Lentivirally transduced CAR T cells specific for CD7; IV infusion at escalating doses; designed for MHC-independent cytotoxicity against CD7+ T-cell malignancies.
Autologous/allogeneic T cells are lentivirally engineered to express a chimeric antigen receptor specific for CD7. Upon binding CD7 on malignant T cells, the CAR provides MHC-independent activation (CD3ζ/co-stimulatory signaling), driving T-cell expansion and cytotoxicity via perforin/granzyme release and cytokine-mediated killing of CD7+ tumor cells.
CD7-specific CAR T cells bind CD7 on target cells, become activated via CD3zeta/co-stimulatory signaling, form an immunologic synapse, and directly lyse CD7+ cells through perforin/granzyme release (with additional death-receptor and cytokine-mediated apoptosis).
Autologous T cells genetically modified via lentiviral transduction to express a B7-H3–targeting chimeric antigen receptor with CD28/CD3ζ signaling domains and membrane 4-1BB ligand to enhance costimulation and persistence; administered locoregionally via CNS reservoir to treat B7-H3 (CD276)-positive pediatric CNS tumors.
Autologous T cells are lentivirally engineered to express a B7-H3-specific chimeric antigen receptor with CD28/CD3zeta signaling. Binding to B7-H3 (CD276) on tumor cells triggers T-cell activation, cytokine release, and cytotoxic killing. Coexpressed membrane 4-1BB ligand provides costimulation to enhance expansion and persistence. Administered locoregionally into the CNS for B7-H3-positive pediatric brain tumors.
B7-H3–specific CAR T cells recognize B7-H3 on target cells and directly kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and death receptor pathways such as Fas/FasL).
Anti-CD38 IgG1 monoclonal antibody that binds CD38 on leukemic T cells to mediate ADCC, CDC, and ADCP and induce direct apoptosis; also inhibits CD38 ectoenzyme (NADase/cyclase) activity to reduce adenosine-mediated immunosuppression.
Isatuximab is an IgG1 monoclonal antibody against CD38. It binds CD38 on malignant T cells to induce Fc-mediated cytotoxicity (ADCC, CDC) and phagocytosis (ADCP) and can trigger direct apoptosis. It also inhibits CD38 ectoenzyme (NADase/cyclase) activity, lowering adenosine production and reducing adenosine-mediated immunosuppression.
Isatuximab binds CD38 on target cells and induces Fc-mediated killing (ADCC, CDC, ADCP) and can trigger direct apoptosis of CD38+ cells.
An anti-CD19 antibody–drug conjugate (Zynlonta) that delivers a pyrrolobenzodiazepine dimer to CD19+ B cells, causing DNA crosslinking and apoptosis.
Anti-CD19 antibody–drug conjugate that binds CD19 on B cells, is internalized, and releases a pyrrolobenzodiazepine (PBD) dimer payload via a cleavable linker; the PBD binds the DNA minor groove to form interstrand crosslinks, blocking DNA replication and inducing apoptosis in CD19-expressing tumor cells.
The anti-CD19 ADC binds CD19, is internalized, and releases a PBD dimer that crosslinks DNA, blocking replication and inducing apoptosis in CD19+ cells.
Chimeric IgG1 monoclonal antibody against EGFR that inhibits downstream signaling to reduce proliferation and survival and mediates antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody targeting EGFR that binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to reduce tumor cell proliferation and survival; its Fc region also mediates antibody-dependent cellular cytotoxicity (ADCC).
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on immune effector cells (e.g., NK cells), triggering antibody‑dependent cellular cytotoxicity; complement‑dependent cytotoxicity may also occur, and EGFR signaling blockade can promote apoptosis.