Ursodiol | Ursodeoxycholic Acid | CAS#128-13-2 | Synthetically-Derived Bile Acid

MedKoo Cat#: 203091 | Name: Ursodiol

Description:

WARNING: This product is for research use only, not for human or veterinary use.

Ursodiol, also known as Ursodeoxycholic acid, is a synthetically-derived form of ursodiol, a bile acid produced by the liver and secreted and stored in the gallbladder. Also produced by the Chinese black bear liver, ursodiol has been used in the treatment of liver disease for centuries. This agent dissolves or prevents cholesterol gallstones by blocking hepatic cholesterol production and decreasing bile cholesterol. Ursodiol also reduces the absorption of cholesterol from the intestinal tract.

Chemical Structure

Ursodiol

CAS#128-13-2 (free acid)

Theoretical Analysis

MedKoo Cat#: 203091

Name: Ursodiol

CAS#: 128-13-2 (free acid)

Chemical Formula: C24H40O4

Exact Mass: 392.2927

Molecular Weight: 392.57

Elemental Analysis: C, 73.43; H, 10.27; O, 16.30

Price and Availability

Size	Price	Availability
5g	USD 90.00	Ready to ship
10g	USD 150.00	Ready to ship
25g	USD 300.00	Ready to ship
50g	USD 450.00	Ready to ship
100g	USD 750.00	Ready to ship

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Related CAS #

128-13-2 (free acid) 2898-95-5 (sodium)

Synonym

Ursodiol, Ursodeoxycholic acid, Actigall, URSO, Deursil, Ursosan, Ursofalk, Urso Forte

IUPAC/Chemical Name

(R)-4-((3R,5S,7S,8R,9S,10S,13R,14S,17R)-3,7-dihydroxy-10,13-dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-17-yl)pentanoic acid

InChi Key

RUDATBOHQWOJDD-UZVSRGJWSA-N

InChi Code

InChI=1S/C24H40O4/c1-14(4-7-21(27)28)17-5-6-18-22-19(9-11-24(17,18)3)23(2)10-8-16(25)12-15(23)13-20(22)26/h14-20,22,25-26H,4-13H2,1-3H3,(H,27,28)/t14-,15+,16-,17-,18+,19+,20+,22+,23+,24-/m1/s1

SMILES Code

C[C@@H]([C@H]1CC[C@@]2([H])[C@]3([H])[C@@H](O)C[C@]4([H])C[C@H](O)CC[C@]4(C)[C@@]3([H])CC[C@]12C)CCC(O)=O

Appearance

White Solid Powder

Purity

>98% (or refer to the Certificate of Analysis)

Shipping Condition

Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.

Storage Condition

Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

Solubility

Soluble in DMSO, not in water

Shelf Life

>2 years if stored properly

Drug Formulation

This drug may be formulated in DMSO

Stock Solution Storage

0 - 4 C for short term (days to weeks), or -20 C for long term (months).

HS Tariff Code

2934.99.9001

More Info

Ursodiol, also known as ursodeoxycholic acid and the abbreviation UDCA, is one of the secondary bile acids, which are metabolic byproducts of intestinal bacteria. Ursodeoxycholic acid goes by the trade names Actigall, Ursosan, Ursofalk, Urso, and Urso Forte. In Italy and Switzerland, it is marketed under the name Deursil. Ursodeoxycholic acid can be chemically synthesized and was brought to market by the Montreal-based Axcan Pharma in 1998, which continues to market the drug. The drug reduces cholesterol absorption and is used to dissolve (cholesterol) gallstones in patients who want an alternative to surgery. The drug is very expensive, however, and if the patient stops taking it, the gallstones tend to recur if the condition that gave rise to their formation does not change. For these reasons, it has not supplanted surgical treatment by cholecystectomy. It is the only FDA approved drug to treat primary biliary cirrhosis. See: http://en.wikipedia.org/wiki/Ursodiol .

Product Data

Product Data

Certificate of Analysis

View CoA: current batch, Lot#BBC51014

QC Data

View QC data: current batch, Lot#BBC51014

Safety Data Sheet (SDS)

View Safety Data Sheet (SDS)

Instruction

View handling instruction

Biological target:

Ursodiol (Ursodeoxycholic acid; UDCA) is a potent liver-specific fatty acid transport protein 5 (FATP5) inhibitor that inhibits LCFA uptake by primary hepatocytes in a FATP5-dependent manner.

