Cat. No.: HY-N10612

Petasin

Petasin is an orally active, potent inhibitor of mitochondrial electron transport chain complex I (ETCC1) with an IC₅₀ of 3.55 μM. Petasin functionally activates AMPK by inhibiting mitochondrial respiration and increasing the intracellular AMP/ATP ratio. Petasin inhibits leukotriene production and eosinophil effector responses, as well as tumor cell proliferation, migration, invasion, and in vivo tumor growth and metastasis. Petasin is also a natural sesquiterpene ester that can be found in plants of the Petasites genus, such as Petasites japonicus and Petasites hybridus. Petasin can be used in studies related to cancer metabolism, glucose and lipid metabolism, and inflammation.

For research use only. We do not sell to patients.

CAS No.: 26577-85-5
Formula: C₂₀H₂₈O₃
Molecular Weight:316.43

Storage:

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

Data Sheet (300 KB)

Petasin Chemical Structure

CAS No.: 26577-85-5

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target

^[5]

ETCC1

3.55 μM (IC₅₀)

All AMPK Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
SW-620	IC50	30.07 μM	Cytotoxicity against human colon carcinoma SW-620 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay. Cytotoxicity against human colon carcinoma SW-620 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.	30896562
Caco-2	IC50	209.67 μM	Cytotoxicity against human colon carcinoma Caco-2 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay. Cytotoxicity against human colon carcinoma Caco-2 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.	30896562
LoVo	IC50	228.59 μM	Cytotoxicity against human colon carcinoma LoVo cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay. Cytotoxicity against human colon carcinoma LoVo cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.	30896562
HT-29	IC50	78.08 μM	Cytotoxicity against human colon carcinoma HT-29 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay. Cytotoxicity against human colon carcinoma HT-29 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.	30896562

In Vitro

Lipid MetabolismAnti-cancerApoptosisEMT / MetastasisOncogenic Signaling (PI3K, MAPK, Wnt, JAK-STAT)Carbohydrate MetabolismMitochondrial Oxidative PhosphorylationLipid Inflammatory MediatorsInnate ImmunityMitochondrial Function

Lipid Metabolism

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].

Anti-cancer

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].

Anti-cancer

Apoptosis

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].

Anti-cancer

EMT / Metastasis

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].

Anti-cancer

Apoptosis

EMT / Metastasis

Oncogenic Signaling (PI3K, MAPK, Wnt, JAK-STAT)

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].

Carbohydrate Metabolism

Lipid Metabolism

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].

Mitochondrial Oxidative Phosphorylation

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].

Lipid Inflammatory Mediators

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].

Lipid Inflammatory Mediators

Innate Immunity

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].

Innate Immunity

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].

Anti-cancer

Mitochondrial Function

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.

Cell Differentiation Assay^[1]

Cell Line:

3T3-F442A preadipocytes
Concentration:

0.25-2 μM; 2 μM (structure-activity relationship testing)
Incubation Time:

6 days
Result:

Potently inhibited lipid accumulation in differentiating cells in a dose-dependent manner, with an IC₅₀ value of 0.95 μM.
Reduced relative lipid accumulation to approximately 40% of the control level at 2 μM.
Showed no inhibitory effect at 2 μM for analogs isopetasin and petasol.

Real Time qPCR^[1]

Cell Line:

3T3-F442A adipocytes
Concentration:

0.5-2 μM; 2 μM (structure-activity relationship testing)
Incubation Time:

6 days
Result:

Suppressed the mRNA expression of mature adipocyte markers (PPARγ, C/EBPα, aP2) in a dose-dependent manner, with near-complete inhibition at 2 μM.
Suppressed the expression of lipid synthesis factors (ACC1, FAS, SCD1) in a dose-dependent manner, with significant reductions observed at concentrations as low as 0.5 μM.
Showed no effect on the expression of any of these genes at 2 μM for analogs isopetasin and petasol.

