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Chenodeoxycholic Acid

Q: Are there different variations or types of Chenodeoxycholic Acid?

While Chenodeoxycholic Acid is the primary form, there are other bile acid variations that may have slightly different properties and applications. Researchers often investigate the efficacy of these related compounds in order to optimize treatment options and find the most effective approaches for specific clinical scenarios.

Chenodeoxycholic Acid is a primary bile acid produced in the liver.
It plays a crucial role in the digestion and absorption of fats, cholesterol, and fat-soluble vitamins.
Chenodeoxycholic Acid can be used to treat certain liver and gallbladder disorders, such as gallstones and primary biliary cirrhosis.
Reseach on the effective use of Chenodeoxycholic Acid in theraupatic applications is an active area of study.
PubCompare.ai's AI-driven platform can help researchers locate the best protocols from literature, preprints, and patents, using intelligent comparisons to identify the most reliable and effective methods for Chenodeoxycholic Acid reasearch.
Experience the power of data-driven insights for your Chenodeoxycholic Acid studiy.

Most cited protocols related to «Chenodeoxycholic Acid»

Quantitative Bile Acid and SCFA Analysis

For BA analysis, samples (≈40 mg of caecal content) were homogenised with acetonitrile using zirconia/silica beads (0.1 mm diameter). After discarding stool particles, the supernatant was evaporated in a vacuum centrifuge and solubilised in a volume of methanol to a final concentration of 1 μL mg⁻¹ of gut content. Chromatographic separation was performed on Agilent 1290 Infinity UHPLC using a 150 mm × 2.1 mm internal diameter (i.d.) Phenomenex Kinetex® C18 core-shell column, packed with 2.6-μm particles. HPLC was carried out with mobile phase A (0.1% formic acid in aqueous solution) and mobile phase B (0.1% formic acid in acetonitrile) at a total flow rate of 0.5 mL min⁻¹. Gradient program was increased linearly from 5% mobile phase B and 95% mobile phase A to 100% mobile phase B for 9.5 min. Bile acid identities were established in negative ion mode using a mass MSMS instrument (Agilent QTOF 6540) and the following pure standards: cholic acid (C1129, SIGMA), deoxycholic acid (D4297, SIGMA), lithocholic acid (L6250, SIGMA), chenodeoxycholic acid (C1050000, European Pharmacopoeia Reference Standard), cholic acid 7-sulphate (9002532, Cayman Chemical), α-muricholic acid (C1890-000, Steraloids), β-muricholic acid (sc-477731, Santa Cruz), ω-muricholic acid (C1888-000, Steraloids), ursodeoxycholic acid (C1020-000, Steraloids), hyodeoxycholic acid (H0535, TCI), taurocholic acid (sc-220189, Santa Cruz) and taurodeoxycholic acid (15935, Cayman Chemical). Peak integration and analysis was performed using ProFinder (software version B.06.00, Agilent Technologies) and a customised spectral library.
For SCFA profiling, samples were spiked with 5 nmol of ¹³C-sodium acetate (279293, SIGMA) and 5 nmol of 2-ethyl butyric acid (109959, SIGMA) as internal standards and were homogenised in isopropanol. After centrifugation, 1 μL of the supernatant was injected into a HP 6890 Series GC System, equipped with an Agilent 5973 Network Mass Selective Detector in splitless mode. Samples were separated on a Stabilwax®-DA (Shimadzu) column (30 m × 0.25 mm i.d.) coated with a 0.25-μm-thick film. The carrier gas was helium at a flow rate of 1 mL min⁻¹. The initial oven temperature of 90 °C was held for 2 min, then increased to 240 °C at 5 °C min⁻¹ and maintained for additional 2 min. The temperature of the quadrupole, MS source and inlet were 150, 230 and 250 °C, respectively. Identities and retention times of the SCFA were established using the volatile-free acid mix (46975-U, Supelco). Peaks were automatically integrated using MSD ChemStation (version D.03.00.611). SCFA concentration was estimated using the internal references ¹³C-sodium acetate (for acetic acid) or 2-ethyl butyric acid (for all the others SCFA tested). Data were calculated as nanomoles per microlitre serum or per milligram caecal content from at least three biological replicates within each different group.

