CTEXLI chenodiol 250 mg Tablet, Film Coated, 100-count
🆔 Identity & classification
Where does this data come from?
🏷️ RxNorm drug class
This medicine belongs to the Bile acids and derivatives class.
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🏭 Manufacturer & labeler
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🩺 Clinical
Chenodiol is used to help dissolve a certain type of gallstones treat people with cerebrotendinous xanthomatosis (CTX; a condition that causes high cholesterol) Chenodiol is in a class of medications called bile acids. It works by breaking down cholesterol that forms gallstones and by lowering the amount of cholesterol made by the liver.
Read the full MedlinePlus article ↗Patient education
Supplement & herbal interactions
Some supplements/herbs that may interact with Chenodiol — tap one for details:
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💊 What it looks like
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🧪 Inactive Ingredients / Excipients
Inactive ingredients, also called excipients, are components of the drug product other than the active ingredient. They may include fillers, dyes, coatings, preservatives, flavors, or other formulation ingredients.
💡 Tap an ingredient (hover on desktop) to see what it is and why it’s used.
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UNII PDC6A3C0OX
Glycerin is a clear, thick liquid derived from plant oils or fats. It acts as a humectant to retain moisture, a sweetener, and a solvent in medications.
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UNII 70097M6I30
Magnesium stearate is a salt made from magnesium and stearic acid, a fatty substance. It's used in tablets and capsules as a lubricant and glidant to help ingredients flow smoothly during manufacturing and prevent sticking.
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UNII 4GFU244C4J
Methylcellulose is a plant-based thickening agent made from cellulose. It acts as a binder to hold pill ingredients together and as a bulking agent to add texture and consistency to liquid or semi-solid medicines.
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UNII OP1R32D61U
Microcrystalline cellulose is a purified form of cellulose, a natural fiber from plant sources. It acts as a binder and filler in tablets and capsules, helping hold ingredients together and give the medicine its shape and size.
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UNII ETJ7Z6XBU4
Silicon dioxide is a naturally occurring mineral used as a glidant and anti-caking agent. It helps powder ingredients flow smoothly and prevents clumping during manufacturing and storage.
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UNII 368GB5141J
A detergent and foaming agent derived from coconut or palm oil. In medications, it helps break down and mix oil and water-based ingredients, aids in tablet disintegration, and improves how the drug dissolves and spreads in the mouth or digestive system.
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UNII 5856J3G2A2
A starch-based powder made from potatoes and processed with sodium. It acts as a disintegrant, helping the tablet or capsule break apart quickly in the stomach so the medicine can be absorbed.
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UNII O8232NY3SJ
A plant-based carbohydrate derived from corn kernels. It acts as a filler to add bulk, a binder to hold ingredients together, and a disintegrant to help the tablet break apart in your stomach for absorption.
8 inactive ingredients listed in the exact product block matched to this NDC.
Where does this data come from?
ingredient classCode="IACT" elements from the exact product block matched by this NDC. Label-section narrative from DailyMed / the openFDA label index is shown separately when available.Inactive ingredient FAQ
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💲 Pricing
A drug doesn't have one price. Each row is a different public payment system, and none is what you'd pay at the counter — that depends on your insurance. The ⓘ on each row explains what it measures.
| Price system | Per each | Per package |
|---|---|---|
| Retail pharmacies payNADAC · weekly | Not in the retail survey — common for institutional, discontinued, or low-volume packs. | |
| Medicaid paysCMS SDUD · 12 mo | $610.99 | $61,099.07 / 100 tablets |
| Medicare drug plans payPart D · Q2 2026 | $679.51 | $67,950.68 / 100 tablets |
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🔁 Therapeutic equivalents
| Product | Labeler | Pack | NADAC/unit | TE | Status | Price vs. this |
|---|---|---|---|---|---|---|
| Chenodal 250 mg 68974-0876-40 | Travere | 100 tablets | — | — | FDA listed | — |
| Ctexli 250 mgthis 79378-0310-90 | Mirum | 100 tablets | — | — | FDA listed | — |
Where does this data come from?
⏳ Availability & generic status
The FDA lists approved generic versions of this medicine, but that does not always mean a pharmacy can get one today. Patent rules, launch agreements, supply and pricing can affect when generics actually arrive.
