Anti-CD20 monoclonal antibody that mediates B-cell depletion via CDC, ADCC, and apoptosis.
Anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and kills via complement-dependent cytotoxicity (MAC lysis), antibody-dependent cellular cytotoxicity by FcγR-bearing effector cells, and direct apoptosis upon crosslinking.
Autologous cellular immunotherapy comprising dendritic cells and activated effector T cells; dendritic cells present tumor antigens via MHC I/II to prime tumor-specific T cells, and infused T cells mediate cytotoxicity via perforin/granzyme and IFN-γ.
Autologous dendritic cells loaded with tumor antigens present peptides via MHC I/II to prime and expand tumor-specific T cells, while co-infused activated effector T cells mediate tumor cell killing through perforin/granzyme release and IFN-γ–driven Th1 cytotoxic responses.
Vaccine-primed/infused CD8+ T cells recognize the tumor peptide–HLA class I complex via the TCR and kill target cells via perforin/granzyme-mediated cytotoxicity (±Fas–FasL), supported by IFN-γ–driven Th1 responses.
Antibody–drug conjugate (human IgG1 mAb targeting Nectin-4) linked to the cytotoxic payload monomethyl auristatin E (MMAE). After Nectin-4 binding and internalization, MMAE is released to inhibit tubulin polymerization, inducing G2/M arrest and apoptosis; given 1.25 mg/kg IV on days 1, 8, and 15 of 28-day cycles.
Enfortumab vedotin is a human IgG1 monoclonal antibody targeting Nectin-4 conjugated via a protease-cleavable linker to the cytotoxic payload monomethyl auristatin E (MMAE). After binding Nectin-4 on tumor cells and internalization, the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M cell-cycle arrest and apoptotic cell death; a local bystander effect may occur.
ADC binds Nectin-4 on tumor cells, is internalized, and releases MMAE after linker cleavage; MMAE inhibits tubulin polymerization causing G2/M arrest and apoptotic cell death (with possible bystander effect).
Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
Vγ9Vδ2 T cells express NKG2D, which binds ULBP5 on target cells, triggering cytotoxic degranulation with perforin/granzymes and killing the target.
Human IgG1κ anti-CD38 monoclonal antibody immunotherapy that depletes CD38+ cells via ADCC, CDC, ADCP, and direct apoptosis/immune modulation; administered subcutaneously.
Human IgG1κ monoclonal antibody against CD38 that binds CD38 on malignant and immunosuppressive CD38+ cells, inducing cell death via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and direct apoptotic/immune-modulatory effects; administered subcutaneously.
Anti-CD38 IgG1 binds CD38 on target cells and elicits Fc-mediated ADCC (NK cells), ADCP (phagocytes), complement-dependent cytotoxicity, and can trigger direct apoptotic signaling.