N-Tetracosanoyl-D-erythro-dihydrosphingosine

CATALOG # 2093
Amount 5 mg
Price $325.00
Qty
 
N-Tetracosanoyl-D-erythro-dihydrosphingosine
  • Catalog #:2093
  • Scientific Name:N-Tetracosanoyl-D-erythro-dihydrosphingosine
  • Common Name:N-C24:0-D-erythro-dihydroceramide; N-Tetracosanoyl-D-erythro-sphinganine; N-Lignoceryl-D-erythro-dihydrosphingosine
  • Empirical Formula:C42H85NO3
  • SDSView Safety Data Sheet
  • Data Sheet:View Data Sheet
  • Formula Weight:652
  • Unit:5 mg
  • Solvent:none
  • Source:synthetic
  • Purity:98+%
  • Analytical Methods:TLC; HPLC; identity confirmed by MS
  • Solubility:chloroform/methanol 2:1
  • Physical Appearance:solid
  • Storage:-20°C
  • Dry Ice:No
  • Hazardous:No
  • Literature References:Application Notes:

    Dihydroceramide is a critical intermediate in the de novo synthesis of ceramide, leading to many complex sphingolipids. It is synthesized by the acylation of dihydrosphingosine and is subsequently converted to ceramide via the enzyme dihydroceramide desaturase or into phytosphingosine via the enzyme C4-hydroxylase.1 Inhibition of ceramide synthase by some fungal toxins (such as fumonisin B1) causes an accumulation of dihydrosphingosine and sphinganine-1- phosphate and a decrease in dihydroceramide and other dihydrosphingolipids, leading to a number of diseases including oesophageal cancer.2 The dihydroceramide desaturase inhibitor N-(4-Hydroxyphenyl) retinamide (4-HPR) has been tested as an anti-cancer agent; it inhibits the dihydroceramide desaturase enzyme in cells resulting in a high concentration of dihydroceramide and dihydro-sphingolipids and this is thought to be the cause of its anti-cancer effects.3 Oxidative stress in cells causes an increase in the amount of dihydroceramide by potently inhibiting the desaturase enzyme.4 Dihydroceramide inhibits the formation of channels by ceramides and may thus reduce ceramide induced apoptosis in cells.5 Skin cells contain significant amounts of long chain ceramides, such as dihydroceramides, that are vital for maintaining skin barrier functions.6

    Selected References:
    1. Y. Mizutani, A. Kihara, and Y. Igarashi “Identifcation of the human sphingolipid C4-hydroxylase, hDES2, and its up-regulation during keratinocyte differentiation” FEBS Letters, vol. 563 pp. 93-97, 2004
    2. J. Soriano et al. “Mechanism of action of sphingolipids and their metabolites in the toxicity of fumonisin B1” Progress in Lipid Research, Vol. 44 pp. 345-356, 2005
    3. W. Zheng “Fenretinide increases dihydroceramide and dihydrosphingolipids due to inhibition of dihydroceramide desaturase” Georgia Institute of Technology, 2006
    4. J. Idkowiak-Baldys et al. “Dihydroceramide Desaturase Activity is Modulated by Oxidative Stress” Biochem. J., Vol. 427(2) pp. 265-274, 2010
    5. J. Stiban et al. “Dihydroceramide hinders ceramide channel formation: Implications on apoptosis” Apoptosis, Vol. 11(5) pp. 773-780, 2006
    6. S. Grond et al., "PNPLA1 Deficiency in Mice and Humans Leads to a Defect in the Synthesis of Omega-O-Acylceramides" J Invest Dermatol. Vol. 137(2) pp. 394-402, 2017