Polyclonal antilymphocyte/antithymocyte globulin that depletes T cells.
Polyclonal anti–T-lymphocyte immunoglobulin that binds multiple T‑cell surface antigens and induces complement-dependent cytotoxicity and Fc-mediated clearance (ADCC/phagocytosis), leading to rapid T‑cell depletion and immunosuppression.
NO
INDIRECT
ATG depletes T cells by binding multiple T‑cell antigens (e.g., CD2/CD3/CD4/CD8) and inducing complement-mediated lysis and Fc-dependent ADCC/phagocytosis; HLA‑B is not the cytotoxic target.
Polyclonal antilymphocyte/antithymocyte globulin that depletes T cells.
Polyclonal anti–T-lymphocyte immunoglobulin that binds multiple T‑cell surface antigens and induces complement-dependent cytotoxicity and Fc-mediated clearance (ADCC/phagocytosis), leading to rapid T‑cell depletion and immunosuppression.
NO
INDIRECT
ATG does not target HLA-C; it binds T-cell–specific surface antigens and depletes T cells via complement-dependent lysis and Fc-mediated ADCC/phagocytosis.
Aumolertinib (HS-10296; almonertinib) is an oral, third-generation, irreversible EGFR tyrosine kinase inhibitor selective for activating EGFR mutations, inhibiting downstream MAPK and PI3K/AKT signaling.
Third-generation, irreversible EGFR tyrosine kinase inhibitor selective for mutant EGFR (e.g., Ex19del, L858R, T790M). Covalently inhibits EGFR kinase activity, blocking autophosphorylation and downstream MAPK and PI3K/AKT signaling, resulting in growth inhibition and apoptosis of EGFR-mutant tumor cells.
YES
DIRECT
Aumolertinib covalently inhibits mutant EGFR (exon 19 deletion), blocking autophosphorylation and MAPK/PI3K-AKT signaling, leading to growth inhibition and apoptosis of EGFR-mutant tumor cells.
Aumolertinib (HS-10296; almonertinib) is an oral, third-generation, irreversible EGFR tyrosine kinase inhibitor selective for activating EGFR mutations, inhibiting downstream MAPK and PI3K/AKT signaling.
Third-generation, irreversible EGFR tyrosine kinase inhibitor selective for mutant EGFR (e.g., Ex19del, L858R, T790M). Covalently inhibits EGFR kinase activity, blocking autophosphorylation and downstream MAPK and PI3K/AKT signaling, resulting in growth inhibition and apoptosis of EGFR-mutant tumor cells.
YES
DIRECT
Aumolertinib covalently inhibits mutant EGFR (L858R), blocking autophosphorylation and downstream MAPK/PI3K-AKT signaling, which triggers growth arrest and apoptosis of the EGFR-mutant tumor cells.
Autologous cellular immunotherapy using ex vivo–generated dendritic cells pulsed with patient-specific tumor neoantigen peptides to prime/expand neoantigen-specific CD8+ and CD4+ T cells.
Autologous dendritic cells are generated ex vivo and pulsed with patient-specific tumor neoantigen peptides. After infusion, the DCs migrate to lymphoid tissues and present these neoantigens on HLA class I and II, providing costimulation (e.g., CD80/CD86) and cytokines to prime and expand neoantigen-specific CD8+ cytotoxic T cells and CD4+ helper T cells, thereby promoting tumor-specific immune responses and immunologic memory.
YES
INDIRECT
Ex vivo–pulsed dendritic cells prime neoantigen-specific T cells; vaccine-activated CD4+ (and supportive CD8+) T cells recognize the neoantigen on HLA class II–positive tumor cells and kill via perforin/granzyme and/or Fas–FasL–mediated apoptosis.