A human afucosylated IgG1 monoclonal antibody (AMG 451; KHK4083) administered subcutaneously that targets OX40 (CD134), blocks OX40–OX40L signaling to reduce T-cell activation and survival, and mediates ADCC to deplete OX40-positive activated T cells.
Human afucosylated IgG1 monoclonal antibody targeting OX40 (CD134) that blocks OX40–OX40L co-stimulatory signaling to reduce T-cell activation and survival, with enhanced ADCC to deplete OX40-positive activated T cells.
Binds OX40 on activated T cells and, via its afucosylated IgG1 Fc, engages FcγRIIIa on NK cells to trigger ADCC, directly depleting OX40+ cells.
A HER2-targeted antibody–drug conjugate with a cleavable linker to a topoisomerase I inhibitor payload; binds HER2, internalizes, and releases the payload to induce DNA damage while retaining HER2 blockade and ADCC.
HER2-targeted monoclonal antibody conjugated via a cleavable linker to a topoisomerase I inhibitor; binds HER2 on tumor cells, internalizes, and releases the cytotoxic payload to inhibit Topo I and induce DNA damage–mediated cell death, while also blocking HER2 signaling and engaging ADCC.
HER2-targeted ADC binds HER2, is internalized, and releases a topoisomerase I inhibitor payload that induces DNA damage–mediated cell death; it can also promote ADCC.
A HER2-targeted antibody–drug conjugate delivering the maytansinoid DM1 (microtubule inhibitor) via a non-cleavable linker; inhibits mitosis and mediates HER2 signaling blockade and ADCC.
HER2-targeted monoclonal antibody-drug conjugate (trastuzumab linked via a non-cleavable linker to the maytansinoid DM1). After binding HER2, it is internalized and degraded to release a DM1 catabolite that inhibits microtubules, causing mitotic arrest and apoptosis; the trastuzumab component also blocks HER2 signaling and mediates ADCC.
T-DM1 binds HER2, is internalized, and lysosomal processing releases a DM1 catabolite that inhibits microtubules, causing mitotic arrest and apoptosis; Fc may also mediate ADCC.
MicAbody adaptor protein (bispecific antibody; also known as ASP101G) that binds CD20 and carries an orthogonal NKG2D ligand to dock and activate ASP2802 convertible CAR T cells, enabling titratable on/off targeting.
MA-20 (ASP101G) is a MicAbody bispecific adaptor that binds CD20 on B cells and carries an orthogonal NKG2D ligand to engage and activate ASP2802 convertible CAR T cells. By bridging CD20+ tumor cells to the engineered CAR T receptor, it enables titratable, on/off CAR T cytotoxic activity against CD20-positive malignancies.
MA-20 binds CD20 on target cells and engages ASP2802 convertible CAR T cells via an orthogonal NKG2D ligand, bridging them to CD20+ cells and triggering CAR T–mediated killing (perforin/granzyme-dependent lysis).
Long-acting (LS-engineered) human IgG1 broadly neutralizing monoclonal antibody targeting the HIV-1 Env gp120 CD4-binding site; neutralizes free virions, blocks Env–CD4/coreceptor-mediated entry, and can recruit Fc-mediated effector functions.
LS-engineered human IgG1 broadly neutralizing monoclonal antibody targeting the HIV-1 Env gp120 CD4-binding site; neutralizes free virions and blocks Env–CD4/coreceptor-mediated entry. The Fc domain can recruit effector functions (e.g., ADCC/ADCP) against Env-expressing infected cells, and LS mutations enhance FcRn binding to extend serum half-life.
The IgG1 bNAb binds gp120 on Env-expressing infected cells and its Fc recruits effector functions—primarily NK cell–mediated ADCC and macrophage/monocyte ADCP; it may also trigger complement (CDC)—resulting in killing of the target cells.