Description
TTFA(326-91-0) blocks the respiratory chain complex II causing inhibition of mitochondrial respiration. Respiratory chain complex II inhibition is caused via binding of TTFA to two ubiquinone binding sites, Qp and Qd.1Inhibition of Complex II by TFA has been shown to cause a delay in overall cell cycle progression leading to oxidative stress.2,3TTFA also was found to inhibit porcine liver carboxylesterase (IC50= 0.54 μM).4
Chemical Properties
light yellow to beige to brown crystalline powder,
Uses
Thenoyltrifluoroacetone is one of the most proved extracting agents in solventextraction analysis. It is equally suitable for the separation and selective enrichment of metal ions.
2-Thenoyltrifluoroacetone (TTFA) is an inhibitor of respiration in animals and bacteria. In animals, TTFA binds at the quinone reduction site of succinate:ubiquinone oxidoreductase (SQR; Complex II), preventing ubiquinone from binding. It inhibits NADH fumarate reductase in bacteria. TTFA also inhibits photosystem II in plants and NADH-ubiquinone oxidoreductase of the virus Vibrio cholerae, decreasing cholera toxin production. This compound is also a chelator of metals, including lanthanum, zirconium, hafnium, and neodymium. Reagent for the determination of actinides and lanthanides.
2-Thenoyltrifluoroacetone is used for the extractive spectrophotometric determination of ruthenium at ph 4.0 (acetate buffer).
Thenoyltrifluoroacetone has also been used as an alternative β-diketone for in-house assay development since NTA was not, until recently, commercially available.
Uses
2-Thenoyltrifluoroacetone is an inhibitor of respiration in animals and bacteria. TTFA binds at the quinone reduction site of succinate ubiquinone oxidoreductase.
reaction suitability
reagent type: derivatization reagent
reaction type: Acylations
Synthesis
The general procedure for the synthesis of 2-thiophenecarbonyltrifluoroacetone from 2-acetylthiophene and ethyl trifluoroacetate was as follows: 1-(thiophen-2-yl)ethanone (20 g, 16 mmol) was added dropwise to a methanolic solution of sodium methanolate (10.3 g, 19 mmol), and the reaction was stirred for 1 hour at room temperature. Subsequently, the reaction mixture was cooled to 0 °C, ethyl 2,2,2-trifluoroacetate (27 g, 19 mmol) was added in batches and the whole reaction mixture was refluxed at 80 °C overnight. Upon completion of the reaction, the organic solvent was removed by vacuum evaporation and the residue was dissolved in water (200 mL), acidified with 1N hydrochloric acid (120 mL) and subsequently extracted three times with ethyl acetate (200 mL). The organic layers were combined, washed with brine, dried over anhydrous sodium sulfate, concentrated and further purified by silica gel column chromatography (petroleum ether/ethyl acetate, 20:1) to afford 4,4,4-trifluoro-1-(thiophen-2-yl)butane-1,3-dione (11 g, 32% yield) as a light red solid.
Purification Methods
Crystallise the dione from hexane or *benzene. (Anaqueous solutions slowly decompose it). It has 1638(C=O), 1657(C=C)cm-1 . The oxime crystallises from H2O or aqueous EtOH. It is used for the determination of Actinides and Lanthanides. [Chaston et al. Aust J Chem 18 673 1956, Jeffrey et al. In Vogel’s Textbook of Qunatitative Chemical Analysis 5thedn J Wiley & Sons, p170 1989, Beilstein 17 III/IV 5989, 17/11 V 128.]
References
[1] FEI SUN. Crystal structure of mitochondrial respiratory membrane protein complex II.[J]. Cell, 2005, 121 7: 1043-1057. DOI:
10.1016/j.cell.2005.05.025[2] HAE-OK BYUN. Mitochondrial dysfunction by complex II inhibition delays overall cell cycle progression via reactive oxygen species production†[J]. Journal of cellular biochemistry, 2008, 104 5: 1747-1759. DOI:
10.1002/jcb.21741[3] ILKA SIEBELS Stefan D. Q-site inhibitor induced ROS production of mitochondrial complex II is attenuated by TCA cycle dicarboxylates[J]. Biochimica et Biophysica Acta-Bioenergetics, 2013, 1827 10: Pages 1156-1164. DOI:
10.1016/j.bbabio.2013.06.005[4] JIN-GANG ZHANG Marc W F. Thenoyltrifluoroacetone, a potent inhibitor of carboxylesterase activity[J]. Biochemical pharmacology, 2002, 63 4: Pages 751-754. DOI:
10.1016/s0006-2952(01)00871-1
