Engineered CAR T cells directed at CD38 using lentiviral transduction; IV infusion with dose escalation; targets CD38+ plasma cell/myeloma malignancies via CAR-mediated T-cell activation and cytotoxicity.
Gene-modified T cells transduced (lentiviral) to express a chimeric antigen receptor that binds CD38 on target cells. CAR engagement triggers T‑cell activation and proliferation with cytokine release and perforin/granzyme-mediated cytotoxicity, leading to MHC-independent killing of CD38-positive plasma cell/myeloma malignancies.
YES
DIRECT
CAR T cells recognize CD38 on target cells, form an immune synapse, and kill via perforin/granzyme-mediated lysis and apoptosis (plus Fas/FasL and cytokine-mediated effects), independent of MHC.
An anti‑HER2 antibody–drug conjugate consisting of a humanized anti‑HER2 monoclonal antibody linked to the microtubule inhibitor MMAE; kills HER2‑expressing tumor cells with a bystander effect.
Humanized anti-HER2 monoclonal antibody conjugated to the microtubule inhibitor MMAE. Binds HER2 on tumor cells, is internalized, and releases MMAE via a cleavable linker to disrupt microtubules, causing G2/M arrest and apoptosis; cytotoxic payload can diffuse for a bystander effect on neighboring cells with lower HER2 expression.
NO
INDIRECT
The ADC binds HER2 on tumor cells, is internalized, and releases MMAE, which binds beta‑tubulin to disrupt microtubules, causing G2/M arrest and apoptosis; MMAE can diffuse for a bystander effect, but beta‑tubulin itself is not the targeting antigen.
An autologous tumor-infiltrating lymphocyte (TIL) therapy manufactured from a patient's tumor, containing polyclonal CD8+ and CD4+ T cells that recognize patient-specific tumor antigens via the TCR–MHC pathway and mediate cytotoxic killing.
Autologous, ex vivo–expanded polyclonal CD8+ and CD4+ tumor-infiltrating T cells that recognize patient-specific tumor antigens via TCR–MHC interactions and kill tumor cells through perforin/granzyme-mediated cytotoxicity. Lymphodepleting chemotherapy enhances engraftment, and high-dose IL-2 supports in vivo expansion and persistence.
YES
DIRECT
Autologous TILs recognize the neoantigen peptide–MHC I via their TCR and directly kill target cells through perforin/granzyme-mediated apoptosis (and Fas–FasL pathways).
An autologous tumor-infiltrating lymphocyte (TIL) therapy manufactured from a patient's tumor, containing polyclonal CD8+ and CD4+ T cells that recognize patient-specific tumor antigens via the TCR–MHC pathway and mediate cytotoxic killing.
Autologous, ex vivo–expanded polyclonal CD8+ and CD4+ tumor-infiltrating T cells that recognize patient-specific tumor antigens via TCR–MHC interactions and kill tumor cells through perforin/granzyme-mediated cytotoxicity. Lymphodepleting chemotherapy enhances engraftment, and high-dose IL-2 supports in vivo expansion and persistence.
YES
DIRECT
TILs (including CD4+ T cells) recognize the neoantigen peptide presented by MHC class II via their TCR and directly kill the presenting cell through perforin/granzyme-mediated cytolysis (and possibly Fas–FasL apoptosis).
An autologous tumor-infiltrating lymphocyte (TIL) therapy manufactured from a patient's tumor, containing polyclonal CD8+ and CD4+ T cells that recognize patient-specific tumor antigens via the TCR–MHC pathway and mediate cytotoxic killing.
Autologous, ex vivo–expanded polyclonal CD8+ and CD4+ tumor-infiltrating T cells that recognize patient-specific tumor antigens via TCR–MHC interactions and kill tumor cells through perforin/granzyme-mediated cytotoxicity. Lymphodepleting chemotherapy enhances engraftment, and high-dose IL-2 supports in vivo expansion and persistence.
YES
DIRECT
TILs recognize the tumor-associated peptide–HLA class I complex via their TCR and directly kill the presenting cell through perforin/granzyme-mediated cytotoxicity (and Fas–FasL apoptosis).