A humanized monoclonal antibody targeting HER2 used to inhibit HER2 signaling and mediate immune effector functions.
Humanized IgG1 monoclonal antibody targeting HER2 (ERBB2); binds the extracellular domain to inhibit HER2 signaling and receptor dimerization, and engages immune effector cells to induce antibody-dependent cell-mediated cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
After binding HER2, trastuzumab engages Fcγ receptors on immune effector cells to trigger ADCC (primarily NK-cell–mediated; also ADCP/CDC), killing HER2+ cells; signaling blockade may also promote apoptosis.
Chimeric anti-CD20 monoclonal antibody; depletes B cells via ADCC, CDC, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them through antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and induction of apoptosis.
Anti-CD20 antibody binds CD20 on B cells and induces killing via ADCC (FcγR-engaged immune cells) and complement-dependent cytotoxicity (CDC), and can also trigger apoptosis of CD20+ cells.
Human IgG1κ anti-CD38 monoclonal antibody; depletes plasmablasts/plasma cells via ADCC, CDC, apoptosis, and immunomodulation.
Human IgG1κ monoclonal antibody targeting CD38; binds CD38 on plasmablasts/plasma cells and other CD38+ cells, inducing cell death via ADCC, ADCP, and CDC, with additional direct apoptosis and immunomodulatory depletion of CD38+ regulatory immune cells (e.g., Tregs, Bregs, MDSCs).
Anti-CD38 mAb binds CD38 on target cells and induces ADCC, ADCP, and complement-dependent cytotoxicity, with additional direct apoptosis.
An antibody–drug conjugate targeting Nectin-4 (PVRL4); upon internalization it releases a monomethyl auristatin E (MMAE)-type microtubule-disrupting payload, inducing mitotic arrest, tumor cell death, and potentially immunogenic cell death.
Targets Nectin-4 on tumor cells; upon binding and internalization, releases the MMAE payload that inhibits tubulin polymerization, leading to G2/M mitotic arrest, apoptosis, and potential immunogenic cell death.
The ADC binds Nectin-4 on tumor cells, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis (potentially immunogenic cell death).
Autologous gene-modified CAR T-cell therapy engineered to express a chimeric antigen receptor targeting DLL3. CAR engagement of DLL3 on tumor cells induces T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of DLL3-positive cancer cells, independent of native TCR; developed for DLL3-expressing neuroendocrine tumors such as small cell lung cancer and large cell neuroendocrine carcinoma.
Autologous gene-modified T cells expressing a DLL3-specific chimeric antigen receptor. Binding to DLL3 on tumor cells activates the T cells, leading to expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of DLL3-positive cancer cells independent of the native TCR.
CAR-T cells recognize DLL3 via the CAR and, upon activation, kill DLL3-positive cells through perforin/granzyme-mediated cytolysis (with cytokine release).