Human IgG1k anti-CD38 monoclonal antibody that depletes CD38-expressing myeloma plasma cells via CDC, ADCC, ADCP, and apoptosis, and modulates CD38+ immunosuppressive cells to reduce free light-chain production.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells, inducing complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), and apoptosis; also depletes CD38+ immunosuppressive cells, thereby reducing free light-chain production and modulating the tumor microenvironment.
Binds CD38 on target cells and triggers complement-dependent cytotoxicity (CDC), NK cell–mediated ADCC, macrophage ADCP, and direct apoptosis upon crosslinking.
IV bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand-driven activation, inhibits PI3K/AKT/mTOR and RAS/RAF/MEK/ERK signaling, promotes receptor internalization/degradation, and induces ADCC/ADCP via Fc engagement; studied in EGFR-amplified glioblastoma.
Bispecific IgG1 monoclonal antibody that binds EGFR and MET extracellular domains to block ligand-driven activation, inhibit downstream PI3K/AKT/mTOR and RAS/RAF/MEK/ERK signaling, promote receptor internalization and degradation, and engage Fcγ receptors to induce ADCC/ADCP by NK cells and macrophages.
Amivantamab binds EGFR on target cells and engages FcγR-expressing effector cells (NK cells, macrophages) to induce ADCC and ADCP, killing EGFR+ cells; it also promotes receptor internalization/degradation.
IV bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand-driven activation, inhibits PI3K/AKT/mTOR and RAS/RAF/MEK/ERK signaling, promotes receptor internalization/degradation, and induces ADCC/ADCP via Fc engagement; studied in EGFR-amplified glioblastoma.
Bispecific IgG1 monoclonal antibody that binds EGFR and MET extracellular domains to block ligand-driven activation, inhibit downstream PI3K/AKT/mTOR and RAS/RAF/MEK/ERK signaling, promote receptor internalization and degradation, and engage Fcγ receptors to induce ADCC/ADCP by NK cells and macrophages.
Amivantamab binds MET on target cells and its IgG1 Fc engages Fcγ receptors on NK cells and macrophages to trigger ADCC and ADCP, resulting in lysis/phagocytosis of MET-expressing cells.
A Nectin-4–directed antibody–drug conjugate (human IgG1 mAb) linked to the microtubule-disrupting payload monomethyl auristatin E (MMAE); delivers MMAE to Nectin-4–expressing tumor cells, disrupting tubulin, causing cell-cycle arrest and apoptosis; exposure to MMAE is associated with peripheral neuropathy.
Nectin-4–directed human IgG1 antibody-drug conjugate; after binding Nectin-4 on tumor cells and internalization, a cleavable linker releases monomethyl auristatin E (MMAE), which inhibits tubulin polymerization, leading to G2/M cell-cycle arrest and apoptosis.
The ADC binds Nectin-4 on target cells, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis.
Personalized cellular immunotherapy using patient-derived tumor-resident T cells (primarily CD8+ and CD4+) expanded ex vivo and reinfused as a single IV infusion (e.g., 2.0×10^7 cells/kg) to recognize tumor/neoantigens via TCR–MHC interactions and mediate cytotoxicity through perforin/granzyme and cytokine release.
Autologous tumor-resident T cells (CD8+/CD4+) expanded ex vivo and reinfused; they recognize patient-specific tumor/neoantigens via native TCR–MHC I/II interactions and mediate cytotoxicity through perforin/granzyme release and cytokine secretion (e.g., IFN-γ, TNF-α), enhancing antitumor immunity within the tumor microenvironment.
Infused TILs recognize TERT peptide–MHC complexes via native TCRs and kill target cells through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis), with supportive cytokine effects.