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M9766

Sigma-Aldrich

4-Methylumbelliferyl α-D-glucopyranoside

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

Synonym(s):

4-Methylumbelliferyl α-D-glucoside

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About This Item

Empirical Formula (Hill Notation):
C16H18O8
CAS Number:
17833-43-1
Molecular Weight:
338.31
Beilstein:
1690776
EC Number:
241-794-0
MDL number:
MFCD00067661
UNSPSC Code:
12352204
PubChem Substance ID:
24897365
NACRES:
NA.32

product name

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

Quality Level

300

description

α-glucosidase substrate

Assay

≥99% (TLC)

form

powder

solubility

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

storage temp.

−20°C

SMILES string

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

InChI key

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.

Biochem/physiol Actions

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.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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
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
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
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
Renata G K Leuschner et al.
Journal of AOAC International, 87(3), 604-613 (2004-08-04)
A standard method for the detection of Enterobacteriaceae was modified for the presumptive detection of Enterobacter sakazakii, and the modified method was validated in an interlaboratory trial with 16 laboratories from 8 European countries. The modification included a differential-elective medium
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