Doxylamine-d5 succinate - CAS 1216840-94-6
Labelled APIs
Molecular Formula:
Molecular Weight:
The succinate salt form of isotope labelled Doxylamine, a histamine receptor antagonist, could be used as a sedative and hypnotic.
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Related CAS:
562-10-7 (unlabelled)
Off-White Solid
10 mM in DMSO
-20ºC Freeze
The succinate salt form of isotope labelled Doxylamine.
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Canonical SMILES:
1.The Combination of α-Tocopheryl Succinate and Sodium Selenite on Breast Cancer: A Merit or a Demerit?
Badr DM1, Hafez HF1, Agha AM2, Shouman SA1. Oxid Med Cell Longev. 2016;2016:4741694. doi: 10.1155/2016/4741694. Epub 2016 Mar 29.
α-Tocopheryl succinate (α-TOS), a mitochondria-targeting agent, induces apoptosis in malignant cells in vitro and in vivo. Selenite is a nutritional supplement that has been shown to stimulate apoptosis in cancer cells. This study was designed to investigate the cytotoxic effect of combined treatment of α-TOS and sodium selenite (SSe) in vitro and in vivo and to explore their effect on apoptosis and autophagy in breast cancer. The type of interaction between α-TOS and SSe was evaluated and levels of oxidative stress and apoptotic and autophagic markers were determined. SSe alone showed varying degrees of cytotoxicity on all the tested cell lines. Its combination with α-TOS was antagonistic in vitro in MCF7 and in vivo in mice bearing Ehrlich tumor compared to α-TOS-treated one. Combination of TOS with 2 μM of SSe increased the level of glutathione without changes in antiapoptotic markers Bcl-2 and Mcl-1 at 16 and 48 hrs. SSe decreased caspase 3 activity and protein level of caspases 7 and 9, while it increased autophagic markers beclin-1 and LC3B protein levels of MCF7 cells treated with α-TOS.
2.3-Bromopyruvic Acid Inhibits Tricarboxylic Acid Cycle and Glutaminolysis in HepG2 Cells.
Jardim-Messeder D1, Moreira-Pacheco F2. Anticancer Res. 2016 May;36(5):2233-41.
BACKGROUND/AIM: 3-bromopyruvate (3BrPA) is an antitumor agent able to inhibit aerobic glycolysis and oxidative phosphorylation, therefore inducing cell death. However, cancer cells are also highly dependent of glutaminolysis and tricarboxylic acid cycle (TCA) regarding survival and 3BrPA action in these metabolic routes is poorly understood.
3.Targeting succinate:ubiquinone reductase potentiates the efficacy of anticancer therapy.
Kruspig B1, Valter K1, Skender B2, Zhivotovsky B3, Gogvadze V4. Biochim Biophys Acta. 2016 Apr 29. pii: S0167-4889(16)30126-4. doi: 10.1016/j.bbamcr.2016.04.026. [Epub ahead of print]
Mitochondria play a pivotal role in apoptosis: permeabilization of the outer mitochondrial membrane and the release of pro-apoptotic proteins from the intermembrane space of mitochondria are regarded as the key event in apoptosis induction. Here we demonstrate how non-toxic doses of the mitochondrial Complex II inhibitor thenoyltrifluoroacetone (TTFA), which specifically inhibits the ubiquinone-binding site of succinate dehydrogenase (SDH), synergistically stimulated cell death, induced by harmless doses of cisplatin in a panel of chemoresistant neuroblastoma cell lines. Apoptotic cell death was confirmed by cytochrome c release from the mitochondria, cleavage of poly ADP-ribose polymerase, processing of caspase-3, which is an important executive enzyme in apoptosis, and caspase-3-like activity. Methyl malonate, an inhibitor of the SDHA subunit partially reversed apoptosis stimulated by TTFA in SK-N-BE(2) neuroblastoma cells (NB), indicating that sensitization requires oxidation of succinate.
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