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.
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.
Biochem/physiol Actions
Cell permeable: no
Primary Target α-glucosidase
Product does not compete with ATP.
Reversible: no
Warning
Toxicity: Harmful (C)
Reconstitution
Unstable in solution; reconstitute just prior to use.
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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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
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
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
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
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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