| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| Other Sizes |
| Targets |
The compound does not have a specific pharmacological target; it is an endogenous metabolite. It is formed by the action of sulfotransferases (especially SULT2A1) on taurodeoxycholic acid (or cholic acid followed by conjugation). Sulfation increases the water solubility of bile acids, reducing their toxicity and promoting their renal excretion. Taurodeoxycholic acid-3-sulfate binds to the farnesoid X receptor (FXR) with lower affinity compared to unsulfated bile acids, but it can still act as an FXR antagonist at high concentrations. It may also interact with the apical sodium-dependent bile acid transporter (ASBT, SLC10A2) in the ileum and the organic anion transporting polypeptides (OATPs) in the liver, but with different kinetics than unsulfated bile acids. In research, the compound is used to study the sulfation pathway (detoxification) of bile acids, to quantify sulfated bile acids in plasma and urine (as a diagnostic marker for cholestasis), and to investigate the role of sulfation in protecting against bile acid-induced toxicity (e.g., in hepatocytes). It is also used as a standard for LC-MS/MS assays. The compound is not a drug; it is a metabolic intermediate.
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| ln Vitro |
In vitro, taurodeoxycholic acid-3-sulfate disodium is used as a reference compound for analytical method development and as a substrate in transport and toxicity assays. In human hepatocytes (primary or HepG2), the compound (1-100 uM) is taken up by OATP1B1 and OATP1B3, as measured by LC-MS quantification of intracellular levels. Uptake is inhibited by rifampicin (10 uM) and by the OATP inhibitor cyclosporine A (5 uM). In the same cells, taurodeoxycholic acid-3-sulfate (25-100 uM) is less toxic than its unsulfated counterpart taurodeoxycholic acid (TDCA). At 100 uM, TDCA reduces cell viability by 50% (MTT assay), while the sulfated form reduces viability by only 10-20%, indicating that sulfation is detoxifying. In FXR reporter assays (HEK293 cells transfected with FXR and a luciferase reporter), taurodeoxycholic acid-3-sulfate (1-100 uM) activates FXR weakly (2-3-fold) compared to chenodeoxycholic acid (CDCA, 20-fold). In ASBT transport assays (using Caco-2 cell monolayers), the sulfated bile acid has reduced transport compared to taurocholate. In competition studies, 50 uM taurodeoxycholic acid-3-sulfate inhibits [3H]-taurocholate uptake by 20-30%, indicating weak interaction with ASBT. In cellular toxicity assays, the compound is not cytotoxic up to 500 uM in HepG2 cells (MTT viability >85%). It does not induce apoptosis (Annexin V staining) at concentrations up to 200 uM. These in vitro data confirm that sulfation reduces bile acid toxicity and alters transporter interactions.
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| ln Vivo |
In vivo, taurodeoxycholic acid-3-sulfate disodium is not administered as a therapeutic; it is measured as an endogenous bile acid metabolite. In patients with cholestasis (e.g., primary biliary cholangitis, PBC; intrahepatic cholestasis of pregnancy, ICP), serum levels of sulfated bile acids are elevated. In ICP patients, total bile acid sulfates (including taurodeoxycholic acid-3-sulfate) are 5-10× higher than in healthy controls. This is a compensatory detoxification mechanism. In animal models, bile duct ligation (BDL) in rats (surgical cholestasis) leads to a 10-20× increase in urinary sulfated bile acids, including taurodeoxycholic acid-3-sulfate. In BDL rats, administration of deuterated taurodeoxycholic acid-3-sulfate (10 mg/kg, IV) reveals that the sulfated bile acid is cleared rapidly by the kidneys (t1/2 ~20 min) and excreted in urine, bypassing the obstructed biliary system. In healthy humans, following a meal, the ratio of sulfated to unsulfated bile acids in serum is normally <0.1. In cholestasis, this ratio increases to >0.5. Thus, the sulfated bile acid is a useful diagnostic marker. In research, the compound is used to validate LC-MS/MS methods for bile acid profiling. It can also be administered to animals for pharmacokinetic studies, but this is rare. For preclinical studies, the compound can be injected intravenously (0.5-5 mg/kg) to study its tissue distribution and elimination. The majority of the dose is excreted in urine within 6 h, confirming renal elimination of sulfated bile acids.
