Investigational HER3/ERBB3 monoclonal antibody given IV; blocks HER3 to inhibit heregulin (NRG1)-driven activation and HER2/EGFR–HER3 heterodimer signaling, suppressing PI3K/AKT and MAPK pathways; as an IgG mAb may mediate ADCC.
Humanized IgG monoclonal antibody targeting HER3/ERBB3 that blocks heregulin (NRG1)-driven activation and HER2/EGFR–HER3 heterodimer signaling, suppressing downstream PI3K/AKT and MAPK pathways; Fc-mediated ADCC may also contribute to antitumor effects.
HER3-binding IgG engages Fcγ receptors on effector cells to trigger ADCC, killing HER3+ cells; signaling blockade may add antiproliferative/pro-apoptotic effects.
EGFR/HER1 monoclonal antibody given IV; binds EGFR to prevent ligand binding and dimerization, promotes receptor downregulation and ADCC, reducing signaling through RAS/RAF/MEK/ERK and PI3K/AKT pathways.
Chimeric IgG1 monoclonal antibody targeting EGFR (HER1). Binds the extracellular domain to block ligand binding and receptor dimerization, promotes receptor internalization/downregulation, suppresses RAS/RAF/MEK/ERK and PI3K/AKT signaling, and can induce Fc-mediated ADCC against EGFR-expressing tumor cells.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on NK cells/macrophages to trigger ADCC (± complement), leading to lysis of EGFR+ cells; EGFR blockade is mainly antiproliferative.
Autologous T cells engineered ex vivo to express a chimeric antigen receptor that recognizes CD70, activating T-cell cytotoxicity to eliminate CD70-positive lymphoma cells.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor that recognizes CD70 on tumor cells. Binding to CD70 triggers CAR signaling (CD3zeta with costimulatory domains), activating and expanding the T cells to release cytotoxic molecules and cytokines, thereby killing CD70-positive lymphoma cells independent of MHC presentation.
CAR-T cells bind CD70 via the CAR, activating the T cells to kill CD70-positive cells through perforin/granzyme-mediated cytolysis and death receptor signaling.
Anti-CD30 antibody-drug conjugate linked to MMAE; binds CD30 on malignant T cells, is internalized, releases MMAE to disrupt microtubules causing G2/M arrest and apoptosis.
Anti-CD30 monoclonal antibody linked via a protease-cleavable valine-citrulline linker to the cytotoxic payload MMAE. After binding CD30 and internalization by CD30-positive tumor cells, MMAE is released intracellularly and inhibits tubulin polymerization, disrupting microtubules, causing G2/M arrest and apoptosis.
The anti-CD30 ADC binds CD30, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization, disrupting microtubules and causing G2/M arrest and apoptosis of CD30+ cells.
Humanized anti-HER2 monoclonal antibody that blocks HER2 signaling and mediates ADCC.
Humanized monoclonal antibody against HER2 (ERBB2) that binds the receptor’s extracellular domain, blocks HER2 signaling and receptor dimerization, and mediates antibody-dependent cell-mediated cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on tumor cells and its Fc engages immune effectors (e.g., NK cells) via Fcγ receptors to trigger ADCC; it can also activate complement (CDC) and inhibit HER2 signaling, promoting apoptosis.