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810222C

Avanti

C6-NBD Glucosyl Ceramide

Avanti Research™ - A Croda Brand 810222C

Sinónimos:

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

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About This Item

Fórmula empírica (notación de Hill):
C36H59N5O11
Número de CAS:
94885-03-7
Peso molecular:
737.88
MDL number:
MFCD00063542
UNSPSC Code:
12352211
NACRES:
NA.25

assay

>99% (TLC)

form

liquid

packaging

pkg of 1 × 1 mL (810222C-250ug)
pkg of 1 × 1 mg (81022C-1MG)

manufacturer/tradename

Avanti Research™ - A Croda Brand 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 Amber Glass Screw Cap Vial (81022C-1MG)
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
GHS06,GHS08

signalword

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

wgk_germany

WGK 3

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Certificados de análisis (COA)

Lot/Batch Number

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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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