Subcutaneous long-peptide therapeutic cancer vaccine targeting PD-L1, designed to elicit PD-L1–specific CD4+ and CD8+ T cells to attack PD-L1–expressing tumor and immunosuppressive cells.
Subcutaneous long-peptide cancer vaccine composed of PD-L1–derived peptides that prime and expand PD-L1–specific CD4+ helper and CD8+ cytotoxic T cells. The induced T cells recognize PD-L1–expressing tumor and immunosuppressive cells and eliminate them, reducing immune suppression and enhancing antitumor immunity. It does not block PD-1/PD-L1 directly like an antibody checkpoint inhibitor.
YES
INDIRECT
A peptide vaccine primes and expands PD-L1–specific CD8+ (and helper CD4+) T cells, which recognize PD-L1–derived peptides presented on MHC of PD-L1–expressing cells and kill them via T cell–mediated cytolysis (perforin/granzyme).
Fully human anti-CD20 monoclonal antibody that depletes CD20+ B cells to reduce antigen presentation, cytokines, and autoantibody activity.
Fully human anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20+ B cells primarily via complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC), thereby reducing antigen presentation, pro-inflammatory cytokines, and autoantibody production.
YES
DIRECT
Ofatumumab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC (and phagocytosis), causing lysis of CD20+ cells.
A humanized anti-CD2 monoclonal antibody (TCD601) that binds CD2 on T cells and NK cells, blocks CD2–LFA-3 (CD58) costimulatory signaling, induces lymphocyte depletion with preferential reduction of CD2high effector/memory T cells, and aims to shift T-cell phenotypes toward a more regulatory profile to preserve β-cell function in recent-onset type 1 diabetes.
Humanized IgG1 anti-CD2 monoclonal antibody that binds CD2 on T cells and NK cells, blocks CD2–CD58 (LFA-3) costimulatory signaling, and engages Fc-mediated effector functions (e.g., ADCC/CDC) to deplete CD2+ lymphocytes—preferentially CD2high effector/memory T cells—shifting the T-cell compartment toward a more regulatory phenotype and suppressing pathogenic T-cell activity.
YES
DIRECT
Anti-CD2 IgG1 binds CD2+ lymphocytes and depletes them via Fc-mediated ADCC and complement-dependent cytotoxicity (CDC), causing lysis/apoptosis.
TROP‑2–directed antibody‑drug conjugate delivering SN‑38 (topoisomerase I inhibitor payload).
Humanized anti-TROP-2 monoclonal antibody (hRS7) conjugated to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells and internalization, linker cleavage releases SN-38, which stabilizes topoisomerase I–DNA complexes, causing DNA breaks, blocking replication, and inducing apoptosis; can also produce a bystander effect.
YES
DIRECT
The ADC binds TROP-2, is internalized, and releases SN-38 (a topoisomerase I inhibitor) inside the cell, causing DNA damage, replication arrest, and apoptosis; can also produce a bystander effect.
TROP‑2–directed antibody‑drug conjugate delivering SN‑38 (topoisomerase I inhibitor payload).
Humanized anti-TROP-2 monoclonal antibody (hRS7) conjugated to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells and internalization, linker cleavage releases SN-38, which stabilizes topoisomerase I–DNA complexes, causing DNA breaks, blocking replication, and inducing apoptosis; can also produce a bystander effect.
YES
INDIRECT
The ADC binds TROP‑2 on tumor cells, is internalized, and releases SN‑38, which inhibits topoisomerase I, stabilizing topo I–DNA complexes and causing DNA breaks and apoptosis (with possible bystander effect).