Chimeric anti-CD20 monoclonal antibody immunotherapy that depletes B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and induction of apoptosis.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity (CDC), recruits Fc receptor–bearing effector cells for antibody-dependent cellular cytotoxicity (ADCC), and can trigger apoptosis via CD20 cross-linking.
Anti-CD38 IgG1 monoclonal antibody targeting CD38 on clonal plasma cells, inducing ADCC, CDC, apoptosis, and immunomodulation.
Human IgG1κ monoclonal antibody targeting CD38 on clonal plasma cells; binding induces Fc-mediated cytotoxicity (ADCC, ADCP, CDC) and direct apoptosis, and depletes CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs) to modulate the tumor microenvironment.
Anti-CD38 IgG1 binds CD38 and triggers Fc-mediated ADCC by NK cells, ADCP by phagocytes, and complement-dependent cytotoxicity; can also induce apoptosis of CD38+ cells.
An antibody–drug conjugate consisting of a humanized anti–Trop-2 monoclonal antibody linked to SN-38 (active metabolite of irinotecan). It delivers a topoisomerase I inhibitor to Trop-2–expressing tumor cells, causing DNA damage and apoptosis with a bystander effect.
Humanized anti–Trop-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor). Binds Trop-2 on tumor cells, is internalized, and releases SN-38 after cleavage, stabilizing topoisomerase I–DNA complexes to cause DNA breaks, inhibit replication, and trigger apoptosis; released payload can exert a bystander effect on neighboring cells.
The ADC binds TROP2 on target cells, is internalized, and releases SN-38, a topoisomerase I inhibitor that causes DNA damage and apoptosis; released payload can also exert a bystander effect on neighboring cells.
Autologous tumor-infiltrating lymphocyte (TIL) therapy expanded ex vivo; adoptive cellular immunotherapy delivering tumor-reactive T cells to mediate antigen-specific cytotoxicity and effector cytokine secretion.
Autologous tumor-infiltrating lymphocytes are isolated from the patient’s tumor, expanded ex vivo, and reinfused. These non-engineered T cells use their native TCRs to recognize tumor antigens presented by MHC on cancer cells, execute antigen-specific cytotoxicity (perforin/granzyme) and secrete effector cytokines (e.g., IFN-γ, TNF-α), enhancing antitumor immune responses.
Infused autologous TILs use native TCRs to recognize the neoantigen peptide–HLA class I complex on tumor cells and directly kill them via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Autologous tumor-infiltrating lymphocyte (TIL) therapy expanded ex vivo; adoptive cellular immunotherapy delivering tumor-reactive T cells to mediate antigen-specific cytotoxicity and effector cytokine secretion.
Autologous tumor-infiltrating lymphocytes are isolated from the patient’s tumor, expanded ex vivo, and reinfused. These non-engineered T cells use their native TCRs to recognize tumor antigens presented by MHC on cancer cells, execute antigen-specific cytotoxicity (perforin/granzyme) and secrete effector cytokines (e.g., IFN-γ, TNF-α), enhancing antitumor immune responses.
Native TCRs on infused TILs recognize the neoantigen peptide–HLA class II complex and directly kill the presenting tumor cell via perforin/granzyme release and Fas/FasL-mediated apoptosis, with supportive effector cytokines.