Cholic acid

Other Names

17β-(1-Methyl-3-carboxypropyl)etiocholane-3α,7α,12α-triol3,7,12-Trihydroxy-cholan-24-oic acid, (3α,5β,7α,12α)-3,7,12-Trihydroxycholan-24-oic acid3-α,7-α,12-α-Trihydroxy-5-β-cholan-24-oic acid3-α,7-α,12-α-Trihydroxycholansaeure3α,7α,12α-Trihydroxy-5β-cholan-24-oic acid3α,7α,12α-Trihydroxy-5β-cholanic acid5β-Cholan-24-oic acid, 3α,7α,12α-trihydroxy-5β-Cholanic acid-3α,7α,12α-triol5β-Cholic acidCACholalic acidCholalinCholan-24-oic acid, 3,7,12-trihydroxy-, (3α,5β,7α,12α)-CholateCholsaeureColalinNSC-6135

Synopsis

Cholic Acid: A Comprehensive Reference

1. Identity and Chemical Characterization

Chemical Names and Formula

Cholic acid, also known by its systematic IUPAC name 3α,7α,12α-trihydroxy-5β-cholan-24-oic acid, is a primary bile acid that is insoluble in water (though soluble in alcohol and acetic acid) and exists as a white crystalline substance. Its molecular formula is C₂₄H₄₀O₅, with a molar mass of approximately 408.6 g/mol. Salts of cholic acid are called cholates.

The name "cholic acid" derives from the Greek khole, meaning bile. It belongs to the broader class of C24 bile acids and is classified as a steroid acid, sharing the four-ring steroid nucleus (cyclopentanoperhydrophenanthrene) with cholesterol and related compounds. Bile acids from different species differ chemically in three structural aspects: side-chain structure; stereochemistry of the A/B ring fusion; and the distribution of the number, position, and stereochemistry of hydroxyl groups in the steroid nucleus. In cholic acid specifically, three hydroxyl groups are positioned at carbons 3α, 7α, and 12α, and the A/B ring junction is in the 5β (cis) configuration, giving the molecule its characteristic concave ("facial amphiphile") shape, with a hydrophilic face bearing the hydroxyl groups and a hydrophobic convex face.

Natural Sources

Cholic acid, along with chenodeoxycholic acid, is one of the two major bile acids produced by the liver, where it is synthesized from cholesterol. These two major bile acids are roughly equal in concentration in humans. The main components in human bile are the C24 compounds chenodeoxycholic (45%), deoxycholic, and cholic acids (31%), with hydroxyl groups of the 3α,7α-, 3α,12α- and 3α,7α,12α-configurations, respectively.

Cholic acid is found naturally in the bile of virtually all vertebrates, including humans, cattle (ox/bovine bile), pigs, and other mammals. Historically, the most important commercial and scientific natural source has been bovine (ox) bile, from which cholic acid can be isolated in relatively large quantities. Ox bile extract is a potent source of bile acids, primarily chenodeoxycholic and cholic acid; these acids are essential for the absorption and emulsification of lipids in the small intestine.

Common Forms and Preparations

Cholic acid exists in multiple forms depending on context:

Free (unconjugated) cholic acid: The parent compound, a white crystalline solid, insoluble in water. Used as a reference standard, research reagent, and pharmaceutical active ingredient.
Conjugated forms: Derivatives are made from cholyl-CoA, which exchanges its CoA with either glycine or taurine, yielding glycocholic acid and taurocholic acid, respectively. These conjugated forms are the predominant circulating and secreted forms under normal physiological conditions.
Pharmaceutical oral capsules: Cholic acid is available as capsules of 50 and 250 mg under the brand name Cholbam. It is a white or off-white powder supplied in 50 mg and 250 mg two-piece gelatin capsules.
Dietary supplement / ox bile extracts: Animal-derived bile extracts standardized to varying concentrations of cholic acid are marketed as digestive supplements, though these preparations are distinct from the pharmaceutical-grade product.

2. Historical and Traditional Use

Ancient Medicine and Humorism

The use of bile — the fluid in which cholic acid is the principal active acid component — in medicine reaches back to antiquity. Among ancient Egyptian medical texts, the Ebers Papyrus (P. Ebers 510) records a remedy that includes ox-bile mixed with honey, potter's clay, and plant juices, to be applied to wounds caused by beatings.

