Sudachitin
Sudachitin is an orally active compound that potently inhibits mouse PDE1C and human PDE4B, with IC50 values of 5.0 μM and 15.0 μM, respectively. Sudachitin upregulates Sirt1 and PGC‑1α expression in skeletal muscle to regulate energy metabolism and promote mitochondrial biogenesis. Sudachitin improves lipid metabolism, glucose tolerance, insulin sensitivity, energy expenditure, and fatty acid β‑oxidation. Sudachitin activates p38MAPK signaling, induces HSP27 phosphorylation and caspase‑dependent apoptosis, and blocks EGF‑driven keratinocyte migration and proliferation. Sudachitin suppresses LPS‑induced TNF‑α, NO, and iNOS expression in macrophages and shows potent anti‑inflammatory activity. Sudachitin can be used for the research of metabolic syndrome, type 2 diabetes, and psoriasis..
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- CAS. Nr.: 4281-28-1
- Formel: C18H16O8
- Molecular Weight:360.31
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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
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Help & FAQs
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Biologische Aktivität
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PDE1C 5 μM (IC50) |
PDE4B 15 μM (IC50) |
SIRT1 |
p38 MAPK |
iNOS |
Sudachitin (30 μmol/L; 48 h) significantly upregulates genes involved in mitochondrial biogenesis and glucose transport, and increases mitochondrial density by 2.5-fold in primary mouse skeletal muscle myocytes[1].
Sudachitin (30-100 μM; 24 h) induces caspase-dependent apoptosis in human keratinocyte HaCaT cells, as evidenced by cleaved Bid, caspase-3, and PARP[2].
Sudachitin (30-100 μM; 2-24 h) induces apoptosis in human keratinocyte HaCaT cells via activation of the MKK3/6-p38MAPK pathway, with sustained p38MAPK phosphorylation up to 24 h at 100 μM[2].
Sudachitin (30 μM; 1 h pretreatment followed by EGF stimulation) suppresses EGF-induced ERK1/2 activation in human keratinocyte HaCaT cells, including inhibiting Raf-1 phosphorylation and Elk-1 transcriptional activity[2].
Sudachitin (30 μM; 1 h pretreatment followed by 24 h EGF exposure) inhibits EGF-induced migration and proliferation of human keratinocyte HaCaT cells[2].
Sudachitin (up to 30 μM; 24 h) does not reduce the viability of mouse macrophage-like RAW264 cells[3].
Sudachitin (10-30 μM; 12 h LPS stimulation) significantly suppresses LPS-induced TNF-α production in mouse macrophage-like RAW264 cells when pretreated before LPS stimulation[3].
Sudachitin (3-30 μM; 12 h LPS incubation) dose-dependently inhibits LPS-induced NO production in mouse macrophage-like RAW264 cells, with 30 μM reducing nitrate levels to near-basal levels[3].
Sudachitin (30 μM; 6 h LPS stimulation) pretreatment markedly inhibits LPS-induced TNF-α and iNOS mRNA expression in mouse macrophage-like RAW264 cells[3].
Sudachitin (0.1-100 μM) inhibits recombinant mouse PDE1C activity with an IC₅₀ of 5.0 μM (1 μM cGMP as substrate) and recombinant human PDE4B activity with an IC₅₀ of 15 μM (1 μM cAMP as substrate)e[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human keratinocyte HaCaT cells
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Concentration:30 μM; 100 μM
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Incubation Time:24 h; 24 h (with Z-VAD-FMK (HY-16658B) pretreatment)
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Result:Reduced full‑length Bid levels while elevating cleaved caspase‑3 levels in a concentration‑dependent manner.
Induced Bid cleavage, caspase‑3 activation, and PARP cleavage concentration‑dependently.
Markedly diminished sudachitin‑triggered PARP cleavage following Z‑VAD‑FMK pretreatment.
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Cell Line:human keratinocyte HaCaT cells
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Concentration:30 μM; 100 μM; 30 μM (with Adezmapimod (HY-10256) pretreatment)
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Incubation Time:4 h (concentration-dependence); 2 h, 4 h, 8 h, 24 h (time-dependence at 100 μM); 4 h, 24 h (with Adezmapimod pretreatment)
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Result:Increased p38MAPK and MKK3/6 phosphorylation concentration- and time-dependently, while decreasing ERK1/2 phosphorylation concentration-dependently.
Adezmapimod pretreatment markedly reduced sudachitin-induced HSP27 phosphorylation and PARP cleavage.
