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.^[1][2][3].

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.

Sudachitin (5 mg/kg, p.o., daily for 12 weeks, with indirect calorimetry performed at 4 weeks) improves fasting glucose, insulin sensitivity, and lipid metabolism while increasing energy expenditure without affecting body weight gain in genetically diabetic db/db mice; in high-fat diet-induced obese and metabolically impaired C57BL/6J mice, the same treatment improves glucose and lipid metabolism, reduces adiposity, and increases energy expenditure by 45%.
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.

360.31

C₁₈H₁₆O₈

4281-28-1

O=C1C=C(C2=CC(OC)=C(O)C=C2)OC3=C1C(O)=C(OC)C(O)=C3OC

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [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.

  [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.

  [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.