Bile, and by extension cholic acid, played a role in ancient medicine through the system of the four humors first put forth by Hippocrates, in which yellow and black bile were identified as two of the primary body fluids. Historians typically credit Hippocrates with the creation of medicinal humors and the widespread belief in blood, yellow bile, black bile, and phlegm. Imbalances in bile were associated in Greco-Roman and medieval medical theory with diseases of the liver and with temperament.

Traditional Chinese Medicine and Other Traditions

Bile has been used in traditional medicine for centuries. In Chinese medicine, bile from various animals is used to treat digestive and liver issues, whereas in European herbal medicine it is used for its digestive and purgative properties.

Early Pharmaceutical and Commercial Use

The first pure isolation of cholic acid from a natural source took place in the nineteenth century. The first description of a bile acid was made in 1848 when cholic acid was discovered in ox-gall. Strecker identified two acidic components in ox bile, one containing nitrogen (glycocholic acid) and the other with nitrogen and sulfur (taurocholic acid), and deduced the correct chemical formula C₂₄H₄₀O₅ for cholic acid.

During the late nineteenth and early twentieth centuries, bile acids were sold as liver tonics and laxatives, but there were no placebo-controlled studies showing efficacy. A tri-oxo derivative of cholic acid (called "dehydrocholic acid") was known to induce bile flow in animals and was occasionally used to stimulate bile flow in patients, but there were no controlled studies showing efficacy in hepatobiliary disease.

A major milestone in cholic acid's commercial history came in 1917. Heinrich Wieland persuaded the Boehringer company to begin the isolation and marketing of cholic acid from ox bile in 1917, making cholic acid of high purity soon available to the scientific community.

Nobel Prize Recognition

In 1927, no prize in chemistry had been awarded because the Nobel Prize Selection Committee could not agree on a suitable candidate. During the following year, the committee decided to award the 1927 prize to Heinrich Wieland and the 1928 prize to Adolf Windaus. In his Nobel lecture, Wieland reviewed his laborious attempts to define the structure of bile acids and presented his current vision of the structure of cholic acid.

The correct structure of the steroid nucleus, however, was not definitively established until 1932 through X-ray diffraction studies. Nitrogen-free cholic acid was isolated as long ago as 1838.

3. Biosynthesis: Key Constituents and Active Compounds

Biosynthetic Pathway

Cholic acid is a primary bile acid formed from cholesterol via a multistep process catalyzed by the cytochrome P450 (CYP) isoforms CYP7A1, CYP8B1, and CYP27A1. The classic pathway, which constitutes 95% of bile acid synthesis, proceeds via cytochrome P450-mediated oxidation of cholesterol requiring NADPH and oxygen, occurring in a series of steps of which the most important is the rate-limiting hydroxylation of the 7th steroid nucleus of cholesterol by cholesterol 7α-hydroxylase (CYP7A1) to create 7α-hydroxycholesterol. In sum, primary bile acid synthesis requires 14 enzymatic steps.

The subsequent conversion of bile acid intermediates from either the classical or alternative pathways to cholic acid or chenodeoxycholic acid is governed by CYP8B1; interaction of these intermediates with this enzyme determines the amount of cholic acid versus chenodeoxycholic acid formed. Hydroxylation via CYP8B1 results in the formation of the more hydrophilic cholic acid molecule. Thus, the cholic acid/chenodeoxycholic acid ratio determines the overall hydrophobicity and biological properties of the bile acid pool.

Conjugation and Metabolism

Cholic acid is conjugated to glycine or taurine by bile acid-CoA:amino acid N-acyltransferase (BAAT) to produce glycocholic acid (GCA) and taurocholic acid (TCA), respectively, in the liver, and is transformed into the secondary bile acid deoxycholic acid (DCA) by intestinal microbiota.

These conjugated cholic acids are stored in the gallbladder until food consumption. After food consumption, bile solution is released from the gallbladder into the intestine, where the conjugated cholic acid molecules are subject to additional chemical modifications mediated by enzymes produced by intestinal microflora. The bacterial enzyme 7α-dehydroxylase converts cholic acid into deoxycholic acid.

Enterohepatic Circulation

In the intestines, bile acids act as detergents and help to emulsify fats, aiding in their digestion and absorption. After participating in digestion in the small bowel, bile acids are almost completely (95%) reabsorbed in the distal ileum and then retaken up from portal blood by the liver — a process called enterohepatic circulation. In humans, the total bile acid pool (3–5 g) recirculates 6–10 times per day, giving rise to a daily uptake of approximately 20–30 g of bile acids.