In vitro activity:

To further explore the physiological and pharmacological implications of hepatic FATP inhibition by secondary bile acids the effects of UDCA (ursodeoxycholic acid) on LCFA uptake were by primary hepatocytes were tested. Using a FACS-based LCFA uptake assay that allows for the gating of viable cells, it was found that UDCA but not TUDCA inhibited LCFA uptake by primary human hepatocytes (Sup. Fig. 5). UDCA also inhibited LCFA uptake by primary mouse hepatocytes from C57Bl/6 animals without any detectable cytotoxic effects (Fig. 5A right). Importantly, this effect was entirely FATP5 dependent, as UDCA (ursodeoxycholic acid) failed to inhibited LCFA uptake by primary hepatocytes from FATP5-null animals (Fig. 5A). While TUDCA did not inhibit FATP2 and -5 mediated uptake, UDCA was identified as a potent inhibitor of FATP5 (Fig. 3) with an IC50 of 5 μM (Tab. 1). Here a novel link is reported between bile acids and metabolism, i.e. the ability of, specific bile acids such as DCA and UDCA to inhibit hepatic LCFA uptake. Hepatology. 2012 Oct; 56(4): 1300–1310. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3445775/

In vivo activity:

To elucidate the mechanism by which UDCA (ursodeoxycholic acid) alters FFA (free fatty acid) profiles in vivo in C57BL/6 mice, the expression of genes involved in TG synthesis and FFA synthesis, oxidation, and uptake in liver, EAT, and BAT were examined. Sterol regulatory element-binding protein 1c (SREBP1c)—a transcription factor that promotes the expression of lipogenic genes including acetyl coenzyme A (CoA) carboxylase 1 (ACC1), FA synthase (FAS), and stearoyl-CoA desaturase-1 (SCD1)—was downregulated by UDCA treatment, with a corresponding decrease in FAS, ACC1, and SCD1 mRNA levels (Figure 5A), indicating that de novo lipogenesis was inhibited. Diacylglycerol acyltransferase (DGAT) is the key enzyme promoting TG formation; it was found here that UDCA suppressed DGAT1 and DGAT2 expressions (Figure 5B), which is consistent with the observed reduction in liver TG content (Figure 1G). The expression of factors involved in FA oxidation including peroxisome proliferator-activated receptor α (PPARα), carnitine palmitoyl transferase 1A (CPT1A), and acy-CoA oxidase-1 (ACOX1) was inhibited by consumption of HFD, but this was reversed by UDCA (Figure 5C). In addition, genes involved in FA uptake in liver including FA transport protein 2 (FATP2), FATP5, and cluster of differentiation 36 (CD36) were downregulated in the UDCA group, whereas FATP2 and CD36 were upregulated in the HFD group (Figure 5D). In EAT and BAT, factors associated with FA uptake and lipogenesis were also suppressed by UDCA administration to varying degrees (Figures 5E–H). These results demonstrate that UDCA alters the FFA profile by inhibiting lipogenesis, promoting FA oxidation, and reducing FA uptake in liver and adipose tissue. Additionally, UDCA repressed the expression of genes regulating TG synthesis, thereby decreasing TG deposition in liver. Front Pharmacol. 2019; 10: 842. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6669341/

	Solvent	mg/mL	mM
Solubility
	DMSO	56.0	142.65

Note: There can be variations in solubility for the same chemical from different vendors or different batches from the same vendor. The following factors can affect the solubility of the same chemical: solvent used for crystallization, residual solvent content, polymorphism, salt versus free form, degree of hydration, solvent temperature. Please use the solubility data as a reference only. Warming and sonication will facilitate dissolving. Still have questions? Please contact our Technical Support scientists.

