78136-16-0

Basic information

• Product Name: (2S,3R,4R,5S)-2,3,4,6-tetrakis(benzyloxy)hexane-1,5-diol
• Synonyms: (2S,3R,4R,5S)-2,3,4,6-tetrakis(benzyloxy)hexane-1,5-diol
• CAS NO: 78136-16-0
• Molecular Weight: 542.672
• Mol File: 78136-16-0.mol

Chemical Properties

• CAS DataBase Reference: (2S,3R,4R,5S)-2,3,4,6-tetrakis(benzyloxy)hexane-1,5-diol(CAS DataBase Reference)
• NIST Chemistry Reference: (2S,3R,4R,5S)-2,3,4,6-tetrakis(benzyloxy)hexane-1,5-diol(78136-16-0)
• EPA Substance Registry System: (2S,3R,4R,5S)-2,3,4,6-tetrakis(benzyloxy)hexane-1,5-diol(78136-16-0)

Safety Data

• Hazardous Substances Data: 78136-16-0(Hazardous Substances Data)

Upstream product

• 78136-16-0 2,3,4,6-tetra-O-benzyl-D-glucitol 
• 4291-69-4 2,3,4,6-Tetra-O-benzyl-D-glucopyranose 
• 1316108-89-0 (2R,3R,4R,5S)-1,3,4,5-tetrakis(benzyloxy)-6-(pivaloyloxy)hexan-2-yl benzoate 
• 1316108-84-5 (2S,3R,4R,5R)-2,3,4,6-tetrakis(benzyloxy)-5-hydroxyhexyl pivalate 
• 14233-52-4 1,3,4,5-O-tetrabenzyl-L-sorbose 
• 3765-95-5 methyl β-L-sorbopyranoside 
• 78136-15-9 methyl 1,3,4,5-tetra-O-benzyl-α-L-sorbopyranoside 
• 470-15-5 α-L-sorbopyranose 
• 78184-86-8 1,3,4,5-tetra-O-benzyl-α-L-sorbopyranoside 
• 4132-28-9 2,3,4,6-tetra-O-benzyl-L-idopyranose 
• 100-39-0 benzyl bromide 
• 97-30-3 methyl-alpha-D-glucopyranoside 
• 3879-79-6 methyl 2,3,4,6-tetra-O-benzyl-α-D-glucopyranoside 
• 83238-55-5 3,4,6-tri-O-benzyl-1,2-O-<(R)-benzylidene>-α-D-glucopyranose 

Downstream Products

• 78890-68-3 1-deoxy-2,3,4,6-tetra-O-benzyl-D-glucopyranose 
• 1221793-46-9 N-(2-hydroxy-ethyl)-2,3,4,6-tetra-O-benzyl-1-deoxynojirimycin 
• 1316108-89-0 (2R,3R,4R,5S)-1,3,4,5-tetrakis(benzyloxy)-6-(pivaloyloxy)hexan-2-yl benzoate 
• 72432-03-2 migitol 
• 149302-60-3 N-benzyl-2,3,4,6-tetra-O-benzyl-1-deoxynojirimycin 
• 1316108-84-5 (2S,3R,4R,5R)-2,3,4,6-tetrakis(benzyloxy)-5-hydroxyhexyl pivalate 
• 1332461-61-6 N-(3-(4-((3-O-methylestradiol)-17β-yl)-1H-1,2,3-triazol-1-yl)propyl)-2,3,4,6-tetra-O-benzyl-1,5-dideoxy-1,5-imino-D-glucitol 
• 1332461-62-7 N-(3-(4-(2-methoxyphenyl)-1H-1,2,3-triazol-1-yl)propyl)-1,5-dideoxy-1,5-imino-D-glucitol 
• 1332461-63-8 N-(3-(4-(4-methoxyphenyl)-1H-1,2,3-triazol-1-yl)propyl)-1,5-dideoxy-1,5-imino-D-glucitol 
• 1332461-64-9 N-(3-(4-(2-fluorophenyl)-1H-1,2,3-triazol-1-yl)propyl)-1,5-dideoxy-1,5-imino-D-glucitol 
• 1332461-67-2 N-(3-(4-(cyclohexanol-1-yl)-1H-1,2,3-triazol-1-yl)propyl)-1,5-dideoxy-1,5-imino-D-glucitol 
• 1332461-73-0 N-(3-(4-(3,4-dichlorophenoxymethyl)-1H-1,2,3-triazol-1-yl)propyl)-2,3,4,6-tetra-O-benzyl-1,5-dideoxy-1,5-imino-D-glucitol 
• 1332461-75-2 N-(3-(4-(3,4-dichlorophenoxymethyl)-1H-1,2,3-triazol-1-yl)propyl)-1,5-dideoxy-1,5-imino-D-glucitol 
• 1332461-76-3 4-{[(1S,2S,4R)-bicyclo[2.2.1]heptan-2-yloxy]methyl}-1-[3-(2,3,4,6-tetra-O-benzyl-(1,5-dideoxy-1,5-imino-D-glucitol)-N-yl)propyl]-1,2,3-triazole 

