TROP2-targeting antibody–drug conjugate that delivers a cleavable topoisomerase I inhibitor payload; binding to TROP2 leads to internalization and payload release, causing DNA damage/replication stress and tumor cell death (potential bystander effect).
Humanized anti‑TROP2 IgG1 ADC linked via a cleavable linker to the topoisomerase I inhibitor tirumotecan. Binding to TROP2 on tumor cells triggers internalization and linker cleavage, releasing the payload to inhibit topoisomerase I, inducing DNA damage/replication stress and apoptosis, with a potential bystander effect on neighboring cells.
NO
INDIRECT
SKB264 binds TROP2 on tumor cells, is internalized, and releases tirumotecan, which inhibits DNA topoisomerase I to cause DNA damage and apoptosis. DNA topoisomerase I is the intracellular payload target, not the antigen that determines cell targeting; killing occurs mainly in TROP2+ cells (with potential bystander effect).
Anti–PD‑L1 IgG1 monoclonal antibody immune checkpoint inhibitor that blocks PD‑L1 to restore T‑cell function and may engage ADCC.
Avelumab is a human IgG1 monoclonal antibody that binds PD-L1 and blocks its interaction with PD-1, releasing inhibitory checkpoint signaling to restore and enhance T‑cell–mediated antitumor activity; its IgG1 Fc can also engage antibody‑dependent cellular cytotoxicity (ADCC) against PD‑L1–expressing cells.
YES
DIRECT
Avelumab binds PD-L1 on target cells and, via its IgG1 Fc, engages Fc-gamma receptors on NK cells (and other effector cells) to mediate antibody-dependent cellular cytotoxicity (ADCC), killing PD-L1-expressing cells.
An IgG1 bispecific antibody that binds CD3 on T cells and BCMA (TNFRSF17) on malignant plasma cells, redirecting T cells to BCMA-expressing myeloma cells to trigger TCR/CD3 signaling, immune synapse formation, and T-cell–mediated cytotoxicity (perforin/granzyme release and cytokine secretion). Administered intravenously with dose escalation.
IgG1 bispecific antibody that binds CD3 on T cells and BCMA (TNFRSF17) on malignant plasma cells, bringing T cells into proximity with BCMA+ myeloma cells to trigger TCR/CD3 signaling, immune synapse formation, and T-cell–mediated cytotoxicity (perforin/granzyme release and cytokine secretion), resulting in lysis of BCMA-expressing tumor cells.
YES
DIRECT
Bispecific engagement of CD3 on T cells and BCMA on target cells forms an immune synapse, activates TCR/CD3 signaling, and induces perforin/granzyme-mediated T-cell cytotoxicity (with cytokine release) against BCMA+ cells.
An IgG1 bispecific antibody that binds CD3 on T cells and BCMA (TNFRSF17) on malignant plasma cells, redirecting T cells to BCMA-expressing myeloma cells to trigger TCR/CD3 signaling, immune synapse formation, and T-cell–mediated cytotoxicity (perforin/granzyme release and cytokine secretion). Administered intravenously with dose escalation.
IgG1 bispecific antibody that binds CD3 on T cells and BCMA (TNFRSF17) on malignant plasma cells, bringing T cells into proximity with BCMA+ myeloma cells to trigger TCR/CD3 signaling, immune synapse formation, and T-cell–mediated cytotoxicity (perforin/granzyme release and cytokine secretion), resulting in lysis of BCMA-expressing tumor cells.
NO
INDIRECT
Binds CD3ε on T cells to activate/redirect them toward BCMA+ tumor cells; activated T cells kill BCMA-expressing cells via perforin/granzyme, not the CD3ε+ T cells themselves.
Patient-derived T cells engineered (retroviral transduction) to express an anti-CD7 chimeric antigen receptor; cellular gene therapy targeting CD7+ T/NK cells.
Autologous T cells are genetically engineered (retroviral transduction) to express an anti‑CD7 chimeric antigen receptor. Engagement of CD7 on target T- and NK-lineage cells activates the CAR T cells, inducing perforin/granzyme-mediated cytotoxicity and inflammatory cytokine release, resulting in selective depletion of CD7+ cells and immune reset.
YES
DIRECT
Anti-CD7 CAR-T cells engage CD7 on target cells, form an immunologic synapse, and kill via perforin/granzyme-mediated cytotoxicity (apoptosis), with supportive cytokine effects.