Adoptive cellular immunotherapy using virus-specific CTL lines engineered with glucocorticoid receptor (GR/NR3C1) knockout to resist steroid-mediated suppression/apoptosis; HLA-restricted recognition of adenovirus, BK virus, CMV, JC virus, or SARS-CoV-2 antigens on infected cells, leading to perforin/granzyme-mediated killing and antiviral cytokine release; administered intravenously with possible repeat dosing.
Adoptively transferred, virus-specific CTLs recognize viral peptides presented on HLA molecules via their native TCRs and eliminate infected cells through perforin/granzyme-mediated cytolysis and antiviral cytokine secretion. The cells are engineered with glucocorticoid receptor (NR3C1) knockout to resist steroid-induced suppression and apoptosis, improving persistence and antiviral activity in immunosuppressed patients.
Virus-specific CTLs recognize BK polyomavirus peptides presented on HLA via their TCR and directly kill infected cells through perforin/granzyme-mediated apoptosis (and Fas/FasL pathways).
Adoptive cellular immunotherapy using virus-specific CTL lines engineered with glucocorticoid receptor (GR/NR3C1) knockout to resist steroid-mediated suppression/apoptosis; HLA-restricted recognition of adenovirus, BK virus, CMV, JC virus, or SARS-CoV-2 antigens on infected cells, leading to perforin/granzyme-mediated killing and antiviral cytokine release; administered intravenously with possible repeat dosing.
Adoptively transferred, virus-specific CTLs recognize viral peptides presented on HLA molecules via their native TCRs and eliminate infected cells through perforin/granzyme-mediated cytolysis and antiviral cytokine secretion. The cells are engineered with glucocorticoid receptor (NR3C1) knockout to resist steroid-induced suppression and apoptosis, improving persistence and antiviral activity in immunosuppressed patients.
Virus-specific CTLs recognize CMV peptide–HLA complexes via their TCR and directly lyse infected cells through perforin/granzyme-mediated cytotoxicity.
Adoptive cellular immunotherapy using virus-specific CTL lines engineered with glucocorticoid receptor (GR/NR3C1) knockout to resist steroid-mediated suppression/apoptosis; HLA-restricted recognition of adenovirus, BK virus, CMV, JC virus, or SARS-CoV-2 antigens on infected cells, leading to perforin/granzyme-mediated killing and antiviral cytokine release; administered intravenously with possible repeat dosing.
Adoptively transferred, virus-specific CTLs recognize viral peptides presented on HLA molecules via their native TCRs and eliminate infected cells through perforin/granzyme-mediated cytolysis and antiviral cytokine secretion. The cells are engineered with glucocorticoid receptor (NR3C1) knockout to resist steroid-induced suppression and apoptosis, improving persistence and antiviral activity in immunosuppressed patients.
Virus-specific CTLs recognize JC polyomavirus peptide–HLA complexes via their TCR and kill infected cells by perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Adoptive cellular immunotherapy using virus-specific CTL lines engineered with glucocorticoid receptor (GR/NR3C1) knockout to resist steroid-mediated suppression/apoptosis; HLA-restricted recognition of adenovirus, BK virus, CMV, JC virus, or SARS-CoV-2 antigens on infected cells, leading to perforin/granzyme-mediated killing and antiviral cytokine release; administered intravenously with possible repeat dosing.
Adoptively transferred, virus-specific CTLs recognize viral peptides presented on HLA molecules via their native TCRs and eliminate infected cells through perforin/granzyme-mediated cytolysis and antiviral cytokine secretion. The cells are engineered with glucocorticoid receptor (NR3C1) knockout to resist steroid-induced suppression and apoptosis, improving persistence and antiviral activity in immunosuppressed patients.
Virus-specific CTLs recognize SARS‑CoV‑2 peptide–HLA complexes via their TCR and kill infected cells through perforin/granzyme-mediated cytolysis (with possible Fas/FasL contribution).
An antibody–drug conjugate (ADC) comprising a humanized anti–TROP-2 IgG1 monoclonal antibody linked to SN-38 (the active metabolite of irinotecan). It targets TROP-2–expressing tumor cells, is internalized, releases SN-38 intracellularly, inhibits topoisomerase I, induces DNA damage and apoptosis, and can cause bystander killing due to membrane-permeable SN-38.
Humanized anti–TROP-2 IgG1 antibody–drug conjugate that delivers SN-38. After binding TROP-2 on tumor cells and internalization, linker cleavage releases SN-38 intracellularly, inhibiting topoisomerase I and stabilizing topo I–DNA complexes to induce DNA damage, S-phase arrest, and apoptosis; membrane-permeable SN-38 can cause bystander killing.
The ADC binds TROP-2, is internalized, and releases SN-38, which inhibits topoisomerase I to cause DNA damage and apoptosis; membrane-permeable SN-38 can also produce bystander killing.