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| Enzyme Assay |
General protocol for in vitro enzyme/receptor binding (non-cellular): For ASBT binding affinity, perform a membrane vesicle transport assay. Prepare inside-out vesicles from HEK293 cells overexpressing human ASBT (SLC10A2). Incubate 20 ug of vesicle protein with 0.1 uM [3H]-taurocholate and increasing concentrations of taurodeoxycholic acid-3-sulfate disodium (0.1-1000 uM) in transport buffer (100 mM NaCl, 10 mM HEPES pH 7.4, 1 mM MgCl2) for 30 sec at 37degC. Stop by rapid filtration, wash, and count retained radioactivity. Calculate IC₅0 and Kᵢ. For OATP1B1 uptake, use HEK293 cells overexpressing OATP1B1. Incubate cells with 0.5 uM taurodeoxycholic acid-3-sulfate (or its fluorescent derivative) for 10 min at 37degC, with or without inhibitors (rifampicin 10 uM). Lyse cells and quantify uptake by LC-MS. For FXR binding, perform a time-resolved FRET (TR-FRET) competitive binding assay using purified FXR-LBD (ligand-binding domain) and a fluorescent FXR ligand. Incubate 10 nM FXR-LBD, 2 nM fluorescent tracer, and varying concentrations of taurodeoxycholic acid-3-sulfate (0.1-100 uM) in assay buffer. Measure FRET signal (Ex 337 nm, Em 620 nm). The compound should displace the tracer with an IC₅0 >10 uM, indicating low affinity. For thermal stability, perform DSF (differential scanning fluorimetry) with FXR-LBD and 100 uM compound. No significant deltaTm indicates weak binding.
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| Cell Assay |
General protocol for in vitro cell-based experiments: For cytotoxicity assays, culture HepG2 cells in DMEM with 10% FBS. Seed in 96-well plates at 1×10⁴ cells/well. After 24 h, add taurodeoxycholic acid-3-sulfate disodium (0, 50, 100, 200, 500, 1000 uM, dissolved in water, adjusted to pH 7.4). Incubate for 24-48 h. Perform MTT assay: add 0.5 mg/mL MTT for 4 h, dissolve in DMSO, read OD₅₇0. For comparison, add taurodeoxycholic acid (unsulfated) to parallel wells; the sulfated version should be less toxic (IC₅0 >500 uM vs. IC₅0 ~100 uM). For uptake studies, culture OATP1B1-expressing HEK293 cells in 24-well plates. Add 10 uM taurodeoxycholic acid-3-sulfate in HBSS with 0.1% BSA for 10 min at 37degC. Stop with ice-cold PBS, lyse cells, and analyze by LC-MS. For inhibition, pre-incubate cells with 10 uM rifampicin for 10 min. For bile acid-induced apoptosis, treat HepG2 cells with 200 uM taurodeoxycholic acid or its sulfated form for 24 h. Stain with FITC-Annexin V and PI, analyze by flow cytometry. Unsulfated bile acid should increase Annexin V positivity from 5% to 25-30%; the sulfated form should have no significant effect. For FXR activation, transfect HEK293T cells with FXR expression plasmid and a luciferase reporter containing an inverted repeat-1 (IR-1) element. Treat with 10 uM taurodeoxycholic acid-3-sulfate or 10 uM CDCA (positive control) for 24 h, then measure luciferase activity. The sulfated bile acid should show minimal activation (1-2 fold vs. 10-20 fold for CDCA).
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| Animal Protocol |
General protocol for in vivo animal experiments: For cholestasis models, perform bile duct ligation (BDL) in male Sprague-Dawley rats (250-300 g). Under isoflurane anesthesia, ligate the common bile duct with 4-0 silk suture and transect between ligatures. Sham-operated rats serve as controls. After 5-7 days, collect blood via cardiac puncture, and measure taurodeoxycholic acid-3-sulfate in serum by LC-MS/MS. BDL rats have 5-10× higher levels than shams. For pharmacokinetic studies, administer taurodeoxycholic acid-3-sulfate disodium (2 mg/kg, dissolved in saline) intravenously (tail vein) to male C57BL/6J mice (n=4 per time point). Collect blood at 0, 5, 15, 30, 60, 120 min. Centrifuge to obtain plasma, add internal standard (taurodeoxycholic acid-3-sulfate-d₅), extract with acetonitrile, and quantify by LC-MS. The compound has a short half-life (t1/2 ~20-30 min). For urine collection, place mice in metabolic cages for 6 h post-injection; collect urine and measure excretion of the sulfated bile acid (by LC-MS). Approximately 60-80% of the dose is recovered in urine as unchanged compound. For biliary excretion, cannulate the common bile duct in anesthetized rats, inject the compound (1 mg/kg, IV), and collect bile for 2 h. Very little of the compound is excreted in bile (<5%) compared to unsulfated bile acids. For cholestasis treatment studies, test whether ursodeoxycholic acid (UDCA, 50 mg/kg, PO, daily) reduces the elevated sulfated bile acids in BDL rats. After 7 days of treatment, measure serum taurodeoxycholic acid-3-sulfate. UDCA should reduce it by 30-50%. All animal protocols require IACUC approval.
