Acanthoic acid
Acanthoic acid (NP1302) is an orally active pimarane-type diterpenoid. Acanthoic acid is isolated from the root bark of Araliaceae family plant Eleutherococcus senticosus (Siberian ginseng). Acanthoic acid activates LXR and FXR. Acanthoic acid activates the AMPK-LKB1, SIRT1, and p38 MAPK signaling pathways and increases the phosphorylation level of ACC. Acanthoic acid downregulates the expression of SREBP-1, CYP2E1, HIF-1α, and PPARγ, and upregulates the expression of PPARα. Acanthoic acid induces Apoptosis by activating Caspase-3, promoting PARP cleavage, and downregulating Bcl-xL. Acanthoic acid exhibits antioxidant, anti-fibrotic, and hepatoprotective effects. It reduces lipid accumulation and lipogenesis. Acanthoic acid is used in studies on non-alcoholic fatty liver disease, alcoholic liver disease, acute promyelocytic leukemia, and Acetaminophen-induced hepatotoxicity.
For research use only. We do not sell to patients.
- CAS No.: 119290-87-8
- Formula: C20H30O2
- Molecular Weight:302.45
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
SIRT1 |
CYP2E1 |
HIF-1α |
PPARγ |
PPARα |
Caspase 3 |
Bcl-xL |
In Vitro
Acanthoic acid (5 μM; 3 days) modulates FXR, LXRα, LXRβ, SREBP-1, and SREBP-1 target gene mRNA levels in PA-stimulated AML-12 hepatocytes, consistent with activation of FXR/LXR signaling and downregulation of lipogenic gene expression[1].
Acanthoic acid (5 μM; 3 days) increases FXR fluorescence intensity in PA-stimulated AML-12 hepatocytes, consistent with activation of FXR signaling[1].
Acanthoic acid (5 μM; 3 days) increases LXRβ fluorescence intensity in PA-stimulated AML-12 hepatocytes, consistent with activation of LXR signaling[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:AML-12 mouse hepatocytes
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Concentration:5 μM
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Incubation Time:3 days
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Result:Decreased the elevated protein expression of SREBP-1 in PA-stimulated AML-12 cells.
Ameliorated the PA-induced reduction of FXR, LXRα, and LXRβ protein levels.
Showed effects consistent with the LXR agonist GW3965 in increasing LXRα, LXRβ, and FXR protein levels and suppressing SREBP-1 protein expression.
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Cell Line:AML-12 mouse hepatocytes
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Concentration:5 μM
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Incubation Time:3 days
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Result:Decreased the elevated mRNA expression of SREBP-1 and its target genes Fasn, Scd, and Acly in PA-stimulated AML-12 cells.
Ameliorated the PA-induced reduction of FXR, LXRα, and LXRβ at the mRNA level.
Showed effects consistent with the LXR agonist GW3965 in increasing FXR, LXRα, and LXRβ mRNA levels and suppressing SREBP-1 and its target gene mRNA expression.
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Cell Line:AML-12 mouse hepatocytes
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Concentration:5 μM
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Incubation Time:3 days
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Result:Enhanced the FXR fluorescence intensity that had been reduced by PA in AML-12 cells.\nEnhanced the LXRβ fluorescence intensity that had been reduced by PA in AML-12 cells.
Showed effects consistent with the LXR agonist GW3965 in increasing LXRβ fluorescence intensity.
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Cell Line:HL-60 human promyelocytic leukaemia cells
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Concentration:50-200 μM (dose-response); 150 μM (time-course)
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Incubation Time:24 h (dose-response); 0-24 h (time-course)
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Result:Reduced HL-60 cell proliferation in a dose- and time-dependent manner.
Exposure to 150 μM for 24 h reduced HL-60 cell proliferation by 86%.
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Cell Line:HL-60 human promyelocytic leukaemia cells
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Concentration:150 μM
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Incubation Time:3 h
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Result:Had little effect on JNK phosphorylation.
Dramatically increased phosphorylation of ERK and p38 MAPK compared to untreated cells.
Did not affect total non-phosphorylated p38 MAPK expression.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (male; 6-week old; 22-24 g; high-fat diet induced)[1]
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Dosage:20 mg/kg; 40 mg/kg
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Administration:p.o.; daily; 12 weeks
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Result:Decreased body weight gain and liver index induced by the high-fat diet.
Reduced serum transaminase (ALT, AST) levels.
Lowered both serum and hepatic triglyceride levels.
Reversed liver enlargement, surface fat accumulation, and softened liver texture.
Ameliorated diffuse hepatic fatty degeneration, inflammatory cell infiltration, and hepatocyte degeneration.
Reduced lipid droplet accumulation in the liver as shown by H&E, Oil Red O, and Nile red staining.
Progressively decreased the protein and mRNA expression of SREBP1 and its target genes Fasn, Scd, and Acly.
Up-regulated PPARα expression.
Down-regulated PPARγ expression in the liver.
Significantly decreased the protein and mRNA expression of hepatic fibrosis markers α-SMA, collagen І, and TIMP-1.
Significantly increased the protein and mRNA expression of LXRα, LXRβ, and FXR.
Enhanced the phosphorylation of AMPKα.
Reduced the phosphorylation of LKB1.
Increased SIRT1 protein expression in the liver.
Showed no significant effects on the above parameters in normal diet-fed mice at 40 mg/kg single administration.
