Lithocholic AcidActivator of vitamin D receptor,PXR and FXR CAS# 434-13-9 |
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Cas No. | 434-13-9 | SDF | Download SDF |
PubChem ID | 9903 | Appearance | Powder |
Formula | C24H40O3 | M.Wt | 376.57 |
Type of Compound | Steroids | Storage | Desiccate at -20°C |
Synonyms | 3α-Hydroxy-5β-cholanic acid | ||
Solubility | DMSO : ≥ 150 mg/mL (398.33 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | (4R)-4-[(3R,5R,8R,9S,10S,13R,14S,17R)-3-hydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoic acid | ||
SMILES | CC(CCC(=O)O)C1CCC2C1(CCC3C2CCC4C3(CCC(C4)O)C)C | ||
Standard InChIKey | SMEROWZSTRWXGI-HVATVPOCSA-N | ||
Standard InChI | InChI=1S/C24H40O3/c1-15(4-9-22(26)27)19-7-8-20-18-6-5-16-14-17(25)10-12-23(16,2)21(18)11-13-24(19,20)3/h15-21,25H,4-14H2,1-3H3,(H,26,27)/t15-,16-,17-,18+,19-,20+,21+,23+,24-/m1/s1 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Lithocholic acid is a toxic secondary bile acid, causes intrahepatic cholestasis, has tumor-promoting activity, its toxic effect can be protected after it activates the vitamin D receptor, PXR and FXR.Lithocholic acid is a vitamin D receptor (VDR) ligand, it can activate the VDR to block inflammatory signals in colon cells. |
Targets | FXR | p65 | NF-kB | IL Receptor | TNF-α |
In vitro | Lithocholic acid, a putative tumor promoter, inhibits mammalian DNA polymerase beta.[Pubmed: 9914784]Jpn J Cancer Res. 1998 Nov;89(11):1154-9.Lithocholic acid (LCA), one of the major components in secondary bile acids, promotes carcinogenesis in rat colon epithelial cells induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), which methylates DNA. Base-excision repair of DNA lesions caused by the DNA methylating agents requires DNA polymerase beta (pol beta). Lithocholic acid as a biomarker of intrahepatic cholestasis of pregnancy during ursodeoxycholic acid treatment.[Pubmed: 19103957 ]Ann Clin Biochem. 2009 Jan;46(Pt 1):44-9.The diagnosis and treatment of intrahepatic cholestasis of pregnancy (ICP) has important implications on fetal health. The biochemical parameter commonly used in the diagnosis of ICP is the determination of the concentration of total serum bile acids (TSBA). However, bile acid profile, especially Lithocholic acid (LCA) analysis is a more sensitive and specific biomarker for differential diagnosis of this pathology and also could be an alternative to evaluate the efficiency of ursodeoxycholic acid (UDCA) for ICP treatment.
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Kinase Assay | Lithocholic acid decreases expression of bile salt export pump through farnesoid X receptor antagonist activity[Reference: WebLink]Journal of Biological Chemistry,2002, 277(35) :31441-7.Bile salt export pump (BSEP) is a major bile acid transporter in the liver. Mutations in BSEP result in progressive intrahepatic cholestasis, a severe liver disease that impairs bile flow and causes irreversible liver damage. BSEP is a target for inhibition and down-regulation by drugs and abnormal bile salt metabolites, and such inhibition and down-regulation may result in bile acid retention and intrahepatic cholestasis. |
Cell Research | Lithocholic acid down-regulation of NF-kappaB activity through vitamin D receptor in colonic cancer cells.[Pubmed: 18515093 ]J Steroid Biochem Mol Biol. 2008 Jul;111(1-2):37-40.Lithocholic acid (LCA), a secondary bile acid, is a vitamin D receptor (VDR) ligand. 1,25-Dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), the hormonal form of vitamin D, is involved in the anti-inflammatory action through VDR. Therefore, we hypothesize that LCA acts like 1,25(OH)(2)D(3) to drive anti-inflammatory signals. |
Lithocholic Acid Dilution Calculator
Lithocholic Acid Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.6555 mL | 13.2777 mL | 26.5555 mL | 53.111 mL | 66.3887 mL |
5 mM | 0.5311 mL | 2.6555 mL | 5.3111 mL | 10.6222 mL | 13.2777 mL |
10 mM | 0.2656 mL | 1.3278 mL | 2.6555 mL | 5.3111 mL | 6.6389 mL |
50 mM | 0.0531 mL | 0.2656 mL | 0.5311 mL | 1.0622 mL | 1.3278 mL |
100 mM | 0.0266 mL | 0.1328 mL | 0.2656 mL | 0.5311 mL | 0.6639 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Lithocholic acid (LCA) is a toxic secondary bile acid, causing intrahepatic cholestasis, which has tumor-promoting activity.
In vitro: Among 17 kinds of bile acids with respect to inhibition of mammalian DNA polymerases, only LCA and its derivatives inhibited DNA polymerases, while other bile acids did not show inhibitory effect [1].
In vivo: Administration of LCA and its conjugates to rodents causes intrahepatic cholestasis, which is a pathogenic state characterized by decreased bile flow and the accumulation of bile constituents in the liver and blood [2].