Relevant articles and documents

Large-scale synthesis of the glucosylceramide synthase inhibitor N-[5-(adamantan-1-yl-methoxy)-pentyl]-1-deoxynojirimycin

A synthetic route for the preparation of glucosylceramide synthase inhibitor N-[5-(adamantan-1-yl-methoxy)-pentyl]-1-deoxynojirimycin methanesulfonic acid salt (AMP-DNM) has been developed. Herein we report the development and optimization of this synthetic route from its initial version in an academic research laboratory at milligram-scale to the final optimized route that was implemented in a cGMP miniplant on kilogram-scale. The definitive route starts with the separate synthesis of building blocks 2,3,4,6-tetra-O- benzyl-1-deoxynojirimycin and 5-(adamantan-1-ylmethoxy)-pentanal. The aldehyde was synthesized from 1,5-pentanediol in five steps and 45% overall yield. Protected 1-deoxynojirimycin was prepared by a successive hemiacetal reduction/Swern oxidation/double reductive amination sequence of 2,3,4,5-tetra-O-benzyl-D-glucopyranose in 52% overall yield. Reductive amination of the two building blocks produced the benzylprotected penultimate that was isolated as its crystalline (+)DTTA salt in 68% yield. Hydrogenolysis of the penultimate and crystallization of the end product as its methanesulfonic acid salt produced AMP-DNM in 76% yield with a purity of >99.5%. The described route enables the production of multikilogram amounts of inhibitor AMP-DNM as a stable crystalline solid with high purity under cGMP control.

Tuning the activity of iminosugars: novel N-alkylated deoxynojirimycin derivatives as strong BuChE inhibitors

We have designed unprecedented cholinesterase inhibitors based on 1-deoxynojirimycin as potential anti-Alzheimer’s agents. Compounds are comprised of three key structural motifs: the iminosugar, for interaction with cholinesterase catalytic anionic site (

Design, synthesis, and activity evaluation of novel N-benzyl deoxynojirimycin derivatives for use as α-glucosidase inhibitors

To obtain α-glucosidase inhibitors with high activity, 19 NB-DNJDs (N-benzyldeoxynojirimycin derivatives) were designed and synthesized. The results indicated that the 19 NBDNJDs displayed different inhibitory activities towards α-glucosidase in vitro. Compound 18a (1- (4-hydroxy-3-methoxybenzyl)-2-(hydroxymethyl) piperidine-3,4,5-triol) showed the highest activity, with an IC50 value of 0.207 ± 0.11 mM, followed by 18b (1-(3-bromo-4-hydroxy-5- methoxybenzyl)-2-(hydroxymethyl) piperidine-3,4,5-triol, IC50: 0.276 ± 0.13 mM). Both IC50 values of 18a and 18b were significantly lower than that of acarbose (IC50: 0.353 ± 0.09 mM). According to the structure-activity analysis, substitution of the benzyl and bromine groups on the benzene ring decreased the inhibition activity, while methoxy and hydroxyl group substitution increased the activity, especially with the hydroxyl group substitution. Molecular docking results showed that three hydrogen bonds were formed between compound 18a and amino acids in the active site of α- glucosidase. Additionally, an arene-arene interaction was also modelled between the phenyl ring of compound 18a and Arg 315. The three hydrogen bonds and the arene-arene interaction resulted in a low binding energy (-5.8 kcal/mol) and gave 18a a higher inhibition activity. Consequently, compound 18a is a promising candidate as a new α-glucosidase inhibitor for the treatment of type II diabetes.

Structure–Activity Studies of N-Butyl-1-deoxynojirimycin (NB-DNJ) Analogues: Discovery of Potent and Selective Aminocyclopentitol Inhibitors of GBA1 and GBA2

Analogues of N-butyl-1-deoxynojirimycin (NB-DNJ) were prepared and assayed for inhibition of ceramide-specific glucosyltransferase (CGT), non-lysosomal β-glucosidase 2 (GBA2) and the lysosomal β-glucosidase 1 (GBA1). Compounds 5 a–6 f, which carry sterically demanding nitrogen substituents, and compound 13, devoid of the C3 and C5 hydroxy groups present in DNJ/NB-DGJ (N-butyldeoxygalactojirimycin) showed no inhibitory activity for CGT or GBA2. Inversion of stereochemistry at C4 of N-(n-butyl)- and N-(n-nonyl)-DGJ (compounds 24) also led to a loss of activity in these assays. The aminocyclopentitols N-(n-butyl)- (35 a), N-(n-nonyl)-4-amino-5-(hydroxymethyl)cyclopentane- (35 b), and N-(1-(pentyloxy)methyl)adamantan-1-yl)-1,2,3-triol (35 f), were found to be selective inhibitors of GBA1 and GBA2 that did not inhibit CGT (>1 mm), with the exception of 35 f, which inhibited CGT with an IC50 value of 1 mm. The N-butyl analogue 35 a was 100-fold selective for inhibiting GBA1 over GBA2 (Ki values of 32 nm and 3.3 μm for GBA1 and GBA2, respectively). The N-nonyl analogue 35 b displayed a Ki value of ?14 nm for GBA1 inhibition and a Ki of 43 nm for GBA2. The N-(1-(pentyloxy)methyl)adamantan-1-yl) derivative 35 f had Ki values of ≈16 and 14 nm for GBA1 and GBA2, respectively. The related N-bis-substituted aminocyclopentitols were found to be significantly less potent inhibitors than their mono-substituted analogues. The aminocyclopentitol scaffold should hold promise for further inhibitor development.