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Animal Model:C57BL/6 (male; 6-week-old; body weight 18-22 g; acute binge model induced by three doses of ethanol 5 g/kg by gavage within 24 h at 12 h intervals)[2]
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Dosage:20 mg/kg; 40 mg/kg
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Administration:p.o.; once daily; 14 consecutive days
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Result:Suppressed acute ethanol-induced increases in serum ALT, AST, LDH, and ALP levels.
Reversed elevated serum and hepatic triglyceride levels.
Reduced massive hepatic steatosis and diminished red-stained lipid droplet accumulation in liver tissue.
Significantly reversed ethanol-induced upregulation of SREBP-1 at both protein and mRNA levels.
Decreased SREBP-1 immunohistochemical positive staining.
At 40 mg/kg, significantly suppressed ethanol-induced CYP2E1 protein elevation.
Markedly inhibited ethanol-induced increases in IL-1β and caspase-1 at both mRNA and protein levels.
Decreased F4/80 expression in liver tissue.
Increased Sirt1 protein expression in both cytoplasm and nucleus.
Elevated phosphorylation levels of LKB1, AMPKα, AMPKβ, and ACC that were reduced by ethanol.
Reversed ethanol-induced decreases in LXRα and LXRβ mRNA levels.
Restored PPARα protein expression.
Decreased ethanol-elevated PPARγ protein expression.
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Animal Model:C57BL/6 (male; 6-7 weeks old; 21-24 g; acetaminophen-induced sub-lethal hepatic toxicity via 300 mg/kg acetaminophen i.p. injection)[4]
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Dosage:50 mg/kg; 100 mg/kg
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Administration:p.o.; once daily; 3 consecutive days
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Result:Reduced serum ALT activity to 138 IU/L at 50 mg/kg and 102 IU/L at 100 mg/kg.
Reduced serum AST activity to 119 IU/L at 50 mg/kg and 94 IU/L at 100 mg/kg.
Reduced serum TNF-α level to 80.0 pg/mL at 50 mg/kg and 65.9 pg/mL at 100 mg/kg.
Reduced liver MDA level to 7.24 nmol/mg prot at 50 mg/kg and 5.05 nmol/mg prot at 100 mg/kg.
Increased liver GSH level to 417.25 mg/g prot at 50 mg/kg and 431.19 mg/g prot at 100 mg/kg.
Increased liver SOD activity to 69.22 U/mg prot at 50 mg/kg and 73.46 U/mg prot at 100 mg/kg.
Increased liver CAT activity to 45.71 U/mg prot at 50 mg/kg and 52.92 U/mg prot at 100 mg/kg.
Increased liver GSH-Px activity to 783.39 U/L at 50 mg/kg and 847.13 U/L at 100 mg/kg.
Reduced caspase-3 expression in liver tissue at both doses.
Reduced HIF-1α expression in liver tissue in a dose-dependent manner.
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Animal Model:C57BL/6 (male; 6-7 weeks old; 21-24 g; acetaminophen-induced lethal hepatic toxicity via 500 mg/kg APAP i.p. injection)[4]
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Dosage:50 mg/kg; 100 mg/kg
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Administration:p.o.; once daily; 3 consecutive days (final dose 2 h before APAP challenge)
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Result:Increased 24 h survival rate to 52% at 50 mg/kg after lethal APAP challenge.
Increased 24 h survival rate to 74% at 100 mg/kg after lethal APAP challenge.
- Kinase activity and phosphorylation assays
- Western Blot
- RNA extraction experimental
- 3T3-L1 preadipocyte-to-adipocyte differentiation
- Detection of Apoptosis
- TUNEL staining for apoptotic DNA fragmentation
- Annexin V plus membrane-impermeant dye apoptosis staining
- Apoptosis Solutions
- Protocol for Kinase activity and phosphorylation assays
- Hepatotoxicity Study
- Research Protocol for Metabolic Diseases
- Lipid Droplets: Oil Red O/Sudan Dye Lipid Staining
Chemical Information
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CAS No. 119290-87-8
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Molecular Weight 302.45
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Formula C20H30O2
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SMILES
C[C@]12[C@@](CC[C@]3([H])C2=CC[C@@](C)(C3)C=C)([H])[C@@](C)(CCC1)C(O)=O
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Synonyms
NP1302
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
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Data Sheet (298 KB)
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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)
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Handling Instructions (2659 KB)
References
[3]. Kim KN, et al. Acanthoic acid induces cell apoptosis through activation of the p38 MAPK pathway in HL-60 human promyelocytic leukaemia. Food chemistry. 2012 Dec 01;135(3):2112-7. [Content Brief]
[4]. Wu YL, et al. Acanthoic acid, a diterpene in Acanthopanax koreanum, protects acetaminophen-induced hepatic toxicity in mice. Phytomedicine : international journal of phytotherapy and phytopharmacology. 2010 May;17(6):475-9. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Acanthoic acid Related Classifications
HY-116136 Related Classifications
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Keywords
- Acanthoic acid
- 119290-87-8
- NP1302
- NP 1302
- NP-1302
- LXR
- FXR
- AMPK
- Sirtuin
- p38 MAPK
- Acetyl-CoA Carboxylase
- Cytochrome P450
- HIF/HIF Prolyl-Hydroxylase
- PPAR
- Caspase
- PARP
- Bcl-2 Family
- Apoptosis
- nonalcoholic fatty liver disease
- AML-12 hepatocytes
- SIRT1
- Acanthopanax koreanum
- acetaminophen-induced hepatic toxicity
- HL-60 human promyelocytic leukaemia cells
- AMPK-LKB1
- Inhibitor
- inhibitor
- inhibit