Feedback Regulation

Cholic acid downregulates cholesterol-7α-hydroxylase (the rate-limiting step in bile acid synthesis), while cholesterol does the opposite. This constitutes the principal negative feedback mechanism of bile acid homeostasis. FXR signaling has been proposed as a mechanism of feedback regulation of the rate-limiting enzyme for bile acid synthesis, cholesterol 7α-hydroxylase (CYP7A1).

4. Mechanisms of Action

Emulsification and Lipid Absorption

Bile acids are potent "digestive surfactants" that promote absorption of lipids (including fat-soluble vitamins), acting as emulsifiers. Bile acids act in bile to solubilize cholesterol (which is totally insoluble in water) with phospholipids in mixed micelles. Once secreted into the intestine, bile acids help to emulsify fats and aid in their digestion. The pKa of conjugated bile acids is lower (between 1–4), meaning they are present in their deprotonated form in the duodenum, which makes them significantly more water-soluble and thus able to function as emulsifiers in the digestion process.

Farnesoid X Receptor (FXR) Signaling

FXR is a bile acid-activated nuclear receptor that regulates the homeostasis of bile acids, lipids, and glucose. Endogenous ligands of FXR include bile acids such as cholic acid (CA), chenodeoxycholic acid (CDCA), deoxycholic acid (DCA), lithocholic acid (LCA), and ursodeoxycholic acid (UDCA). Cholic acid is also a potent signaling molecule and acts as a weak FXR agonist, resulting in a decrease in bile acid synthesis and a parallel increase in cholesterol. Because of this FXR agonism, exogenous cholic acid suppresses endogenous bile acid synthesis through feedback inhibition. For these reasons, cholic acid is not effective in gallstone dissolution.

TGR5 Receptor and Metabolic Signaling

Bile acids activate farnesoid X receptor (FXR) and G protein-coupled bile acid receptor-1 (TGR5) to regulate bile acid metabolism and glucose and insulin sensitivity. Activation of FXR induces TGR5 to stimulate glucagon-like peptide-1 (GLP-1) secretion to improve insulin sensitivity and hepatic metabolism. Animal research has demonstrated a potential metabolic role: administration of cholic acid to high-fat diet-fed mice results in body weight reduction and enhanced energy expenditure through a TGR5–cAMP pathway characterized in brown adipose tissue and skeletal muscle. However, these findings come from preclinical animal models, and their translation to human physiology has not been confirmed in controlled clinical trials.

Cholesterol Catabolism

Bile acids represent the primary pathway for cholesterol catabolism and account for approximately 50% of the daily turnover of cholesterol. By converting cholesterol to bile acids, the liver maintains cholesterol homeostasis. Impairing enterohepatic circulation of bile acids decreases cholesterol because the liver is driven to use more cholesterol to make more. This state is the basis behind treating hyperlipidemia with bile acid resins like cholestyramine, colestipol, and colesevelam, which bind bile acids in the gut, preventing their reabsorption.

Suppression of Toxic Bile Acid Intermediates

The absence of cholic acid in patients with bile acid synthesis disorders leads to reduced bile flow, accumulation of potentially toxic bile acid intermediates in the liver (cholestasis), and malabsorption of fats and fat-soluble vitamins in the diet. Exogenous cholic acid replacement is thought to work by restoring normal bile acid pool composition, restoring bile flow, suppressing the accumulation of aberrant and hepatotoxic intermediates, and providing physiological feedback inhibition of the defective synthesis pathway. Endogenous bile acids including cholic acid enhance bile flow and provide the physiologic feedback inhibition of bile acid synthesis. Cholic acid enhances absorption of lipids from the intestine and has additional metabolic effects.

Broad Physiological Roles

The physiological functions of bile acids include emulsification of dietary fat, absorption of fat and fat-soluble vitamins, maintaining glucose, lipid, and energy homeostasis, sustenance of intestinal epithelial integrity and epithelial cell proliferation, reducing inflammation in the intestine, and prevention of enteric infection due to antimicrobial properties.

5. Body Systems and Health Areas of Association

Hepatobiliary System

Cholic acid is primarily a molecule of the liver and biliary system. It is synthesized in hepatocytes and is a major constituent of human bile. Bile acids secreted by hepatocytes are stored in the gallbladder and released postprandially into the proximal small bowel, where they carry out their well-known digestive functions such as emulsification and formation of micelles aiding in the absorption of fat and fat-soluble vitamins. Deficiencies in the enzymes needed for cholic acid synthesis cause progressive cholestatic liver disease (see Clinical Evidence section).

