complement (CDC).
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.
Mesothelin-specific CAR T cells bind mesothelin on target cells and kill them via T-cell cytotoxic pathways (perforin/granzyme release and death-receptor signaling); IL-21–anti-PD-1 scFv enhances activation/persistence.
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.
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.
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.