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MTOB is an intermediate in the methionine salvage pathway.1 It is also a substrate of the dehydrogenase domain of C-terminal-binding protein 1 (CtBP1) and CtBP2 that inhibits the transcriptional corepressor activity of CtBP1 and -2 at concentrations in the millimolar range.2 MTOB reduces cell viability in p53 wild-type and p53 knockout HCT116 colorectal cancer cells and induces apoptosis in p53 knockout HCT116 cells. It inhibits growth of MCF-7 breast cancer, MDA-MB-231 breast cancer, and U2OS osteosarcoma cells in a concentration-dependent manner. MTOB reduces tumor mass and ascites volume in a mouse xenograft model using HCT116 cells lacking p53 when administered at a dose of 750 mg/kg. It also reduces the neurological severity score (NSS) and the loss of righting reflex duration in a mouse model of traumatic brain injury.3
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1. Methylthioadenosine phosphorylase regulates ornithine decarboxylase by production of downstream metabolites. The Journal of Biological Chemisty 278(50), 49868-49873 (2003).
2. Therapeutic targeting of C-
3. C-