Third-generation, irreversible covalent EGFR tyrosine kinase inhibitor selective for mutant EGFR (including T790M), blocking EGFR signaling to inhibit proliferation and induce death of EGFR-mutant tumor cells and overcome T790M-mediated resistance.
A fully humanized IgG1 antibody-drug conjugate targeting B7-H3 (CD276). After binding and internalization into B7-H3–expressing tumor cells, it releases a cytotoxic payload to kill the cells. Administered IV every 3 weeks; evaluated as monotherapy for relapsed/refractory osteosarcoma and other sarcomas.
Fully humanized IgG1 ADC targeting B7-H3 (CD276); upon binding to B7-H3 on tumor cells and internalization, it releases a topoisomerase inhibitor payload that inhibits DNA topoisomerase activity, blocks DNA replication, and induces cell cycle arrest and apoptosis in B7-H3–expressing tumor cells.
The ADC binds B7-H3 on target cells, is internalized, and releases a topoisomerase inhibitor payload that inhibits DNA topoisomerase, blocks DNA replication, and induces cell-cycle arrest and apoptosis.
Autologous CD39+CD103+ CD8+ tumor-infiltrating lymphocytes (TIL) enriched and expanded ex vivo (AGX148); adoptive cellular therapy targeting tumor antigens via the TCR.
Autologous CD39+CD103+ CD8+ TILs are enriched and expanded ex vivo and reinfused to provide tumor‑reactive cytotoxic T cells that recognize patient-specific tumor antigens via their endogenous TCRs and mediate HLA-restricted killing of tumor cells.
Infused autologous CD8+ TILs recognize the tumor neoantigen peptide–HLA class I complex via their endogenous TCR and directly kill target cells through HLA-restricted cytotoxicity (perforin/granzyme release and death receptor pathways).
Autologous CD39+CD103+ CD8+ tumor-infiltrating lymphocytes (TIL) enriched and expanded ex vivo (AGX148); adoptive cellular therapy targeting tumor antigens via the TCR.
Autologous CD39+CD103+ CD8+ TILs are enriched and expanded ex vivo and reinfused to provide tumor‑reactive cytotoxic T cells that recognize patient-specific tumor antigens via their endogenous TCRs and mediate HLA-restricted killing of tumor cells.
Endogenous TCRs on reinfused CD8+ TILs recognize tumor-associated peptide–HLA class I (pMHC), triggering cytotoxic T-cell killing via perforin/granzyme release and death receptor pathways (e.g., Fas–FasL), HLA-I–restricted.
Anti-HER2 monoclonal antibody that inhibits HER2 signaling and mediates ADCC.
Humanized monoclonal antibody targeting HER2 (ERBB2); binds the receptor on tumor cells to inhibit HER2 signaling/dimerization and triggers immune effector functions, mediating antibody-dependent cell-mediated cytotoxicity (ADCC) against HER2-overexpressing cells.
Trastuzumab binds HER2 on target cells and engages Fcγ receptor–bearing effector cells to mediate ADCC, leading to killing of HER2+ cells (with possible contribution from CDC and apoptosis).