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Cell Line:human keratinocyte HaCaT cells
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Concentration:30 μM
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Incubation Time:1 h pretreatment, followed by 24 h incubation with EGF
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Result:Reduced EGF-stimulated cell migration, with migration area decreased to 0.9-fold relative to EGF-only control over 24 h.
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Cell Line:human keratinocyte HaCaT cells
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Concentration:10 μM
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Incubation Time:1 h pretreatment, followed by 24 h incubation with EGF
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Result:Reduced EGF-stimulated BrdU incorporation to 0.9-fold, relative to EGF-only control over 24 h.
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Cell Line:LPS-stimulated mouse macrophage-like RAW264 cells
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Concentration:10 μM, 30 μM (pretreated before LPS stimulation)
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Incubation Time:12 h (incubated with LPS)
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Result:Significantly inhibited LPS-stimulated TNF-α production at both tested concentrations, with stronger inhibition observed at 30 μM than at 10 μM, and showed stronger inhibition than licochalcone A at 10 μM.
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Cell Line:LPS-stimulated mouse macrophage-like RAW264 cells
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Concentration:30 μM (pretreated before LPS stimulation)
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Incubation Time:6 h (incubated with LPS)
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Result:Significantly suppressed LPS-stimulated iNOS expression by more than 50%.\nSignificantly reduced LPS-induced TNF-α expression.
Sudachitin (10 mg/kg; p.o.; daily; 7 days) enhances antigen-specific cellular and humoral immune responses in BALB/c mice, with 1.8-fold increased interferon-γ production, 2.1-fold increased IgG1 titers, and 1.7-fold increased IgG2a titers[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 J (male, 4 weeks of age, high-fat diet-induced obesity and metabolic syndrome)[1]
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Dosage:5 mg/kg (12-week studies); 5 mg/kg (4-week indirect calorimetry studies)
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Administration:p.o.; daily; 12 weeks; 4 weeks (indirect calorimetry)
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Result:Reduced body weight gain, serum triglyceride and free fatty acid levels, fasting glucose and insulin, total body fat, subcutaneous fat, visceral fat, and adipocyte size in high-fat diet-fed mice.
Improved glucose tolerance and insulin sensitivity, and elevated plasma adiponectin levels.
Increased mRNA expression of GLUT4, UCP1, UCP3 in white adipose tissue and UCP2, PGC-1α, Sirt1 in skeletal muscle.
Enhanced skeletal muscle ATP content and citrate synthase activity, and raised oxygen consumption and total daily energy expenditure by 45% after 4 weeks of treatment.
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Animal Model:db/db (4 weeks of age, genetic leptin receptor deficiency-induced type 2 diabetes)[1]
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Dosage:5 mg/kg (12-week studies); 5 mg/kg (4-week indirect calorimetry studies)
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Administration:p.o.; daily; 12 weeks; 4 weeks (indirect calorimetry)
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Result:Did not affect body weight gain within 12 weeks. Reduced fasting blood glucose, serum triglyceride, and non‑esterified fatty acid levels.
Improved insulin sensitivity by decreasing the AUC of insulin tolerance test.
Enhanced oxygen consumption and total daily energy expenditure after 4 weeks of treatment.
Chemical Information
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CAS. Nr. 4281-28-1
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Molecular Weight 360.31
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Formel C18H16O8
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SMILES
O=C1C=C(C2=CC(OC)=C(O)C=C2)OC3=C1C(O)=C(OC)C(O)=C3OC
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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
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Data Sheet (285 KB)
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SDS (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
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- Español - ES (252 KB)
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- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
Verweise
[1]. Tsutsumi R, et al. Sudachitin, a polymethoxylated flavone, improves glucose and lipid metabolism by increasing mitochondrial biogenesis in skeletal muscle. Nutr Metab (Lond). 2014;11:32. Published 2014 Jul 4. [Content Brief]
[2]. Abe S, et al. Sudachitin, a polymethoxyflavone from Citrus sudachi, induces apoptosis via the regulation of MAPK pathways in human keratinocyte HaCaT cells. Biochem Biophys Res Commun. 2019;519(2):344-350. [Content Brief]
[3]. Yuasa K, et al. Sudachitin, a polymethoxyflavone from Citrus sudachi, suppresses lipopolysaccharide-induced inflammatory responses in mouse macrophage-like RAW264 cells. Biosci Biotechnol Biochem. 2012;76(3):598-600. [Content Brief]
[4]. Abe S, et al. Sudachitin, a polymethoxyflavone from Citrus sudachi, induces apoptosis via the regulation of MAPK pathways in human keratinocyte HaCaT cells. Biochem Biophys Res Commun. 2019 Nov 5;519(2):344-350. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
Sudachitin Related Classifications
HY-N11262 Related Classifications
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