S-Petasin 

S-Petasin is a phosphodiesterase (PDE) inhibitor with IC₅₀ values of 25.5 μM and 17.5 μM for PDE3 and PDE4, respectively. S-Petasin inhibits cholesterol side-chain cleavage enzyme, 11β-hydroxylase, PPAR-γ, and iNOS induction at RNA and protein levels. S-Petasin induces apoptosis, activates caspases, cleaves PARP, modulates mitochondrial membrane permeability, and regulates BCL2/BAX, p53, Bcl-XL, MMP-2, MMP-9, p21, CDK4, and cyclin D1 expression. S-Petasin reduces inflammatory cell accumulation, cytokine and IgE levels, and enhances serum IgG2a levels. S-Petasin relaxes isolated sensitized guinea pig trachealis and exhibits gastrointestinal anti-spasmodic activity. S-Petasin reduces tonsillitis severity and asthmatic attack frequency. S-Petasin can be used for the research of prostate cancer, obesity, melanoma, allergic asthma, asthma, and peritonitis^{[1][2][3][4][5]}.

S-Petasin (10 nM-10 μM; 3-4 days) dose-dependently inhibits proliferation of LNCaP, DU145, and PC3 human prostate cancer cells, but not PC3 cells^[1].
S-Petasin (0.1-10 μM; 12-18 h) activates caspase cascades and induces PARP cleavage in LNCaP, DU145, and PC3 human prostate cancer cells, consistent with induction of apoptosis^[1].
S-Petasin (0.1-10 μM; 8-12 h) induces mitochondrial membrane permeability disruption, cytochrome c release, and modulates expression of BCL2 family proteins and p53 in LNCaP, DU145, and PC3 human prostate cancer cells, triggering mitochondria-mediated apoptosis^[1].
S-petasin (0.31-1.55 μM; 8 days) dose-dependently inhibits 3T3-L1 pre-adipocyte differentiation, reducing lipid accumulation to 30.18% at the highest tested concentration^[2].
S-petasin (0.31-1.55 μM; 8 days) dose-dependently inhibits triglyceride accumulation in differentiated 3T3-L1 adipocytes, reducing TG content to 61.04% at the highest tested concentration^[2].
S-petasin (0.31-1.55 μM) dose-dependently inhibits PPAR-γ expression in 3T3-L1 cells, with greater inhibition observed after 8 days of differentiation treatment than after 24 h^[2].
S-petasin (0.31-1.55 μM; 8 days) dose-dependently inhibits the expression of PPAR-γ target genes (HMGCR, FAS, CD36, Glut4, A-FABP, LPL) in differentiated 3T3-L1 adipocytes^[2].
S-Petasin (2-160 μM; 24 h) potently inhibits proliferation of B16F10 cells (IC₅₀ = 42.16 μM) and A375 cells (IC₅₀ = 36.90 μM) after 24 h of treatment, as measured by MTT assay^[3].
S-Petasin (10-40 μM; 24 h) induces apoptosis of B16F10 cells and A375 cells in a concentration-dependent manner after 24 h of treatment, as measured by Annexin V/PI flow cytometry^[3].
S-Petasin (10-40 μM; 24 h) induces apoptosis of B16F10 cells and A375 cells after 24 h of treatment by downregulating pro-apoptotic precursors and upregulating activated cleavage products of caspase 9, caspase 3, and PARP-1^[3].
S-Petasin (10-40 μM; 24 h) regulates downstream p53 target genes in B16F10 cells and A375 cells after 24 h of treatment by decreasing nuclear NF-κB, MMP-2, MMP-9, Bcl-2, Bcl-xL, CDK4, and cyclin D₁ expression, and increasing Bax and p21 expression, all in a concentration-dependent manner^[3].
S-Petasin (4-40 μM; up to 24 h) inhibits migration of B16F10 cells and A375 cells in a concentration-dependent manner over 24 h, as measured by wound healing assay^[3].
S-Petasin (4-40 μM; 24 h) inhibits invasion of B16F10 cells and A375 cells through Max Gel ECM in a concentration-dependent manner after 24 h of treatment^[3].
S-Petasin (10-40 μM; 24 h) activates p53 expression at mRNA and protein levels in a concentration-dependent manner in B16F10 cells and A375 cells after 24 h of treatment^[3].
S-Petasin (1-100 μM; 30 min) competitively inhibits PDE3 and PDE4 from guinea pig lungs and hearts with IC₅₀ values of 25.5 μM and 17.5 μM, respectively, and does not inhibit PDE1, PDE2, or PDE5 at concentrations up to 100 μM^[4].
S-Petasin potently inhibits antigen-induced degranulation in RBL-2H3 mast cells with an IC₅₀ of ~1 nM^[5].
S-Petasin (1-10 μM; 1 h preincubation, 24 h LPS stimulation) concentration-dependently inhibits LPS-induced iNOS protein and mRNA expression, NO and PGE2 production in mouse peritoneal macrophages, with significant effects at 1, 3, 5, and 10 μM^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

S-Petasin (10-30 μmol/kg (3.3-9.9 mg/kg); s.c.; 2 hours before, 6 and 24 hours after secondary OVA provocation) dose-dependently and significantly attenuates airway hyperresponsiveness, reduces inflammatory cell infiltration, suppresses pro-inflammatory cytokine production, and modulates immunoglobulin levels in a murine model of allergic asthma^[4].
S-Petasin (1 mg/kg; i.p.; 1 h before each ovalbumin nebulization) inhibits ovalbumin-induced accumulation of eosinophils, macrophages, and lymphocytes in BALB/c mouse bronchoalveolar lavage fluid, reducing total cell counts by 80% relative to untreated asthmatic mice^[5].
S-Petasin (1 mg/kg; i.p.; single dose 1 h prior to LPS injection) reduces LPS-induced accumulation of total peritoneal cells, polymorphonuclear leukocytes, and mononuclear leukocytes in C57BL/6 mice^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

334.47

C₁₉H₂₆O₃S

70238-51-6

C[C@@H]([C@@H](CCC1=CC2=O)OC(/C=C\SC)=O)[C@@]1(C)C[C@H]2C(C)=C

Room temperature in continental US; may vary elsewhere.

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

• [1]. Wang ZH, et al. Cytotoxic effect of s-petasin and iso-s-petasin on the proliferation of human prostate cancer cells. Anticancer Res. 2015;35(1):191-199.  [Content Brief]

  [2]. Guo L, et al. S-Petasin isolated from Petasites japonicus exerts anti-adipogenic activity in the 3T3-L1 cell line by inhibiting PPAR-γ pathway signaling. Food Funct. 2019 Jul 17;10(7):4396-4406.  [Content Brief]

  [3]. Guo L, et al. S-petasin induces apoptosis and inhibits cell migration through activation of p53 pathway signaling in melanoma B16F10 cells and A375 cells. Arch Biochem Biophys. 2020;692:108519.  [Content Brief]

  [4]. Shih CH, et al. S-Petasin, the Main Sesquiterpene of Petasites formosanus, Inhibits Phosphodiesterase Activity and Suppresses Ovalbumin-Induced Airway Hyperresponsiveness. Evid Based Complement Alternat Med. 2011;2011:132374.  [Content Brief]

  [5]. Lee KP, et al. Therapeutic effects of s-petasin on disease models of asthma and peritonitis. Biomol Ther (Seoul). 2015;23(1):45-52.  [Content Brief]