Preparing Stock Solutions

The following data is based on the product molecular weight 392.57 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Concentration / Solvent Volume / Mass	1 mg	5 mg	10 mg
1 mM	1.15 mL	5.76 mL	11.51 mL
5 mM	0.23 mL	1.15 mL	2.3 mL
10 mM	0.12 mL	0.58 mL	1.15 mL
50 mM	0.02 mL	0.12 mL	0.23 mL

Formulation protocol:

1. Nie B, Park HM, Kazantzis M, Lin M, Henkin A, Ng S, Song S, Chen Y, Tran H, Lai R, Her C, Maher JJ, Forman BM, Stahl A. Specific bile acids inhibit hepatic fatty acid uptake in mice. Hepatology. 2012 Oct;56(4):1300-10. doi: 10.1002/hep.25797. PMID: 22531947; PMCID: PMC3445775. 2. Hu J, Hong W, Yao KN, Zhu XH, Chen ZY, Ye L. Ursodeoxycholic acid ameliorates hepatic lipid metabolism in LO2 cells by regulating the AKT/mTOR/SREBP-1 signaling pathway. World J Gastroenterol. 2019 Mar 28;25(12):1492-1501. doi: 10.3748/wjg.v25.i12.1492. PMID: 30948912; PMCID: PMC6441910. 3.Nie B, Park HM, Kazantzis M, Lin M, Henkin A, Ng S, Song S, Chen Y, Tran H, Lai R, Her C, Maher JJ, Forman BM, Stahl A. Specific bile acids inhibit hepatic fatty acid uptake in mice. Hepatology. 2012 Oct;56(4):1300-10. doi: 10.1002/hep.25797. PMID: 22531947; PMCID: PMC3445775. 4. Hu J, Hong W, Yao KN, Zhu XH, Chen ZY, Ye L. Ursodeoxycholic acid ameliorates hepatic lipid metabolism in LO2 cells by regulating the AKT/mTOR/SREBP-1 signaling pathway. World J Gastroenterol. 2019 Mar 28;25(12):1492-1501. doi: 10.3748/wjg.v25.i12.1492. PMID: 30948912; PMCID: PMC6441910.

In vitro protocol:

In vivo protocol:

1. Zhang Y, Zheng X, Huang F, Zhao A, Ge K, Zhao Q, Jia W. Ursodeoxycholic Acid Alters Bile Acid and Fatty Acid Profiles in a Mouse Model of Diet-Induced Obesity. Front Pharmacol. 2019 Jul 25;10:842. doi: 10.3389/fphar.2019.00842. PMID: 31402868; PMCID: PMC6669341. 2. Chen YS, Liu HM, Lee TY. Ursodeoxycholic Acid Regulates Hepatic Energy Homeostasis and White Adipose Tissue Macrophages Polarization in Leptin-Deficiency Obese Mice. Cells. 2019 Mar 16;8(3):253. doi: 10.3390/cells8030253. PMID: 30884843; PMCID: PMC6468643.

1: Hansen JD, Kumar S, Lo WK, Poulsen DM, Halai UA, Tater KC. Ursodiol and colorectal cancer or dysplasia risk in primary sclerosing cholangitis and inflammatory bowel disease: a meta-analysis. Dig Dis Sci. 2013 Nov;58(11):3079-87. doi: 10.1007/s10620-013-2772-0. Epub 2013 Jul 30. Review. PubMed PMID: 23896754. 2: San Luis VA, Btaiche IF. Ursodiol in patients with parenteral nutrition-associated cholestasis. Ann Pharmacother. 2007 Nov;41(11):1867-72. Epub 2007 Oct 2. Review. PubMed PMID: 17911205. 3: Brentnall TA. Ursodiol: good drug makes good. Gastroenterology. 2003 Apr;124(4):1139-40. Review. PubMed PMID: 12671906. 4: Comcowich SA, Spitzer TR, Tsunoda SM. Ursodiol to prevent hepatic venoocclusive disease. Ann Pharmacother. 1997 Oct;31(10):1249-52. Review. PubMed PMID: 9337452. 5: O'Brien CB, Shields DS, Saul SH, Reddy KR. Drug-induced vanishing bile duct syndrome: response to ursodiol. Am J Gastroenterol. 1996 Jul;91(7):1456-7. Review. PubMed PMID: 8678017. 6: Rubin RA, Kowalski TE, Khandelwal M, Malet PF. Ursodiol for hepatobiliary disorders. Ann Intern Med. 1994 Aug 1;121(3):207-18. Review. PubMed PMID: 8017748. 7: Vondracek TG, Seifert CF. Use of ursodiol in a patient with biliary cirrhosis. Clin Pharm. 1992 Aug;11(8):672-3. Review. PubMed PMID: 1511539. 8: Rosenbaum CL, Cluxton RJ Jr. Ursodiol: a cholesterol gallstone solubilizing agent. Drug Intell Clin Pharm. 1988 Dec;22(12):941-5. Review. PubMed PMID: 3072172.