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Merck
CN

M9766

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
NACRES:
NA.32
PubChem Substance ID:
24897365
UNSPSC Code:
12352204
EC Number:
241-794-0
MDL number:
MFCD00067661
Beilstein/REAXYS Number:
1690776

Key Documents

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Product Name

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

InChI key

YUDPTGPSBJVHCN-JZYAIQKZSA-N

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

SMILES string

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

description

α-glucosidase substrate

assay

≥99% (TLC)

form

powder

solubility

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

storage temp.

−20°C

Quality Level

300

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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

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)

Regulatory Information

涉药品监管产品
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Certificates of Analysis (COA)

Lot/Batch Number
0000519445
0000519437
0000519439
0000519439
0000519437

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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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