Caparrós-Martín J.A., Lareu R.R., Ramsay J.P., Peplies J., Jerry Reen F., Headlam H.A., Ward N.C., Croft K.D., Newsholme P., Hughes J.D, & O’Gara F. (2017). Statin therapy causes gut dysbiosis in mice through a PXR-dependent mechanism. Microbiome, 5, 95.

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Publication 2017

Acetic Acid acetonitrile Acids ARID1A protein, human Bile Acids Biopharmaceuticals Butyric Acid Caimans cDNA Library Cecum Centrifugation Chenodeoxycholic Acid Cholic Acid Chromatography Deoxycholic Acid Europeans Feces formic acid Helium High-Performance Liquid Chromatographies hyodeoxycholic acid Isopropyl Alcohol Lithocholic Acid Methanol muricholic acid Retention (Psychology) Serum Silicon Dioxide Sodium Acetate Sulfates, Inorganic Taurocholic Acid Taurodeoxycholic Acid Ursodiol Vacuum zirconium oxide

Bile Acid Dynamics Modeling in Rats

The BA submodel in DILIsym comprises several components. It includes (i) the synthesis and metabolism of BAs in hepatocytes, (ii) the basolateral and canalicular active transport of BAs, (iii) the release of BAs from the gallbladder in humans, (iv) the synthesis of secondary BAs and deconjugation of BAs in the gut, (v) the recirculation of BAs from the gut and subsequent active uptake by the liver, and (vi) the regulatory effects of BAs on transporter expression and BA synthesis. The model contains representations of LCA and CDCA and its conjugates, the BA species most frequently linked to toxicity in in vitro experiments,^{20 (link),21 (link),33 (link),34 (link)} and a “bulk” BA representation that contains the other BAs. A more detailed description of the BA homeostasis model and its parameterization is presented in the Supplementary Materials online.
To represent BA dynamics in humans, the model was optimized to the known profile of BAs in serum published by Trottier et al.,^{35 (link)} as well as to overall concentrations of BAs in the liver measured by Setchell^{36 (link)} and García-Cañaveras et al.^{37 (link)} There were 47 system variables that were either unknown or expected to vary within the human population that were fit to the BA profile; a list of the variables used in the optimization is provided in the Supplementary Materials online. The optimization of the model based on the published BA profile was performed in a manner similar to the SimPops method outlined in previous publications, wherein a genetic algorithm was used to generate values of variable parameters that lead to model outcomes (in this case, BA profiles) that are within the range of experimental data.^{27 (link),28 (link)} Using this optimization method allowed the selection of a population of 2,400 individuals with reasonable baseline BA concentrations for the large human sample population. A smaller, 10-parameter, 331-individual SimPops was also constructed for the purpose of model validation. While the large population was given artificially wide parameter ranges for the purpose of the sensitivity analysis, the small human sample population was constructed with more constrained parameter ranges for the purpose of approximating a plausible population of humans. For example, the transporter V_max ranges included four orders of magnitude in the large population, but were constrained to ranges suggested by transporter expression profiles from Meier et al.^{25 (link)} in the small population.
A smaller SimPops was constructed in rats for the validation against the experimental data. A population of 191 rats using a more limited 11 variable set (Supplementary Table S4 online) was generated. This population was intended to represent rats with both plausible serum BA concentrations and plausible values for the parameters that were varied. The baseline rat model was optimized to the BA profile from the control rats in the present experiment, and the SimPops was constructed around this baseline.
Details on the simulations performed for the model validation and for the model exploration can be found in the Supplementary Materials online. Multivariate analysis on the population sample was performed using JMP 9 from SAS (Cary, NC).