Why the date isn’t exact: Generic timing can change because patents may be challenged, settled, licensed, added, removed, or worked around with a narrower label — and FDA approval does not always mean a pharmacy can get the generic today.
🛈 What do these terms mean?
- Patent
- Legal protection listed in the Orange Book that may delay generic approval or launch. Issued by the U.S. Patent & Trademark Office.
- Substance patent
- Covers the active drug molecule itself — the hardest to design around. A generic generally can’t launch until it expires.
- Formulation (product) patent
- Covers a specific formulation or dosage form. A generic can sometimes work around it with a different formulation.
- Method-of-use patent
- A patent covering one specific approved use of the drug — not necessarily the whole molecule. A generic can sometimes launch with a “skinny label” that carves out the protected use and keeps the others.
- Skinny label
- A generic label that omits a still-patented use when the FDA allows it — letting a generic reach the market for the unprotected uses.
- Exclusivity
- FDA-granted marketing protection, separate from patents — e.g. 5-yr new chemical entity, 7-yr orphan drug, or a +6-month pediatric extension.
- Paragraph IV
- A generic applicant’s formal challenge to a listed patent. It can potentially lead to earlier generic entry, but often involves litigation or a settlement.
- RLD / RS
- Reference Listed Drug — the brand product the FDA uses as the reference for generic applications. Reference Standard — the product the FDA expects generics to compare against in bioequivalence testing.
- TE / AB rating
- FDA therapeutic-equivalence rating. An AB rating generally means the FDA considers a generic therapeutically equivalent to — and substitutable for — the brand.
- LOE (loss of exclusivity)
- The latest patent or exclusivity currently listed — the loss-of-exclusivity / latest-listed-protection date shown on this page. Paragraph-IV challenges and settlements can move the real date earlier; FDA approval and a manufacturer’s decision to market can move it later.
Built from the FDA Orange Book. The bars above are scaled to each protection’s expiry; the red LOE marker is the last one to lapse.
| Code | What it grants | Expires |
|---|---|---|
| NP | New Product | Feb 21, 2028 |
| ODE-523 | Orphan Drug Exclusivity (7-year) | Feb 21, 2032 |
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🗺️ Medicaid utilization & spend
📊 Medicare Part D spend CMS · PART D · 2026 (Q1)
📦 Packaging — all sizes for this product
| Package NDC | Description | Marketing start | Status |
|---|---|---|---|
| 79378-0310-90 You're viewing this | 100 TABLET, FILM COATED in 1 BOTTLE (79378-310-90) | 2025-04-04 | Active |
🧭 About this NDC listing & data coverage
What data is (and isn’t) available for this NDC — tap to expand
| NDC identity (package / product / labeler codes) | ✓ Available |
| Labeler | ✓ Available |
| Product & package description | ✓ Available |
| Marketing category & status | ✓ Available |
| Active ingredient / dosage form / route | ✓ Available |
| FDA label (SPL via DailyMed) | ✓ Available |
| Package photos | ✓ Available |
| Inactive ingredients (structured) | ✓ Available |
| NADAC pharmacy acquisition price (CMS) | — Not published for this NDC CMS publishes NADAC only for NDCs reported in its retail-pharmacy survey. |
| Orange Book / therapeutic-equivalence data | ✓ Available |
| HCPCS J-code billing crosswalk | — Not published for this NDC Most self-administered / retail products have no J-code — that is normal. |
| Medicaid utilization (CMS SDUD) | ✓ Available |
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📄 Full prescribing information FDA SPL
🎯 Indications and Usage ▾
1 INDICATIONS AND USAGE CTEXLI is indicated for the treatment of cerebrotendinous xanthomatosis (CTX) in adults. CTEXLI is a bile acid indicated for treatment of cerebrotendinous xanthomatosis (CTX) in adults. ( 1 )
⏱️ Dosage and Administration ▾
2 DOSAGE AND ADMINISTRATION • Before initiating CTEXLI, obtain baseline liver transaminase (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) and total bilirubin levels in all patients. ( 2.1 ) • The recommended dosage is 250 mg orally three times daily. ( 2.2 )
2.1Important Recommendation Prior to CTEXLI Treatment Initiation Before initiating CTEXLI, obtain baseline liver transaminase (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) and total bilirubin levels in all patients [see Warnings and Precautions ( 5.1 )] .