Cell Viability Assay^[7]

Cell Line:

SW-620, Caco-2, LoVo, HT-29
Concentration:

1 μM, 5 μM, 25 μM
Incubation Time:

24 h, 48 h, 72 h
Result:

Exerted dose-dependent cytotoxicity on all four cell lines.
Reduced SW-620 cell growth by 21.16% at 24 h, 38.52% at 48 h, and 47.15% at 72 h when used at 25 μM.
Achieved IC₅₀ values of 30.07 μM for SW-620, 209.67 μM for Caco-2, 228.59 μM for LoVo, and 78.08 μM for HT-29 at 48 h.

Apoptosis Analysis^[7]

Cell Line:

SW-620
Concentration:

25 μM
Incubation Time:

48 h
Result:

Increased the percentage of apoptotic SW-620 cells from 6.01% to 31.03%.
Induced clear nuclear condensation and structural changes in treated cells.

Cell Invasion Assay^[7]

Cell Line:

SW-620
Concentration:

25 μM
Incubation Time:

24 h
Result:

Reduced the number of invasive SW-620 cells from 268 to 61 per microscope field.

Western Blot Analysis^[7]

Cell Line:

SW-620
Concentration:

25 μM
Incubation Time:

24 h
Result:

Reduced Akt/mTOR/P70S6K phosphorylation and altered apoptosis- and invasion-associated proteins.

Western Blot Analysis^[4]

Cell Line:

H4IIE rat hepatoma cells
Concentration:

0.1, 0.3, 0.5, 1, 5, 10 μM
Incubation Time:

1 h
Result:

Induced a dose-dependent increase in phosphorylated AMPKα (Thr172) and phosphorylated ACC (Ser79) levels, with increases observed at concentrations of at least 0.3 μM.

Western Blot Analysis^[4]

Cell Line:

C2C12 mouse myotubes
Concentration:

1, 10, 25, 50, 100, 200 μM
Incubation Time:

2 h
Result:

Induced a dose-dependent increase in phosphorylated AMPKα (Thr172) and phosphorylated ACC (Ser79) levels, with increases observed at concentrations of at least 5 μM.

Western Blot Analysis^[4]

Cell Line:

differentiated 3T3-L1 mouse adipocytes
Concentration:

1, 5, 10, 25, 50, 100 μM
Incubation Time:

2 h
Result:

Induced a dose-dependent increase in phosphorylated AMPKα (Thr172) and phosphorylated ACC (Ser79) levels, with increases observed at concentrations of at least 10 μM.

In Vivo

Anti-cancerApoptosisCarbohydrate MetabolismLipid MetabolismEMT / MetastasisCell Cycle Regulation

Anti-cancer

Apoptosis

Petasin (10 mg/kg; p.o.; twice daily; for 28 consecutive days) reduces the volume of subcutaneous SW-620 colon tumors in Balb/c nude mice and induces apoptosis in tumor tissues, with apoptotic DNA fragmentation observed in 36.0% of tumor cells^[7].

Carbohydrate Metabolism

Lipid Metabolism

Petasin (200 mg/kg; p.o.; single administration) activates AMPK and its downstream signaling pathways in the liver, white adipose tissue and skeletal muscle of healthy mice^[4].

Carbohydrate Metabolism

Petasin (100-200 mg/kg; p.o.; single administration) is administered to fasted C57BL/6J mice 1 h prior to glucose loading, which significantly reduces the blood glucose AUC after glucose loading and enhances glucose tolerance^[4].

Anti-cancer

Petasin (50 mg/kg; i.p.; once daily; for 4 consecutive days) significantly inhibits tumor growth in a B16F10 melanoma mouse model^[5].
Petasin (50 mg/kg; i.p.; once daily; for 14 consecutive days) significantly reduces pulmonary tumor colonies in the B16F10 lung colonization model^[5].

Anti-cancer

EMT / Metastasis

Cell Cycle Regulation

Petasin (50 mg/kg; i.p.; daily; for 14 consecutive days) potently inhibits spontaneous pulmonary metastasis and lymph node metastasis of Jyg-MCB breast cancer in mice, without affecting primary tumor growth or causing obvious acute toxicity^[5].

