Autologous T cells retrovirally transduced to express a glypican-3 (GPC3)–specific chimeric antigen receptor, engineered to provide autocrine IL-15 and IL-21 signaling and to include an inducible caspase-9 (iCasp9) safety switch.
Autologous T cells are engineered to express a glypican-3 (GPC3)-specific chimeric antigen receptor that recognizes GPC3 on tumor cells and activates T-cell cytotoxicity; co-expression of IL-15 and IL-21 provides autocrine signaling to enhance proliferation, survival, and persistence; an inducible caspase-9 (iCasp9) safety switch enables rapid elimination of the cells upon administration of a dimerizer drug.
GPC3-specific CAR T cells bind GPC3 on target cells and induce T-cell–mediated killing via perforin/granzyme-mediated apoptosis (with possible Fas/FasL contribution).
Long-acting LS-engineered human IgG1 broadly neutralizing monoclonal antibody targeting the HIV-1 gp120 CD4-binding site to block attachment/entry; extended half-life via enhanced FcRn binding and may mediate Fc-effector functions (e.g., ADCC/ADCP).
Long-acting LS-engineered human IgG1 broadly neutralizing monoclonal antibody that binds the HIV-1 gp120 CD4-binding site, blocking attachment to CD4 and preventing viral entry; LS Fc modifications enhance FcRn binding to extend half-life and may enable Fc-mediated effector functions (e.g., ADCC/ADCP) against Env-expressing cells.
Antibody binds gp120 on Env-expressing (HIV‑infected) cells and engages Fcγ receptors on effector cells to trigger ADCC/ADCP (± complement), leading to killing of the target cells.
Autologous T cells retrovirally transduced to express a glypican-3 (GPC3)–specific chimeric antigen receptor, engineered to provide autocrine IL-15 and IL-21 signaling and to include an inducible caspase-9 (iCasp9) safety switch.
Autologous T cells are engineered to express a glypican-3 (GPC3)-specific chimeric antigen receptor that recognizes GPC3 on tumor cells and activates T-cell cytotoxicity; co-expression of IL-15 and IL-21 provides autocrine signaling to enhance proliferation, survival, and persistence; an inducible caspase-9 (iCasp9) safety switch enables rapid elimination of the cells upon administration of a dimerizer drug.
Upon administration of a dimerizer drug, iCasp9 in the engineered CAR T cells is activated, triggering the caspase cascade and inducing rapid apoptosis of the iCasp9-expressing cells.
Small-molecule dimerizer used to activate the inducible caspase-9 safety switch to rapidly eliminate CAR T cells in the event of toxicity.
Rimiducid (AP1903) is a small-molecule dimerizer that binds engineered FKBP12(F36V) domains fused to inducible caspase-9 in gene-modified T cells, inducing caspase-9 dimerization and activation, which triggers downstream caspase-3/7–mediated apoptosis to rapidly eliminate the modified cells as a safety switch in case of toxicity.
Rimiducid binds the engineered FKBP12(F36V) domains in the iCasp9 switch, dimerizing and activating caspase-9 and triggering downstream caspase-3/7–mediated apoptosis of the modified cells.
Glycoengineered chimeric IgG1 anti-CD20 monoclonal antibody (TG-1101/BRIUMVI). Afucosylation enhances FcγRIIIa binding and antibody-dependent cellular cytotoxicity; also induces complement-dependent cytotoxicity and apoptosis, leading to rapid, sustained depletion of CD20+ B cells in relapsing multiple sclerosis.
Glycoengineered, afucosylated chimeric IgG1 monoclonal antibody targeting CD20 on B cells; enhanced FcγRIIIa binding drives potent antibody-dependent cellular cytotoxicity (ADCC), also triggers complement-dependent cytotoxicity (CDC) and apoptosis, resulting in rapid and sustained depletion of CD20+ B cells.
Binds CD20 on B cells and engages immune effectors via its Fc to induce ADCC (enhanced via FcγRIIIa), activates complement for CDC, and can trigger apoptosis, leading to depletion of CD20+ cells.