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M9766

Sigma-Aldrich

4-Methylumbelliferyl α-D-glucopyranoside

α-glucosidase substrate, fluorogenic, ≥99% (TLC), powder

Synonyme(s) :

4-Methylumbelliferyl α-D-glucoside

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About This Item

Formule empirique (notation de Hill):
C16H18O8
Numéro CAS:
17833-43-1
Poids moléculaire :
338.31
Beilstein:
1690776
Numéro CE :
241-794-0
Numéro MDL:
MFCD00067661
Code UNSPSC :
12352204
ID de substance PubChem :
24897365
Nomenclature NACRES :
NA.32
Le tarif et la disponibilité ne sont pas disponibles actuellement.

Nom du produit

4-Methylumbelliferyl α-D-glucopyranoside, α-glucosidase substrate

Niveau de qualité

300

Description

α-glucosidase substrate

Essai

≥99% (TLC)

Forme

powder

Solubilité

pyridine: 50 mg/mL, clear, colorless to faintly yellow

Température de stockage

−20°C

Chaîne SMILES 

CC1=CC(=O)Oc2cc(O[C@H]3O[C@H](CO)[C@@H](O)[C@H](O)[C@H]3O)ccc12

InChI

1S/C16H18O8/c1-7-4-12(18)23-10-5-8(2-3-9(7)10)22-16-15(21)14(20)13(19)11(6-17)24-16/h2-5,11,13-17,19-21H,6H2,1H3/t11-,13-,14+,15-,16+/m1/s1

Clé InChI

YUDPTGPSBJVHCN-JZYAIQKZSA-N

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Application

4-Methylumbelliferyl ǥ-D-glucopyranoside has been used to assay acid alpha-glucosidase (GAA) activity in tissue homogenates.[1][1][2]

Actions biochimiques/physiologiques

4-Methylumbelliferyl ǥ-D-glucopyranoside serves as a fluorogenic substrate for the ǥ-glucosidase enzyme. The product, 4-methylumbelliferyl, shows a peak at 440nm in the fluorescence spectra.[3]

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Équipement de protection individuelle

Eyeshields, Gloves, type N95 (US)

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Certificats d'analyse (COA)

Lot/Batch Number
0000381627
0000365208
0000397525
0000375592
0000375593

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Consulter la Bibliothèque de documents

Darin J Falk et al.
Molecular therapy : the journal of the American Society of Gene Therapy, 21(9), 1661-1667 (2013-06-05)
Pompe disease is a neuromuscular disease resulting from deficiency in acid α-glucosidase (GAA), results in cardiac, skeletal muscle, and central nervous system (CNS) pathology. Enzyme replacement therapy (ERT) has been shown to partially correct cardiac and skeletal muscle dysfunction. However
Omid Motabar et al.
Analytical biochemistry, 390(1), 79-84 (2009-04-18)
Mutations in alpha-glucosidase cause accumulation of glycogen in lysosomes, resulting in Pompe disease, a lysosomal storage disorder. Small molecule chaperones that bind to enzyme proteins and correct the misfolding and mistrafficking of mutant proteins have emerged as a new therapeutic
Ryoga Hamura et al.
Cancer science, 112(6), 2335-2348 (2021-05-02)
Lysosomal degradation plays a crucial role in the metabolism of biological macromolecules supplied by autophagy. The regulation of the autophagy-lysosome system, which contributes to intracellular homeostasis, chemoresistance, and tumor progression, has recently been revealed as a promising therapeutic approach for
Phillip A Doerfler et al.
Human gene therapy, 27(1), 43-59 (2015-11-26)
Pompe disease is a progressive neuromuscular disorder caused by lysosomal accumulation of glycogen from a deficiency in acid alpha-glucosidase (GAA). Replacement of the missing enzyme is available by repeated protein infusions; however, efficacy is limited by immune response and inability
Nao Yamakawa et al.
Biochimie, 89(11), 1396-1408 (2007-05-29)
Sulfated sialic acid (SiaS) is a unique sialic acid (Sia) derivative in which an additional anionic group is attached to a carboxylated monosaccharide. Very little is known about the occurrence and biologic function of SiaS, due to the limitations of
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