Autologous, gene-modified anti-CD19 CAR T-cell therapy with CD28 costimulation; CAR engagement of CD19 triggers T-cell activation (CD3ζ/CD28), cytotoxic killing, and cytokine release.
Autologous T cells are gene-modified to express an anti-CD19 chimeric antigen receptor with CD28 costimulation and CD3ζ signaling. Upon binding CD19 on B-cell malignancies, the CAR activates T-cell signaling, driving proliferation, cytokine release, and targeted cytotoxic killing of CD19-positive tumor cells.
Anti-CD19 CAR T cells bind CD19, triggering CD3ζ/CD28 signaling and T-cell activation, leading to perforin/granzyme-mediated cytolysis and apoptosis of CD19+ cells.
A human IgG1 monoclonal antibody immune checkpoint inhibitor targeting PD-L1; it blocks PD-L1 interactions with PD-1 and B7.1 to restore T‑cell activation and antitumor immunity and, via its Fc-competent IgG1, can mediate antibody-dependent cellular cytotoxicity (ADCC) through NK cells.
Human IgG1 monoclonal antibody against PD-L1 that blocks PD-L1 interactions with PD-1 and B7.1 to release T-cell inhibition and restore antitumor immunity; its Fc-competent IgG1 can also engage NK cells to mediate ADCC against PD-L1–expressing tumor cells.
Avelumab binds PD-L1 on target cells and, via its IgG1 Fc, engages NK cells (CD16) to trigger antibody-dependent cellular cytotoxicity (ADCC), directly killing PD-L1-positive cells; PD-1/PD-L1 blockade also enhances T-cell killing (indirect).
Human IgG1κ monoclonal antibody targeting CD38; depletes CD38+ plasma cells via ADCC, CDC, ADCP, and apoptosis, with additional immunomodulatory effects.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on plasma cells and other CD38+ immune cells, inducing cell death via ADCC, CDC, ADCP, and apoptosis, thereby depleting CD38+ pathogenic and immunosuppressive cells and exerting immunomodulatory effects.
Binding of daratumumab to CD38 on cells triggers antibody-mediated killing via ADCC, CDC, ADCP, and can induce apoptosis of CD38+ cells.
Human anti-CD2 monoclonal antibody biologic that binds CD2 on T cells and NK cells, blocks LFA-3/CD2 costimulation, and preferentially depletes/modulates CD2hi effector-memory T cells while relatively sparing regulatory T cells.
Human anti-CD2 monoclonal antibody that binds CD2 on T cells and NK cells, blocks LFA-3/CD2 costimulation, and preferentially depletes/modulates CD2hi effector-memory T cells while relatively sparing regulatory T cells, suppressing alloreactive responses.
Anti-CD2 IgG engages Fc effector functions to deplete CD2+ cells via ADCC/ADCP and possibly complement-mediated lysis; may also trigger apoptosis, while also blocking LFA-3/CD2 costimulation.
Armored, glypican-3 (GPC3)-targeted autologous CAR T-cell therapy for advanced/recurrent GPC3-positive hepatocellular carcinoma. Patient T cells are engineered to express a CAR that binds GPC3, triggering T-cell activation, cytokine release, and cytotoxic killing of GPC3+ tumor cells. The armored design is intended to enhance T-cell persistence and function within the solid tumor microenvironment. Administered as a single IV infusion.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds glypican-3 (GPC3) on tumor cells, leading to T-cell activation, cytokine release, and direct cytotoxic killing of GPC3-positive cells; the armored design enhances T-cell persistence and function within the immunosuppressive solid tumor microenvironment.
GPC3-specific CAR T cells bind GPC3 on target cells, become activated, and kill them via T-cell cytotoxic pathways (perforin/granzyme and Fas–FasL–mediated apoptosis).