Anti-CD52 monoclonal antibody used for T-cell depletion to prevent rejection and GVHD.
Humanized anti-CD52 IgG1 monoclonal antibody that binds CD52 on lymphocytes and induces complement-dependent cytotoxicity and antibody-dependent cell-mediated cytotoxicity, leading to depletion of CD52+ T and B cells (and other leukocytes) to reduce rejection and GVHD.
Alemtuzumab binds CD52 on leukocytes and induces complement-dependent cytotoxicity and Fc-mediated ADCC (and phagocytosis), leading to lysis/depletion of CD52+ cells.
Izalontamab brengitecan (BMS-986507), an EGFR/HER3-directed bispecific antibody–drug conjugate that internalizes upon binding and releases the topoisomerase I inhibitor brengitecan to induce DNA strand breaks and bystander killing.
Bispecific EGFR/HER3-targeting antibody-drug conjugate that binds EGFR and HER3 on tumor cells, internalizes, and releases the topoisomerase I inhibitor brengitecan to induce DNA strand breaks, leading to tumor cell death and bystander killing.
An EGFR/HER3-targeting ADC binds HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA strand breaks and apoptosis; bystander killing may also occur.
An intravenous anti-human CD38 IgG monoclonal antibody that depletes CD38+ long-lived plasma cells to reduce pathogenic anti-platelet autoantibody production in refractory/relapsed primary ITP.
Anti-CD38 IgG monoclonal antibody that binds CD38 on plasma cells and induces ADCC, CDC, and antibody-dependent phagocytosis to deplete CD38+ long-lived plasma cells, reducing pathogenic autoantibody production; it may also inhibit CD38 ectoenzyme activity.
Anti-CD38 IgG binds CD38 on target cells; the Fc region engages NK cells/macrophages and complement to mediate ADCC, ADCP, and CDC, and can also trigger apoptosis, resulting in depletion of CD38+ cells.
An adenoviral vector-based gene therapy delivering an hTERT-targeted trans-splicing ribozyme to redirect hTERT mRNA to express HSV-1 thymidine kinase selectively in tumor cells, enabling suicide gene therapy.
A replication-deficient adenoviral vector delivers an hTERT-targeted trans-splicing ribozyme that redirects hTERT mRNA to express HSV-1 thymidine kinase selectively in tumor cells. Upon administration of valganciclovir, HSV-TK converts it into cytotoxic nucleotides, inducing tumor cell death with bystander and immunogenic effects (suicide gene therapy).
Cells expressing hTERT mRNA are reprogrammed by a trans-splicing ribozyme to express HSV-1 thymidine kinase; upon valganciclovir dosing, HSV-TK converts the prodrug into toxic nucleotides that induce DNA damage and apoptosis in those cells (with a bystander effect).
An oral prodrug of ganciclovir that is phosphorylated by HSV-1 thymidine kinase to cytotoxic metabolites, killing hTERT-expressing tumor cells in the suicide gene strategy.
Oral prodrug of ganciclovir; once converted to ganciclovir and phosphorylated (here by HSV‑1 thymidine kinase supplied by the suicide gene), it forms ganciclovir triphosphate that is incorporated into DNA, inhibiting DNA polymerase and DNA synthesis, leading to death of HSV‑TK–expressing tumor cells with a bystander effect.
Valganciclovir is converted to ganciclovir, which HSV-1 thymidine kinase phosphorylates; the resulting triphosphate is incorporated into DNA, inhibiting DNA polymerase and DNA synthesis, killing the HSV-TK–expressing cells (with a bystander effect).