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Tormentic acid
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Product Name Tormentic acid
Price: $238 / 10mg
CAS No.: 13850-16-3
Catalog No.: CFN99434
Molecular Formula: C30H48O5
Molecular Weight: 488.7 g/mol
Purity: >=98%
Type of Compound: Triterpenoids
Physical Desc.: Powder
Source: The herbs of Potentilla tormentilla
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
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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: Tormentic acid has anticancer, anti-inflammatory, anti-atherogenic , anti-allodynic, and hepatoprotective properties, it can inhibit markedly the neuropathic allodynia induced by partial ligation of the sciatic nerve. Tormentic acid potently inhibits the production of nitric oxide (NO) in RAW 264.7 cells, also suppresses the LPS-stimulated degradation and phosphorylation of inhibitor of kappa B-α (IκB-α), suggests that the anti-inflammatory activity of TA is associated with the down-regulation of iNOS, COX-2, and TNF-α through the negative regulation of the NF-κB pathway in RAW 264.7 cells.
Targets: NO | HO-1 | GLUT | NOS | NF-kB | Bcl-2/Bax | Caspase | COX | IL Receptor | PGE | PPAR | TNF-α | AMPK
In vivo:
Int Immunopharmacol. 2014 Apr;19(2):365-72.
Protective effect of tormentic acid from Potentilla chinensis against lipopolysaccharide/D-galactosamine induced fulminant hepatic failure in mice.[Pubmed: 24560903]
A compound was isolated from Potentilla chinensis, and it was identified as Tormentic acid (TA) based on its physicochemical properties and spectral data.
METHODS AND RESULTS:
The hepatoprotective effect of Tormentic acid was evaluated using an acute liver failure model induced by lipopolysaccharide (LPS)/D-galactosamine (D-GalN). The results revealed that Tormentic acid significantly prevented LPS/D-GalN-induced fulminant hepatic failure, as evidenced by the decrease in serum aminotransferase and total bilirubin activities and the attenuation of histopathological changes. Tormentic acid alleviated the pro-inflammatory cytokines including TNF-α and NO/iNOS by inhibiting nuclear factor-κB (NF-κB) activity. Moreover, Tormentic acid strongly inhibited lipid peroxidation, recruited the anti-oxidative defense system, and increased HO-1 activity. In addition, Tormentic acid significantly attenuated increases in TUNEL-positive hepatocytes through decreasing the levels of cytochrome c, as well as caspases-3, 8 and 9, while augmenting the expression of Bcl-2.
CONCLUSIONS:
In conclusion, Tormentic acid protects hepatocytes against LPS/D-GalN-induced injury by blocking NF-κB signaling pathway for anti-inflammatory response and attenuating hepatocellular apoptosis. Consequently, Tormentic acid is a potential agent for preventing acute liver injury and may be a major bioactive ingredient of Potentilla chinensis.
Eur J Pharmacol. 2002 Oct 25;453(2-3):203-8.
Anti-allodynic action of the tormentic acid, a triterpene isolated from plant, against neuropathic and inflammatory persistent pain in mice.[Pubmed: 12398905]

METHODS AND RESULTS:
The inhibition observed was 82+/-9% and 100+/-11%, respectively. Interestingly, Tormentic acid did not inhibit paw oedema formation following Complete Freund's Adjuvant plantar injection. Tormentic acid (30 mg/kg, p.o.) and gabapentin (70 mg/kg, p.o.), given twice a day, inhibited markedly the neuropathic allodynia induced by partial ligation of the sciatic nerve, with inhibition of 91+/-19% and 71+/-16%, respectively. The anti-allodynic action of Tormentic acid was not associated with impairment of the motor activity of the animals.
CONCLUSIONS:
Together, the present results indicate that Tormentic acid or its derivatives might be of potential interest in the development of new clinically relevant drugs for the management of persistent neuropathic and inflammatory allodynia.
Tormentic acid Description
Source: The herbs of Potentilla tormentilla
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.
doi: 10.1016/j.cell.2017.12.019.
IF=36.216(2019)

PMID: 29328914

Cell Metab. 2020 Mar 3;31(3):534-548.e5.
doi: 10.1016/j.cmet.2020.01.002.
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PMID: 32004475

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PMID: 29149595

ACS Nano. 2018 Apr 24;12(4): 3385-3396.
doi: 10.1021/acsnano.7b08969.
IF=13.903(2019)

PMID: 29553709

Nature Plants. 2016 Dec 22;3: 16206.
doi: 10.1038/nplants.2016.205.
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PMID: 28005066

Sci Adv. 2018 Oct 24;4(10): eaat6994.
doi: 10.1126/sciadv.aat6994.
IF=12.804(2019)

