Tetraethylammonium bromide explained

Tetraethylammonium bromide (TEAB) is a quaternary ammonium compound with the chemical formula C₈H₂₀N⁺Br⁻, often written as "Et₄N⁺Br⁻" in the chemical literature. It has been used as the source of tetraethylammonium ions in pharmacological and physiological studies, but is also used in organic chemical synthesis.

Chemistry

Synthesis

TEAB is commercially available, but can be prepared by the reaction between tetraethylammonium hydroxide and hydrobromic acid:

Et₄N⁺HO⁻ + HBr → Et₄N⁺Br⁻ + H₂O

Evaporation of the water and recrystallization from acetonitrile yields a crystalline sample of TEAB.^[1]

Structure

The crystal structure of TEAB has been determined and found to exhibit a distorted tetrahedral symmetry with respect to the geometry of the C atoms around the central N.^[2]

Synthetic applications

Examples include:

• TEAB catalyzes the high-yield oxidation of organic sulfides to sulfoxides by o-iodoxybenzoic acid (IBX) in chloroform/water at room temperature,^[3] e.g.

(C₂H₅)₂S → (C₂H₅)₂S=O

• TEAB has been used for the in situ preparation of tetraethylammonium superoxide from potassium superoxide for the conversion of primary alkyl halides to dialkyl peroxides.^[4] The overall reaction is:

2R¹Br + 2KO₂ → R¹-O-O-R¹ + 2KBr + O₂

Biology

In common with tetraethylammonium chloride and tetraethylammonium iodide, TEAB has been used as a source of tetraethylammonium ions for numerous clinical and pharmacological studies, which are covered in more detail under the entry for tetraethylammonium. Briefly, TEAB has been explored clinically for its ganglionic blocking properties,^[5] although it is now essentially obsolete as a drug, and it is still used in physiological research for its ability to block K⁺ channels in various tissues.^[6]

Toxicity

The toxicity of TEAB is primarily due to the tetraethylammonium ion, which has been studied extensively. The acute toxicity of TEAB is comparable to that of tetraethylammonium chloride and tetraethylammonium iodide. These data, taken from a study by Randall and co-workers,^[7] are provided for comparative purposes; additional details may be found in the entry for Tetraethylammonium.

LD₅₀ for mouse: 38 mg/kg, i.v.; 60 mg/kg, i.p.; >2000 mg/kg, p.o.

See also

• Tetraethylammonium
• Tetraethylammonium chloride
• Tetraethylammonium iodide

References

1. D. N. Kevill and N. H. Cromwell (1961). "Elimination reactions of α-halogenated ketones. V. Kinetics of the bromide ion promoted elimination reaction of 2-benzyl-2-bromo-4,4-dimethyl-1-tetralone in solvent acetonitrile". J. Am. Chem. Soc. 83 3812-3815.
2. M. Ralle, J. C. Bryan, A. Habenschuss and B. Wunderlich (1997). "Low-temperature phase of tetraethylammonium bromide." Acta Crystallogr. Sect. C C53 488–490.
3. V. G. Shukla, P. D. Salgaonkar and K. G. Akamanchi (2003). "A mild, chemoselective oxidation of sulfides to sulfoxides using o-iodoxybenzoic acid and tetraethylammonium bromide as catalyst." J. Org. Chem. 68 5422-5425.
4. T. A. Foglia and L. S. Silbert (1992)."Preparation of di-n-alkyl peroxides: phase-transfer reaction of potassium superoxide with primary alkyl bromides." Synthesis 545-547.
5. A. M. Boyd et al. (1948). "Action of tetraethylammonium bromide." Lancet 251 15-18.
6. C. M. Armstrong and B. Hille (1972). "The inner quaternary ammonium receptor in potassium channels of the node of Ranvier." J. Gen. Physiol. 59 388-400.
7. L. O. Randall, W. G. Peterson and G. Lehmann (1949). "The ganglionic blocking actions of thiophanium derivatives." J. Pharmacol. Exp. Ther. 97 48-57.