A biological, cell-based immunotherapy administered by intravenous infusion at 3.0×10^8 or 6.0×10^8 cells (up to three monthly infusions) for refractory colorectal or pancreatic cancer; intended to elicit immune-mediated antitumor cytotoxicity. Specific cell type/engineering and target antigens are not disclosed.
Genetically modified human T lymphocytes engineered to express a chimeric antigen receptor that recognizes two undisclosed tumor-associated antigens. Upon binding antigen on colorectal or pancreatic tumor cells, the CAR activates T-cell effector functions (cytokine release, proliferation, and perforin/granzyme-mediated lysis), producing selective immune-mediated antitumor cytotoxicity and aiming to reduce antigen-escape through dual targeting.
CAR-T cells bind the antigen and trigger T-cell effector cytotoxicity, primarily perforin/granzyme-mediated lysis (and related apoptosis) of antigen-positive tumor cells.
Oral BH3-mimetic BCL-2 inhibitor that promotes mitochondrial apoptosis in myeloid blasts.
Selective BH3-mimetic BCL-2 inhibitor that binds the BCL-2 hydrophobic groove, neutralizes its anti‑apoptotic function, and restores BAX/BAK-mediated mitochondrial outer membrane permeabilization and apoptosis in malignant myeloid cells (sparing BCL-XL).
Venetoclax binds and inhibits BCL-2, neutralizing its anti-apoptotic function and enabling BAX/BAK-mediated mitochondrial outer membrane permeabilization, caspase activation, and apoptosis in BCL-2–dependent cells.
Anti-HER2 antibody–drug conjugate linking a monoclonal antibody to MMAE via an enzyme-specific linker; binds HER2, is internalized, and releases MMAE to inhibit microtubules and induce tumor cell death.
Anti-HER2 monoclonal antibody linked to MMAE via a cleavable linker; binds HER2 on tumor cells, is internalized, and releases MMAE intracellularly to inhibit microtubule polymerization, causing G2/M arrest and apoptosis in HER2-expressing cells.
ADC binds HER2, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of HER2+ cells.
CT-P13 is a chimeric human–murine IgG1 monoclonal antibody biosimilar to infliximab (Remicade). It is an anti–TNF-α mAb that binds soluble and transmembrane TNF-α, blocking TNFR1/TNFR2 signaling, reducing NF-κB/MAPK pathway activation and downstream pro‑inflammatory cytokines (e.g., IL‑1, IL‑6) and adhesion molecules; it can induce apoptosis and CDC/ADCC against TNF‑expressing cells. Administered intravenously (IV) or subcutaneously (SC).
Chimeric IgG1 monoclonal antibody biosimilar to infliximab that binds soluble and transmembrane TNF-α, neutralizing TNF-α and preventing TNFR1/TNFR2 signaling. This reduces NF-κB/MAPK pathway activation and downstream pro‑inflammatory cytokines and adhesion molecules; can also induce apoptosis and mediate CDC/ADCC against TNF‑expressing cells.
By binding transmembrane TNF-α, CT-P13 triggers reverse-signaling apoptosis and engages Fc-mediated effector functions (ADCC via NK cells and CDC), killing TNF-α–expressing cells.
Oral small-molecule BCL-2 inhibitor that restores mitochondrial apoptosis in leukemic blasts.
Selective oral BCL-2 inhibitor (BH3 mimetic) that binds the hydrophobic groove of BCL-2, blocks its anti-apoptotic function, and restores mitochondrial apoptosis in malignant cells; minimal BCL-XL inhibition.
Venetoclax directly inhibits BCL-2 (BH3 mimetic), freeing pro-apoptotic proteins to activate BAX/BAK, inducing mitochondrial outer membrane permeabilization, caspase activation, and apoptosis of BCL-2–dependent cells.