PMID: 30417089
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:
Neuroscience. 2015 Feb 26;287:9-14.
Tormentic acid reduces inflammation in BV-2 microglia by activating the liver X receptor alpha.[Pubmed: 25497374 ]
Tormentic acid (TA) has been reported to have anticancer, anti-inflammatory and anti-atherogenic properties. However, the effects of Tormentic acid on neuroinflammation have not been reported.
METHODS AND RESULTS:
In this study, we investigated whether TA inhibited lipopolysaccharide (LPS)-induced inflammatory response in BV2 microglia cells. BV2 microglia cells were treated with Tormentic acid for 1h before exposure to LPS. The expression of inducible nitric oxide synthase (iNOS), Cyclooxygenase-2 (COX-2), Nuclear factor κB (NF-κB) and liver X receptor alpha (LXRα) was detected by western blotting. The expression of cytokines Tumor necrosis factor-alpha (TNF-α) and interleukin 1beta (IL-1β) was detected by enzyme-linked immunosorbent assays (ELISA). Results showed that Tormentic acid inhibited nitric oxide (NO), prostaglandin E2 (PGE2) production by inhibiting iNOS and COX-2 expression. Tormentic acid also inhibited LPS-induced inflammatory cytokines TNF-α and IL-1β expression. Furthermore, Tormentic acid could activate LXRα and inhibit LPS-induced NF-κB activation. Knowdown of LXRα reversed the anti-inflammatory effects of Tormentic acid.
CONCLUSIONS:
In conclusion, our results indicate that Tormentic acid exerts an anti-inflammatory effect on LPS-stimulated BV2 microglia cells by activating LXRα.
Cell Research:
Anticancer Agents Med Chem. 2013 Jun;13(5):768-76.
Antiproliferative activities on renal, prostate and melanoma cancer cell lines of Sarcopoterium spinosum aerial parts and its major constituent tormentic acid.[Pubmed: 23157592]
The search for improved cytotoxic agents continues to be an important line in the discovery of modern anticancer drugs. Sarcopoterium spinosum (L.) Spach is mentioned in ethnobotanical surveys as a medicinal plant used for the treatment of cancer. The aim of this study is to investigate and to compare the aerial parts of S. spinosum collected in Italy and Lebanon for their chemical composition and their antiproliferative activity against ACHN, C32, A375, MCF-7, LNCaP and HeLa human cancer cell lines using SRB assay.
METHODS AND RESULTS:
The main constituent Tormentic acid was isolated by MPLC and characterized by spectroscopic techniques (NMR, MS). Non polar compounds were analyzed by GC and GC-MS. S. spinosum showed an interesting antiproliferative activity against ACHN and C32 cell lines with IC(50) values of 2.4 and 2.7 μg/ml for S. spinosum from Italy and Lebanon, respectively. Remarkable results were obtained also against A375 and LNCaP cell lines. The cytotoxicity against ACHN cell line could be partially attributed to Tormentic acid that demonstrated a higher cytotoxicity than the positive control vinblastine. Close association between the radical scavenging activity (evaluated by DPPH and ABTS assay) and cytotoxicity was also demonstrated.
CONCLUSIONS:
This investigation demonstrated the potential cytotoxic activity of S. spinosum taking into account also that none of the tested extracts, fractions and isolated compound affected the proliferation of normal cell line 142BR. Tormentic acid, the major constituent isolated from S. spinosum, play an important role in the cytotoxicity exhibited by the extract.
Animal Research:
J Agric Food Chem. 2014 Nov 5;62(44):10717-26.
Tormentic acid, a major component of suspension cells of Eriobotrya japonica, suppresses high-fat diet-induced diabetes and hyperlipidemia by glucose transporter 4 and AMP-activated protein kinase phosphorylation.[Pubmed: 25317836]
This study was designed to evaluate the effects and mechanism of Tormentic acid (PTA) on diabetes and dyslipidemia in high-fat (HF)-fed mice.
METHODS AND RESULTS:
Feeding C57BL/6J mice with a HF diet for 12 weeks induced type 2 diabetes and hyperlipidemia. During the last 4 weeks, the mice were given orally Tormentic acid (at two dosages) or rosiglitazone (Rosi) or water. In this study, the HF diet increased glucose, triglyceride, insulin, and leptin levels, whereas Tormentic acid effectively prevented these phenomena and ameliorated insulin resistance. Tormentic acid reduced visceral fat mass and hepatic triacylglycerol contents; moreover, Tormentic acid significantly decreased both the area of adipocytes and ballooning degeneration of hepatocytes. Tormentic acid caused increased skeletal muscular AMP-activated protein kinase (AMPK) phosphorylation and Akt phosphorylation and glucose transporter 4 (GLUT4) proteins, but reduced the hepatic expressions of phosphenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6 Pase) genes. Tormentic acid enhanced skeletal muscular Akt phosphorylation and increased insulin sensitivity. Tormentic acid also enhanced phospho-AMPK in the liver. Therefore, it is possible that the activation of AMPK by Tormentic acid results in decreasing hepatic glucose production while increasing skeletal muscular GLUT4 contents, thus contributing to attenuating the diabetic state. Moreover, Tormentic acid exhibits an antihyperlipidemic effect by down-regulations of the hepatic sterol regulatory element binding protein-1c (SREBP-1c) and apolipoprotein C-III (apo C-III) and an increased peroxisome proliferator activated receptor (PPAR)-α expression, thus resulting in decreases in blood triglycerides.
CONCLUSIONS:
These findings demonstrated that Tormentic acid was effective for the treatment of diabetes and hyperlipidemia in HF-fed mice.
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