Neokestose
Neokestose is an orally active 6G-series fructooligosaccharide with both sucrase inhibitor and antiproliferative activities. Neokestose inhibits the activity of the NF-κB signaling pathway, reduces the expression of cyclin D1 and COX-2, induces apoptosis, and disrupts the cell cycle. Neokestose can be used in research related to melanoma, colorectal cancer, obesity and diabetes.
For research use only. We do not sell to patients.
- CAS No.: 3688-75-3
- Formula: C18H32O16
- Molecular Weight:504.44
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Endogenous Metabolite Isoforms
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Biological Activity
Neokestose (1-100 μg; 5 min) dose-dependently inhibits purified Candida sp. invertase activity, with 14.7% inhibition at the 100 μg concentration tested[1].
Neokestose (100 μg; 1 h for crude intestinal enzyme; 1-100 μg; 5 min for invertase) is stable to enzymatic digestion by crude α-glycosidase solution from rat intestinal acetone powder and purified Candida sp. invertase under the tested conditions[1].
Neokestose (80 μg/mL; 0-240 min) is hydrolyzed in pH 1 artificial gastric juice at 37 °C, with ~80% decomposed after 240 min, producing glucose, fructose, sucrose, and blastose (peaking at 1.2 μM at 180 min)[1].
Neokestose (0.5-2.5 mg/mL; 48 h) dose-dependently reduces the viability of human colorectal cancer Caco-2 cells, with viability dropping to ~59% at the highest tested concentration of 2.5 mg/mL following 48 h of treatment[3].
Neokestose (0.5-2.5 mg/mL; 48 h) dose-dependently increases the sub-G1 phase population of human colorectal cancer Caco-2 cells, reaching 45% at 2.5 mg/mL following 48 h of treatment, indicating induced apoptosis[3].
Neokestose (0.5-2.5 mg/mL; 48 h) dose-dependently increases the percentage of late apoptotic human colorectal cancer Caco-2 cells, reaching 31.2% at 2.5 mg/mL following 48 h of treatment[3].
Neokestose (0.5-2.5 mg/mL; 48 h) dose-dependently inhibits the expression of NF-κB and COX-2 proteins in human colorectal cancer Caco-2 cells following 48 h of treatment[3].
Neokestose (10% (w/v) sucrose; 24 h inoculum, 18 h fermentation) was produced at 107.63 g/L by Xanthophyllomyces dendrorhous TISTR 5730 fermenting longan fruit pulp extract, achieving a productivity of 5.98 g/L•h[4].
Neokestose (0.5% (w/v) sucrose inoculum, 20% (v/v) cell pellet; 96 h) was purified from fermented longan fruit pulp extract by Candida orthopsilosis FLA44.2 to 98.3% purity, with 97.5% neokestose recovery and no detectable glucose or sucrose[4].
Neokestose (2 min oral, 3 h gastric, 270 h intestinal phases) is resistant to simulated human gastrointestinal digestion, retaining over 95% of its initial content after exposure to oral, gastric, and intestinal conditions[4].
Neokestose (20 g/L; 48 h) is readily fermentable by Lacticaseibacillus casei TISTR 1500, L. casei TISTR 1463, and Lactiplantibacillus plantarum TISTR 1465, supporting growth equivalent to glucose and being fully consumed within 24-36 h of incubation[4].
Neokestose (5-20% (w/v); 48 h) is non-cytotoxic to HIEC-6 human small intestinal epithelial cells, showing no significant reduction in cell viability after 48 h incubation[4].
Neokestose (10 g/L; 24 h) is preferentially utilized by Bifidobacterium breve NCFB 2257, Bifidobacterium longum NCFB 2259, Bifidobacterium adolescentis NCFB 2230, and Bifidobacterium infantis NCFB 2205 under anaerobic conditions, supporting significantly higher biomass production (1.14-1.17 g/L) than facultative anaerobes or Lactobacillus salivarius NCFB 1555, with utilization rates ranging from 68.7-98.9%[5].
