Autologous, gene-modified T cells engineered with the Sleeping Beauty transposon/transposase system to stably express patient-specific, tumor-reactive T-cell receptors targeting mutation-derived neoantigen peptides presented on HLA; upon infusion, these cells activate TCR-CD3 signaling to mediate cytotoxic killing (perforin/granzyme) and may generate immunologic memory.
Autologous T cells are gene-modified with the Sleeping Beauty transposon/transposase system to stably express patient-specific, tumor-reactive TCRs that recognize mutation-derived neoantigen peptides presented on HLA (primarily MHC I). Upon infusion, engagement of the TCR-CD3 complex triggers activation, clonal expansion, cytokine release, and cytotoxic killing of tumor cells via perforin/granzyme, with potential development of immunologic memory.
Engineered TCR-T cells recognize the neoantigen peptide–HLA-A complex via TCR/CD3, form an immune synapse, and induce apoptosis of target cells through perforin/granzyme release (and Fas–FasL).
Autologous, gene-modified T cells engineered with the Sleeping Beauty transposon/transposase system to stably express patient-specific, tumor-reactive T-cell receptors targeting mutation-derived neoantigen peptides presented on HLA; upon infusion, these cells activate TCR-CD3 signaling to mediate cytotoxic killing (perforin/granzyme) and may generate immunologic memory.
Autologous T cells are gene-modified with the Sleeping Beauty transposon/transposase system to stably express patient-specific, tumor-reactive TCRs that recognize mutation-derived neoantigen peptides presented on HLA (primarily MHC I). Upon infusion, engagement of the TCR-CD3 complex triggers activation, clonal expansion, cytokine release, and cytotoxic killing of tumor cells via perforin/granzyme, with potential development of immunologic memory.
TCR-engineered T cells bind the specific neoantigen peptide–HLA-B complex, activate via TCR-CD3, and kill the target cell via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Autologous, gene-modified T cells engineered with the Sleeping Beauty transposon/transposase system to stably express patient-specific, tumor-reactive T-cell receptors targeting mutation-derived neoantigen peptides presented on HLA; upon infusion, these cells activate TCR-CD3 signaling to mediate cytotoxic killing (perforin/granzyme) and may generate immunologic memory.
Autologous T cells are gene-modified with the Sleeping Beauty transposon/transposase system to stably express patient-specific, tumor-reactive TCRs that recognize mutation-derived neoantigen peptides presented on HLA (primarily MHC I). Upon infusion, engagement of the TCR-CD3 complex triggers activation, clonal expansion, cytokine release, and cytotoxic killing of tumor cells via perforin/granzyme, with potential development of immunologic memory.
TCR-engineered T cells recognize the neoantigen peptide–HLA-C complex and directly lyse the presenting cell via perforin/granzyme release (and Fas/FasL-mediated apoptosis).
An antibody–drug conjugate that targets Nectin‑4 on urothelial cancer cells and delivers the microtubule inhibitor MMAE, leading to microtubule disruption, G2/M arrest, and apoptosis.
Monoclonal antibody targeting Nectin-4 linked to the microtubule inhibitor MMAE via a cleavable linker; after binding and internalization in Nectin-4–expressing tumor cells, MMAE is released to inhibit tubulin polymerization, leading to microtubule disruption, G2/M arrest, and apoptosis.
ADC binds Nectin-4 on tumor cells, is internalized, linker is cleaved to release MMAE, which inhibits tubulin polymerization leading to microtubule disruption, G2/M arrest, and apoptosis.
Antibody–drug conjugate (Blenrep) comprising an anti-BCMA IgG1 monoclonal antibody linked to monomethyl auristatin F (MMAF); binds BCMA on myeloma cells, is internalized, releases MMAF to disrupt microtubules and induce apoptosis, and can mediate ADCC/ADCP.
Anti-BCMA IgG1 antibody linked to monomethyl auristatin F (MMAF). After binding BCMA on myeloma cells, the complex is internalized and releases MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the afucosylated Fc can also mediate ADCC/ADCP.
The ADC binds BCMA, is internalized, and releases MMAF that inhibits tubulin polymerization causing G2/M arrest and apoptosis; its afucosylated Fc also mediates ADCC/ADCP against BCMA+ cells.