cis-THSG
cis-THSG is a selective and orally active DNA topoisomerase II inhibitor with no activity against DNA topoisomerase I. cis-THSG suppresses transcription of PEPCK. cis-THSG reduces blood glucose levels, ameliorates glucose intolerance, and alleviates insulin resistance in high fat diet-induced diabetic male CF-1 mice. cis-THSG can be used for the research of type 2 diabetes mellitus.
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- CAS. Nr.: 928205-59-8
- Formel: C20H22O9
- Molecular Weight:406.38
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
- Protokoll
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
Alle Topoisomerase Isoform-spezifische Produkte anzeigen
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Biologische Aktivität
Beschreibung
IC50 & Target
[1]|
Topoisomerase II |
In Vitro
cis-THSG (100 μM; 30 min) exhibits weak inhibitory activity against human DNA topoisomerase II, with 46% inhibition at 100 μM, and no activity against DNA topoisomerase I[1].
cis-THSG shows no cytotoxicity against HT-29, MCF-7, and HepG2 cell lines[1].
Cis-THSG (30-100 μM; 8 h) suppresses Dexamethasone (HY-14648)/8-CTP-cAMP -induced PEPCK mRNA expression in HepG2 cells, with maximum inhibition (61.7% reduction) observed at 30 μM for 8 h[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:CF-1 (male; HFD-induced type 2 diabetes mellitus)[2]
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Dosage:0.01% in drinking water
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Administration:ad libitum; daily; 12 weeks
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Result:Significantly decreased serum glucose levels in HFD-induced diabetic mice.
Significantly lowered elevated serum insulin levels and reduced calculated HOMA-IR by 102.7% compared to the trans-THSG treatment group.
Greatly suppressed the sharp rise in blood glucose at 30 minutes post-intraperitoneal glucose injection and reduced the sustained high blood glucose levels observed at 120 minutes, effectively ameliorating glucose intolerance.
Chemical Information
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CAS. Nr. 928205-59-8
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Molecular Weight 406.38
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Formel C20H22O9
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SMILES
O[C@H]([C@H]([C@@H]([C@@H](CO)O1)O)O)[C@@H]1OC2=C(/C=C\C3=CC=C(O)C=C3)C=C(O)C=C2O
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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.
Protokoll
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Reinheit & Dokumentation
Verweise
[1]. Xu ML, et al. A new stilbene glucoside from the roots of Polygonum multiflorum Thunb. Arch Pharm Res. 2006;29(11):946-951. [Content Brief]
[2]. Tang W, et al. Anti-diabetic activities of cis- and trans-2,3,5,4'-tetrahydroxystilbene 2-O-β-glucopyranoside from Polygonum multiflorum. Mol Nutr Food Res. 2017 Aug;61(8). [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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