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Asiatic acid
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Product Name Asiatic acid
Price: $40 / 20mg
CAS No.: 464-92-6
Catalog No.: CFN98688
Molecular Formula: C30H48O5
Molecular Weight: 488.7 g/mol
Purity: >=98%
Type of Compound: Triterpenoids
Physical Desc.: Powder
Source: The herbs of Centella asiatica.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
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Similar structural: Comparison (Web)  (SDF)
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
Description: Asiatic acid shows antihyperlipidemic, anti-inflammatory, antioxidant, and anti-tumorigenesis effects, it inhibits NLRP3 inflammasome activation, NO and COX-2 signals. Asiatic acid inhibits the expression NDR1/2 kinase and promotes the stability of p21WAF1/CIP1 protein through attenuating NDR1/2 dependent phosphorylation of p21WAF1/CIP1 in HepG2 cells.
Targets: TNF-α | IFN-γ | IL Receptor | Caspase | p21 | NOS | NADPH-oxidase | NO | HMG-CoA reductase | COX
In vivo:
Int Immunopharmacol. 2015 Feb;24(2):232-8.
Asiatic acid ameliorates dextran sulfate sodium-induced murine experimental colitis via suppressing mitochondria-mediated NLRP3 inflammasome activation.[Pubmed: 25523461]
In the present study, the effect of Asiatic acid, a natural triterpenoid compound, on murine experimental colitis induced by dextran sulfate sodium (DSS) and its possible mechanism were examined in vivo and vitro.
METHODS AND RESULTS:
Oral administration of Asiatic acid dose-dependently attenuated the loss of body weight and shortening of colon length induced by DSS. The disease activity index, histopathologic scores of musco and myeloperoxidase activity were also significantly reduced by Asiatic acid treatment. Protein and mRNA levels of DSS-induced pro-inflammatory cytokines in colon, including TNF-α, IL-1β, IL-6 and IFN-γ, were markedly suppressed by Asiatic acid. At the same time, decreased activation of caspase-1 in peritoneal macrophages was detected in Asiatic acid-treated mice, which suggested that the NLRP3 inflammasome activation was suppressed. In addition, we also found that Asiatic acid dose-dependently inhibited IL-1β secretion, caspase-1 activation as well as inflammasome assembling in vitro. Furthermore, the mechanism of Asiatic acid was related to the inhibition of mitochondrial reactive oxygen species generation and prevention of mitochondrial membrane potential collapse.
CONCLUSIONS:
Taken together, our results demonstrate the ability of Asiatic acid to inhibit NLRP3 inflammasome activation and its potential usage in the treatment of inflammatory bowel diseases.
Nutrients. 2014 Jan 16;6(1):355-70.
Asiatic acid alleviates hemodynamic and metabolic alterations via restoring eNOS/iNOS expression, oxidative stress, and inflammation in diet-induced metabolic syndrome rats.[Pubmed: 24441717 ]
Asiatic acid is a triterpenoid isolated from Centella asiatica. The present study aimed to investigate whether Asiatic acid could lessen the metabolic, cardiovascular complications in rats with metabolic syndrome (MS) induced by a high-carbohydrate, high-fat (HCHF) diet.
METHODS AND RESULTS:
Male Sprague-Dawley rats were fed with HCHF diet with 15% fructose in drinking water for 12 weeks to induce MS. MS rats were treated with Asiatic acid (10 or 20 mg/kg/day) or vehicle for a further three weeks. Plasma nitrate and nitrite (NOx) were markedly high with upregulation of inducible nitric oxide synthase (iNOS) expression, but dowregulation of endothelial nitric oxide synthase (eNOS) expression (p<0.05). Asiatic acid significantly improved insulin sensitivity, lipid profiles, hemodynamic parameters, oxidative stress markers, plasma TNF-α, NOx, and recovered abnormality of eNOS/iNOS expressions in MS rats (p<0.05).
CONCLUSIONS:
In conclusion, Asiatic acid improved metabolic, hemodynamic abnormalities in MS rats that could be associated with its antioxidant, anti-inflammatory effects and recovering regulation of eNOS/iNOS expression.
Phytomedicine. 2014 Feb 15;21(3):225-32.
Antidiabetic and antihyperlipidemic activity of asiatic acid in diabetic rats, role of HMG CoA: in vivo and in silico approaches.[Pubmed: 24075211]
Hyperlipidemia is an associated complication of diabetes and also a major risk factor for cardiovascular diseases.
METHODS AND RESULTS:
The present study was designed to examine the antihyperlipidemic effect of Asiatic acid (AA) in streptozotocin (STZ) induced diabetic rats. Diabetes was induced in male Wistar rats by a single intraperitoneal injection of STZ (40 mg/kg b.w.). Diabetic rats show increased plasma glucose, total cholesterol, triglycerides, free fatty acids, phospholipids, low density lipoprotein, very low density liprotein, atherogenic index and decreased insulin and high density lipoprotein in diabetic rats. The activity of 3-hydroxy 3-methylglutaryl coenzyme A (HMG CoA) reductase increased significantly in contrast to the activities of lipoprotein lipase and lecithin cholesterol acyltransferase. In addition, the molecular docking of AA against HMG CoA reductase involved in cholesterol biosynthesis using Argus software. Diabetic rats were treated with AA shifted all these parameters towards normalcy. AA has shown best ligand binding energy 11.8122 kcal/mol. The antihyperlipidemic effect of AA was compared with glibenclamide; a well-known antihyperglycemic drug.
