Ursodeoxycholic Acid (UDCA)

Product Story

Ursodeoxycholic acid was first isolated in 1902 by Swedish chemist Olof Hammarsten from the bile of the Chinese black bear (Ursus thibetanus) — the name "urso" comes from the Latin word for bear. For centuries before this isolation, traditional Chinese medicine had used bear bile for liver ailments, but Hammarsten's work was the first to identify UDCA as a distinct chemical entity. In 1954, Japanese scientist Kanji Shoda achieved the first chemical synthesis of UDCA, opening a path to industrial production without reliance on bear bile extraction. The therapeutic breakthrough came in 1975 when Fumio Nakayama demonstrated that UDCA could dissolve cholesterol gallstones in human patients — a non-surgical alternative to cholecystectomy that transformed hepatology practice. The U.S. FDA approved UDCA as Actigall for gallstone dissolution in 1987, and by the late 1990s it had become the first-line therapy for primary biliary cholangitis (PBC), one of the few treatments proven to extend transplant-free survival in that disease.

UDCA's mechanism of action centers on bile acid pool remodeling. In cholestatic conditions, toxic hydrophobic bile acids like chenodeoxycholic acid and lithocholic acid accumulate in the liver, where their detergent properties damage hepatocyte membranes and trigger apoptosis. UDCA, being hydrophilic, displaces these toxic bile acids, shifting the bile acid pool to a less cytotoxic composition. At therapeutic doses (13-15 mg/kg/day), UDCA constitutes 40-60% of circulating bile acids. Beyond simple displacement, UDCA incorporates directly into hepatocyte membranes, stabilizing them against oxidative stress, and stimulates bicarbonate-rich bile flow through the "bicarbonate umbrella" mechanism, physically flushing toxic bile acids from the biliary tree.

UDCA's unique advantage among bile acid therapeutics is its exceptional safety profile. Unlike chenodeoxycholic acid (CDCA), the alternative bile acid used before UDCA's adoption, UDCA does not cause diarrhea, hepatotoxicity, or LDL cholesterol elevation at therapeutic doses. CDCA was largely abandoned for gallstone dissolution after UDCA proved equally effective with far fewer adverse effects. Compared to obeticholic acid (OCA), the newer FXR agonist approved for PBC, UDCA does not induce pruritus — the dose-limiting side effect that affects up to 58% of OCA patients. This tolerability advantage, combined with decades of pharmacovigilance data, makes UDCA the cornerstone of cholestatic liver disease therapy.

The global UDCA market reached approximately USD 644 million in 2025 and continues to grow, driven by rising PBC diagnosis rates, expanding geriatric populations, and increasing use in non-alcoholic fatty liver disease (NAFLD) protocols. China accounts for over 70% of global UDCA API production, with major manufacturing hubs in Guangdong, Jiangsu, Zhejiang, and Shandong provinces. Innovation in enzymatic synthesis using engineered 7-beta-hydroxysteroid dehydrogenase (7-beta-HSDH) now achieves over 94% conversion yields from CDCA, supplanting traditional multi-step chemical synthesis. KingWish, as a leading China-based UDCA API manufacturer, supplies over 40 MT annually to pharmaceutical formulation companies across 100+ countries.

Manufacturing Process

KingWish's UDCA is produced through a four-stage synthetic route starting from cholic acid extracted from bovine bile — a byproduct of the cattle industry that creates a sustainable, non-endangered supply chain fully compliant with CITES requirements. The process is carried out in GMP-certified facilities in Zhongshan, Guangdong province:

Regulatory Certifications

Quality Specifications

Applications

• Gallstone dissolution therapy: UDCA 8-10 mg/kg/day for radiolucent cholesterol gallstones <20mm in patients with functioning gallbladders. Non-surgical dissolution over 6-24 months with 30-60% complete dissolution rates.
• Primary Biliary Cholangitis (PBC): First-line treatment at 13-15 mg/kg/day. Shown to slow histological progression, normalize liver enzymes, and delay need for liver transplantation. Response assessed by Paris-II or Toronto criteria after 12 months.
• Primary Sclerosing Cholangitis (PSC): Used at 20-30 mg/kg/day, particularly for reducing the risk of colonic dysplasia in PSC patients with concomitant ulcerative colitis.
• Hepatoprotective formulations: UDCA in combination therapies for autoimmune hepatitis, drug-induced liver injury, intrahepatic cholestasis of pregnancy, and non-alcoholic steatohepatitis. Reduces ALT, AST, and GGT levels and slows fibrosis progression.