A NECTIN-4–targeted antibody–drug conjugate delivering MMAE, a microtubule inhibitor that causes cell-cycle arrest and apoptosis.
Nectin-4–targeted monoclonal antibody–drug conjugate that binds Nectin-4 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE after linker cleavage, leading to tubulin depolymerization, G2/M cell-cycle arrest, and apoptosis in Nectin-4–expressing cancer cells.
ADC binds Nectin-4 on target cells, is internalized, linker is cleaved to release MMAE, which depolymerizes microtubules causing G2/M arrest and apoptosis of the Nectin-4–expressing cells.
Anti-HER2 antibody–drug conjugate delivering the microtubule inhibitor MMAE to HER2 (ERBB2)-expressing tumor cells, leading to internalization and microtubule disruption.
Disitamab vedotin is an anti-HER2 (ERBB2) antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE via a cleavable linker. Released MMAE disrupts tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander killing of adjacent tumor cells.
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits microtubule polymerization causing G2/M arrest and apoptosis (with possible bystander killing).
Autologous T lymphocytes genetically modified ex vivo (typically via retroviral or lentiviral vectors) to express a chimeric antigen receptor targeting tumor antigens; adoptively transferred for durable in vivo persistence and anti-cancer activity.
Autologous T cells are genetically modified ex vivo (commonly via retroviral or lentiviral vectors) to express a chimeric antigen receptor that binds tumor surface antigens independent of MHC; CAR signaling (CD3ζ with costimulatory domains such as CD28 or 4-1BB) activates T cells to proliferate, persist, release cytokines, and mediate cytotoxic killing of tumor cells.
CAR T cells bind the target antigen via the CAR and directly lyse antigen-expressing cells through perforin/granzyme release and death receptor (e.g., Fas/FasL) pathways.
Autologous T cells genetically engineered ex vivo to express a tumor‑specific T‑cell receptor, enabling antigen-specific recognition and cytotoxicity after adoptive transfer; designed for persistent gene expression.
Autologous T cells are genetically engineered ex vivo to express a tumor-specific T-cell receptor, enabling HLA-restricted recognition of peptide–MHC on tumor cells and TCR-mediated activation that drives cytotoxic killing (perforin/granzyme) and cytokine release; integrated viral vectors support durable TCR expression after adoptive transfer.
Engineered TCR-T cells recognize the tumor antigen peptide–HLA class I complex and, upon TCR engagement, directly kill target cells via perforin/granzyme-mediated cytolysis and death receptor pathways.
A monoclonal antibody immunotherapy targeting MICA/MICB on tumor cells to enhance NKG2D-mediated immune recognition, reduce shedding of soluble MICA/MICB, and engage Fcγ receptors to promote ADCC/ADCP in relapsed/refractory multiple myeloma.
CLN-619 is a human IgG1 monoclonal antibody that binds the alpha3 domain of MICA/MICB on tumor cells, preventing their proteolytic shedding and reducing soluble MICA/MICB. This preserves and enhances NKG2D-mediated recognition by NK cells and cytotoxic T cells, activating antitumor immunity. Its Fc domain engages Fcγ receptors to promote antibody-dependent cell-mediated cytotoxicity and phagocytosis (ADCC/ADCP).
CLN-619 binds MICA on tumor cells and opsonizes them; its Fc engages Fcγ receptors on NK cells/macrophages to trigger ADCC/ADCP. By blocking MICA shedding, it also enhances NKG2D-dependent killing by NK and cytotoxic T cells.