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Merck
CN

M3633

Sigma-Aldrich

4-甲基伞形酮基β-D-葡萄糖苷

β-glucosidase substrate, fluorogenic, ≥99% (HPLC), powder

别名:

MUD

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About This Item

经验公式(希尔记法):
C16H18O8
CAS号:
分子量:
338.31
Beilstein:
94672
EC 号:
MDL编号:
UNSPSC代码:
12352204
PubChem化学物质编号:
NACRES:
NA.32

产品名称

4-甲基伞形酮基β-D-葡萄糖苷, β-glucosidase substrate

质量水平

方案

≥99% (HPLC)

表单

powder

溶解性

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

荧光

λex 316 nm; λem 372 nm (pH 9.1)
λex 360 nm; λem 449 nm (Reaction product)

储存温度

−20°C

SMILES字符串

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-YMILTQATSA-N

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应用

4-甲基伞形酮基β-D-葡萄糖苷可用来作为以下反应的底物:
  • 原发性海马神经元富含溶菌酶部分葡糖神经酰胺酶β 酶活性分析
  • 酵母发酵过程中β-葡萄糖苷酶分析
  • 巨噬细胞细胞系(RAW)中的葡萄糖脑苷脂酶1(GBA1)-相关葡萄糖苷酶活性分析

生化/生理作用

4-甲基伞形酮基β-D-葡萄糖苷是一种合成糖苷酶底物。它可用作来自肠球菌的葡萄糖苷酶底物。

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Gloves, type N95 (US)

法规信息

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分析证书(COA)

Lot/Batch Number

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访问文档库

Assessing microbial safety of drinking water improving approaches and methods: Improving approaches and methods, 253-253 (2003)
Florent Malard et al.
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation, 21(6), 1059-1067 (2015-02-25)
This retrospective report compared the 4-year outcomes of allogeneic stem cell transplantation (allo-SCT) in 651 adult patients with acute myeloid leukemia receiving a reduced-intensity (RIC) or nonmyeloablative conditioning (NMA) regimen according to the type of unrelated donors. These were either
Determinants on an efficient cellulase recycling process for the production of bioethanol from recycled paper sludge under high solid loadings
Gomes D, et al.
Biotechnology for Biofuels, 11(1), 111-111 (2018)
Samantha G Scharenberg et al.
Nature communications, 11(1), 3327-3327 (2020-07-06)
Gaucher disease is a lysosomal storage disorder caused by insufficient glucocerebrosidase activity. Its hallmark manifestations are attributed to infiltration and inflammation by macrophages. Current therapies for Gaucher disease include life-long intravenous administration of recombinant glucocerebrosidase and orally-available glucosylceramide synthase inhibitors.
Mitochondrial dysfunction and mitophagy defect triggered by heterozygous GBA mutations
Li H, et al.
Autophagy, 15(1), 113-130 (2019)

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