Bispecific antibodies that bind CD20 on B cells and CD3 on T cells to redirect T-cell cytotoxicity against CD20-positive malignant B cells.
Bispecific antibodies that bind CD20 on B cells and CD3 on T cells, bringing T cells into close proximity with CD20+ malignant B cells to form an immunologic synapse and activate T-cell cytotoxicity (perforin/granzyme), leading to MHC-independent killing of target B cells.
NO
INDIRECT
CD3ε on T cells is engaged to recruit/activate T cells; these T cells then kill CD20+ B cells via perforin/granzyme. CD3ε+ cells are not directly targeted or killed.
A gene-modified cellular therapy of gamma-delta (γδ) T cells engineered with a BCMA-targeted chimeric antigen receptor (CAR). Administered as a single infusion to treat relapsed/refractory multiple myeloma by recognizing BCMA (TNFRSF17) on malignant plasma cells and mediating MHC-independent cytotoxicity.
Gamma-delta T cells engineered with a BCMA-targeted CAR bind BCMA (TNFRSF17) on myeloma cells, triggering MHC-independent activation and cytotoxicity (perforin/granzyme release, cytokine secretion, proliferation) to eliminate BCMA+ malignant plasma cells.
YES
DIRECT
BCMA-targeted CAR γδ T cells bind BCMA on target cells, become activated, and directly lyse them via perforin/granzyme–mediated cytotoxicity (MHC-independent), with supportive cytokine-mediated effects.
An anti-HER2 antibody–drug conjugate (RC48) that targets HER2 (ERBB2), internalizes, and releases the cytotoxic payload MMAE to disrupt microtubules and induce apoptosis; may also mediate ADCC and bystander killing.
Anti-HER2 antibody–drug conjugate that binds HER2 (ERBB2) on tumor cells, is internalized, and releases the cytotoxic payload MMAE to inhibit microtubule polymerization, causing G2/M arrest and apoptosis; may also mediate ADCC and bystander killing.
YES
DIRECT
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE that inhibits microtubule polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC and bystander killing may also contribute.
An anti-HER2 antibody–drug conjugate (RC48) that targets HER2 (ERBB2), internalizes, and releases the cytotoxic payload MMAE to disrupt microtubules and induce apoptosis; may also mediate ADCC and bystander killing.
Anti-HER2 antibody–drug conjugate that binds HER2 (ERBB2) on tumor cells, is internalized, and releases the cytotoxic payload MMAE to inhibit microtubule polymerization, causing G2/M arrest and apoptosis; may also mediate ADCC and bystander killing.
NO
INDIRECT
The ADC binds HER2 on tumor cells, is internalized, and releases MMAE; MMAE then binds beta-tubulin to inhibit microtubule polymerization, causing mitotic arrest and apoptosis. Beta-tubulin expression itself is not the targeting determinant.
Anti-CD22 antibody-drug conjugate that delivers calicheamicin to CD22-positive blasts, causing DNA double-strand breaks and apoptosis.
Humanized anti-CD22 monoclonal antibody linked to calicheamicin; upon binding CD22 on B-cell blasts, the ADC is internalized and releases calicheamicin that binds the DNA minor groove, causing double-strand breaks and apoptosis.
NO
INDIRECT
The ADC binds CD22 on B cells, is internalized, then releases calicheamicin that binds the DNA minor groove to cause double‑strand breaks and apoptosis. Killing is determined by CD22 expression, not by DNA minor‑groove expression.