Anti-HER2 monoclonal antibody that inhibits HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti-HER2 monoclonal antibody that binds HER2 (ErbB2) on tumor cells, inhibits HER2-driven signaling and proliferation, and induces antibody-dependent cellular cytotoxicity via Fc gamma receptor–bearing effector cells.
Trastuzumab binds HER2 on tumor cells and its Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells) to trigger antibody-dependent cellular cytotoxicity, killing HER2+ cells; it also inhibits HER2 signaling.
Autologous CD8+ and CD4+ T cells genetically engineered to express a high-affinity T-cell receptor specific for the KRAS G12V peptide presented by HLA-A*11:01, designed to recognize and kill KRAS G12V–positive tumor cells (adoptive cellular therapy).
Autologous CD8+ and CD4+ T cells engineered to express a high-affinity TCR specific for the KRAS G12V peptide presented by HLA-A*11:01. Upon HLA-restricted recognition of KRAS G12V on tumor cells, the transgenic TCR triggers T-cell activation, cytokine release, and perforin/granzyme-mediated cytotoxicity, selectively eliminating KRAS G12V–positive tumor cells.
Engineered TCR T cells recognize the HLA-A*11:01–presented KRAS G12V peptide on tumor cells, activating cytotoxic T cells to kill via perforin/granzyme-mediated apoptosis (± Fas/FasL).
An antibody–drug conjugate (ADC) consisting of a humanized anti–Trop-2 monoclonal antibody linked to SN-38 (the active metabolite of irinotecan), a topoisomerase I inhibitor. After binding Trop-2 on tumor cells, the ADC is internalized and releases SN-38 to inhibit topoisomerase I, leading to DNA damage and apoptosis. Administered IV at 10 mg/kg on days 1 and 8 of a 21-day cycle.
Humanized anti–Trop-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor). After binding Trop-2 on tumor cells, the ADC is internalized and releases SN-38, which stabilizes Topo I–DNA complexes, causing DNA damage, S-phase arrest, and apoptosis; membrane-permeable SN-38 can produce a bystander effect.
After ADC delivery to Trop-2–positive cells, the SN-38 payload inhibits topoisomerase I by stabilizing Topo I–DNA complexes, causing DNA damage, S-phase arrest, and apoptosis (with possible bystander effect).
Anti-CD20 monoclonal antibody that depletes B cells via CDC, ADCC, and apoptosis.
Anti-CD20 chimeric monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity (CDC), Fc-mediated antibody-dependent cellular cytotoxicity/phagocytosis (ADCC/ADCP), and direct induction of apoptosis.
Rituximab binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP by immune effector cells; CD20 ligation can also induce apoptosis.
Investigational anti-HIV monoclonal antibody intended to directly target HIV (likely the envelope) to help control viremia via neutralization and immune effector engagement.
Investigational anti-HIV monoclonal antibody that binds the viral envelope to neutralize virions and block entry, while engaging Fc-mediated effector functions (e.g., ADCC/ADCP/CDC) to help clear virus and infected cells, thereby reducing viremia.
The anti-Env antibody binds HIV-1 Env on infected cells and engages Fc effector functions—NK cell–mediated ADCC, macrophage ADCP, and complement-dependent cytotoxicity—leading to killing/clearance of Env-expressing cells.