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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
Oral small-molecule BCL-2 inhibitor that triggers mitochondrial apoptosis in leukemic cells.
Selective BH3-mimetic that inhibits BCL-2 by binding its hydrophobic groove, neutralizing its anti-apoptotic function and restoring mitochondrial apoptosis (MOMP and caspase activation) in BCL-2–dependent tumor cells; minimal BCL-XL inhibition reduces thrombocytopenia risk.
YES
DIRECT
Venetoclax inhibits BCL-2 in BCL-2–dependent cells, enabling BAX/BAK activation and mitochondrial outer membrane permeabilization, leading to caspase-mediated apoptosis.