Neokestose (10 g/L; 5-24 h) preferentially stimulates the growth of beneficial bifidobacteria and lactobacilli in human faecal microbiota batch cultures, reduces populations of potentially harmful coliforms, bacteroides, clostridia, and gram-positive cocci after 24 h[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human colorectal cancer Caco-2 cell line
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Concentration:0.5 mg/mL; 1.0 mg/mL; 2.5 mg/mL
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Incubation Time:48 h
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Result:Caused a significant, dose-dependent reduction in Caco-2 cell viability.
Decreased cell viability from 100% in untreated controls to ~59% with 2.5 mg/mL treatment.
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Cell Line:human colorectal cancer Caco-2 cell line
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Concentration:0.5 mg/mL; 1.0 mg/mL; 2.5 mg/mL
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Incubation Time:48 h
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Result:Caused a significant, dose-dependent increase in the sub-G1 phase population of Caco-2 cells, a marker of apoptosis.
Increased the sub-G1 population from 8% in untreated controls to 22% with 0.5 mg/mL, 28% with 1.0 mg/mL, and 45% with 2.5 mg/mL treatment.
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Cell Line:human colorectal cancer Caco-2 cell line
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Concentration:0.5 mg/mL; 1.0 mg/mL; 2.5 mg/mL
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Incubation Time:48 h
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Result:Caused a significant, dose-dependent increase in the percentage of late apoptotic Caco-2 cells (Annexin V-FITC/PI double positive).
Increased late apoptotic cell percentages from 15.3% in untreated controls to 25.3% with 0.5 mg/mL, 27.2% with 1.0 mg/mL, and 31.2% with 2.5 mg/mL treatment.
Kept early apoptotic cell percentages relatively stable across treatment groups.
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Cell Line:human colorectal cancer Caco-2 cell line
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Concentration:0.5 mg/mL; 1.0 mg/mL; 2.5 mg/mL
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Incubation Time:48 h
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Result:Caused a significant, dose-dependent reduction in the protein expression levels of NF-κB and COX-2 in Caco-2 cells.
Decreased expression levels as neokestose concentration increased from 0.5 to 2.5 mg/mL.
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Cell Line:human small intestinal epithelial cells (HIEC-6, ATCC® CRL-3266™)
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Concentration:5-20% (w/v)
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Incubation Time:48 h
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Result:Did not significantly reduce cell viability compared to the control (no sugar).
Maintained viability above 90% for 5% and 10% concentrations.
Maintained viability above 85% for 20% concentration.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar (male, 7 weeks old at study initiation, streptozotocin-induced diabetic)[1]
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Dosage:11.1 mg/kg
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Administration:p.o.; single co-administration with 1.5 g/kg sucrose
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Result:Delayed the time to peak plasma glucose (ΔPG) concentration compared to rats receiving only sucrose.
Reduced ΔPG concentrations significantly at 30, 60, and 120 minutes post-administration.
Reduced the area under the ΔPG concentration-time curve (AUCΔPG) significantly relative to the sucrose-only group.
Chemical Information
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CAS No. 3688-75-3
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Molecular Weight 504.44
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Formula C18H32O16
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SMILES
OC[C@]1(O[C@@H]([C@H]([C@@H]1O)O)CO)O[C@H]2O[C@@H]([C@H]([C@@H]([C@H]2O)O)O)CO[C@@]3(O[C@@H]([C@H]([C@@H]3O)O)CO)CO
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
[1]. Sato K, et al. Neokestose suppresses the increase in plasma glucose caused by oral administration of sucrose in a streptozotocin‑induced diabetic rat. Scientific reports. 2024 Jul 19;14(1):16658. [Content Brief]
[2]. Wu JS, et al. Neokestose suppresses the growth of human melanoma A2058 cells via inhibition of the nuclear factor‑κB signaling pathway. Molecular medicine reports. 2017 Jul;16(1):295-300. [Content Brief]
[3]. Lee SM, et al. Antineoplastic effect of a novel chemopreventive agent, neokestose, on the Caco-2 cell line via inhibition of expression of nuclear factor-κB and cyclooxygenase-2. Molecular medicine reports. 2015 Jul;12(1):1114-8. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)