A chimeric (mouse/human) anti-CD20 monoclonal antibody that depletes CD20-positive B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis; used as a biologic DMARD in rheumatoid arthritis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre‑B and mature B lymphocytes (not plasma cells) and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby reducing autoantibody production and B-cell–mediated immune activation.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity (CDC), Fc-mediated antibody-dependent cellular cytotoxicity (ADCC) by NK cells/macrophages, and can trigger apoptosis of the bound cells.
Anti-HER2 antibody-drug conjugate (RC48) that delivers MMAE to HER2-expressing tumor cells, causing microtubule disruption; may also induce ADCC and bystander killing.
Anti-HER2 antibody-drug conjugate that binds HER2 on tumor cells; upon internalization, delivers the microtubule inhibitor MMAE, leading to microtubule disruption, G2/M arrest, and apoptosis; may also trigger ADCC and bystander killing.
ADC binds HER2 on tumor cells, is internalized, and releases MMAE, which inhibits microtubule polymerization causing G2/M arrest and apoptosis; can also induce ADCC and bystander killing.
An antibody–drug conjugate targeting PSMA; a humanized IgG1κ anti-PSMA monoclonal antibody linked to two AS269 microtubule-disrupting payloads that internalize and release cytotoxic payload to induce mitotic arrest and cell death.
Humanized anti-PSMA IgG1 kappa monoclonal antibody delivers two amberstatin (AS269) microtubule-disrupting payloads to PSMA-expressing tumor cells; after binding and internalization, the payload inhibits tubulin polymerization, leading to G2/M arrest and apoptotic cell death.
ADC binds PSMA on tumor cells, is internalized, and releases amberstatin payload that inhibits tubulin polymerization, causing G2/M arrest and apoptotic cell death.
An autologous anti‑CD19 CAR T‑cell therapy (Breyanzi; liso‑cel) composed of CD4+ and CD8+ T cells with a 4‑1BB costimulatory domain, targeting CD19+ malignant B cells.
Autologous CD4+ and CD8+ T cells engineered to express an anti‑CD19 chimeric antigen receptor with 4‑1BB costimulation and CD3ζ signaling. Upon infusion, the CAR T cells bind CD19 on malignant B cells, become activated, expand, and mediate cytotoxic killing and cytokine release to eliminate CD19+ tumor cells; the 4‑1BB domain enhances T‑cell proliferation and persistence. A truncated EGFR tag enables in vivo tracking and potential elimination of the cells if needed.
Anti-CD19 CAR T cells bind CD19 on target cells, become activated, and kill them via cytolytic mechanisms (perforin/granzyme, Fas–FasL) with associated cytokine release.
A CD19-directed autologous chimeric antigen receptor (CAR) T-cell therapy in which a patient’s T cells are genetically engineered to express an anti-CD19 CAR, enabling targeted cytotoxic killing of CD19-positive B cells.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor comprising an anti-CD19 scFv with CD28 costimulatory and CD3ζ signaling domains. After infusion, these CAR T cells bind CD19 on B cells, become activated, expand, release cytotoxic molecules and cytokines, and selectively kill CD19-positive malignant B cells.
CD19-specific CAR T cells bind CD19 on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis and apoptosis.