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M9766

Sigma-Aldrich

4-Methylumbelliferyl α-D-Glucopyranosid

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

Synonym(e):

4-Methylumbelliferyl-α-D-glucosid

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10 MG
€ 69,00
25 MG
€ 130,00
100 MG
€ 327,00
250 MG
€ 648,00
1 G
€ 1.110,00

€ 69,00

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Alle Fotos(4)

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10 MG
€ 69,00
25 MG
€ 130,00
100 MG
€ 327,00
250 MG
€ 648,00
1 G
€ 1.110,00

About This Item

Empirische Formel (Hill-System):
C16H18O8
CAS-Nummer:
17833-43-1
Molekulargewicht:
338.31
Beilstein:
1690776
EG-Nummer:
241-794-0
MDL-Nummer:
MFCD00067661
UNSPSC-Code:
12352204
PubChem Substanz-ID:
24897365
NACRES:
NA.32

€ 69,00

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Produktbezeichnung

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

Beschreibung

α-glucosidase substrate

Assay

≥99% (TLC)

Form

powder

Löslichkeit

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

Lagertemp.

−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

InChIKey

YUDPTGPSBJVHCN-JZYAIQKZSA-N

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Anwendung

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

Biochem./physiol. Wirkung

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]

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Persönliche Schutzausrüstung

Eyeshields, Gloves, type N95 (US)

Hier finden Sie alle aktuellen Versionen:

Analysenzertifikate (COA)

Lot/Batch Number
0000424209
0000424208
0000424207
0000424207
0000424208

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Die Dokumentenbibliothek aufrufen

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
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
J van Lieshout et al.
Archaea (Vancouver, B.C.), 1(4), 285-292 (2005-04-07)
Pyrococcus furiosus laminarinase (LamA, PF0076) is an endo-glycosidase that hydrolyzes beta-1,3-glucooligosaccharides, but not beta-1,4-gluco-oligosaccharides. We studied the specificity of LamA towards small saccharides by using 4-methylumbelliferyl beta-glucosides with different linkages. Besides endo-activity, wild-type LamA has some exo-activity, and catalyzes the
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