Autologous anti-CD19 CAR T-cell therapy (gene-modified T cells) for CD19+ B-cell malignancies.
Autologous T cells are genetically modified with a gamma-retroviral vector to express an anti-CD19 chimeric antigen receptor containing a CD28 costimulatory domain and CD3ζ signaling domain. After infusion, these CAR T cells recognize CD19 on B-cell malignancies, become activated, expand, secrete cytokines, and kill CD19+ tumor cells via perforin/granzyme-mediated cytotoxicity.
Anti-CD19 CAR T cells recognize CD19 on target cells and kill them via immune-synapse–mediated perforin/granzyme cytotoxicity (and death-receptor pathways).
Chimeric anti-CD20 monoclonal antibody that depletes B cells via CDC/ADCC and apoptosis.
Chimeric anti‑CD20 IgG1 monoclonal antibody that binds CD20 on normal and malignant B cells and induces B‑cell depletion primarily via complement‑dependent cytotoxicity (CDC), antibody‑dependent cellular cytotoxicity/phagocytosis (ADCC/ADCP), and direct apoptotic signaling.
Rituximab binds CD20 on B cells, activating complement for CDC (MAC lysis) and engaging FcγR-bearing effectors (NK cells/macrophages) for ADCC/ADCP; cross-linking can also trigger apoptosis.
A HER2-targeted bispecific antibody–drug conjugate (ADC) administered IV every 3 weeks; binds two HER2 epitopes to enhance internalization and delivers an intracellular cytotoxic payload while also inhibiting HER2 signaling and potentially mediating ADCC.
TQB2102 is a bispecific anti‑HER2 antibody–drug conjugate that binds two distinct HER2 epitopes to enhance receptor engagement and internalization. After HER2-mediated uptake, it releases an intracellular cytotoxic payload to kill tumor cells. The antibody component can also inhibit HER2 signaling and may trigger Fc‑mediated effector functions such as ADCC.
The HER2-targeted ADC binds HER2, is internalized, and releases an intracellular cytotoxic payload that kills the HER2-expressing cell; Fc functions may also trigger ADCC.
A single-dose allogeneic anti-CD19 chimeric antigen receptor T-cell (CAR-T) therapy using donor-derived T cells engineered to target CD19 on B cells, inducing profound B-cell depletion to suppress autoantibody production and reset humoral immunity in refractory SLE; administered after lymphodepleting chemotherapy.
Allogeneic donor-derived T cells engineered with an anti-CD19 chimeric antigen receptor recognize and kill CD19+ B cells/plasmablasts, causing profound B-cell depletion, suppression of autoantibody production, and reset of humoral immunity; administered after lymphodepleting chemotherapy.
Anti-CD19 CAR-T cells recognize CD19 on B cells and directly induce killing via immune synapse formation with perforin/granzyme-mediated apoptosis (and Fas–FasL pathways).
An autologous, ex vivo–expanded T‑cell therapy composed of cytotoxic T lymphocytes engineered/selected to recognize personalized tumor‑specific antigens (neoantigens) via native TCRs; administered intraventricularly to target pediatric embryonal brain tumors.
Autologous, ex vivo–expanded cytotoxic T cells selected for reactivity to patient-specific tumor antigens/neoantigens via native TCRs. After intraventricular administration, TCR recognition of peptide–MHC on tumor cells activates CTLs to kill targets through perforin/granzyme release and cytokine-mediated immune responses in the CNS.
TSA-T cells recognize the patient-specific neoantigen peptide–HLA-I complex via their TCRs and directly kill target cells by perforin/granzyme-mediated apoptosis (and possibly Fas/FasL).