An anti-HER2 antibody–drug conjugate (humanized IgG1) given IV every 2 weeks. It binds HER2 (ERBB2) on tumor cells, is internalized, and a cleavable linker releases the cytotoxic payload monomethyl auristatin E (MMAE), a microtubule inhibitor that induces G2/M arrest and apoptosis; the IgG1 Fc can trigger ADCC and released MMAE may produce a bystander effect.
Humanized anti-HER2 (ERBB2) IgG1 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and via a cleavable linker releases the cytotoxic payload MMAE, a microtubule inhibitor causing G2/M arrest and apoptosis; the IgG1 Fc can mediate ADCC, and released MMAE may produce a bystander effect.
Binds HER2 and is internalized; cleavable linker releases MMAE, a microtubule inhibitor, causing G2/M arrest and apoptosis of HER2+ cells. The IgG1 Fc can also mediate ADCC, with possible bystander killing from released MMAE.
Autologous tumor-infiltrating lymphocyte (TIL) cell therapy in which patient tumor T cells are expanded ex vivo and reinfused after lymphodepleting chemotherapy to mediate tumor-specific cytotoxicity and enhance persistence.
Autologous T cells isolated from the patient’s tumor are expanded ex vivo and reinfused after lymphodepleting chemotherapy to reconstitute a large pool of tumor‑reactive T cells. These TILs recognize native tumor antigens via their endogenous TCRs and mediate tumor cell killing through cytotoxic effector functions, supporting durable antitumor immunity.
Infused TILs use their endogenous TCRs to recognize tumor neoantigen peptide–HLA class I complexes and directly kill target cells via perforin/granzyme release and death receptor (Fas–FasL) pathways.
Autologous tumor-infiltrating lymphocyte (TIL) cell therapy in which patient tumor T cells are expanded ex vivo and reinfused after lymphodepleting chemotherapy to mediate tumor-specific cytotoxicity and enhance persistence.
Autologous T cells isolated from the patient’s tumor are expanded ex vivo and reinfused after lymphodepleting chemotherapy to reconstitute a large pool of tumor‑reactive T cells. These TILs recognize native tumor antigens via their endogenous TCRs and mediate tumor cell killing through cytotoxic effector functions, supporting durable antitumor immunity.
Autologous TILs recognize tumor-associated peptide–HLA class I complexes via their TCRs and directly kill target cells by perforin/granzyme release and Fas–FasL–mediated apoptosis.
Autologous tumor-infiltrating lymphocyte (TIL) cell therapy in which patient tumor T cells are expanded ex vivo and reinfused after lymphodepleting chemotherapy to mediate tumor-specific cytotoxicity and enhance persistence.
Autologous T cells isolated from the patient’s tumor are expanded ex vivo and reinfused after lymphodepleting chemotherapy to reconstitute a large pool of tumor‑reactive T cells. These TILs recognize native tumor antigens via their endogenous TCRs and mediate tumor cell killing through cytotoxic effector functions, supporting durable antitumor immunity.
Reinfused tumor-infiltrating lymphocytes recognize the tumor neoantigen peptide–HLA class II complex via their endogenous TCRs (primarily CD4+ T cells) and directly kill target cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
Autologous tumor-infiltrating lymphocyte (TIL) cell therapy in which patient tumor T cells are expanded ex vivo and reinfused after lymphodepleting chemotherapy to mediate tumor-specific cytotoxicity and enhance persistence.
Autologous T cells isolated from the patient’s tumor are expanded ex vivo and reinfused after lymphodepleting chemotherapy to reconstitute a large pool of tumor‑reactive T cells. These TILs recognize native tumor antigens via their endogenous TCRs and mediate tumor cell killing through cytotoxic effector functions, supporting durable antitumor immunity.
Reinfused TILs recognize the tumor-associated peptide–HLA class II complex via their endogenous TCRs and directly kill the presenting cell through perforin/granzyme release and/or Fas–FasL–mediated apoptosis.