Ex vivo expanded TILs infused to restore antitumor immunity and kill tumor cells via TCR recognition and cytotoxic effector functions.
Autologous TILs are isolated from the tumor, expanded ex vivo, and reinfused as a polyclonal T‑cell product that recognizes tumor antigens via native, HLA‑restricted TCRs and eliminates tumor cells through cytotoxic effector functions (perforin/granzyme) and cytokine release, restoring antitumor immunity without genetic engineering.
TILs recognize tumor-derived peptide–HLA class II via native TCRs and kill the presenting cell through cytotoxic effector functions (perforin/granzyme and/or Fas–FasL).
Ex vivo expanded TILs infused to restore antitumor immunity and kill tumor cells via TCR recognition and cytotoxic effector functions.
Autologous TILs are isolated from the tumor, expanded ex vivo, and reinfused as a polyclonal T‑cell product that recognizes tumor antigens via native, HLA‑restricted TCRs and eliminates tumor cells through cytotoxic effector functions (perforin/granzyme) and cytokine release, restoring antitumor immunity without genetic engineering.
Infused TILs recognize the EBV peptide–HLA class I complex via their native TCRs and directly kill target cells by releasing perforin and granzymes (with possible Fas/FasL-mediated apoptosis).
IgG1 monoclonal antibody targeting CD38; depletes CD38+ cells via ADCC, CDC, and ADCP; can induce direct apoptosis; inhibits CD38 ectoenzyme (NADase/cyclase) activity, reducing adenosine and modulating immune signaling.
Humanized IgG1 anti-CD38 monoclonal antibody that depletes CD38+ cells via ADCC, CDC, and ADCP and can directly induce apoptosis; also inhibits CD38 ectoenzyme (NADase/cyclase) activity, reducing adenosine and modulating immune signaling.
Isatuximab binds CD38 on target cells and triggers Fc-mediated ADCC (NK cells), CDC (complement), and ADCP (phagocytes), and can also directly induce apoptosis of CD38+ cells.
Teclistamab (Tecvayli) is an anti-BCMA×CD3 bispecific IgG4 monoclonal antibody T-cell engager that binds BCMA on multiple myeloma cells and CD3 on T cells to activate TCR/CD3 signaling and drive T-cell–mediated cytotoxicity against BCMA-positive myeloma cells.
Teclistamab is a bispecific IgG4 antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to form an immune synapse. This activates TCR/CD3 signaling, leading to T‑cell proliferation, cytokine release, and cytotoxic effector activity (perforin/granzymes) that selectively lyses BCMA‑positive myeloma cells.
Teclistamab bridges CD3 on T cells to BCMA on target cells, forming an immune synapse and activating TCR/CD3 signaling, leading to perforin/granzyme-mediated cytotoxic lysis of BCMA-positive cells.
Virus-like particle–drug conjugate (bel-sar; AU-011) linked to an IRDye 700DX photosensitizer that selectively binds heparan sulfate proteoglycans on tumor cells; activation by near-infrared laser triggers localized photochemical membrane damage causing rapid necrotic and immunogenic cell death.
Virus-like particle–photosensitizer conjugate that binds heparan sulfate proteoglycans on tumor cells; activation by near‑infrared light triggers IRDye 700DX to generate reactive oxygen species and induce localized photochemical membrane damage, leading to rapid necrotic and immunogenic cell death while sparing surrounding healthy tissue.
Bel-sar binds HSPGs on tumor cells; near-infrared light activates the IR700 photosensitizer to generate ROS and cause photochemical membrane damage, leading to rapid necrotic/immunogenic cell death.