CONCLUSIONS:
In conclusion, this study indicates that AA showed an antihyperlipidemic effect in addition to its antidiabetic effect in experimental diabetes.
Asiatic acid Description
Source: The herbs of Centella asiatica.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

Cell. 2018 Jan 11;172(1-2):249-261.e12.
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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.0462 mL 10.2312 mL 20.4625 mL 40.9249 mL 51.1561 mL
5 mM 0.4092 mL 2.0462 mL 4.0925 mL 8.185 mL 10.2312 mL
10 mM 0.2046 mL 1.0231 mL 2.0462 mL 4.0925 mL 5.1156 mL
50 mM 0.0409 mL 0.2046 mL 0.4092 mL 0.8185 mL 1.0231 mL
100 mM 0.0205 mL 0.1023 mL 0.2046 mL 0.4092 mL 0.5116 mL
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Kinase Assay:
Biol Pharm Bull. 2007 Jan;30(1):176-9.
Inhibitory effects of asiatic acid on 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol 13-acetate-induced tumor promotion in mice.[Pubmed: 17202682]
Asiatic acid, a pentacyclic triterpene, has been reported to induce apoptosis of various human cancer cells.
METHODS AND RESULTS:
In the present study, we assessed the anti-tumor promoting effect of Asiatic acid against 12-O-tetradecanoylphorbol 13-acetate (TPA)-mediated skin tumorigenesis in 7,12-dimethylbenz[a]anthracene (DMBA)-initiated ICR mice. Topical application of Asiatic acid prior to each application of TPA resulted in a significant reduction in skin tumor formation. We also found that pre-application of Asiatic acid alleviated TPA-induced [3H]thymidine incorporation, which is a conventional marker for skin tumor promotion. In addition, Asiatic acid inhibited the TPA-induced generation of nitric oxide (NO) and expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), which are known to play important roles in tumor growth, especially in the promotion stage. In addition, topical application of aminoguanidine (AG), a selective iNOS inhibitor, and N(G)-nitro-L-arginine-methyl ester (NAME), another iNOS inhibitor, 30 min prior to TPA treatment significantly inhibited the TPA-induced COX-2 expression.
CONCLUSIONS:
These results suggest that Asiatic acid may exert anti-tumorigenesis through inhibitory actions in NO and COX-2 signals.
Animal Research:
Asian Pac J Cancer Prev. 2014;15(2):963-7.
Asiatic acid promotes p21(WAF1/CIP1) protein stability through attenuation of NDR1/2 dependent phosphorylation of p21(WAF1/ CIP1) in HepG2 human hepatoma cells.[Pubmed: 24568526 ]
Asiatic acid is a triterpenoid isolated from Centella asiatica.
METHODS AND RESULTS:
The present study aimed to investigate whether Asiatic acid could lessen the metabolic, cardiovascular complications in rats with metabolic syndrome (MS) induced by a high-carbohydrate, high-fat (HCHF) diet. Male Sprague-Dawley rats were fed with HCHF diet with 15% fructose in drinking water for 12 weeks to induce MS. MS rats were treated with Asiatic acid (10 or 20 mg/kg/day) or vehicle for a further three weeks. MS rats had an impairment of oral glucose tolerance, increases in fasting blood glucose, serum insulin, total cholesterol, triglycerides, mean arterial blood pressure, heart rate, and hindlimb vascular resistance; these were related to the augmentation of vascular superoxide anion production, plasma malondialdehyde and tumor necrosis factor-alpha (TNF-α) levels (p<0.05). Plasma nitrate and nitrite (NOx) were markedly high with upregulation of inducible nitric oxide synthase (iNOS) expression, but dowregulation of endothelial nitric oxide synthase (eNOS) expression (p<0.05). Asiatic acid significantly improved insulin sensitivity, lipid profiles, hemodynamic parameters, oxidative stress markers, plasma TNF-α, NOx, and recovered abnormality of eNOS/iNOS expressions in MS rats (p<0.05).
CONCLUSIONS:
In conclusion, Asiatic acid improved metabolic, hemodynamic abnormalities in MS rats that could be associated with its antioxidant, anti-inflammatory effects and recovering regulation of eNOS/iNOS expression.
Phytother Res. 2014 Oct;28(10):1506-12.
Asiatic acid reduces blood pressure by enhancing nitric oxide bioavailability with modulation of eNOS and p47phox expression in L-NAME-induced hypertensive rats.[Pubmed: 24723332]
We investigated the effect of Asiatic acid (AA) on hemodynamic status, vascular function, oxidative stress markers, endothelial nitric oxide synthase (eNOS), and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit expression in Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertensive rats.
METHODS AND RESULTS:
Male Sprague-Dawley rats treated with L-NAME (40 mg/kg/day) in drinking water for 5 weeks showed significant increases in mean arterial pressure, heart rate, hindlimb vascular resistance, vascular dysfunction, superoxide anion (O2(•-)) production, and plasma malondialdehyde. Moreover, NO metabolite (NOx) levels were reduced, aortic eNOS expression was downregulated, and NADPH oxidase subunit p47(phox) was upregulated in hypertensive rats (p < 0.05). Hypertensive rats that were administered AA (10 or 20 mg/kg/day) for the last 2 weeks of the study showed significant improvement in hemodynamic status and vascular function. The antihypertensive effects of AA were associated with elevated plasma NOx levels, together with upregulation of eNOS expression. Decreased vascular O2(•-) production, consistent with downregulation of p47(phox) expression, was also observed after AA treatment.
CONCLUSIONS:
Our results are therefore consistent with a model whereby AA reduces blood pressure by enhancing NO bioavailability.
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