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

Animal Model:

Balb/c athymic (nu+/nu+) (male, 4 weeks old, colon cancer model via SW-620 cell hypodermic injection)^[7]
Dosage:

10 mg/kg
Administration:

intragastrically; twice a day; 28 days
Result:

Reduced tumor volume to 289.22 mm³ at day 21.
Reduced tumor volume to 577.67 mm³ at day 28.
Induced apoptosis in 36.0% of tumor cells.

Animal Model:

C57BL/6J (male, 10 weeks old)^[4]
Dosage:

200 mg/kg
Administration:

p.o.; single dose
Result:

Increased phosphorylation of AMPKα in liver, white adipose tissue, and skeletal muscle.
Increased phosphorylation of ACC (Ser79) in liver and white adipose tissue.
Increased relative mRNA expression of PGC-1α in skeletal muscle.

Animal Model:

C57BL/6J (male, 10 weeks old)^[4]
Dosage:

100 mg/kg; 200 mg/kg
Administration:

p.o.; single dose
Result:

Reduced blood glucose levels after glucose loading compared to vehicle controls.
Lowered AUC values compared to vehicle controls.

Animal Model:

C57BL/6 (orthotopic syngeneic B16F10 melanoma model)^[5]
Dosage:

50 mg/kg
Administration:

i.p.; once daily for 4 d
Result:

Significantly inhibited tumor growth.

Animal Model:

immunocompromised (subcutaneous xenograft A2058 melanoma and NB-1 neuroblastoma models)^[5]
Dosage:

50 mg/kg
Administration:

i.p.; daily; 14 days
Result:

Significantly reduced tumor volume in both A2058 melanoma and NB-1 neuroblastoma xenograft models.
Caused no severe weight loss or apparent toxicity over the 14-day period.

Animal Model:

syngeneic (spontaneous metastatic Jyg-MCB mammary carcinoma model)^[5]
Dosage:

50 mg/kg
Administration:

i.p.; 6 administrations over 16 d
Result:

Significantly reduced the number of lung metastatic lesions and the weight of enlarged axillary lymph nodes.
Reduced p-FAKY397-positive lung metastatic colonies and lowered percentages of Ki-67 and p-histone H3S10-positive proliferating cells in lung metastatic tissues.
Caused no significant growth inhibition of primary tumors and no severe weight loss or apparent toxicity.

Related Protocols :

Chemical Information

CAS No. 26577-85-5
Molecular Weight 316.43
Formula C₂₀H₂₈O₃
SMILES

C[C@@]12C(CC[C@H]([C@@H]2C)OC(/C(C)=C\C)=O)=CC([C@@H](C1)C(C)=C)=O
Structure Classification
- Others
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

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

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (300 KB)
SDS (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Uesugi S, et al. Petasin is the main component responsible for the anti-adipogenic effect of Petasites japonicus. Fitoterapia. 2022 Mar;157:105130. [Content Brief]

[2]. Thomet OA, et al. Differential inhibition of inflammatory effector functions by petasin, isopetasin and neopetasin in human eosinophils. Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology. 2001 Aug;31(8):1310-20.

[3]. Thomet OA, et al. Role of petasin in the potential anti-inflammatory activity of a plant extract of petasites hybridus. Biochemical pharmacology. 2001 Apr 15;61(8):1041-7.

[4]. Adachi Y, et al. Petasin activates AMP-activated protein kinase and modulates glucose metabolism. Journal of natural products. 2014 Jun 27;77(6):1262-9.

[5]. Heishima K, et al. Petasin potently inhibits mitochondrial complex I-based metabolism that supports tumor growth and metastasis. The Journal of clinical investigation. 2021 Sep 01;131(17):e139933.

[6]. Kleeberg-Hartmann J, et al. Petasin and isopetasin reduce CGRP release from trigeminal afferents indicating an inhibitory effect on TRPA1 and TRPV1 receptor channels. The journal of headache and pain. 2021 Apr 13;22(1):23.

[7]. Lyu X, et al. Inhibitory effects of petasin on human colon carcinoma cells mediated by inactivation of Akt/mTOR pathway. Chinese medical journal. 2019 May 05;132(9):1071-1078.

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Petasin

All AMPK Isoforms