Autologous T cells genetically engineered with a murine-derived anti-CD19 chimeric antigen receptor to target CD19 on B-ALL blasts, triggering CD3ζ-mediated activation, cytokine release, and cytotoxic killing; induces B-cell aplasia.
Autologous T cells genetically engineered to express a murine-derived anti-CD19 chimeric antigen receptor bind CD19 on B-cell leukemia cells. CAR engagement triggers CD3zeta-mediated signaling (with costimulation), activating T cells to proliferate, release cytokines, and exert cytotoxic killing, leading to depletion of CD19+ B cells (B-cell aplasia).
CD19 CAR T cells bind CD19 on target cells; CAR activation triggers T‑cell cytotoxicity via perforin/granzyme degranulation and death‑receptor (e.g., Fas/FasL) pathways, killing CD19+ cells.
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.
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.
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.
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.
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 HER2-directed antibody–drug conjugate composed of a humanized anti-HER2 IgG1 (disitamab) linked to the microtubule inhibitor monomethyl auristatin E (MMAE, vedotin). After binding HER2 on tumor cells and internalization, MMAE is released to disrupt microtubules, inducing G2/M arrest and apoptosis, with potential bystander effect and Fc-mediated ADCC.
Humanized anti-HER2 IgG1 (disitamab) linked to the microtubule inhibitor MMAE (vedotin). After binding HER2 on tumor cells and internalization, the linker is cleaved to release MMAE, which disrupts microtubules, causing G2/M arrest and apoptosis; membrane-permeable MMAE can exert a bystander effect, and the IgG1 Fc may mediate ADCC.
The ADC binds HER2, is internalized, and releases MMAE intracellularly to disrupt microtubules, causing G2/M arrest and apoptosis; additional bystander killing and Fc-mediated ADCC may contribute.