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810222C

Avanti

C6-NBD Glucosyl Ceramide

Avanti Polar Lipids 810222C

Synonym(s):

N-[6-[(7-nitro-2-1,3-benzoxadiazol-4-yl)amino]hexanoyl]-D-glucosyl-β1-1′-sphingosine

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About This Item

Empirical Formula (Hill Notation):
C36H59N5O11
CAS Number:
Molecular Weight:
737.88
UNSPSC Code:
12352211
NACRES:
NA.25

Assay

>99% (TLC)

form

liquid

packaging

pkg of 1 × 1 mL (810222C-250ug)

manufacturer/tradename

Avanti Polar Lipids 810222C

concentration

0.25 mg/mL (810222C-250ug)

shipped in

dry ice

storage temp.

−20°C

General description

C6-NBD Glucosyl Ceramide is a fluorescent derivative of biologically active compound, glucosyl ceramide. Glucosyl ceramide belongs to the class of sphingolipids that are synthesized in the cis/medial-Golgi apparatus by the glycosylation of ceramide.

Application

C6-NBD Glucosyl Ceramide may be used as a substrate for glucocerebrosidase (GCase) activity assay in Drosophila melanogaster and mice.

Biochem/physiol Actions

Glucosylceramide is the precursor of different glycosphingolipids including gangliosides and sulfatides. Glucosyl ceramide is also known to be responsible for axon growth of neural cells. The accumulation of glucosyl ceramide is associated with an inherited lysosomal storage disorder, Gaucher′s disease.

Packaging

5 mL Clear Glass Sealed Ampule (810222C-250ug)

Legal Information

Avanti Research is a trademark of Avanti Polar Lipids, LLC

Pictograms

Skull and crossbonesHealth hazard

Signal Word

Danger

Hazard Classifications

Acute Tox. 3 Inhalation - Acute Tox. 4 Oral - Carc. 2 - Eye Irrit. 2 - Repr. 2 - Skin Irrit. 2 - STOT RE 1 - STOT SE 3

Target Organs

Central nervous system

Storage Class Code

6.1D - Non-combustible, acute toxic Cat.3 / toxic hazardous materials or hazardous materials causing chronic effects

WGK

WGK 3

Flash Point(F)

does not flash

Flash Point(C)

does not flash


Certificates of Analysis (COA)

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H Zhao et al.
Cellular and molecular life sciences : CMLS, 59(4), 694-707 (2002-05-23)
Gaucher disease is an autosomal recessive trait and the most common lysosomal storage disease. The pathogenesis evolves from the diminished activity of the lysosomal hydrolase, acid beta-glucosidase and the resultant accumulation of glucosylceramide within lysosomes. The pathogenic mechanisms are poorly

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