Autologous, non–genetically engineered, ex vivo–expanded polyclonal multi–tumor-associated antigen (multiTAA)–specific T-cell therapy that recognizes multiple shared TAAs on pancreatic adenocarcinoma via native, MHC-restricted TCRs to mediate cytotoxic killing and cytokine-driven immune activation.
Autologous, ex vivo-expanded polyclonal CD4+/CD8+ T cells with native, MHC-restricted TCRs specific for multiple shared tumor-associated antigens on pancreatic adenocarcinoma. After infusion, these T cells recognize antigen-MHC complexes on tumor cells and mediate cytotoxic killing (perforin/granzyme) and cytokine-driven immune activation; multi-antigen targeting reduces antigen-loss escape and may improve durability.
YES
DIRECT
Native, MHC-restricted TCRs on the infused multiTAA-specific CD4+/CD8+ T cells recognize PRAME-derived peptides presented on HLA and directly lyse target cells via perforin/granzyme (with supportive cytokine-mediated effects).
Autologous CD8+ T cells genetically engineered (gene-edited, TCR-transduced) with a personalized, multi-target, tumor-specific TCR set; administered as sequential IV infusions to redirect T-cell receptor specificity to patient-specific HLA class I–presented tumor antigens and drive cytotoxic effector activity (cytokine release, perforin/granzyme-mediated killing).
Autologous CD8+ T cells are gene-edited and TCR-transduced to express a personalized set of tumor-specific T-cell receptors that recognize patient-specific peptide–HLA class I complexes on tumor cells, activating TCR signaling and cytotoxic effector functions (cytokine release, perforin/granzyme-mediated killing) to eliminate cancer cells.
YES
DIRECT
Engineered CD8+ T cells recognize the patient-specific peptide–HLA class I complex via their transduced TCRs and directly kill target cells through TCR-triggered cytotoxic effector functions (perforin/granzyme release and Fas–FasL–mediated apoptosis).
First-in-human investigational immunotherapy designed to target the NY‑ESO‑1 antigen presented by HLA‑A2, aiming to elicit antigen-specific T‑cell–mediated anti-tumor responses in HLA‑A2–positive and/or NY‑ESO‑1–positive tumors.
A TCR-mimetic bispecific that targets the NY‑ESO‑1 peptide presented by HLA‑A2 on tumor cells and engages T cells to drive antigen‑specific cytotoxic killing of HLA‑A2/NY‑ESO‑1–positive tumors.
YES
DIRECT
A TCR-mimetic bispecific binds the NY-ESO-1/HLA-A*02 peptide-MHC on tumor cells and CD3 on T cells, creating an immunological synapse that activates T cells to kill the target cell via perforin/granzyme-mediated apoptosis (and Fas/FasL pathways).
First-in-human investigational immunotherapy designed to target the NY‑ESO‑1 antigen presented by HLA‑A2, aiming to elicit antigen-specific T‑cell–mediated anti-tumor responses in HLA‑A2–positive and/or NY‑ESO‑1–positive tumors.
A TCR-mimetic bispecific that targets the NY‑ESO‑1 peptide presented by HLA‑A2 on tumor cells and engages T cells to drive antigen‑specific cytotoxic killing of HLA‑A2/NY‑ESO‑1–positive tumors.
NO
INDIRECT
DS-2243a bridges NY-ESO-1/HLA-A2 on tumor cells with CD3ε on T cells, activating T cells to kill the antigen-positive tumor cells (perforin/granzyme-mediated lysis); CD3ε-expressing T cells are effectors, not targets of killing.
An antibody-drug conjugate comprising an anti-HER2 IgG1 (trastuzumab) linked to a membrane-permeable topoisomerase I inhibitor payload (DXd). It binds HER2 (including low expression), is internalized, releases DXd to inhibit TOP1 and induce DNA damage/apoptosis with bystander effect; the trastuzumab component can inhibit HER2 signaling and mediate ADCC.
Anti-HER2 IgG1 (trastuzumab) linked to a membrane‑permeable topoisomerase I inhibitor payload (DXd). After binding HER2 (including low expression) and internalization, the linker is cleaved to release DXd, which inhibits TOP1, causing DNA damage and apoptotic cell death with a bystander effect; the antibody component can also inhibit HER2 signaling and mediate ADCC.
YES
DIRECT
ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage and apoptotic death of HER2+ cells; trastuzumab component can also mediate ADCC and bystander killing.