Autologous, gene-modified T cells engineered to express an anti-CD7 chimeric antigen receptor; administered as a single infusion of 2×10^8 CAR+ T cells to target CD7-expressing malignant cells in r/r T-ALL/LBL and CD7-positive AML. Mechanism involves CAR-mediated CD3ζ/costimulatory signaling leading to MHC-independent activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxicity; expected on-target depletion of normal CD7+ T/NK cells (T-cell aplasia).
Autologous T cells engineered to express an anti‑CD7 chimeric antigen receptor. CAR binding to CD7 triggers CD3ζ and costimulatory signaling, driving MHC‑independent T‑cell activation, expansion, cytokine release, and perforin/granzyme‑mediated killing of CD7‑positive malignant cells (r/r T‑ALL/LBL and CD7+ AML), with expected on‑target depletion of normal CD7+ T/NK cells (T‑cell aplasia).
Anti-CD7 CAR-T cells bind CD7 and, upon CAR activation, directly kill CD7-positive cells via MHC-independent perforin/granzyme-mediated cytotoxicity (and associated death-receptor pathways).
Humanized anti-EGFR monoclonal antibody that blocks EGFR ligand binding and downstream signaling (RAS/RAF/MEK/ERK; PI3K/AKT) and may induce ADCC.
Humanized anti-EGFR monoclonal antibody that binds EGFR, blocks ligand binding and downstream signaling (RAS/RAF/MEK/ERK and PI3K/AKT), inhibiting tumor cell proliferation and survival; may also induce antibody-dependent cellular cytotoxicity (ADCC).
Anti-EGFR IgG1 binding engages Fcγ receptor–bearing immune cells (e.g., NK cells) to mediate ADCC; EGFR signaling blockade can also promote apoptosis.
Humanized IgG1 monoclonal antibody that binds HER2/ERBB2 domain IV, blocks HER2 signaling and receptor activation/dimerization, and promotes immune-mediated tumor cell killing via antibody‑dependent cellular cytotoxicity (ADCC).
Trastuzumab binds HER2 domain IV on tumor cells and engages FcγR-bearing immune effectors (e.g., NK cells) to induce antibody-dependent cellular cytotoxicity (ADCC), leading to lysis/apoptosis of HER2+ cells; signaling blockade is mainly cytostatic.
Humanized monoclonal antibody that binds HER2 extracellular domain II, blocking HER2–HER3 dimerization and downstream PI3K–AKT/MAPK signaling to inhibit tumor cell growth and promote apoptosis; also mediates ADCC.
Pertuzumab binds HER2 and recruits Fcγ receptor–bearing immune cells to mediate ADCC against HER2+ cells; blockade of HER2–HER3 signaling can also induce apoptosis.
HER2-targeted antibody–drug conjugate of trastuzumab linked to the maytansinoid DM1 microtubule inhibitor; delivers cytotoxic payload to HER2-overexpressing cells while retaining trastuzumab activity.
Ado-trastuzumab emtansine (T-DM1) is a HER2-targeted antibody–drug conjugate in which trastuzumab is linked to the microtubule inhibitor DM1. It binds HER2 on tumor cells, is internalized, and releases DM1 to disrupt microtubules and induce cell death, while trastuzumab concurrently inhibits HER2 signaling and mediates ADCC.
T-DM1 binds HER2, is internalized, and releases the DM1 payload that inhibits microtubules, causing mitotic arrest and apoptosis; the trastuzumab component can also trigger ADCC.