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Key Documents

234599

Sigma-Aldrich

Conduritol B Epoxide

≥98% (HPLC), solid, Glucocerebrosidase inhibitor, Calbiochem®

Sinónimos:

Conduritol B Epoxide, CBE, 1,2-Anhydro-myo-inositol

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About This Item

Fórmula empírica (notación de Hill):
C6H10O5
Número de CAS:
6090-95-5
Peso molecular:
162.14
Código UNSPSC:
12352119
NACRES:
NA.77

product name

Conduritol B Epoxide, Conduritol B Epoxide, CAS 6090-95-5, is an irreversible Inhibitor of glucocerebrosidase in neurons. Also inhibits α-glucosidase activity in a variety of species.

Nivel de calidad

100

Análisis

≥98% (HPLC)

formulario

solid

fabricante / nombre comercial

Calbiochem®

condiciones de almacenamiento

OK to freeze
desiccated

color

white

solubilidad

DMSO: soluble
water: soluble

Condiciones de envío

ambient

temp. de almacenamiento

−20°C

InChI

1S/C6H10O5/c7-1-2(8)4(10)6-5(11-6)3(1)9/h1-10H/t1-,2-,3+,4+,5-,6+/m0/s1

Clave InChI

ZHMWOVGZCINIHW-FTYOSCRSSA-N

Descripción general

Inhibits α-glucosidase activity in mammals, snails, sweet almonds and yeast. An irreversible, potent, and specific inhibitor of glucocerebrosidase in cultured neurons. Has also been shown to inhibit α-glucosidase from yeast, and rabbit intestinal sucrase-isomaltase complex.
Inhibits α-glucosidase activity in mammals, snails, sweet almonds, and yeast. An irreversible, potent, and specific inhibitor of glucocerebrosidase in cultured neurons. Has also been shown to inhibit α-glucosidase from yeast and rabbit intestinal sucrase-isomaltase complex.

Acciones bioquímicas o fisiológicas

Cell permeable: no
Primary Target
α-glucosidase
Product does not compete with ATP.
Reversible: no

Advertencia

Toxicity: Harmful (C)

Reconstitución

Unstable in solution; reconstitute just prior to use.

Otras notas

2024 CiteAb Award Winner for Supplier Succeeding in Parkinson′s Research

Información legal

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Código de clase de almacenamiento

11 - Combustible Solids

Clase de riesgo para el agua (WGK)

WGK 3

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Oeystein Roed Brekk et al.
Proceedings of the National Academy of Sciences of the United States of America, 117(44), 27646-27654 (2020-10-17)
Neurons are dependent on proper trafficking of lipids to neighboring glia for lipid exchange and disposal of potentially lipotoxic metabolites, producing distinct lipid distribution profiles among various cell types of the central nervous system. Little is known of the cellular
Kelly E Glajch et al.
Proceedings of the National Academy of Sciences of the United States of America, 118(31) (2021-07-31)
Loss-of-function mutations in acid beta-glucosidase 1 (GBA1) are among the strongest genetic risk factors for Lewy body disorders such as Parkinson's disease (PD) and Lewy body dementia (DLB). Altered lipid metabolism in PD patient-derived neurons, carrying either GBA1 or PD
Azucena Perez-Canamas et al.
Brain communications, 3(1), fcaa200-fcaa200 (2021-04-03)
TMEM106B is a transmembrane protein localized to the endo-lysosomal compartment. Genome-wide association studies have identified TMEM106B as a risk modifier of Alzheimer's disease and frontotemporal lobar degeneration, especially with progranulin haploinsufficiency. We recently demonstrated that TMEM106B loss rescues progranulin null
Electra Brunialti et al.
Journal of neuroinflammation, 18(1), 220-220 (2021-09-24)
Homozygotic mutations in the GBA gene cause Gaucher's disease; moreover, both patients and heterozygotic carriers have been associated with 20- to 30-fold increased risk of developing Parkinson's disease. In homozygosis, these mutations impair the activity of β-glucocerebrosidase, the enzyme encoded
Iva Stojkovska et al.
Neuron, 110(3), 436-451 (2021-11-19)
Neurodegenerative disorders are characterized by a collapse in proteostasis, as shown by the accumulation of insoluble protein aggregates in the brain. Proteostasis involves a balance of protein synthesis, folding, trafficking, and degradation, but how aggregates perturb these pathways is unknown.

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