Autologous, genetically engineered convertible CAR T-cell therapy expressing an inert NKG2D-based receptor; requires an adaptor (MicAbody) to engage tumor targets and activate T cells.
Autologous T cells engineered with an inert NKG2D-based convertible CAR that requires an adaptor antibody (MA-20/ASP101G MicAbody). The adaptor binds CD20 on tumor cells and presents a ULBP2 ligand to the CAR, triggering T-cell activation and cytotoxicity against CD20-positive B-cell malignancies; without the adaptor, the CAR T cells remain inactive.
The adaptor MicAbody (MA-20/ASP101G) binds CD20 on target cells and engages the NKG2D-based convertible CAR on ASP2802 T cells via a ULBP2 ligand, activating the CAR T cells to kill CD20+ cells via cytotoxic T-cell mechanisms (e.g., perforin/granzyme-mediated lysis).
Chimeric IgG1 monoclonal antibody against EGFR; blocks EGFR signaling (MAPK/ERK, PI3K/AKT) and can mediate ADCC.
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream MAPK/ERK and PI3K/AKT signaling and tumor cell proliferation; Fc region can mediate ADCC.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages FcγR-bearing effector cells (e.g., NK cells) to trigger ADCC (and potentially CDC), killing EGFR+ cells; it also blocks EGFR signaling (anti-proliferative).
A bispecific T‑cell engager (BiTE) antibody that simultaneously binds CD3 on T cells and CD19 on B‑lineage cells to redirect cytotoxic T cells to kill CD19+ B cells, depleting autoreactive B cells and reducing pathogenic autoantibodies.
Bispecific T‑cell engager antibody that binds CD3 on T cells and CD19 on B‑lineage cells, bringing them into proximity to trigger cytotoxic T‑cell–mediated killing of CD19+ B cells, thereby depleting autoreactive B cells and reducing pathogenic autoantibodies.
Blinatumomab links CD3 on T cells to CD19 on target B cells, triggering T‑cell activation and immune‑synapse formation, leading to perforin/granzyme‑mediated apoptosis of CD19+ cells.
Autologous CD19-directed CAR T-cell therapy (also known as relma-cel/JWCAR029) in which a patient’s T cells are genetically engineered to express a chimeric antigen receptor targeting CD19 on B cells, leading to MHC-independent T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD19+ malignant cells; expected on-target B-cell aplasia.
Autologous T cells are engineered to express a chimeric antigen receptor that binds CD19 on B cells, driving MHC-independent T-cell activation, expansion, cytokine release, and cytotoxic killing of CD19-positive malignant cells, with expected on-target B-cell aplasia.
CD19-directed CAR T cells bind CD19 on target B cells, triggering T-cell activation and cytolytic killing via perforin/granzyme-mediated apoptosis.
Disitamab vedotin, an anti-HER2 antibody–drug conjugate (ADC) carrying the microtubule inhibitor MMAE. It binds HER2 (ERBB2) on tumor cells, is internalized, and releases MMAE to disrupt microtubules and induce cell death; the antibody component may also mediate ADCC and a bystander effect.
Disitamab vedotin (RC48) is an anti-HER2 antibody–drug conjugate that binds HER2 (ERBB2) on tumor cells, is internalized, and releases the microtubule inhibitor MMAE. MMAE inhibits tubulin polymerization, leading to microtubule disruption, G2/M arrest, and apoptosis. The antibody component may also mediate ADCC and a bystander effect.
The ADC binds HER2, is internalized, and releases MMAE, which inhibits tubulin polymerization leading to microtubule disruption, G2/M arrest, and apoptosis; the antibody may also trigger ADCC.