Digestive and Absorptive System

The digestive role of cholic acid is central to the absorption of all dietary fats, fat-soluble vitamins (A, D, E, and K), and cholesterol. Without an adequate bile acid pool, fats pass undigested into the colon (steatorrhea), and deficiencies of fat-soluble vitamins develop. Bile acids facilitate fat digestion and absorption by forming mixed micelles, and facilitate absorption of fat-soluble vitamins in the intestine.

Gut Microbiome

The primary bile acids synthesized in the liver are transformed to secondary bile acids by the gut microbiota. The gut-to-liver axis plays a critical role in the regulation of bile acid synthesis, composition and circulating bile acid pool size, which in turn regulates glucose, lipid, and energy metabolism. The conversion of cholic acid to deoxycholic acid by gut bacteria is a major route of secondary bile acid production, and is heavily influenced by the composition of the microbiome. Dysregulation of bile acid metabolism and FXR signaling in the gut-to-liver axis contributes to metabolic diseases including obesity and diabetes.

Metabolic Regulation

Over the last decade, it has become clear that bile acids are not simply digestive detergents and the primary route governing cholesterol catabolism. Bile acids are now recognized as hormones involved in the regulation of various metabolic processes. Through activation of various signaling pathways, bile acids regulate not only their own synthesis and enterohepatic circulation, but also triglyceride, cholesterol, glucose, and energy homeostasis.

Nervous System / Neurological Association

A study in rats concluded that cholic acid and other unconjugated bile acids are present in brain tissue at the same concentrations as in the circulation, suggesting passive diffusion of these lipophilic bile acids. Bile acids can penetrate the blood-brain barrier and bind to nuclear receptors in the brain. However, the functional significance of this in humans remains under investigation.

6. Scientific Evidence by Area of Use

6.1 Bile Acid Synthesis Disorders Due to Single Enzyme Defects (SEDs) — Strongest Evidence

The FDA has approved oral cholic acid (Cholbam) for treatment of children and adults with bile acid synthesis disorders caused by single enzyme defects and for adjunctive treatment of peroxisomal disorders such as Zellweger spectrum disorders in patients who have liver disease, steatorrhea, or complications from fat-soluble vitamin malabsorption. In 2015, the US Food and Drug Administration approved cholic acid as an orphan drug for this treatment.

Patients with these rare inborn errors of bile acid metabolism cannot synthesize primary bile acids such as cholic acid, resulting in reduced bile flow, decreased absorption of fat and fat-soluble vitamins, and development of liver disease, which can be fatal.

Clinical trial evidence: The safety and efficacy of Cholbam in patients with bile acid synthesis deficiency disorders were evaluated in a nearly 20-year open-label, single-arm, investigator-initiated trial at Cincinnati Children's Hospital and Medical Center. The efficacy of Cholbam for the treatment of patients with bile acid synthesis disorders due to single enzyme defects was assessed in an uncontrolled trial involving 50 patients treated over an 18-year period. On average, patients were 4 years of age at the start of cholic acid treatment (range 3 weeks to 36 years). Overall, treatment improved baseline liver function in 64% of evaluated patients, who ranged in age from 3 weeks to 36 years at the beginning of the trial. Administration of cholic acid appeared to decrease hepatic injury and increase height and weight; 67% of patients with bile acid synthesis disorders treated in the clinical trials survived for more than 3 years. Some of these survivors have been treated successfully for more than 20 years.

Evidence strength: The pivotal evidence is from a long-term, uncontrolled, single-arm open-label trial — not a randomized controlled trial. However, given the rarity and severity of the disease, and the consistent, durable clinical responses observed over nearly two decades, the FDA granted full orphan drug approval. The evidence is strong within its design limitations for this specific orphan indication.

6.2 Peroxisomal Disorders (Including Zellweger Spectrum Disorders) — Moderate Evidence, Adjunctive Use

The efficacy of Cholbam for the treatment of peroxisomal disorders, including Zellweger spectrum disorders, was assessed in an uncontrolled treatment trial involving 29 patients treated over an 18-year period. An extension trial followed 10 of these patients and enrolled an additional two patients. The majority of patients were less than 2 years of age at the start of cholic acid treatment. Overall, 46% of patients responded and 42% of patients survived for three years or more.

Evidence strength: Uncontrolled, open-label, small-sample evidence. FDA approval for this indication is adjunctive (not primary), based on improvements in liver function. Evidence is preliminary and limited by absence of a control group.

