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.
YES
DIRECT
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 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.
NO
INDIRECT
ARX517 binds PSMA on tumor cells; after internalization, its AS269 payload binds beta-tubulin to block microtubule polymerization, causing G2/M arrest and apoptosis. Beta-tubulin is not the targeted antigen.
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.
YES
DIRECT
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.
Recombinant SIRPα-Fc fusion protein that binds CD47 to block the CD47–SIRPα 'don't-eat-me' signal, enhancing macrophage-mediated phagocytosis and antigen presentation.
Recombinant SIRPα–Fc fusion protein that binds CD47 on tumor cells, blocking the CD47–SIRPα innate immune checkpoint to remove the “don’t‑eat‑me” signal, thereby enhancing macrophage-mediated phagocytosis and downstream antigen presentation/T‑cell priming.
YES
INDIRECT
Blocks the CD47–SIRPα “don’t‑eat‑me” signal on target cells, enabling macrophage-mediated phagocytosis (Fc-dependent ADCP), which kills CD47+ cells; downstream T-cell priming may follow.
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.
YES
DIRECT
CD19-specific CAR T cells bind CD19 on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis and apoptosis.