2,4,6-Tri-tert-butylphenol

Solid. Insoluble in water; soluble in most organic solvents. Combustible.

2,4,6-Tri-tert-butylphenol is an antioxidant; used in preparation method of high-temperature resistant electromagnetic shielding electromagnetic bushing.

Non flammable

CDK5 is a member of the Cyclin-Dependent Kinase family th at is most abundant in the mammalian brain. Active form of CDK5, which has also been called neuronal cdc2-like kinase, is a heterodimer of CDK5 and a 25 kDa protein which is derived proteolytically from a 35 kDa brain and neuron-specific protein and is essential for the kinase activity of CDK5. CDK5 has emerged as a crucial regulator of neuronal migration in the developing central nervous system. CDK5 phosphorylates a diverse list of substrates, implicating it in the regulation of a range of cellular processes - from adhesion and motility, to synaptic plasticity and drug addiction.

Distil the phenol under reduced pressure and/or recrystallise it from n-hexane or several times from 95% EtOH until the EtOH solution is colourless [Balasubramanian & Bruice J Am Chem Soc 108 5495 1986]. It has also been purified by sublimation [Yuan & Bruice J Am Chem Soc 108 1643 1986, Wong et al. J Am Chem Soc 109 3428 1987]. Purification has also been achieved by passage through a silica gel column followed by recrystallisation from n-hexane [Kajii et al. J Phys Chem 91 2791 1987]. [Beilstein 6 III 2094, 6 IV 3539.]

In order to study the chronic toxicity of 2,4,6-tri-tert-butylphenol (TTBP), groups of 40 Slc: Wistar rats of either sex were fed a diet containing 0, 30, 100, 300, or 1000 ppm of TTBP for up to 24 months. Hematological, biochemical, and histopathological examinations performed periodically revealed slight microcytic anemia, changes in some biochemical parameters relating to liver function, and focal necrosis of liver cells following TTBP administration, and these changes observed in females were more severe than those in males. No neoplastic responses following TTBP administration were noted. Hence, it was concluded that TTBP causes liver injury characterized by focal necrosis with microcytic anemia and elevations of serum phospholipids and cholesterol levels, presumably occurring as secondary effects following the liver injury[1].

[1] Matsumoto, Kiyoshi , et al. "Chronic toxicity of 2,4,6-tri-tert-butylphenol in rats." Journal of Toxicological Sciences 16.4(1991):167.