An antibody-drug conjugate (STRO-002, Luvelta) targeting folate receptor-α (FOLR1). It consists of an anti-FOLR1 IgG1 (SP8166) linked via a cathepsin-cleavable linker to a 3-aminophenyl hemiasterlin payload (SC209) that inhibits tubulin polymerization, causing mitotic arrest and cell death.
Anti-FOLR1 IgG1 antibody (SP8166) binds folate receptor-α on tumor cells, is internalized, and a cathepsin-cleavable linker releases the 3-aminophenyl hemiasterlin payload (SC209), which inhibits tubulin polymerization, inducing mitotic arrest and cell death in FOLR1-expressing cells.
An anti-FOLR1 antibody-drug conjugate binds folate receptor alpha, is internalized, and releases a hemiasterlin payload that inhibits tubulin polymerization, causing mitotic arrest and apoptotic cell death in FOLR1-expressing cells.
An anti-HER2 antibody–drug conjugate (Enhertu) composed of humanized IgG1 trastuzumab linked to a topoisomerase I inhibitor payload (DXd). It binds HER2 on tumor cells, is internalized, and releases DXd to inhibit topoisomerase I, causing DNA damage and bystander killing; it also retains trastuzumab functions such as ADCC and HER2 signaling blockade.
Humanized anti-HER2 monoclonal antibody (trastuzumab) linked to a topoisomerase I inhibitor (DXd). Binds HER2 on tumor cells, is internalized, and releases DXd to inhibit topoisomerase I, causing DNA damage, replication arrest, and apoptosis with a bystander-killing effect; retains trastuzumab functions including HER2 signaling blockade and antibody-dependent cell-mediated cytotoxicity (ADCC).
The anti-HER2 ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage and apoptosis; it also elicits Fc-mediated ADCC and can produce a bystander-killing effect.
Patient-derived TIL product consisting of >=5 x 10^9 autologous ex vivo-expanded T cells administered intravenously to mediate antigen-specific tumor cytotoxicity.
Autologous ex vivo‑expanded tumor-infiltrating T cells that recognize patient-specific tumor antigens via native TCRs and kill tumor cells through cytotoxic effector functions (perforin/granzyme and cytokines); conditioning/IL-2 support engraftment and persistence.
TILs recognize the patient-specific peptide–HLA complex via native TCRs and directly kill target cells through cytotoxic effector functions (perforin/granzyme-mediated apoptosis; also Fas–FasL and inflammatory cytokines).
Patient-derived TIL product consisting of >=5 x 10^9 autologous ex vivo-expanded T cells administered intravenously to mediate antigen-specific tumor cytotoxicity.
Autologous ex vivo‑expanded tumor-infiltrating T cells that recognize patient-specific tumor antigens via native TCRs and kill tumor cells through cytotoxic effector functions (perforin/granzyme and cytokines); conditioning/IL-2 support engraftment and persistence.
Native TCRs on infused TILs recognize the tumor-associated peptide–HLA complex and directly kill the presenting cell via perforin/granzyme release and Fas–FasL–mediated apoptosis.
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement activation, and apoptosis to reduce platelet/HLA alloantibody-producing cells.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, thereby reducing alloantibody-producing B cells (anti-platelet/HLA).
Rituximab binds CD20 on B cells and triggers Fc-dependent ADCC by NK/macrophages, complement-dependent cytotoxicity (C1q/MAC), and can induce apoptosis via CD20 crosslinking.