Humanized IgG1 monoclonal antibody targeting the HER2 extracellular dimerization domain; prevents HER2 dimerization—especially HER2/HER3—thereby blocking downstream PI3K/AKT/MAPK signaling to inhibit tumor growth and promote apoptosis; can also mediate ADCC.
Pertuzumab binds HER2, blocks HER2/HER3 signaling to trigger apoptosis, and its IgG1 Fc engages FcγR+ effector cells (e.g., NK cells) to mediate ADCC (±CDC), killing HER2+ cells.
Anti-HER2 IgG1 monoclonal antibody that inhibits HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting HER2 (ERBB2); binds the receptor’s extracellular domain to inhibit HER2 signaling and dimerization (especially HER2/HER3) and engages Fcγ receptors to elicit antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on tumor cells and engages Fc gamma receptors on immune effector cells (e.g., NK cells) to trigger antibody-dependent cellular cytotoxicity (ADCC), killing HER2-expressing cells.
An antibody-drug conjugate (ADC) composed of a humanized anti-HER2 monoclonal antibody linked via a cleavable linker to monomethyl auristatin E (MMAE); binds HER2, is internalized, and releases MMAE to disrupt microtubules and induce tumor cell death, with a bystander killing effect.
Humanized anti-HER2 (ERBB2) monoclonal antibody linked via a cleavable linker to the microtubule-disrupting payload MMAE. After binding HER2 on tumor cells and internalization, the linker is cleaved to release MMAE, which binds tubulin and inhibits microtubule polymerization, causing G2/M arrest and apoptosis; the membrane-permeable payload enables bystander killing of adjacent cells.
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE intracellularly via a cleavable linker; MMAE inhibits microtubule polymerization, causing G2/M arrest and apoptosis (with a membrane-permeable payload enabling bystander killing).
Autologous, humanized anti-CD22 chimeric antigen receptor (CAR) T-cell therapy using a humanized scFv against CD22 linked to CD3ζ signaling and a 4-1BB costimulatory domain to target and eliminate CD22-positive B-lineage malignant cells.
Autologous T cells are lentivirally transduced to express a humanized anti-CD22 CAR with a 4-1BB costimulatory domain and CD3ζ signaling. After infusion, the CAR T cells bind CD22 on B-lineage malignant cells, activate, expand, and mediate cytotoxic killing and cytokine release; 4-1BB supports activation, persistence, and antitumor activity.
Anti-CD22 CAR T cells bind CD22 on target cells and, after CD3zeta signaling with 4-1BB costimulation, kill via perforin/granzyme-mediated cytolysis and death-receptor pathways.
Autologous, humanized anti-CD19 chimeric antigen receptor (CAR) T-cell therapy using a humanized scFv against CD19 linked to CD3ζ signaling and a 4-1BB costimulatory domain to target and eliminate CD19-positive B-lineage malignant cells.
Autologous T cells engineered to express a humanized anti‑CD19 CAR containing CD3ζ signaling and 4‑1BB costimulation. Upon binding CD19 on B‑lineage malignant cells, the CAR activates and co‑stimulates T cells to proliferate, persist, and mediate cytotoxic killing of CD19‑positive tumor cells.
Anti-CD19 CAR T cells bind CD19 on target cells, become activated, and kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis).