Ursodeoxycholic Acid

Synonyms: Acide Ursodéoxycholique; Acide ursodésoxycholique; Ácido ursodeoxicólico; Acidum ursodeoxycholicum; Kyselina ursodeoxycholová; UDCA; Ursodeoksicholio ru _ gštis; Ursodeoksikolik Asit; Ursodeoksikoolihappo; Ursodeoxicholsyra; Ursodesoxycholic Acid; Ursodiol droxy-5
Cyrillic synonym: Урсодезоксихолевая Кислота.

💊 Chemical information

Chemical formula: C24H40O4 = 392.6.
CAS — 128-13-2.
ATC — A05AA02.
ATC Vet — QA05AA02.


In Chin., Eur., Jpn, and US.

Ph. Eur. 6.2

(Ursodeoxycholic Acid). A white or almost white powder. Practically insoluble in water and in dichloromethane; freely soluble in alcohol; slightly soluble in acetone.

USP 31

(Ursodiol). A white or almost white, crystalline powder. Practically insoluble in water; freely soluble in alcohol and in glacial acetic acid; sparingly soluble in chloroform; slightly soluble in ether. Store in airtight containers.


References. 1. Mallett MS, et al. Stability of ursodiol 25 mg/mL in an extemporaneously prepared oral liquid. Am J Health-Syst Pharm 1997; 54: 1401–4. 2. Johnson CE, Streetman DD. Stability of oral suspensions of ursodiol made from tablets. Am J Health-Syst Pharm 2002; 59: 361–3.

💊 Adverse Effects and Precautions

Ursodeoxycholic acid may cause nausea, vomiting, and other gastrointestinal disturbances; diarrhoea is reported to occur less frequently than with chenodeoxycholic acid. Increased liver enzyme values are also less likely. Pruritus may occur. Treatment with ursodeoxycholic acid may cause more calcification of cholesterol stones than chenodeoxycholic acid. Ursodeoxycholic acid should not be given to patients with intestinal and hepatic disorders that interfere with entero-hepatic circulation of bile salts (but see Chronic Liver Disease below). It is ineffective for the dissolution of calcified and pigment gallstones and is of no value in patients without a patent and functioning gallbladder. Licensed product information recommends that its use should be avoided in pregnancy.
1. Hempfling W, et al. Systematic review: ursodeoxycholic acid— adverse effects and drug interactions. Aliment Pharmacol Ther 2003; 18: 963–72.

💊 Interactions

Ursodeoxycholic acid should not be used with drugs that increase bile cholesterol such as oestrogenic hormones and cholesterol-lowering drugs such as clofibrate. Use with bile-acid binding drugs including antacids, charcoal, and colestyramine should be avoided since this may reduce the effectiveness of therapy with ursodeoxycholic acid. For references to the possible effects of ursodeoxycholic acid on ciclosporin.

💊 Pharmacokinetics

Ursodeoxycholic acid is absorbed from the gastrointestinal tract and undergoes enterohepatic recycling. It is partly conjugated in the liver before being excreted into the bile. Under the influence of intestinal bacteria the free and conjugated forms undergo 7 αdehydroxylation to lithocholic acid, some of which is excreted directly in the faeces and the rest absorbed and mainly conjugated and sulfated by the liver before excretion in the faeces. However, in comparison with chenodeoxycholic acid, less ursodeoxycholic acid undergoes such bacterial degradation.
1. Crosignani A, et al. Clinical pharmacokinetics of therapeutic bile acids. Clin Pharmacokinet 1996; 30: 333–58.

💊 Uses and Administration

Ursodeoxycholic acid is a naturally occurring bile acid present in small quantities in human bile. Ursodeoxycholic acid suppresses the synthesis and secretion of cholesterol by the liver and inhibits intestinal absorption of cholesterol. It is used for the dissolution of cholesterol-rich gallstones in patients with functioning gallbladders (see below). The licensed dose is 6 to 12 mg/kg daily as a single bedtime dose or in 2 or 3 divided doses; obese patients may require up to 15 mg/kg daily. The daily dose may be divided unequally and the larger dose given before bedtime to counteract the increase in biliary cholesterol concentration seen overnight. The time required for dissolution of gallstones is likely to be between 6 and 24 months depending on stone size and composition. Treatment should be continued for 3 to 4 months after radiological disappearance of the stones. A dose of 300 mg twice daily has been suggested for the prevention of gallstones in patients undergoing rapid weight loss. Ursodeoxycholic acid has also been given in reduced doses in combination with chenodeoxycholic acid. Ursodeoxycholic acid is also used in primary biliary cirrhosis. The usual dose is 10 to 15 mg/kg daily in 2 to 4 divided doses. Ursodeoxycholic acid has been tried in the treatment of primary sclerosing cholangitis. The more hydrophilic derivative, tauroursodeoxycholic acid, has also been used.

Chronic liver disease.

The use of ursodeoxycholic acid in chronic liver diseases has been summarised.1-5 There have been differing opinions of its value in primary biliary cirrhosis (below). Response has been reported in obstetric cholestasis of pregnancy,6-10 primary sclerosing cholangitis,11 chronic active hepatitis,12 and viral hepatitis.13,14 Although ursodeoxycholic acid is widely used in the treatment of obstetric cholestasis, data on its safety and efficacy in this indication are lacking, and its possible role therefore remains unclear until further larger studies have been done.15 See also Adverse Effects and Precautions, above. Ursodeoxycholic acid appears to be of benefit in liver disease associated with cystic fibrosis16-18 and in the UK the BNFC recommends a dose of 10 to 15 mg/kg twice daily in children and adolescents with this condition; alternatively the total daily dose may be given in 3 divided doses. Ursodeoxycholic acid had initially shown some promise in the treatment of nonalcoholic steatohepatitis,19 but a randomised, controlled study20 failed to confirm this. There has also been some interest in the use of ursodeoxycholic acid to treat refractory graft-versus-host disease of the liver in transplant patients,21 and possibly as an adjuvant to immunosuppressant therapy22-24 after orthotopic liver transplantation. It may also be of benefit in the prevention of hepatic complications following allogeneic bone marrow transplantation.25,26 Ursodeoxycholic acid has shortened the clinical course of parenteral nutrition-associated cholestasis in very-low-birth-weight infants,27 and the BNFC recommends a dose of 10 mg/kg three times daily for this purpose. Benefit has also been reported28 in parenteral-nutrition associated cholestasis in children and adults, although the optimal timing and duration of therapy remains to be evaluated. Ursodeoxycholic acid has also been associated with a lower incidence of colonic dysplasia in patients with ulcerative colitis and primary sclerosing cholangitis.29,30 For sclerosing cholangitis in children and adolescents, the BNFC recommends a dose of 5 to 10 mg/kg 2 or 3 times daily up to a maximum of 15 mg/kg 3 times daily depending on response. In children with biliary atresia, ursodeoxycholic acid may be used to treat associated cholestasis. The BNFC suggests a dose of 5 mg/kg three times daily in neonates and children up to 2 years of age, the dose and frequency adjusted according to response up to a maximum of 10 mg/kg three times daily.
1. de Caestecker JS, et al. Ursodeoxycholic acid in chronic liver disease. Gut 1991; 32: 1061–5
2. Rubin RA, et al. Ursodiol for hepatobiliary disorders. Ann Intern Med 1994; 121: 207–18
3. Kowdley KV. Ursodeoxycholic acid therapy in hepatobiliary disease. Am J Med 2000; 108: 481–6
4. Trauner M, Graziadei IW. Review article: mechanisms of action and therapeutic applications of ursodeoxycholic acid in chronic liver diseases. Aliment Pharmacol Ther 1999; 13: 979–95
5. Lazaridis KN, et al. Ursodeoxycholic acid ‘mechanisms of action and clinical use in hepatobiliary disorders’. J Hepatol 2001; 35: 134–46
6. Palma J, et al. Ursodeoxycholic acid in the treatment of cholestasis of pregnancy: a randomized, double-blind study controlled with placebo. J Hepatol 1997; 27: 1022–8
7. Roncaglia N, et al. A randomised controlled trial of ursodeoxycholic acid and S-adenosyl-l-methionine in the treatment of gestational cholestasis. Br J Obstet Gynaecol 2004; 111: 17–21
8. Kondrackiene J, et al. Efficacy and safety of ursodeoxycholic acid versus cholestyramine in intrahepatic cholestasis of pregnancy. Gastroenterology 2005; 129: 894–901
9. Glantz A, et al. Intrahepatic cholestasis of pregnancy: a randomized controlled trial comparing dexamethasone and ursodeoxycholic acid. Hepatology 2005; 42: 1399–1405
10. Zapata R, et al. Ursodeoxycholic acid in the treatment of intrahepatic cholestasis of pregnancy: a 12-year experience. Liver Int 2005; 25: 548–54
11. Lindor KD, et al. Ursodiol for primary sclerosing cholangitis. N Engl J Med 1997; 336: 691–5
12. Rolandi E, et al. Effects of ursodeoxycholic acid (UDCA) on serum liver damage indices in patients with chronic active hepatitis: a double-blind controlled study. Eur J Clin Pharmacol 1991; 40: 473–6
13. Puoti C, et al. Ursodeoxycholic acid and chronic hepatitis C infection. Lancet 1993; 341: 1413–14
14. Angelico M, et al. Recombinant interferon-α and ursodeoxycholic acid versus interferon-α alone in the treatment of chronic hepatitis C: a randomized clinical trial with long-term followup. Am J Gastroenterol 1995: 90: 263–9
15. Royal College of Obstetricians and Gynaecologists. Obstetric Cholestasis. RCOG Guideline No. 43 (issued January 2006). Available at: http://www.rcog.org.uk/resources/Public/pdf/ obstetric_cholestasis43.pdf (accessed 01/07/08
16. Colombo C, et al. Effects of ursodeoxycholic acid therapy for liver disease associated with cystic fibrosis. J Pediatr 1990; 117: 482–9
17. Cotting J, et al. Effects of ursodeoxycholic acid treatment on nutrition and liver function in patients with cystic fibrosis and longstanding cholestasis. Gut 1990; 31: 918–21
18. Scher H, et al. Ursodeoxycholic acid improves cholestasis in infants with cystic fibrosis. Ann Pharmacother 1997; 31: 1003–5
19. Laurin J, et al. Ursodeoxycholic acid or clofibrate in the treatment of non-alcohol-induced steatohepatitis: a pilot study. Hepatology 1996; 23: 1464–7
20. Lindor KD, et al. Ursodeoxycholic acid for treatment of nonalcoholic steatohepatitis: results of a randomized trial. Hepatology 2004; 39: 770–8
21. Fried RH, et al. Ursodeoxycholic acid treatment of refractory chronic graft-versus-host disease of the liver. Ann Intern Med 1992; 116: 624–9
22. Persson H, et al. Ursodeoxycholic acid for prevention of acute rejection in liver transplant recipients. Lancet 1990; ii: 52–3
23. Friman S, et al. Adjuvant treatment with ursodeoxycholic acid reduces acute rejection after liver transplantation. Transplant Proc 1992; 24: 389–90
24. Clavien P-A, et al. Evidence that ursodeoxycholic acid prevents steroid-resistant rejection in adult liver transplantation. Clin Transplant 1996; 10: 658–62
25. Essell JH, et al. Ursodiol prophylaxis against hepatic complications of allogeneic bone marrow transplantation: a randomized, double-blind, placebo-controlled trial. Ann Intern Med 1998; 128: 975–81
26. Ruutu T, et al. Ursodeoxycholic acid for the prevention of hepatic complications in allogeneic stem cell transplantation. Blood 2002; 100: 1977–83
27. Chen C-Y, et al. Ursodeoxycholic acid (UDCA) therapy in verylow-birth-weight infants with parenteral nutrition-associated cholestasis. J Pediatr 2004; 145: 317–21
28. San Luis VA, Btaiche IF. Ursodiol in patients with parenteral nutrition-associated cholestasis. Ann Pharmacother 2007; 41: 1867–72
29. Tung BY, et al. Ursodiol use is associated with lower prevalence of colonic neoplasia in patients with ulcerative colitis and primary sclerosing cholangitis. Ann Intern Med 2001; 134: 89–95
30. Pardi DS, et al. Ursodeoxycholic acid as a chemopreventive agent in patients with ulcerative colitis and primary sclerosing cholangitis. Gastroenterology 2003; 124: 889–93.
PRIMARY BILIARY CIRRHOSIS. Primary biliary cirrhosis (PBC) is a chronic liver disease of unknown aetiology that develops due to progressive destruction of small and intermediate bile ducts within the liver, subsequently evolving to fibrosis and cirrhosis. Over 90% of patients are female, usually aged between 40 and 60 years. The disease is thought to be auto-immune in nature. Most patients develop antimitochondrial antibodies that may be evident even before disease is clinically apparent.1,2 Genetic factors and hormonal stimulation may play a role in precipitating PBC.1,2 Infectious agents such as Chlamydophila pneumoniae (Chlamydia pneumoniae)2 or retroviruses3 may be involved in the pathogenesis. Clinical manifestations include pruritus, fatigue, jaundice, hepatomegaly, and hypercholesterolaemia leading to xanthoma formation. In late disease portal hypertension, bleeding oesophageal varices and liver failure may develop. Impaired calcium and vitamin D absorption may result in osteomalacia or osteoporosis, and fat-soluble vitamin deficiencies may occur. There may be accumulation of copper in the liver.4 Other disorders including rheumatoid arthritis, scleroderma, thyroiditis, and Sjögren’s syndrome may be associated with PBC.1,5 The disease is slowly progressive, with a mean survival of 8 years for symptomatic patients, and 16 years for asymptomatic individuals.1,6 Despite its presumed auto-immune aetiology, few immunosuppressive drugs have shown any benefit,5,7 although newer drugs such as mycophenolate mofetil, sirolimus, and tacrolimus have yet to be fully evaluated.7 The best-studied treatment for PBC is ursodeoxycholic acid, which is thought to replace toxic endogenous bile acids, stimulate bile acid secretion, and exert local immunosuppressive and cytoprotective effects.1,4,5,7-9 The value of ursodeoxycholic acid is controversial: its reported therapeutic benefits in terms of delaying disease progression and the need for liver transplantation5,10 have not been confirmed by meta-analysis or systematic review.11,12 Both of these were, however, criticised13,14 on the grounds that most of the studies included had follow-up periods of only 2 years. In consequence, some do not recommend its use,12,15 but others still believe it to be the treatment of choice.1,7,13,14,16 Its advocates consider that it appears to be efficacious for about 10 years and improves longterm survival by delaying the progression of hepatic fibrosis, development of oesophageal varices, and the need for liver transplantation. However, it is not effective in the presence of extensive fibrosis or cirrhosis in advanced disease.13,14,16 Both penicillamine and azathioprine have been used in PBC, but trials have failed to show any benefit from treatment5-7 and their use has declined. A systematic review17 identified a significant increase in the occurrence of adverse effects with penicillamine and concluded that its use could not be supported for patients with PBC. Corticosteroids, colchicine, ciclosporin, and chlorambucil have also been tried, but toxicity has restricted their use.5,7They may be of benefit2,4,6,7 when used with ursodeoxycholic acid, although some guidelines5 do not recommend their use. A systematic review18 of studies with methotrexate concluded that it tended to increase mortality or the need for liver transplantation and should not therefore be used in patients with PBC outside clinical trials. Budesonide7 and bezafibrate1,7 have also been tried. Symptomatic treatment includes the use of bile acid sequestrants, such as colestyramine, to treat both pruritus and hypercholesterolaemia. Ursodeoxycholic acid may also improve pruritus in up to 40% of patients, and rifampicin, phenobarbital, and opioid antagonists are used as second-line therapies.1,4,5,8 Vitamin D and calcium supplementation will prevent osteomalacia; supplementation with vitamins A, E, and K may also be necessary.1,4,5,8 Liver transplantation is recommended for liver failure, although PBC can recur in the allograft.5,13,14,16
1. Nishio A, et al. Primary biliary cirrhosis: lessons learned from an organ-specific disease. Clin Exp Med 2001; 1: 165–78
2. Kaplan MM. Primary biliary cirrhosis: past, present, and future. Gastroenterology 2002; 123: 1392–4
3. Mason A, Nair S. Primary biliary cirrhosis: new thoughts on pathophysiology and treatment. Curr Gastroenterol Rep 2002; 4: 45–51
4. Poupon R, Poupon RE. Treatment of primary biliary cirrhosis. Baillieres Best Pract Res Clin Gastroenterol 2000; 14: 615–28
5. Heathcote EJ. Management of primary biliary cirrhosis. Hepatology 2000; 31: 1005–13
6. Heathcote EJ. Evidence-based therapy of primary biliary cirrhosis. Eur J Gastroenterol Hepatol 1999; 11: 607–15
7. Holtmeier J, Leuschner U. Medical treatment of primary biliary cirrhosis and primary sclerosing cholangitis. Digestion 2001; 64: 137–50
8. Prince MI, Jones DE. Primary biliary cirrhosis: new perspectives in diagnosis and treatment. Postgrad Med J 2000; 76: 199–206
9. Lindor K. Ursodeoxycholic acid for the treatment of primary biliary cirrhosis. N Engl J Med 2007; 357: 1524–9
10. Lindor KD, et al. Ursodeoxycholic acid for primary biliary cirrhosis. Lancet 2000; 355: 657–8
11. Gluud C, Christensen E. Ursodeoxycholic acid for primary biliary cirrhosis. Available in The Cochrane Database of Systematic Reviews; Issu
4. Chichester: John Wiley; 2001 (accessed 04/04/06)
12. Goulis J, et al. Randomised controlled trials of ursodeoxycholic-acid therapy for primary biliary cirrhosis: a meta-analysis. Lancet 1999; 354: 1053–60
13. Talwalkar JA, Lindor KD. Primary biliary cirrhosis. Lancet 2003; 362: 53–61
14. Kaplan MM, Gershwin ME. Primary biliary cirrhosis. N Engl J Med 2005; 353: 1261–73. Correction. ibid. 2006; 354: 313
15. Anonymous. Ursodeoxycholic acid for primary biliary cirrhosis. Drug Ther Bull 1999; 37: 30–2
16. Oo YH, Neuberger J. Options for treatment of primary biliary cirrhosis. Drugs 2004; 64: 2261–71
17. Gong Y, et al. -Penicillamine for primary biliary cirrhosis. Available in The Cochrane Database of Systematic Reviews; Issu
4. Chichester: John Wiley; 2004 (accessed 04/04/06)
18. Gong Y, Gluud C. Methotrexate for primary biliary cirrhosis. Available in the Cochrane Database of Systematic Reviews; Issu
3. Chichester: John Wiley; 2005 (accessed 04/04/06).


Gallstones (cholelithiasis) occur when mechanisms for the solubilisation of cholesterol or bilirubin fail or are overcome. They may be divided into those formed of pure cholesterol, which are usually solitary; pigment stones, largely made up of bilirubin or its derivatives; and mixed stones of cholesterol, bile pigment, and calcium salts, which form the great majority of cases seen in the West. Gallstones are generally more common in women than in men. The prevalence also increases with age and obesity, although rapid weight loss as a result of dieting or surgery is associated with an increased risk. As many as two-thirds of patients with gallstones are asymptomatic. Symptoms usually relate to the site of the stone although biliary colic is often present regardless of whether the stone is in the gallbladder or biliary tract. If the stone blocks the exit from the gallbladder, inflammation and bacterial infection may follow (acute cholecystitis), sometimes leading to perforation and subsequent peritonitis. Less commonly, obstruction of the common bile duct by gallstones (choledocholithiasis) may lead to cholestasis and jaundice; infection of the bile ducts and septicaemia may follow. Pancreatitis may also be associated with gallstone disease, and there may be an increased risk of developing malignant neoplasms of the gallbladder. Treatment. Asymptomatic gallstones discovered during other investigations should not be treated, and even mildly symptomatic patients may be managed with analgesics and subsequent observation. Potent analgesics such as morphine may be needed in more severe cases. In symptomatic patients the preferred treatment for gallstones is surgical removal of the gallbladder; laparoscopic cholecystectomy causes less postoperative morbidity than open surgery, and has largely replaced other methods of treatment. In patients unsuited to, or unwilling to undergo, surgery for gallbladder stones, drug therapy, alone or with lithotripsy, may be considered. Exogenous bile acids have been tried in an attempt to dissolve the cholesterol component of gallstones. Ursodeoxycholic acid is more effective and is associated with fewer adverse effects than chenodeoxycholic acid. Combination therapy has also been tried but this is no more effective than ursodeoxycholic acid alone. Dissolution of gallstones is slow but can be achieved in about one-third of cases with the best results seen with small stones. However, about half of all successfully treated patients will develop further gallstones within 10 years. Studies of prophylactic bile acid therapy have mostly yielded disappointing results, although such therapy may be of benefit in patients on very-lowcalorie diets, after surgery for weight loss, and in those receiving treatment with octreotide. Somewhat larger stones may respond to extracorporeal shockwave lithotripsy, or fluoroscopically guided laser lithotripsy, which may be more effective. Oral bile acids should then be given to dissolve the stone fragments. Another method that has been used is the direct instillation of a solvent (usually methyl tert-butyl ether) into the gallbladder, which dissolves stones within a matter of hours, and is effective against almost all cholesterol-based stones regardless of size and number. Care is required to avoid overflow of the solvent into the common bile duct or the duodenum, where it can cause inflammation. Other solvents, such as ethyl propionate have been investigated as potentially less toxic alternatives, and edetic acid has been suggested as a possible solvent for non-cholesterol gallstones. As with all non-surgical methods, recurrence is likely. Patients with stones in the common bile duct or acute cholecystitis require prompt therapy because of the risk of serious complications; endoscopic sphincterotomy and physical retrieval of the stones with a basket or balloon appears to be the preferred treatment, with open surgery as an alternative. A biliary stent to allow bile flow around the stone has been used as a temporary measure in patients with stones too large to remove by endoscopic sphincterotomy. Lithotripsy or infusion of a solvent such as monoctanoin or methyl tert-butyl ether are possible alternatives in patients unfit for surgery. In patients who develop cholecystitis or cholangitis antibacterial therapy may be required.
1. Johnston DE, Kaplan MM. Pathogenesis and treatment of gallstones. N Engl J Med 1993; 328: 412–21
2. Ransohoff DF, Gracie WA. Treatment of gallstones. Ann Intern Med 1993; 119: 606–19
3. May GR, et al. Efficacy of bile acid therapy for gallstone dissolution: a meta-analysis of randomized trials. Aliment Pharmacol Ther 1993; 7: 139–48
4. Hofmann AF, et al. Pathogenesis and treatment of gallstones. N Engl J Med 1993; 328: 1854–5
5. Anonymous. Managing patients with gallstones. Drug Ther Bull 1994; 32: 33–5
6. Lanzini A, Northfield TC. Pharmacological treatment of gallstones: practical guidelines. Drugs 1994; 47: 458–70
7. Tait N, Little JM. The treatment of gall stones. BMJ 1995; 311: 99–105
8. Jakobs R, et al. Fluoroscopically guided laser lithotripsy versus extracorporeal shock wave lithotripsy for retained bile duct stones: a prospective randomised study. Gut 1997; 40: 678–82
9. Toouli J, Wright TA. Gallstones. Med J Aust 1998; 169: 166–71
10. Bateson MC. Gallbladder disease. BMJ 1999; 318: 1745–8
11. Ahmed A, et al. Management of gallstones and their complications. Am Fam Physician 2000; 61: 1673–80
12. Bellows CF, et al. Management of gallstones. Am Fam Physician 2005; 72: 637–42
13. Portincasa P, et al. Cholesterol gallstone disease. Lancet 2006; 368: 230–9
14. Caddy GR, Tham TCK. Symptoms, diagnosis and endoscopic management of common bile duct stones. Best Pract Res Clin Gastroenterol 2006; 20: 1085–1101.

💊 Preparations

BP 2008: Ursodeoxycholic Acid Capsules; Ursodeoxycholic Acid Tablets; USP 31: Ursodiol Capsules.

Proprietary Preparations

Arg.: Dexo; Solutrat; UDCA; Ursidesox; Ursomax; Urzac; Austral.: Ursofalk; Austria: Ursofalk; Belg.: Ursochol; Ursofalk; Braz.: Ursacol; Canad.: Urso; Chile: Solvobil; Ursofalk; Cz.: Ursochol; Ursofalk; Ursosan; Fin.: Adursal; Fr.: Delursan; Ursolvan; Ger.: Cholit-Ursan; Cholofalk; UDC; Urso†; Ursochol; Ursofalk; Gr.: Ursofalk; Hong Kong: Ursofalk; Ursosan; Hung.: Ursofalk; India: Udiliv; Indon.: Estazor; Pramur; Urdafalk; Urdahex; Irl.: Ursofalk; Israel: Ursofalk; Ursolit; Ital.: Benursil†; Biliepar; Coledos†; Desocol; Desoxil; Deursil; Dissolursil; Epasol†; Fraurs; Galmax†; Lentorsil†; Litoff; Litursol; Tauro; Tudcabil†; Urdes; Ursacol; Ursilon; Ursobil; Ursodamor; Ursodexil†; Ursodiol; Ursofalk†; Ursoflor; Ursolac†; Ursolisin; Ursoproge†; Jpn: Urso; Ursosan†; Malaysia: Ursofalk; Mex.: Ursofalk; Neth.: Ursochol; Ursofalk; Norw.: Ursofalk; NZ: Actigall; Ursofalk; Philipp.: Ursofalk; Pol.: Proursan; Ursocam; Ursofalk; Ursopol; Port.: Destolit; Ursofalk; Rus.: Ursosan (Урсосан); S.Afr.: Ursotan†; Singapore: Ursofalk; Spain: Ursobilane; Ursochol; Swed.: Ursofalk; Switz.: De-ursil; Ursochol; Ursofalk; Thai.: Udihep; Ursofalk; Ursolin; Turk.: Ursofalk; UK: Destolit; Urdox; Ursofalk; Ursogal; USA: Actigall; Urso. Multi-ingredient: Austria: Lithofalk†; Ger.: Lithofalk; Urso Mix†; Gr.: Lithiofalk†; Ital.: Bilenor; Jpn: Cabe 2; Eki Cabe.
Published May 08, 2019.