Concise synthesis of 1-epi-castanospermine

1-epi-Castanospermine (5) was synthesized from readily available 2,3,4,6-tetra-O-benzyl-1-deoxynojirimycin (11) in 9 steps and 21% overall yield, with selective debenzylation, Barbier reaction and reductive amination as the main reaction steps.

A Fluorescence Polarization Activity-Based Protein Profiling Assay in the Discovery of Potent, Selective Inhibitors for Human Nonlysosomal Glucosylceramidase

Human nonlysosomal glucosylceramidase (GBA2) is one of several enzymes that controls levels of glycolipids and whose activity is linked to several human disease states. There is a major need to design or discover selective GBA2 inhibitors both as chemical tools and as potential therapeutic agents. Here, we describe the development of a fluorescence polarization activity-based protein profiling (FluoPol-ABPP) assay for the rapid identification, from a 350+ library of iminosugars, of GBA2 inhibitors. A focused library is generated based on leads from the FluoPol-ABPP screen and assessed on GBA2 selectivity offset against the other glucosylceramide metabolizing enzymes, glucosylceramide synthase (GCS), lysosomal glucosylceramidase (GBA), and the cytosolic retaining β-glucosidase, GBA3. Our work, yielding potent and selective GBA2 inhibitors, also provides a roadmap for the development of high-throughput assays for identifying retaining glycosidase inhibitors by FluoPol-ABPP on cell extracts containing recombinant, overexpressed glycosidase as the easily accessible enzyme source.

Selenoureido-iminosugars: A new family of multitarget drugs

Herein we report the synthesis of N-alkylated deoxynojirimycin derivatives decorated with a selenoureido motif at the hydrocarbon tether as an example of unprecedented multitarget agents. Title compounds were designed as dual drugs for tackling simultaneously the Gaucher disease (by selective inhibition of β-glucosidase, Ki= 1.6–5.5 μM, with improved potency and selectivity compared to deoxynojirimycin) and its neurological complications (by inhibiting AChE, Kiup to 5.8 μM). Moreover, an excellent mimicry of the selenoenzyme glutathione peroxidase was also found for the catalytic scavenging of H2O2(Kcat/Kuncatup to 640) using PhSH as a cofactor, with improved activity compared to known positive controls, like (PhSe)2and ebselen; therefore, such compounds are also excellent scavengers of peroxides, an example of reactive oxygen species present at high concentrations in patients of Gaucher disease and neurological disorders.

High sugar composition for treatment and method

The invention relates to the compounds of formula (I) or its pharmaceutical acceptable salts, as well as polymorphs, solvates, enantiomers, stereoisomers and hydrates thereof The pharmaceutical compositions comprising an effective amount of compounds of formula (I), and methods for the treatment of hyperglycemia may be formulated for oral, buccal, rectal, topical, transdermal, transmucosal, intravenous, parenteral administration, syrup, or injection. Such compositions may be used to treatment of insulin resistance, diabetes mellitus, diabetes insipidus, type 1 diabetes, type 2 diabetes, microvascular complications, macrovascular complications, lipid disorders, prediabetes, obesity, arrhythmia, myocardial infarction, stroke, neuropathy, renal complications, hypertriglyceridemia, cardiovascular complications, and post prandial hyperglycemia.

Chemical synthesis of 1-deoxy-L-fructose and L-sorbose through carbonyl translocation

Two rare sugars - 1-deoxy-L-fructose and L-sorbose - were synthesized from inexpensive starting materials by a carbonyl translocation method developed in our laboratory. Reduction of a known starting compound gave a 1,5-diol derivative. Selective protecti

Compositions and methods for the treatment of hyperglycemia

The invention relates to the compounds of formula I or its pharmaceutical acceptable salts, as well as polymorphs, solvates, enantiomers, stereoisomers and hydrates thereof. The pharmaceutical compositions comprising an effective amount of compounds of formula I, and methods for the treatment of hyperglycemia may be formulated for oral, buccal, rectal, topical, transdermal, transmucosal, intravenous, parenteral administration, syrup, or injection. Such compositions may be used to treatment of insulin resistance, diabetes mellitus, diabetes insipidus, type 1 diabetes, type 2 diabetes, microvascular complications, macrovascular complications, lipid disorders, prediabetes, obesity, arrhythmia, myocardial infarction, stroke, neuropathy, renal complications, hypertriglyceridemia, cardiovascular complications, and post prandial hyperglycemia.