Oral small‑molecule BCL‑2 inhibitor that induces intrinsic (mitochondrial) apoptosis in BCL‑2–dependent lymphoma cells.
Selective oral BCL-2 inhibitor (BH3 mimetic) that binds the hydrophobic groove of BCL-2, blocking its anti-apoptotic function and restoring mitochondrial (intrinsic) apoptosis in BCL-2–dependent tumor cells; spares BCL-XL.
Venetoclax directly inhibits BCL-2 (BH3 mimetic), releasing pro-apoptotic factors to activate BAX/BAK, trigger mitochondrial outer membrane permeabilization, cytochrome c release, and caspase-mediated apoptosis in BCL-2–dependent cells.
A B7-H3 (CD276)–targeted antibody-drug conjugate that binds B7-H3 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor cell death.
BGB-C354 is a B7-H3 (CD276)-targeted antibody-drug conjugate. The antibody binds B7-H3 on tumor cells, is internalized, and releases a topoisomerase-1 inhibitor payload that inhibits topo I, blocking DNA replication and inducing cell cycle arrest and apoptosis in B7-H3–expressing tumor cells.
The ADC binds B7-H3 on target cells, is internalized, and releases a topoisomerase-1 inhibitor that blocks DNA replication, leading to cell cycle arrest and apoptosis.
Autologous, non–genetically engineered, ex vivo–expanded polyclonal multi–tumor-associated antigen (multiTAA)–specific T-cell therapy that recognizes multiple shared TAAs on pancreatic adenocarcinoma via native, MHC-restricted TCRs to mediate cytotoxic killing and cytokine-driven immune activation.
Autologous, ex vivo-expanded polyclonal CD4+/CD8+ T cells with native, MHC-restricted TCRs specific for multiple shared tumor-associated antigens on pancreatic adenocarcinoma. After infusion, these T cells recognize antigen-MHC complexes on tumor cells and mediate cytotoxic killing (perforin/granzyme) and cytokine-driven immune activation; multi-antigen targeting reduces antigen-loss escape and may improve durability.
Infused autologous T cells recognize MAGE-A4–derived peptides presented on MHC via native TCRs and directly lyse target cells through perforin/granzyme-mediated cytotoxicity.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting B7‑H3 (CD276); activation via CD3ζ/co-stimulatory signaling induces cytokine release and perforin/granzyme-mediated cytotoxicity against B7‑H3–positive glioma cells. Administered intracavitary and/or intraventricular with dose escalation.
Autologous T cells engineered to express a chimeric antigen receptor targeting B7-H3 (CD276) bind B7-H3 on tumor cells, triggering CD3zeta and co-stimulatory signaling that activates T cells to release cytokines and kill targets via perforin/granzyme-mediated cytotoxicity; administered locally (intracavitary/intraventricular) for B7-H3–positive glioma.
CAR-T cells recognize B7-H3 and, upon CAR (CD3ζ/co-stimulatory) activation, kill target cells via perforin/granzyme-mediated cytotoxicity.
Anti-CD38 IgG1 monoclonal antibody targeting CD38 on malignant plasma cells; mediates ADCC/CDC/ADCP, induces apoptosis, and inhibits CD38 ectoenzyme activity to reduce immunosuppressive adenosine.
Unconjugated anti-CD38 IgG1 monoclonal antibody that binds CD38 on malignant plasma cells and induces cell death via Fc-mediated ADCC, CDC, and ADCP; also directly triggers apoptosis and inhibits CD38 ectoenzyme activity, reducing immunosuppressive adenosine and depleting CD38+ tumor cells.
Binds CD38 on target cells and induces killing via Fc-mediated ADCC, complement-dependent cytotoxicity, antibody-dependent phagocytosis, and can also directly trigger apoptosis.