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.
YES
DIRECT
HER3-binding IgG engages Fcγ receptors on effector cells to trigger ADCC, killing HER3+ cells; signaling blockade may add antiproliferative/pro-apoptotic effects.
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.
NO
INDIRECT
SIBP-03 binds HER3 on tumor cells; its Fc engages CD16A on NK cells to trigger ADCC against HER3-positive targets. CD16A-expressing cells are effectors, not killed.
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.