Autologous T cells genetically engineered with a humanized anti-CD22 chimeric antigen receptor to target CD22 on B-ALL blasts, triggering CD3ζ-mediated activation, cytokine release, and cytotoxic killing; used sequentially with CD19 CAR T cells to mitigate antigen-loss escape.
Autologous T cells engineered to express a humanized anti-CD22 chimeric antigen receptor redirect T cells to CD22 on B-ALL blasts. CAR engagement triggers CD3ζ signaling (with costimulatory signaling), leading to T-cell activation, cytokine release, proliferation, and perforin/granzyme-mediated cytotoxic killing of CD22+ leukemia cells; used sequentially with CD19 CAR T cells to reduce antigen-loss escape.
YES
DIRECT
CD22 CAR T cells bind CD22 on target cells, triggering CD3ζ/costimulatory signaling and T‑cell cytotoxicity via perforin/granzyme release, inducing apoptosis of CD22+ cells.
An antibody-drug conjugate linking the anti-HER2 monoclonal antibody trastuzumab to the maytansinoid cytotoxin DM1, delivering DM1 to HER2-overexpressing tumor cells after receptor-mediated internalization; inhibits HER2 signaling and mediates ADCC while the released DM1 disrupts microtubules causing mitotic arrest and cell death.
HER2-directed monoclonal antibody trastuzumab linked to the maytansinoid DM1. Trastuzumab binds HER2, inhibiting HER2 signaling and mediating ADCC; after receptor-mediated internalization, DM1 is released to disrupt microtubules, causing mitotic arrest and tumor cell death.
YES
DIRECT
T-DM1 binds HER2, is internalized, and releases DM1 intracellularly to disrupt microtubules, causing mitotic arrest and apoptosis; it can also mediate ADCC via the trastuzumab Fc.
An antibody-drug conjugate linking the anti-HER2 monoclonal antibody trastuzumab to the maytansinoid cytotoxin DM1, delivering DM1 to HER2-overexpressing tumor cells after receptor-mediated internalization; inhibits HER2 signaling and mediates ADCC while the released DM1 disrupts microtubules causing mitotic arrest and cell death.
HER2-directed monoclonal antibody trastuzumab linked to the maytansinoid DM1. Trastuzumab binds HER2, inhibiting HER2 signaling and mediating ADCC; after receptor-mediated internalization, DM1 is released to disrupt microtubules, causing mitotic arrest and tumor cell death.
NO
INDIRECT
T-DM1 targets HER2, is internalized, and releases DM1, which binds beta-tubulin to disrupt microtubules, causing mitotic arrest and cell death. Cells expressing beta-tubulin alone are not selectively killed; only HER2+ cells receive the cytotoxic payload.
A humanized monoclonal antibody that binds HER2/ERBB2 to inhibit HER2 signaling and mediate antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody that binds the extracellular domain of HER2/ERBB2, inhibiting HER2 signaling and tumor cell proliferation, reducing receptor activation, and engaging Fc receptors to mediate antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing cells.
YES
DIRECT
Trastuzumab binds HER2 and its Fc engages Fcγ receptors on NK cells and other effectors to mediate antibody-dependent cellular cytotoxicity (and phagocytosis), killing HER2-expressing cells; signaling blockade contributes but cytotoxicity is via ADCC.
A humanized anti-HER2 monoclonal antibody that binds HER2 domain IV, inhibits signaling, and mediates ADCC.
Humanized monoclonal antibody targeting HER2 that binds domain IV on the HER2 receptor, inhibiting HER2-driven signaling (e.g., PI3K/AKT/MAPK) and preventing receptor activation/shed extracellular domain; its Fc engages immune effector cells via Fcγ receptors to mediate antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
NO
INDIRECT
Trastuzumab binds HER2 on tumor cells; its Fc engages CD16a on NK cells to trigger ADCC, leading NK cells to kill HER2+ targets. CD16a-expressing cells themselves are not killed.