6.3 AMACR Deficiency and Other Rare Bile Acid Defects — Emerging Evidence

A more recent open-label, non-randomized trial examined cholic acid in patients with α-methylacyl-CoA racemase (AMACR) deficiency. An open-label, non-randomized trial with cholic acid supplementation included six patients with AMACR deficiency and one patient with 3β-hydroxy-Δ5-C27-steroid oxidoreductase deficiency. Patients received up to 20 mg/kg/day for 3.5 years, adjusted for biochemical response, side effects, and clinical evaluation. Bile acid metabolites, liver enzymes, liver stiffness, and neurological symptoms were evaluated at baseline and during follow-up. Children's transaminase levels normalized during treatment, while adults' levels remained normal throughout. C₂₇-bile acids and C₂₉-dicarboxylic acid decreased with treatment, while pristanic acid fluctuated and remained elevated. No clinically relevant changes were observed in liver elasticity, fat-soluble vitamin levels, neurological assessment, or growth in children.

Evidence strength: Small sample, non-randomized, open-label. Biochemical improvements were observed but clinical endpoints were mixed. Evidence is preliminary.

6.4 Smith-Lemli-Opitz Syndrome (SLOS) — Investigational

Cholbam is approved by the FDA for the treatment of bile acid synthesis disorders due to single enzyme defects (SEDs) and for adjunctive treatment of peroxisomal disorders. Owing to their inherited defect in cholesterol and bile acid synthesis, SLOS subjects are considered to be SEDs. Research on cholic acid in SLOS is ongoing (clinical trial NCT03720990), but definitive efficacy data from completed randomized trials are not yet available in the published literature.

6.5 Alzheimer's Disease and Neurodegeneration — Observational/Biomarker Only

Several observational and metabolomics studies have identified associations between cholic acid levels and Alzheimer's disease (AD), but no clinical trials of cholic acid supplementation for AD have been completed.

Serum levels of 15 primary and secondary bile acids and their conjugated forms were measured in 1,464 subjects including 370 cognitively normal older adults, 284 with early mild cognitive impairment, 505 with late mild cognitive impairment, and 305 AD cases enrolled in the AD Neuroimaging Initiative. Significantly lower serum concentrations of primary bile acid cholic acid and increased levels of the bacterially produced secondary bile acid deoxycholic acid and its glycine and taurine conjugated forms were found in AD patients compared to healthy subjects.

Using LC-MS/MS, one study profiled 22 bile acids in brain extracts and blood plasma from AD patients (n = 10) and age-matched control subjects (n = 10). In human plasma, significantly lower cholic acid (p = 0.03) was detected in AD patients than age-matched control subjects. In human brain with AD pathology (Braak stages V–VI), taurocholic acid was significantly lower (p = 0.01) than in age-matched control subjects.

Researchers analyzed 2,114 post-mortem brain transcriptomes and identified genes in the alternative bile acid synthesis pathway expressed in the brain. A targeted metabolomic analysis of primary and secondary bile acids measured from post-mortem brain samples of 111 individuals supported these results. Metabolic network analysis suggests that taurine transport, bile acid synthesis, and cholesterol metabolism differ in AD and cognitively normal individuals.

Evidence strength: All current evidence for a cholic acid–AD relationship is observational, associative, and largely cross-sectional or derived from post-mortem tissue analyses. No causal relationship has been established. No intervention trials have been completed. The levels of bile acids are clearly disturbed during the development of AD pathology and, since some bile acids are being proposed as potential AD therapeutics, more work is needed to advance bile acid therapeutics. Evidence in this area is preliminary and should not be interpreted as a basis for supplementation.

6.6 Metabolic Disease (Obesity, Diabetes, NAFLD) — Preclinical Only

The TGR5 and FXR receptor signaling data (see Mechanisms section) have generated hypotheses about cholic acid's role in metabolic regulation. Administration of cholic acid to high-fat diet-fed mice results in body weight reduction and enhanced energy expenditure through a TGR5–cAMP pathway characterized in brown adipose tissue and skeletal muscle. However, this is animal data only. No controlled human trials have established clinical efficacy of cholic acid supplementation for obesity, type 2 diabetes, or NAFLD.

7. Dosage Forms and Reported Dosages

Cholic acid is available as capsules of 50 and 250 mg under the brand name Cholbam.

The typical dose is 10 to 15 mg/kg once daily.