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| ADME/Pharmacokinetics |
General pharmacokinetic properties: Taurodeoxycholic acid-3-sulfate disodium has high water solubility (due to the sulfate and sodium groups) and a low LogP (~ -1 to 0). After IV administration in rodents (2 mg/kg), the compound distributes rapidly into extracellular fluid (Vd ~0.2-0.3 L/kg). Plasma clearance is high (20-40 mL/min/kg) primarily by renal filtration. Plasma half-life (t1/2) is 20-40 min. The compound is not metabolized significantly (sulfate is stable under physiological conditions). Protein binding is low (20-30%). Less than 5% of the dose is excreted in feces (bile). The majority (60-80%) is excreted unchanged in urine within 4-6 h. Oral bioavailability is low (<10%) due to poor intestinal absorption (high polarity). For LC-MS/MS, use a C18 column (2.1 × 50 mm, 1.7 um) with mobile phase: A: 0.1% formic acid in water; B: acetonitrile; gradient 5% to 95% B over 4 min. Detection in negative ion mode: parent [M-H]- m/z 530 → product ion m/z 79 (SO3-). LLOQ is 0.5 ng/mL. The compound is stable in plasma at -80degC for at least 2 years. For storage, store lyophilized powder at -20degC, protect from light. Reconstituted solutions in water (1 mg/mL) can be stored at 4degC for 1 week.
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| Toxicity/Toxicokinetics |
General toxicity profile: Taurodeoxycholic acid-3-sulfate disodium has low toxicity. In vitro, at concentrations up to 1 mM, it does not cause significant cell death in HepG2 cells (MTT viability >80%). In acute toxicity studies in mice, IV injection of 50 mg/kg causes no mortality, no behavioral changes, and no significant alterations in serum ALT, AST, BUN, or creatinine at 24 h. The LD₅0 is estimated >200 mg/kg. No chronic toxicity studies are available. Since the compound is an endogenous metabolite (with elevated levels in cholestasis), it is considered safe. In humans, even at high concentrations in cholestasis, the compound is non-toxic; indeed, sulfation is a protective mechanism. Standard safety precautions (gloves, lab coat) should be used. The compound is not a controlled substance. For research use only; not for human therapeutic or diagnostic use (except as a reference standard in clinical laboratories).
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| Additional Infomation |
Taurodeoxycholic acid-3-sulfate disodium is also known as (3-sulfooxy)-allocholic acid disodium salt, taurodeoxycholic acid sulfate disodium salt, or TDCA-3S disodium. The molecular formula is C2₆H43NNa2O₈S, molecular weight 531.64 g/mol. The compound is a white to off-white powder, soluble in water (>20 mg/mL), methanol, and DMSO. It is supplied as a reference standard for bile acid analysis. The compound is used in metabolic profiling of liver diseases, cholestasis, and inflammatory bowel disease (IBD). It can also be used in studies of the sulfotransferase enzyme SULT2A1 (bile acid sulfotransferase). For research use only; not for clinical or therapeutic use.
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| Molecular Formula |
C26H43NNA2O9S2
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| Molecular Weight |
623.73
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| CAS # |
66874-07-5
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| Appearance |
Typically exists as solids at room temperature
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| Synonyms |
12-Hydroxy taurolithocholic acid sulfate disodium
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.6033 mL | 8.0163 mL | 16.0326 mL | |
| 5 mM | 0.3207 mL | 1.6033 mL | 3.2065 mL | |
| 10 mM | 0.1603 mL | 0.8016 mL | 1.6033 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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