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.
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- CAS. Nr.: 3688-75-3
- Formel: C18H32O16
- Molecular Weight:504.44
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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. Nr. 3688-75-3
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Molecular Weight 504.44
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Formel 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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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
[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
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)