2.2Recommended Dosage The recommended dosage of CTEXLI is 250 mg administered orally three times daily. Administer CTEXLI with or without food. Swallow tablets whole. Missed Dose If a dose of CTEXLI is missed, advise the patient to skip the missed dose and to resume taking the prescribed dose at the next scheduled time. Patients should not take a double dose.
2.3Administration Modification and Monitoring If liver transaminase (ALT, AST) levels are elevated > 3 times the upper limit of normal (ULN) or total bilirubin level is >2 times ULN, interrupt treatment with CTEXLI until the levels have returned to baseline values. Monitor liver transaminase and total bilirubin levels yearly and as clinically indicated [see Warnings and Precautions ( 5.1 )].
💊 Dosage Forms and Strengths ▾
3 DOSAGE FORMS AND STRENGTHS Tablets: 250 mg of chenodiol as white film-coated tablets imprinted with “MP” on one side and "250" on the other side. CTEXLI tablets: 250 mg. ( 3 )
⛔ Contraindications ▾
4 CONTRAINDICATIONS None. None. ( 4 )
⚠️ Warnings and Cautions ▾
5 WARNINGS AND PRECAUTIONS Hepatotoxicity : Obtain baseline liver transaminase and total bilirubin levels in all patients and monitor yearly and as clinically indicated. Interrupt treatment until the levels have returned to baseline values. For persistent or recurrent liver test abnormalities, consider discontinuing CTEXLI. ( 5.1 )
5.1Hepatotoxicity Chenodiol, including CTEXLI, has been associated with hepatotoxicity [see Adverse Reactions ( 6 )] . In Trial 1, one CTEXLI-treated patient (7%) had increased ALT levels > 3 times ULN, which led to treatment interruption. Patients with pre-existing liver disease or bile duct abnormalities may be at higher risk for hepatotoxicity during treatment with CTEXLI.
Published reports suggest patients who are poor sulfators of lithocholic acid are more likely to develop chenodiol-induced serum aminotransferase elevations [see Clinical Pharmacology ( 12.3 )] . Obtain baseline liver transaminase (ALT, AST) and total bilirubin levels in all patients prior to treatment initiation with CTEXLI. If liver transaminase levels are elevated > 3 times ULN or total bilirubin level is >2 times ULN, interrupt treatment with CTEXLI until the levels have returned to baseline values.
Monitor liver transaminase and total bilirubin levels yearly and as clinically indicated. For persistent or recurrent liver test abnormalities, consider discontinuing CTEXLI. Inform the patient of the symptoms of hepatotoxicity (e.g., abdominal pain, bruising, dark-colored urine, fatigue, bleeding, jaundice, nausea, and pruritus).
If clinical signs and symptoms consistent with hepatotoxicity occur, have the patient discontinue CTEXLI immediately.
🤒 Adverse Reactions ▾
6 ADVERSE REACTIONS The following clinically significant adverse reaction is described elsewhere in the labeling: • Hepatotoxicity [see Warnings and Precautions ( 5.1 )] The most common adverse reactions (incidence > 14%) are diarrhea, headache, abdominal pain, constipation, hypertension, muscular weakness, and upper respiratory tract infection. ( 6.1 ) To report SUSPECTED ADVERSE REACTIONS, contact Mirum Pharmaceuticals at 1-855-MRM-4YOU or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
6.1Clinical Trials Experience Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice. The safety of CTEXLI was evaluated in a randomized, double blind, placebo-controlled, 2-period, 2-treatment crossover trial in 14 patients (16 to 55 years of age) with CTX (Trial 1). CTEXLI is not approved for use in pediatric patients.
The dosage of CTEXLI was 250 mg orally three times a day [see Clinical Studies ( 14 )]. The mean (SD) chenodiol exposure during Trial 1 was 139.1 (26.7) days. The most common adverse reactions which occurred in two or more patients ( > 14%) during CTEXLI treatment (including the two 8-week open-label treatment periods) were diarrhea (36%), headache (21%), and abdominal pain (including abdominal pain upper) (14%), constipation (14%), hypertension (14%), muscular weakness (14%), and upper respiratory tract infection (14%).
In Trial 1, one CTEXLI-treated patient (7%) had increased ALT levels > 3x ULN, which led to treatment interruption.
6.2Postmarketing Experience The following adverse reactions have been identified during post approval use of chenodiol. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure. • Hepatobiliary Disorders: Hepatotoxicity [see Warnings and Precautions ( 5.1 )] • Immune System Disorders: Hypersensitivity reactions such as facial swelling, pruritus, rash, urticaria.
🔄 Drug Interactions ▾
7 DRUG INTERACTIONS • Bile acid sequestering agents and aluminum-based antacids: Avoid concomitant use with CTEXLI. ( 7.1 ) • Coumarin and its derivatives: Monitor prothrombin time and adjust dosage accordingly. ( 7.2 )
7.1Effect of Other Drugs on CTEXLI Co-administration of bile acid sequestering agents, such as cholestyramine and colestipol, or aluminum-based antacids may decrease absorption of CTEXLI in the intestine and may result in decreased efficacy of CTEXLI. Avoid concomitant use of bile acid sequestering agents or aluminum-based antacids with CTEXLI.
7.2Effect of CTEXLI on Other Drugs Due to potential hepatotoxicity, CTEXLI may affect the pharmacodynamics of coumarin and its derivatives, causing unexpected prolongation of the prothrombin time and hemorrhage. If concomitant use of CTEXLI with coumarin or its derivatives is unavoidable, monitor prothrombin time. Adjust the dosage of coumarin or its derivatives in accordance with its approved product labeling.
👥 Use in Specific Populations ▾
8 USE IN SPECIFIC POPULATIONS
8.1Pregnancy Risk Summary Available data from published case reports over decades of use with chenodiol during pregnancy have not identified an increased risk of major birth defects, miscarriage, or other adverse maternal or fetal outcomes. Serious hepatic, renal and adrenal lesions occurred in fetuses of female Rhesus monkeys treated at doses 1 to 2 times the recommended human dose based on body surface area (mg/m 2 ). Hepatic lesions also occurred at doses comparable to the human dose based on body surface area in neonatal baboons born to mothers administered chenodiol during pregnancy ( see Data ).
The animal study findings have not been demonstrated with human use. The background risk of major birth defects and miscarriage for the indicated population is unknown. All pregnancies have a background risk of birth defect, loss, or other adverse outcomes.
In the US general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively. Data Animal Data Hepatic lesions were reported in neonatal baboons whose mothers had received 18 to 38 mg/kg of chenodiol throughout pregnancy (0.6 to 1.4 times the recommended human dose based on body surface area). Serious hepatic, renal and adrenal lesions were also reported in fetuses of female Rhesus monkeys given 60 to 90 mg/kg/day from GD 21-45 of pregnancy (1 to 2 times the recommended human dose based on body surface area).
Non-human primates form sulfate conjugates of the known hepatotoxic bacterial metabolite of chenodiol, lithocholic acid, to a lesser extent than reported in humans, which may exaggerate the toxicity of orally dosed chenodiol compared to humans. However, there is also evidence that the hepatobiliary toxicity is partly due to the parent drug, chenodiol.
8.2Lactation Risk Summary There are no data on the presence of chenodiol in either human or animal milk, the effects on the breastfed infant, or the effects on milk production. The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for CTEXLI and any potential adverse effects on the breastfed infant from CTEXLI or the underlying maternal condition.
8.4Pediatric Use The safety and effectiveness of CTEXLI for the treatment of CTX have not been established in pediatric patients.
8.5Geriatric Use Trial 1 of CTEXLI in patients with CTX did not include patients aged 65 years and older.
🤰 Pregnancy ▾
8.1Pregnancy Risk Summary Available data from published case reports over decades of use with chenodiol during pregnancy have not identified an increased risk of major birth defects, miscarriage, or other adverse maternal or fetal outcomes. Serious hepatic, renal and adrenal lesions occurred in fetuses of female Rhesus monkeys treated at doses 1 to 2 times the recommended human dose based on body surface area (mg/m 2 ). Hepatic lesions also occurred at doses comparable to the human dose based on body surface area in neonatal baboons born to mothers administered chenodiol during pregnancy ( see Data ).
