Autologous, gene-modified CAR T-cell therapy engineered to express a CAR that binds NKG2D ligands; administered as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells are genetically modified to express a chimeric antigen receptor that recognizes NKG2D ligands (e.g., MICA, MICB, ULBP/RAET1) on tumor cells; CAR engagement activates the T cells to kill NKG2DL-positive cells and release effector cytokines. Administered after lymphodepleting chemotherapy.
LEU011 CAR T cells recognize NKG2D ligands such as ULBP4 on target cells; CAR engagement activates T-cell cytotoxicity, leading to perforin/granzyme-mediated lysis (and death receptor–mediated apoptosis) of the bound cells.
Autologous, gene-modified CAR T-cell therapy engineered to express a CAR that binds NKG2D ligands; administered as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells are genetically modified to express a chimeric antigen receptor that recognizes NKG2D ligands (e.g., MICA, MICB, ULBP/RAET1) on tumor cells; CAR engagement activates the T cells to kill NKG2DL-positive cells and release effector cytokines. Administered after lymphodepleting chemotherapy.
NKG2D-based CAR T cells bind ULBP5 on target cells, activate, form an immunologic synapse, and kill via perforin/granzyme-mediated cytolysis (and Fas/FasL), leading to apoptosis of ULBP5+ cells.
Autologous, gene-modified CAR T-cell therapy engineered to express a CAR that binds NKG2D ligands; administered as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells are genetically modified to express a chimeric antigen receptor that recognizes NKG2D ligands (e.g., MICA, MICB, ULBP/RAET1) on tumor cells; CAR engagement activates the T cells to kill NKG2DL-positive cells and release effector cytokines. Administered after lymphodepleting chemotherapy.
CAR T cells engineered with an NKG2D-ligand–binding CAR recognize ULBP6 on target cells, leading to T-cell activation and direct cytotoxicity via perforin/granzyme release (and death receptor pathways).
Gene-modified autologous CD19-directed CAR T-cell therapy manufactured on the PrimeCAR platform (~3-day process) with high T-naive content; administered as a single IV infusion after lymphodepletion to target and kill CD19+ B-lineage leukemia cells via CAR-mediated TCR/co-stimulatory signaling, T-cell activation, cytokine release, and cytotoxicity.
Autologous T cells are gene-modified to express a CD19-directed chimeric antigen receptor. CAR engagement of CD19 on B-lineage leukemia cells triggers CD3ζ and co-stimulatory signaling, activating T cells to proliferate, release cytokines, and execute perforin/granzyme-mediated cytotoxicity, resulting in targeted depletion of CD19+ malignant (and normal) B cells after lymphodepletion and single IV infusion.
CD19-directed CAR T cells engage CD19 on B cells, triggering T-cell activation and perforin/granzyme-mediated killing of CD19+ target cells.
Human IgG1 broadly neutralizing monoclonal antibody targeting the HIV-1 Env CD4-binding site; LS modification extends half-life; mediates neutralization and Fc effector functions.
Broadly neutralizing human IgG1 antibody that binds the HIV-1 Env CD4-binding site to block viral attachment and entry, neutralizing circulating virions; Fc region mediates effector functions (e.g., ADCC/ADCP, complement) and contains LS (M428L/N434S) mutation to enhance FcRn binding and extend serum half-life.
IgG1 binds gp120 on infected cell surfaces and, via its Fc, engages NK cells/macrophages (ADCC/ADCP) and activates complement (CDC) to lyse the target cells.