Takeda Oncology (Millennium Pharmaceuticals, Inc) is a wholly owned subsidiary of Takeda Pharmaceutical Company Limited, developing therapies for the treatment of cancer.
In May 2008, Millennium was acquired by Takeda Pharmaceutical for $8.8 billion USD and is operating as an independent wholly owned subsidiary of Takeda.
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Takeda Oncology Active Oncology Pipeline Drug Description
- Pevonedistat, a first in class NEDD8-activating enzyme (NAE) inhibitor, could be the first novel treatment for Higher-Risk Myelodysplastic Syndromes patients in more than a decade, expanding treatment options that have so far been limited to hypomethylating agent (HMA) monotherapy alone.
- Mobocertinib is a potent, small-molecule TKI specifically designed to selectively target EGFR and HER2 exon 20 insertion mutations.
- TAK-007, an allogenic CAR-NK cell therapy for CD19+ hematological malignancies
- TAK-169, a novel CD38-specific immunotoxin ETB, armed with a deimmunized (DI) Shiga-like toxin A subunit (SLTA) payload, has been designed with this idea. TAK-169 induces irreversible ribosome inactivation of target cells with no dependency on immune effector cells.
- Engineered Toxin Bodies (ETBs) are developed by modifying a bacterial toxin to reduce its immunogenicity and allow for its PEGylation. This bacterial toxin scaffold has been fused to randomized scFv fragments and expressed on phage display to create screen able libraries of immunotoxins ETBs. These ETBs retain the parent toxin’s ability and have an improved and predictable pharmacokinetic.
- TAK-573 is a first-in-class, humanized, anti-CD38, IgG4 monoclonal antibody genetically fused to 2 attenuated interferon alpha-2b (IFNα2b) molecules.
- TAK-940 is a next-generation CD19 targeting CAR-T, having signaling domain developed with MD Anderson Sloan Kettering Cancer Center for Relapsed/ Refractory B-Cell Malignancies.
- TAK-981 is a first-in-class, small molecule inhibitor of SUMOylation, a reversible post-translational modification that regulates protein function by covalent attachment of small ubiquitin-like modifier (SUMO) proteins to a protein substrate.
- SUMOylation has a key role in restraining Type I interferon (IFN) responses. In-vivo preclinical studies have demonstrated that inhibition of SUMOylation by TAK-981 promotes innate and adaptive antitumor immune responses dependent on induction of Type I IFN signaling.
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