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Merck
모든 사진(4)

주요 문서

M9766

Sigma-Aldrich

4-Methylumbelliferyl α-D-glucopyranoside

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

동의어(들):

4-Methylumbelliferyl α-D-glucoside

로그인조직 및 계약 가격 보기

크기 선택

10 MG
₩116,218
25 MG
₩143,115
100 MG
₩327,744
250 MG
₩703,395
1 G
₩2,209,351

₩116,218


구입 가능 여부는 고객센터에 문의하십시오.


크기 선택

보기 변경
10 MG
₩116,218
25 MG
₩143,115
100 MG
₩327,744
250 MG
₩703,395
1 G
₩2,209,351

About This Item

실험식(Hill 표기법):
C16H18O8
CAS Number:
Molecular Weight:
338.31
Beilstein:
1690776
EC Number:
MDL number:
UNSPSC 코드:
12352204
PubChem Substance ID:
NACRES:
NA.32

₩116,218


구입 가능 여부는 고객센터에 문의하십시오.

제품명

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

설명

α-glucosidase substrate

분석

≥99% (TLC)

양식

powder

solubility

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

저장 온도

−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

유사한 제품을 찾으십니까? 방문 제품 비교 안내

애플리케이션

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

생화학적/생리학적 작용

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]

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable

개인 보호 장비

Eyeshields, Gloves, type N95 (US)


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문서 라이브러리 방문

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
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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