Anti‑CD20 monoclonal antibody that depletes B cells via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and mediates B‑cell depletion via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and kills them via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity, and apoptosis upon CD20 cross-linking.
Fully human IgG1 monoclonal antibody targeting CA19-9 (sialyl-Lewis A) on tumor cells; mediates ADCC and CDC.
Fully human IgG1 monoclonal antibody targeting CA19-9 (sialyl-Lewis A) on tumor cells; binding triggers Fc-mediated antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), leading to lysis of CA19-9-expressing cancer cells.
IgG1 antibody binds CA19-9 on tumor cells and engages immune effectors via Fc to induce ADCC and activates complement (CDC), leading to lysis of CA19-9–expressing cells.
Autologous, gene-modified CAR T-cell therapy engineered to express chimeric antigen receptors targeting CD19 and CD22; administered as a single IV infusion. CAR engagement triggers CD3zeta/co-stimulatory signaling leading to T-cell activation, expansion, cytokine release, and cytotoxic killing of malignant B-lineage lymphoblasts. Manufactured via the T-Charge process.
Autologous T cells are gene-modified to express chimeric antigen receptors targeting CD19 and CD22. Upon antigen engagement, CAR-mediated CD3ζ and co‑stimulatory signaling activates and expands the T cells, driving cytokine release and cytotoxic killing of CD19/CD22‑positive malignant B‑lineage lymphoblasts.
CAR T cells recognize CD19, become activated via CD3zeta/co-stimulatory signaling, and kill target cells through perforin/granzyme release and death-receptor (e.g., Fas/FasL) pathways.
Autologous, gene-modified CAR T-cell therapy engineered to express chimeric antigen receptors targeting CD19 and CD22; administered as a single IV infusion. CAR engagement triggers CD3zeta/co-stimulatory signaling leading to T-cell activation, expansion, cytokine release, and cytotoxic killing of malignant B-lineage lymphoblasts. Manufactured via the T-Charge process.
Autologous T cells are gene-modified to express chimeric antigen receptors targeting CD19 and CD22. Upon antigen engagement, CAR-mediated CD3ζ and co‑stimulatory signaling activates and expands the T cells, driving cytokine release and cytotoxic killing of CD19/CD22‑positive malignant B‑lineage lymphoblasts.
Autologous CD22‑targeted CAR T cells bind CD22 on tumor cells and directly induce cytolysis via immune synapse formation with perforin/granzyme release (and death receptor pathways), leading to apoptosis.
A fibroblast activation protein (FAP)-targeted radiopharmaceutical in which the FAP-binding ligand LNC1004 is labeled with the beta-emitting radionuclide lutetium-177; it binds FAP on cancer-associated fibroblasts and delivers localized beta radiation, causing DNA damage with cross-fire effects on nearby tumor cells.
EB-modified FAP inhibitor LNC1004 is chelated with DOTA and labeled with lutetium-177; after binding to fibroblast activation protein on cancer-associated fibroblasts, the complex is internalized and delivers beta radiation that induces DNA damage and cell death in FAP-expressing stromal cells with cross-fire effects killing adjacent tumor cells.
Radiolabeled FAP inhibitor binds FAP on cancer-associated fibroblasts, is internalized, and 177Lu beta emissions induce DNA double-strand breaks, leading to cell death; cross-fire can also affect nearby cells.