Intravenous anti–PD-L1 IgG1 monoclonal antibody immune checkpoint inhibitor; blocks PD-L1 from engaging PD-1/B7.1 to restore T-cell activity and can trigger NK cell–mediated ADCC via its Fc.
Human IgG1 anti–PD-L1 immune checkpoint inhibitor that blocks PD-L1 interaction with PD-1/B7.1 to release inhibitory signaling and restore T‑cell activity; its Fc can engage Fcγ receptors to trigger NK cell–mediated ADCC against PD-L1–expressing cells.
NO
INDIRECT
Avelumab’s Fc binds CD16a on NK cells to activate them for ADCC against PD‑L1–expressing targets; CD16a+ cells are effectors, not killed by the drug.
An intravenous CD30-targeted antibody–drug conjugate that is internalized upon CD30 binding and releases a camptothecin-based topoisomerase I inhibitor payload, inhibiting Topo I, disrupting DNA replication, and inducing DNA damage/apoptosis; studied as monotherapy in adults with advanced CD30+ lymphomas.
PF-08046044/SGN-35C is a CD30-targeted antibody–drug conjugate. After binding CD30 on tumor cells and internalization, it releases a camptothecin-based topoisomerase I inhibitor payload that inhibits Topo I, disrupts DNA replication, and induces DNA damage leading to apoptosis.
YES
DIRECT
The CD30-targeted ADC binds CD30 on tumor cells, is internalized, and releases a camptothecin-based topoisomerase I inhibitor payload that disrupts DNA replication and induces DNA damage, leading to apoptotic cell death.
An intravenous CD30-targeted antibody–drug conjugate that is internalized upon CD30 binding and releases a camptothecin-based topoisomerase I inhibitor payload, inhibiting Topo I, disrupting DNA replication, and inducing DNA damage/apoptosis; studied as monotherapy in adults with advanced CD30+ lymphomas.
PF-08046044/SGN-35C is a CD30-targeted antibody–drug conjugate. After binding CD30 on tumor cells and internalization, it releases a camptothecin-based topoisomerase I inhibitor payload that inhibits Topo I, disrupts DNA replication, and induces DNA damage leading to apoptosis.
NO
INDIRECT
The ADC binds CD30 on tumor cells, is internalized, and releases a camptothecin topoisomerase I inhibitor that causes DNA damage and apoptosis; killing is directed by CD30 expression, not by Topoisomerase I expression.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, reducing B-cell antigen presentation, T-cell co-stimulation, autoantibody production, and pro-inflammatory cytokines to attenuate compartmentalized CNS inflammation in SPMS.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby lowering B-cell antigen presentation, T-cell costimulation, autoantibody production, and pro-inflammatory cytokines.
YES
DIRECT
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC by NK cells/macrophages, and can trigger apoptosis, leading to lysis of CD20+ cells.
Autologous, ex vivo–prepared dendritic cells (1×10^7 cells) administered post–radical surgery to induce tumor-specific T-cell immunity (CD8+ cytotoxic and CD4+ helper responses) via antigen presentation and costimulation; intended to prevent recurrence/metastasis in survivin- or p53-positive solid tumors.
Autologous ex vivo–prepared dendritic cells present tumor antigens (e.g., survivin/p53) via MHC I/II with costimulatory signals (CD80/CD86) to activate tumor-specific CD8+ cytotoxic and CD4+ helper T cells, enhancing Th1/CTL responses to eliminate residual disease and prevent recurrence/metastasis.
YES
INDIRECT
Ex vivo–prepared dendritic cells present survivin peptides with costimulation to prime survivin-specific CD8+ T cells, which then recognize survivin peptide–MHC on tumor cells and kill them via perforin/granzyme (and Fas–FasL) pathways.