Clinical trials: Currently no clinical data are available.
References:
[1] Ogawa A, Murate T, Suzuki M, Nimura Y, Yoshida S. Lithocholic acid, a putative tumor promoter, inhibits mammalian DNA polymerase beta. Jpn J Cancer Res. 1998 Nov;89(11):1154-9.
[2] Staudinger JL, Goodwin B, Jones SA, Hawkins-Brown D, MacKenzie KI, LaTour A, Liu Y, Klaassen CD, Brown KK, Reinhard J, Willson TM, Koller BH, Kliewer SA. The nuclear receptor PXR is a lithocholic acid sensor that protects against liver toxicity. Proc Natl Acad Sci U S A. 2001 Mar 13;98(6):3369-74.
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Lithocholic acid down-regulation of NF-kappaB activity through vitamin D receptor in colonic cancer cells.[Pubmed:18515093]
J Steroid Biochem Mol Biol. 2008 Jul;111(1-2):37-40.
Lithocholic Acid (LCA), a secondary bile acid, is a vitamin D receptor (VDR) ligand. 1,25-Dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), the hormonal form of vitamin D, is involved in the anti-inflammatory action through VDR. Therefore, we hypothesize that LCA acts like 1,25(OH)(2)D(3) to drive anti-inflammatory signals. In present study, we used human colonic cancer cells to assess the role of LCA in regulation of the pro-inflammatory NF-kappaB pathway. We found that LCA treatment increased VDR levels, mimicking the effect of 1,25(OH)(2)D(3). LCA pretreatment inhibited the IL-1beta-induced IkappaBalpha degradation and decreased the NF-kappaB p65 phosphorylation. We also measured the production of IL-8, a well-known NF-kappaB target gene, as a read-out of the biological effect of LCA expression on NF-kappaB pathway. LCA significantly decreased IL-8 secretion induced by IL-1beta. These LCA-induced effects were very similar to those of 1,25(OH)(2)D(3.) Thus, LCA recapitulated the effects of 1,25(OH)(2)D(3) on IL-1beta stimulated cells. Mouse embryonic fibroblast (MEF) cells lacking VDR have intrinsically high NF-kappaB activity. LCA pretreatment was not able to prevent TNFalpha-induced IkappaBalpha degradation in MEF VDR (-/-), whereas LCA stabilized IkappaBalpha in MEF VDR (+/-) cells. Collectively, our data indicated that LCA activated the VDR to block inflammatory signals in colon cells.
Lithocholic acid as a biomarker of intrahepatic cholestasis of pregnancy during ursodeoxycholic acid treatment.[Pubmed:19103957]
Ann Clin Biochem. 2009 Jan;46(Pt 1):44-9.
BACKGROUND: The diagnosis and treatment of intrahepatic cholestasis of pregnancy (ICP) has important implications on fetal health. The biochemical parameter commonly used in the diagnosis of ICP is the determination of the concentration of total serum bile acids (TSBA). However, bile acid profile, especially Lithocholic Acid (LCA) analysis is a more sensitive and specific biomarker for differential diagnosis of this pathology and also could be an alternative to evaluate the efficiency of ursodeoxycholic acid (UDCA) for ICP treatment. METHODS: Serum bile acid (SBA) profiles including LCA determination, were studied in 28 ICP patients using a capillary electrophoresis method. The effects of UDCA treatment on bile acid profile, were analysed in 23 out of 28 ICP patients and the two samples obtained before and 15 days after treatment were compared. Two samples taken as controls were also obtained from each of five patients without therapy. RESULTS: A dramatic decrease in LCA concentrations and maintenance of TSBA concentrations were found in all patients after UDCA therapy, whereas SBA profiles together with LCA values did not change in patients without therapy. CONCLUSION: We propose LCA as an alternative biomarker and a more sensitive parameter than TSBA to evaluate the effectiveness of UDCA treatment, at least in ICP patients from Argentina.
Lithocholic acid, a putative tumor promoter, inhibits mammalian DNA polymerase beta.[Pubmed:9914784]
Jpn J Cancer Res. 1998 Nov;89(11):1154-9.
Lithocholic Acid (LCA), one of the major components in secondary bile acids, promotes carcinogenesis in rat colon epithelial cells induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), which methylates DNA. Base-excision repair of DNA lesions caused by the DNA methylating agents requires DNA polymerase beta (pol beta). In the present study, we examined 17 kinds of bile acids with respect to inhibition of mammalian DNA polymerases in vitro. Among them, only LCA and its derivatives inhibited DNA polymerases, while other bile acids were not inhibitory. Among eukaryotic DNA polymerases alpha, beta, delta, epsilon, and gamma, pol beta was the most sensitive to inhibition by LCA. The inhibition mode of pol beta was non-competitive with respect to the DNA template-primer and was competitive with the substrate, dTTP, with the Ki value of 10 microM. Chemical structures at the C-7 and C-12 positions in the sterol skeleton are important for the inhibitory activity of LCA. This inhibition could contribute to the tumor-promoting activity of LCA.