Autologous, gene-modified TCR-engineered T cells (TCR-T; T-Plex) expressing a high-affinity TCR specific for MAGE-A1 peptide presented by HLA-A*01:01; targets peptide–HLA on tumor cells to induce TCR/CD3-mediated cytotoxic killing after lymphodepletion.
Autologous T cells are gene-modified to express a high-affinity TCR specific for the MAGE-A1 peptide presented by HLA-A*01:01. After lymphodepletion, these TCR-T cells recognize the peptide–HLA complex on tumor cells, activate TCR/CD3 signaling, and mediate targeted cytotoxic killing.
Engineered TCR-T cells bind the MAGE-A1 peptide presented by HLA-A*01:01 on target cells, activating TCR/CD3 signaling and cytolytic degranulation (perforin/granzymes) to induce apoptosis.
Autologous, gene-modified TCR-engineered T cells (TCR-T; T-Plex) expressing a high-affinity TCR specific for MAGE-C2 peptide presented by HLA-B*07:02; recognizes peptide–HLA on tumor cells to trigger TCR/CD3 signaling and cytotoxicity following lymphodepletion.
Autologous T cells are gene-modified to express a high-affinity TCR specific for the MAGE-C2 peptide presented by HLA-B*07:02. Binding to the peptide–HLA complex on tumor cells triggers TCR/CD3 signaling, activating the T cells to mediate cytokine release and targeted cytotoxic killing of antigen-positive tumor cells following lymphodepletion.
Engineered TCR-T cells bind the MAGE-C2 peptide presented by HLA-B*07:02 on tumor cells, triggering TCR/CD3 activation and perforin/granzyme (and Fas/FasL)–mediated killing of antigen-positive cells.
Autologous, gene-modified TCR-engineered T cells (TCR-T; T-Plex) expressing a high-affinity TCR specific for MAGE-A4 peptide presented by HLA-A*02:01; mediates recognition of peptide–HLA on tumor cells and TCR/CD3-driven cytotoxic killing after lymphodepletion.
Autologous T cells are gene-modified to express a high-affinity TCR specific for the MAGE-A4 peptide presented by HLA-A*02:01. Upon recognizing the peptide–HLA complex on tumor cells, the introduced TCR triggers TCR/CD3 signaling, leading to T-cell activation and cytotoxic killing of target cells. Activity is HLA-A*02:01–restricted and antigen-dependent, and therapy is administered after lymphodepletion to enhance engraftment and function.
Engineered TCR-T cells recognize the MAGE-A4 peptide presented on HLA-A*02:01, activate via TCR/CD3, and kill target cells via perforin/granzyme release (and death-receptor pathways).
A bispecific T-cell engager (BiTE) antibody that binds CD19 on B cells and CD3 on T cells to redirect cytotoxic T cells against CD19+ B cells and modulate aberrant humoral immunity.
A single‑chain bispecific antibody that binds CD19 on B cells and CD3 on T cells, forming an immunologic synapse that activates cytotoxic T cells to release perforin/granzymes and lyse CD19+ B cells, resulting in B‑cell depletion and modulation of humoral immunity.
Blinatumomab bridges CD3+ T cells to CD19+ cells, forming an immunologic synapse that activates T-cell cytotoxicity (perforin/granzyme-mediated lysis) of CD19-expressing cells.
HER2-directed antibody–drug conjugate in which a humanized anti‑HER2 antibody is linked via a protease-cleavable vedotin linker to the microtubule inhibitor MMAE. Binding to HER2 triggers internalization and lysosomal release of MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander cytotoxicity to adjacent cells.
ADC binds HER2, is internalized, linker is proteolytically cleaved to release MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis; released payload may also cause bystander killing of adjacent cells.