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Sigma-Aldrich

Conduritol B Epoxide

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

Synonim(y):

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

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About This Item

Wzór empiryczny (zapis Hilla):
C6H10O5
Numer CAS:
6090-95-5
Masa cząsteczkowa:
162.14
Kod 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.

Poziom jakości

100

Próba

≥98% (HPLC)

Postać

solid

producent / nazwa handlowa

Calbiochem®

warunki przechowywania

OK to freeze
desiccated

kolor

white

rozpuszczalność

DMSO: soluble
water: soluble

Warunki transportu

ambient

temp. przechowywania

−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

Klucz InChI

ZHMWOVGZCINIHW-FTYOSCRSSA-N

Opis ogólny

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.

Działania biochem./fizjol.

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

Ostrzeżenie

Toxicity: Harmful (C)

Rekonstytucja

Unstable in solution; reconstitute just prior to use.

Inne uwagi

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

Informacje prawne

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
This page may contain text that has been machine translated.

Kod klasy składowania

11 - Combustible Solids

Klasa zagrożenia wodnego (WGK)

WGK 3

Temperatura zapłonu (°F)

Not applicable

Temperatura zapłonu (°C)

Not applicable

Certyfikaty analizy (CoA)

Poszukaj Certyfikaty analizy (CoA), wpisując numer partii/serii produktów. Numery serii i partii można znaleźć na etykiecie produktu po słowach „seria” lub „partia”.

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Dokumenty związane z niedawno zakupionymi produktami zostały zamieszczone w Bibliotece dokumentów.

Odwiedź Bibliotekę dokumentów

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
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
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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