The recommended dosage of Cholbam is 10 to 15 mg/kg administered orally once daily, or in two divided doses, in pediatric patients and in adults. Cholbam should be taken with food.

In the AMACR deficiency open-label trial, patients received up to 20 mg/kg/day cholic acid for 3.5 years, adjusted for biochemical response, side effects, and clinical evaluation.

Among 15 patients with bile acid synthesis defects treated with oral bile acids (ursodiol and cholic acid initially, and eventually cholic acid alone for all except one patient) at 3–9 mg/kg daily for 5–15 years, all had lasting clinical improvements shown by repeat liver biopsies in 14.

These dosage ranges pertain exclusively to treatment of diagnosed bile acid synthesis defects and related disorders. There are no established therapeutic dosages for other conditions in humans.

8. Safety Considerations and Drug Interactions

General Safety Profile

Cholic acid is a naturally occurring bile acid used to treat patients with genetic deficiencies in the synthesis of bile acids. When given in high doses, cholic acid replacement therapy has been linked to minor elevations in serum aminotransferase levels, but it has not been linked to instances of clinically apparent acute liver injury with jaundice.

Dose-Dependent Side Effects

Side effects are largely dose-related and include diarrhea, indigestion, nausea, abdominal discomfort, fatigue, and skin rash.

In some instances, higher doses of cholic acid were associated with elevations in serum aminotransferase levels. These abnormalities, however, were mild, transient and rapidly reversed with lowering the daily dose.

Cholic acid was well tolerated in children (n = 3), allowing for higher doses. Adults (n = 4) experienced more side effects, primarily diarrhea and other gastrointestinal symptoms.

Overdose of cholic acid was marked by diarrhea, pruritus, and increases in GGT and ALT that responded to dose modification.

Monitoring Considerations

Because higher doses can cause aminotransferase elevations, liver function monitoring is appropriate during therapeutic use. Dose-related gastrointestinal effects typically resolve with dose reduction. A glycine conjugate of cholic acid (glycocholic acid) is currently being evaluated for treatment of bile acid conjugation defects, suggesting further therapeutic derivatives are under active investigation.

Drug Interactions

Patients in a clinical trial also used antihypertensives, antiplatelet medication, bisphosphonates, nonsteroidal anti-inflammatory drugs (NSAIDs), laxatives, and/or antacids for other indications. There are no known interactions between these medications and cholic acid.

Because cholic acid is a bile acid, it has potential for pharmacokinetic interactions with agents that bind bile acids (such as cholestyramine, colestipol, or colesevelam), which could reduce its absorption and thereby its efficacy if administered concurrently. The prescribing information for Cholbam advises that bile acid-binding resins and aluminum-containing antacids may inhibit the absorption of cholic acid and should not be taken at the same time.

Pregnancy and Pediatric Considerations

The indication for Cholbam, which is an oral treatment, is for children aged three weeks and older and for adults. The drug was studied in very young infants (as young as three weeks of age) as well as in adults up to 36 years of age. Data on use in pregnancy are limited and not established in published clinical literature available at this time.

Potential Hepatocellular Risk at High Exposures

One adult in the personalized cholic acid treatment trial developed hepatocellular carcinoma during treatment. The causal relationship to cholic acid in this single case was not established, as it occurred in a patient with pre-existing severe metabolic liver disease; however, this observation underscores the importance of clinical surveillance in treated patients.

9. Regulatory Status

Cholbam (oral cholic acid) is the first drug to be approved in the US for the indications of bile acid synthesis disorders due to single enzyme defects and adjunctive treatment of peroxisomal disorders. It received FDA approval in March 2015 as an orphan drug. Cholic acid was given orphan drug approval for use in the United States for treatment of children and adults with bile acid synthetic defects and Zellweger's syndrome.

As a dietary supplement ingredient derived from ox bile extract, cholic acid-containing products are available in some markets outside the pharmaceutical regulatory framework. These preparations are not approved or evaluated by the FDA for therapeutic use and differ from the pharmaceutical-grade Cholbam product used in clinical trials.

References

Health Conditions

Health conditions that Cholic acid may help support.

Gallbladder HealthScientific
Cholic acid is the most abundant primary human bile acid synthesized from cholesterol in the liver, essential to bile composition and cholesterol solubilization in the gallbladder. It is FDA-approved as Cholbam for bile acid synthesis defects, and as a standardized component of ox bile supplements it supports biliary function in bile-deficient states.

Body Systems

Body systems that Cholic acid may help support.

No body systems available.