Defucosylated humanized IgG1 monoclonal antibody targeting CCR4 on malignant skin-homing T cells and regulatory T cells; enhances NK cell–mediated ADCC and reduces CCR4-dependent trafficking.
Defucosylated humanized IgG1 monoclonal antibody targeting CCR4 that blocks CCR4-mediated chemokine signaling and trafficking while inducing enhanced NK cell–mediated ADCC to deplete CCR4+ malignant T cells and regulatory T cells.
YES
DIRECT
Antibody binds CCR4 on target cells; its defucosylated IgG1 Fc engages FcγRIIIa on NK cells to trigger antibody-dependent cellular cytotoxicity (ADCC), leading to lysis/apoptosis of CCR4+ cells.
Allogeneic (off-the-shelf) bispecific CAR-modified natural killer (NK) cell therapy targeting BCMA and GPRC5D for multiple myeloma; single infusion after lymphodepletion to mediate cytotoxicity against malignant plasma cells.
Allogeneic bispecific CAR-engineered NK cells recognizing BCMA and GPRC5D on myeloma cells; CAR engagement activates NK cytotoxicity (perforin/granzyme, cytokines) to induce apoptosis of malignant plasma cells and mitigate antigen escape.
YES
DIRECT
Bispecific CAR-NK cells bind GPRC5D on target cells, triggering NK degranulation (perforin/granzymes) and death ligand pathways to induce apoptosis/lysis.
Anti-CD30 antibody–drug conjugate that delivers monomethyl auristatin E (MMAE); binds CD30, internalizes, releases MMAE to inhibit microtubule polymerization and induce apoptosis.
Anti-CD30 IgG1 antibody–drug conjugate that binds CD30 on tumor cells, is internalized, and releases monomethyl auristatin E (MMAE) via proteolytic cleavage; MMAE binds tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis (with some Fc-mediated ADCC).
YES
DIRECT
Anti-CD30 antibody–drug conjugate binds CD30, is internalized, and releases MMAE intracellularly, inhibiting microtubule polymerization to cause G2/M arrest and apoptosis (with some Fc-mediated ADCC).
Anti-CD30 antibody–drug conjugate that delivers monomethyl auristatin E (MMAE); binds CD30, internalizes, releases MMAE to inhibit microtubule polymerization and induce apoptosis.
Anti-CD30 IgG1 antibody–drug conjugate that binds CD30 on tumor cells, is internalized, and releases monomethyl auristatin E (MMAE) via proteolytic cleavage; MMAE binds tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis (with some Fc-mediated ADCC).
NO
INDIRECT
The ADC binds CD30 (not beta‑tubulin), is internalized, and releases MMAE, which then binds beta‑tubulin to inhibit microtubule polymerization and trigger G2/M arrest and apoptosis. Thus only CD30+ cells are killed; beta‑tubulin expression alone is not sufficient.
FDA-approved autologous anti-CD19 CAR T-cell therapy with 4-1BB costimulation; patient T cells are engineered to express a CAR recognizing CD19, leading to T-cell activation, cytotoxicity, cytokine release, clearance of malignant B cells, and B-cell aplasia.
Autologous T cells are genetically engineered to express an anti‑CD19 chimeric antigen receptor with 4‑1BB costimulation, enabling recognition of CD19 on B-lineage cells and triggering T‑cell activation, proliferation, cytokine release, and cytotoxic killing of malignant B cells, resulting in clearance of CD19+ disease and B‑cell aplasia.
YES
DIRECT
Anti-CD19 CAR T cells recognize CD19 on target B cells and directly induce cytotoxicity via perforin/granzyme-mediated apoptosis and Fas–FasL signaling, with cytokine release contributing.