An antibody–drug conjugate (RC48) consisting of a humanized anti-HER2 IgG1 linked via a cleavable vedotin linker to monomethyl auristatin E (MMAE), a microtubule-disrupting cytotoxic. It binds HER2 (ERBB2), is internalized, and releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; may also induce ADCC and bystander killing.
Disitamab vedotin is a humanized anti-HER2 IgG1 antibody–drug conjugate (RC48) linked via a cleavable vedotin linker to monomethyl auristatin E (MMAE). It binds HER2 (ERBB2) on tumor cells, is internalized, and releases MMAE intracellularly to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis; it may also induce ADCC and bystander killing.
YES
DIRECT
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE inside the cell to disrupt microtubules, causing G2/M arrest and apoptosis; it may also induce ADCC and bystander killing.
An antibody–drug conjugate (RC48) consisting of a humanized anti-HER2 IgG1 linked via a cleavable vedotin linker to monomethyl auristatin E (MMAE), a microtubule-disrupting cytotoxic. It binds HER2 (ERBB2), is internalized, and releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; may also induce ADCC and bystander killing.
Disitamab vedotin is a humanized anti-HER2 IgG1 antibody–drug conjugate (RC48) linked via a cleavable vedotin linker to monomethyl auristatin E (MMAE). It binds HER2 (ERBB2) on tumor cells, is internalized, and releases MMAE intracellularly to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis; it may also induce ADCC and bystander killing.
NO
INDIRECT
The ADC targets HER2, is internalized, and releases MMAE, which binds beta‑tubulin to block microtubule polymerization, causing G2/M arrest and apoptosis; tubulin expression alone does not make cells targets.
Allogeneic, gene-modified anti-CD20 chimeric antigen receptor T-cell (CAR-T) therapy; donor-derived T cells engineered to target and kill CD20-positive B cells via T-cell activation and cytotoxicity.
Allogeneic donor-derived T cells are genetically engineered to express an anti-CD20 chimeric antigen receptor; upon binding CD20 on malignant B cells, the CAR activates T-cell effector functions (cytokine release and perforin/granzyme-mediated cytotoxicity) to selectively eliminate CD20-positive B cells.
YES
DIRECT
Anti-CD20 CAR-T cells bind CD20 on target cells and induce T-cell cytotoxicity, primarily via perforin/granzyme-mediated apoptosis (with additional Fas/FasL and cytokine-mediated effects).
Anti-GD2 IgG1 monoclonal antibody that binds GD2 on tumor cells to promote ADCC via FcγRIIIa/CD16 and complement-mediated cytotoxicity.
Humanized anti-GD2 IgG1 monoclonal antibody that binds GD2 on tumor cells and recruits immune effectors via its Fc to induce FcγRIIIa/CD16-mediated ADCC and complement-dependent cytotoxicity, resulting in tumor cell lysis.
YES
DIRECT
Anti-GD2 IgG1 binds GD2 on target cells and recruits effector functions via its Fc to trigger NK cell–mediated ADCC (through FcγRIIIa/CD16) and complement-dependent cytotoxicity, leading to lysis of GD2+ cells.
Autologous cellular immunotherapy consisting of patient-derived, tumor-specific T cells (TIL-like) expanded ex vivo via antigen presentation and infused intravenously to recognize leukemia neoantigens/associated antigens via TCR and mediate cytotoxic killing of malignant blasts.
Autologous tumor‑reactive T cells are enriched and expanded ex vivo via antigen presentation and then infused intravenously; they use their endogenous TCRs to recognize leukemia neoantigens/leukemia‑associated antigens in an HLA‑restricted manner and mediate cytotoxic killing of malignant blasts via perforin/granzyme pathways.
YES
DIRECT
Infused autologous T cells use endogenous TCRs to recognize the HLA-presented neoantigen on malignant cells and kill them via perforin/granzyme-mediated cytolysis (and related T cell effector pathways).