Petasin

Petasin (for 6 days) potently inhibits adipocyte differentiation of 3T3-F442A cells, with an IC₅₀ value of 0.95 μM^[1].
Petasin (6 days) dose-dependently inhibits the expression of mature adipocyte markers (PPARγ, C/EBPα, aP2) and lipid synthesis factors (ACC1, FAS, SCD1) in differentiating 3T3-F442A cells^[1].
Petasin (2 μM; 2-6 days) primarily inhibits the late stage of adipogenic differentiation in 3T3-F442A cells^[1].
Petasin (1-25 μM; 24-72 h) dose-dependently inhibits the proliferation of SW-620, Caco-2, LoVo, and HT-29 colon cancer cells; the IC₅₀ values at 48 h are 30.07, 209.67, 228.59, and 78.08 μM, respectively^[7].
Petasin (15-150 nM) inhibits the migration of B16F10 cells, and reduces cell invasion and adhesion prior to the occurrence of energy depletion; Petasin also decreases focal adhesion and downregulates related signaling molecules including p-FAK, ITGA5, and Rac-GTP^[5].
Petasin (25 μM; 48 h) induces apoptosis in human colon cancer SW-620 cells, which is characterized by an increased proportion of apoptotic cells and typical nuclear morphological changes^[7].
Petasin (25 μM; 24 h) significantly inhibits the migration of human colon cancer SW-620 cells^[7].
Petasin (25 μM; 24 h) significantly inhibits the invasive ability of human colon cancer cell line SW-620^[7].
Petasin (25 μM; 24 h) reduces the phosphorylation of Akt, mTOR and P70S6K, increases the levels of Caspase-3 and Caspase-9, and decreases the expression of Bcl-2, MMP-3 and MMP-9 in SW-620 cells^[7].
Petasin activates AMPK in H4IIE, C2C12 and 3T3-L1 cells; AMPK activation is observed at concentrations ≥ 0.3 μM in H4IIE cells, while the effective concentrations are ≥ 5 μM and ≥ 10 μM in C2C12 and 3T3-L1 cells, respectively^[4].
Petasin reduces intracellular ATP levels and increases AMP and ADP levels in cultured cells, leading to dose-dependent increases in the AMP/ATP and ADP/ATP ratios; it also dose-dependently inhibits mitochondrial respiration driven by complex I substrates, without affecting respiration driven by complex II substrates^[4].
Petasin potently inhibits mitochondrial complex I in isolated bovine heart mitochondria, with an IC₅₀ of 3.55 μM^[5].
Petasin (8-40 μg/mL; 15 min pre-incubation, followed by GM-CSF priming and agonist stimulation) dose-dependently inhibits cysteinyl-LT production in human eosinophils stimulated with PAF or C5a after GM-CSF priming, with an IC₅₀ < 24 μg/mL; the inhibition rate reaches 68%-82% at 40 μg/mL^[2].
Petasin (24 μg/mL; 20 min pre-incubation) inhibits cPLA2 activity in A23187-stimulated human eosinophils and prevents the translocation of 5-LO to the nuclear membrane^[2].
Petasin dose-dependently inhibits ECP release from eosinophils stimulated by PAF or C5a, with an IC₅₀ < 8 μg/mL; at 40 μg/mL, it inhibits PAF- and C5a-induced ECP release by 89.1% and 80.7%, respectively^[2].
Petasin (40 μg/mL) inhibits the synthesis of cysteinyl leukotrienes in GM-CSF-prestimulated human eosinophils, as well as the synthesis of LTB₄ in GM-CSF-prestimulated human neutrophils, with an IC₅₀ ≤24 μg/mL; the inhibition rate reaches 68-94% at a concentration of 40 μg/mL^[3].
Petasin (16 μg/mL) completely blocks the PAF- and C5a-induced elevation of intracellular Ca²⁺ in human eosinophils^[2].
Petasin (16 μg/mL) inhibits PAF- and C5a-mediated increases in intracellular calcium concentrations in human eosinophils and human neutrophils in a dose-dependent manner, and completely blocks calcium signals at 16 μg/mL^[3].
Petasin (3 μM; 72 h) potently inhibits the growth of various tumor cells and induces cell cycle arrest; subsequent mitochondrial damage, ATP depletion, and necrotic cell death occur in B16F10 cells, while non-tumor cells are less affected^[5].

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