An anti-HER2 antibody–drug conjugate with a microtubule-inhibiting payload that binds HER2 (ERBB2) and kills HER2-expressing tumor cells.
HER2-directed antibody–drug conjugate that binds ERBB2 on tumor cells; after internalization, a cleavable linker releases the microtubule inhibitor MMAE, which blocks tubulin polymerization, leading to G2/M cell-cycle arrest and apoptosis in HER2-expressing cancer cells.
The anti-HER2 ADC binds HER2 on tumor cells, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis of HER2-expressing cells.
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.
Avelumab binds PD-L1 on target cells and its IgG1 Fc engages Fcγ receptors on NK cells to trigger antibody-dependent cellular cytotoxicity, leading to lysis of PD-L1–expressing cells.
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.
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.
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.
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.
An autologous CD19-directed chimeric antigen receptor (CAR) T-cell therapy in which patient T cells are genetically modified to express a CAR targeting CD19, leading to T-cell activation, proliferation, cytokine release, and cytolysis of CD19+ B cells when infused intravenously.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor; upon binding CD19 on B cells, CAR signaling (CD3 zeta with co-stimulatory domains) activates the T cells, inducing proliferation, cytokine release, and cytolytic killing of CD19-positive malignant and normal B cells.
CD19-specific CAR T cells bind CD19 on B cells, become activated, and kill target cells via perforin/granzyme-mediated cytolysis and apoptosis (with contributions from death receptor and cytokine pathways).