The animal study findings have not been demonstrated with human use. The background risk of major birth defects and miscarriage for the indicated population is unknown. All pregnancies have a background risk of birth defect, loss, or other adverse outcomes.
In the US general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively. Data Animal Data Hepatic lesions were reported in neonatal baboons whose mothers had received 18 to 38 mg/kg of chenodiol throughout pregnancy (0.6 to 1.4 times the recommended human dose based on body surface area). Serious hepatic, renal and adrenal lesions were also reported in fetuses of female Rhesus monkeys given 60 to 90 mg/kg/day from GD 21-45 of pregnancy (1 to 2 times the recommended human dose based on body surface area).
Non-human primates form sulfate conjugates of the known hepatotoxic bacterial metabolite of chenodiol, lithocholic acid, to a lesser extent than reported in humans, which may exaggerate the toxicity of orally dosed chenodiol compared to humans. However, there is also evidence that the hepatobiliary toxicity is partly due to the parent drug, chenodiol.
🧒 Pediatric Use ▾
8.4Pediatric Use The safety and effectiveness of CTEXLI for the treatment of CTX have not been established in pediatric patients.
🧓 Geriatric Use ▾
8.5Geriatric Use Trial 1 of CTEXLI in patients with CTX did not include patients aged 65 years and older.
🆘 Overdosage ▾
10 OVERDOSAGE Cases of intentional overdose with chenodiol have been reported: one patient consumed 3 g to 4.5 g of chenodiol and another patient consumed 30 g of chenodiol. Clinical manifestations experienced by these patients included nausea, dizziness, and diarrhea. In the event of an overdose, discontinue CTEXLI, monitor the patient, and institute general supportive measures if needed.
🧬 Clinical Pharmacology ▾
12 CLINICAL PHARMACOLOGY
12.1Mechanism of Action Endogenous chenodiol (chenodeoxycholic acid) is a primary bile acid, synthesized from cholesterol in the liver. In CTX, the major bile acid synthesis pathways are disrupted due to partial or total deficiency in sterol 27-hydroxylase encoded by the CYP27A1 gene. CTEXLI may act to replace deficient levels of the endogenous bile acid chenodeoxycholic acid in patients with CTX.
Increased chenodiol levels in the enterohepatic bile acid pool restore the activation of farnesoid X receptor (FXR) and downregulate CYP7A1 leading to suppression and reduction of atypical bile acids and bile alcohols including cholestanol and 23S-pentol.
12.2Pharmacodynamics In Trial 1, plasma cholestanol and urine 23S-pentol concentrations were elevated in patients with CTX. Treatment with CTEXLI resulted in reductions of plasma cholestanol and urine 23S-pentol concentrations in the 8-week run-in open label treatment period. Continued treatment with CTEXLI for 4 weeks in the double-blind treatment period resulted in the maintenance of low levels of urine 23S-pentol and additional reductions of plasma cholestanol [see Clinical Studies ( 14 )] .
12.3Pharmacokinetics In CTX patients, the geometric mean (%CV) maximum plasma concentration (C max ), trough plasma concentration (C trough ), and area under the plasma concentration-time curve (AUC 0-8h ) of chenodiol at steady state following the recommended dosage (250 mg administered orally three times daily) were 3.7 mcg/mL (60%), 0.7 mcg/mL (90%), and 12.5 mcg*h/mL (60%), respectively. Absorption The median (range) T max of chenodiol following an oral administration in CTX patients was 3 (0.5‑8) hours. Distribution Due to first-pass hepatic clearance, the body pool of chenodiol resides mainly in the enterohepatic circulation.
The apparent volume of distribution of chenodiol at steady-state was
0.36L/kg. The plasma protein binding of chenodiol was approximately 98%. Elimination The geometric mean total apparent clearance of chenodiol in CTX patients was 20 L/h.
