An anti-CD30 antibody–drug conjugate that delivers MMAE to CD30-positive Hodgkin/Reed–Sternberg cells, causing microtubule disruption and apoptosis.
Anti-CD30 monoclonal antibody conjugated via a protease-cleavable valine-citrulline linker to monomethyl auristatin E (MMAE). After binding CD30 on tumor cells and internalization, the linker is cleaved to release MMAE, which binds tubulin and inhibits microtubule polymerization, leading to G2/M arrest and apoptosis; the linker is plasma-stable, enhancing selectivity for CD30-positive cells.
YES
DIRECT
The ADC binds CD30, is internalized, and releases MMAE via protease cleavage; MMAE disrupts microtubules (tubulin polymerization), causing G2/M arrest and apoptosis of CD30-positive cells.
An anti-CD30 antibody–drug conjugate that delivers MMAE to CD30-positive Hodgkin/Reed–Sternberg cells, causing microtubule disruption and apoptosis.
Anti-CD30 monoclonal antibody conjugated via a protease-cleavable valine-citrulline linker to monomethyl auristatin E (MMAE). After binding CD30 on tumor cells and internalization, the linker is cleaved to release MMAE, which binds tubulin and inhibits microtubule polymerization, leading to G2/M arrest and apoptosis; the linker is plasma-stable, enhancing selectivity for CD30-positive cells.
NO
INDIRECT
Brentuximab vedotin binds CD30 on target cells, is internalized, and releases MMAE, which binds beta-tubulin to inhibit microtubule polymerization, leading to G2/M arrest and apoptosis; beta-tubulin expression alone is not selectively targeted.
Chimeric anti-EGFR monoclonal antibody that inhibits EGFR ligand binding and receptor activation and can engage immune effector functions (ADCC).
Chimeric anti-EGFR monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor activation/dimerization to inhibit downstream RAS-RAF-MEK-ERK signaling and tumor cell proliferation; also mediates immune effector functions via ADCC.
YES
DIRECT
Cetuximab binds EGFR on tumor cells and its Fc engages FcγR-bearing effector cells to mediate ADCC (and can activate complement for CDC), causing lysis/apoptosis; EGFR blockade is antiproliferative.
Type II glycoengineered anti-CD20 monoclonal antibody with enhanced ADCC and direct cell death activity, used to deplete CD20+ B cells.
A type II glycoengineered humanized IgG1 anti-CD20 monoclonal antibody that binds CD20 on B cells and, through enhanced affinity for Fc gamma RIIIa (CD16), mediates strong antibody-dependent cellular cytotoxicity and induces direct, caspase-independent cell death, leading to depletion of CD20-positive B cells (with relatively less complement activation than type I anti-CD20 mAbs).
YES
DIRECT
Binds CD20 on B cells and recruits FcγRIIIa+ effector cells (e.g., NK cells) to trigger strong ADCC; also induces direct, caspase‑independent cell death (with relatively less complement-mediated lysis).
Autologous genetically modified T cells engineered ex vivo to express a chimeric antigen receptor targeting a myeloma-associated surface antigen; administered as a CAR T cell infusion to drive antigen-dependent T-cell activation, proliferation, cytokine release, and cytotoxic killing of malignant plasma cells.
Autologous T cells are genetically engineered ex vivo to express a chimeric antigen receptor recognizing a myeloma-associated surface antigen. Upon antigen binding, CAR signaling (CD3ζ with costimulation) drives antigen-dependent activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant plasma cells in an MHC-independent manner, with in vivo expansion and persistence enabling sustained antitumor activity.
YES
DIRECT
CAR T cells bind the myeloma-associated surface antigen and, upon CAR signaling, kill target cells via perforin/granzyme-mediated cytotoxicity (and death receptor pathways) in an MHC-independent manner.