Metabolism Chenodiol is well absorbed from the small intestine and taken up by the liver where it is converted to its taurine and glycine conjugates and secreted into the bile along with other endogenous bile acids in the enterohepatic circulation. Chenodiol that escapes to the colon is converted by bacterial action to lithocholic acid. Humans have the capacity to form sulfate conjugates of lithocholic acid.
About 80% of the lithocholate is excreted in the feces and the remainder is absorbed and converted in the liver to its poorly absorbed sulfolithocholyl conjugates. Excretion Conjugated chenodiol is either reabsorbed in the terminal ileum, deconjugated before excretion, or decomposed by bacteria to lithocholic acid. Drug Interaction Studies Based on in vitro studies, chenodiol and its glyco- and tauro- conjugates are not expected to inhibit CYPs 1A2, 2B6, 2C8, 2C9, 2C19, 2D6, or 3A4, or induce CYPs 1A2 or 2B6 at the recommended dose of chenodiol of 250 mg TID.
Chenodiol and its tauro- conjugate may upregulate CYP3A4 mRNA in vitro. The clinical significance of this upregulation is unknown. The glyco- and tauro- conjugates of chenodiol are high affinity substrates for BSEP, and in vitro studies suggest that chenodiol may inhibit OATP1B1 and OATP1B3 at the recommended dose of 250 mg TID (clinical significance unknown), but chenodiol and its glyco- and tauro- conjugates are not predicted to inhibit P-gp, BCRP, OATP2B1, OAT1, OAT3, OCT1, OCT2, MATE1, or MATE2-K.
🧬 Mechanism of Action ▾
12.1Mechanism of Action Endogenous chenodiol (chenodeoxycholic acid) is a primary bile acid, synthesized from cholesterol in the liver. In CTX, the major bile acid synthesis pathways are disrupted due to partial or total deficiency in sterol 27-hydroxylase encoded by the CYP27A1 gene. CTEXLI may act to replace deficient levels of the endogenous bile acid chenodeoxycholic acid in patients with CTX.
Increased chenodiol levels in the enterohepatic bile acid pool restore the activation of farnesoid X receptor (FXR) and downregulate CYP7A1 leading to suppression and reduction of atypical bile acids and bile alcohols including cholestanol and 23S-pentol.
📦 How Supplied / Storage and Handling ▾
16 HOW SUPPLIED/STORAGE AND HANDLING How Supplied CTEXLI (chenodiol) tablets are supplied as 250 mg white film-coated tablets imprinted with “MP” on one side and "250" on the other side. NDC 79378-310-90: 100 count bottle Storage and Handling Store CTEXLI at 20°C to 25°C (68°F to 77°F); excursions permitted between 15°C to 30°C (59°F to 86°F) [see USP Controlled Room Temperature].
📋 Description ▾
11 DESCRIPTION CTEXLI (chenodiol) is a bile acid. Chenodiol is a bitter-tasting, white powder consisting of crystalline and amorphous particles that are freely soluble in methanol, acetone and acetic acid, and practically insoluble in water. The chemical name of chenodiol is 3α,7α-dihydroxy-5-β-cholan-24-oic acid.
The molecular formula is C 24 H 40 O 4 and the molecular weight is 392.58 g/mol. The chemical structure is: Each CTEXLI tablet contains 250 mg of chenodiol. Inactive ingredients are magnesium stearate, microcrystalline cellulose, pregelatinized starch, silicon dioxide, and sodium starch glycolate.
The thin-film coating contains opadry YS 2 7035 (consisting of methylcellulose and glycerin) and sodium lauryl sulfate. Chenodiol chemical structure
💬 Information for Patients ▾
17 PATIENT COUNSELING INFORMATION Hepatotoxicity Inform the patient of the symptoms of hepatotoxicity (e.g., abdominal pain, bruising, dark-colored urine, fatigue, bleeding, jaundice, nausea, and pruritus). Instruct the patient to discontinue CTEXLI immediately and seek medical care should symptoms occur [see Warnings and Precautions ( 5.1 )] . Rx only Manufactured for: Mirum Pharmaceuticals, Inc.
Foster City, CA 94404 © 2025 Mirum Pharmaceuticals, Inc. CTEXLI ® is a registered trademark of Mirum Pharmaceuticals, Inc.