Multiple-dose glibenclamide study in ratsFor the BA-profiling experiments, 16 male 8- to 9-week-old CD-1 rats from Charles River Laboratories (Raleigh, NC) weighing between 200 and 300 g were randomized into four groups of four animals each. These groups were administered daily doses of either the vehicle control (0.5% hydroxypropylmethylcellulose /0.1% Tween 80 in water) or glibenclamide (Sigma-Aldrich, St Louis, MO) in vehicle via oral gavage for 7 days at three dose levels (300, 750, and 1,500 mg/kg/day). Details on the treatment of the rats are available in the Supplementary materials online.
Rats underwent a viability check twice per day, and detailed clinical observations were taken at least twice over the course of the study. Blood was drawn for serum BA profiles at 1, 3, 6, and 24 h after dosing on day 1 and day 7, and glibenclamide concentrations were measured for toxicokinetic analysis using the same blood samples from day 7. The animals were euthanized under isoflourane anesthesia on day 8 and underwent necropsy. Clinical and anatomic pathology data were collected from the animals, and these results are reported in the Supplementary Materials online. The serum BA concentrations from day 1 were used for comparison to the simulation results.
BA profiling in serum was performed using liquid chromatography–tandem mass spectrometry analysis at GlaxoSmithKline (Ware, UK). BAs in liver tissue 24 h after the final dose also were profiled; results from this analysis, as well as the liquid chromatography–tandem mass spectrometry analytical method, are presented in the Supplemental Materials online. This study was conducted in accordance with the GlaxoSmithKline Policy on the Care, Welfare and Treatment of Laboratory Animals and was reviewed by the Institutional Animal Care and Use Committee.
For this experiment, doses of glibenclamide were administered every 24 h for 7 days. Systemic exposure data were compared to simulation results for day 7; day 1 BA data were compared to simulated BA concentrations on day 1.
Short-term glibenclamide studies in ratsFor the short-term studies, male Han Wistar rats (substrain AlpkHsdBrlHan:WIST; AstraZeneca, Macclesfield, UK) of 10–12-week age (300–400 g) were used. Details on the treatment of the rats used in this study are available in the Supplemental Materials online. All animals were treated in accordance with approved UK Home Office license requirements.
Two experiments were performed in which total plasma BA concentrations and glibenclamide plasma concentrations were determined. Glibenclamide (Sigma-Aldrich) was formulated as a solution or suspension in hydroxypropyl-β-cyclodextrin (Acros Organics, distributed by Fisher Scientific, Loughborough, UK) in aqueous 0.2 mol/l Na₂CO₃/NaHCO₃ buffer (pH 10). In the first experiment (29 animals), four groups of five animals received a single dose via oral gavage of 50, 250, and 500 mg/kg glibenclamide or 10% (w/v) hydroxypropyl-β-cyclodextrin vehicle alone, and blood samples were taken at 1, 6, and 24 h after dosing; an additional three animals per glibenclamide-treated group received a single dose of 50, 250, and 500 mg/kg glibenclamide, and blood samples were taken at 1, 3, 6, 12, and 24 h after dosing. In the second experiment (20 animals), two groups of five animals each received two oral doses of 250 and 500 mg/kg glibenclamide in 20% (w/v) hydroxypropyl-β-cyclodextrin vehicle at 0 and 4 h, and blood samples were taken predose and at 0.5, 1, 2, and 4 h after dosing; blood samples from an additional five animals per glibenclamide-treated group were taken predose and 1 h after dosing to increase the dataset for this time point. Details on the blood-sampling procedure are located in the Supplementary Materials online. Animals were dosed 2 h into the light cycle.

Woodhead J.L., Yang K., Brouwer K.L., Siler S.Q., Stahl S.H., Ambroso J.L., Baker D., Watkins P.B, & Howell B.A. (2014). Mechanistic Modeling Reveals the Critical Knowledge Gaps in Bile Acid–Mediated DILI. CPT: Pharmacometrics & Systems Pharmacology, 3(7), e123-.

Publication 2014

Anabolism Animals Animals, Laboratory Autopsy Bicarbonate, Sodium Biological Transport, Active BLOOD Buffers Chenodeoxycholic Acid Cyclodextrins Dental Anesthesia Dietary Fiber Gallbladder Glyburide Hepatocyte Homeostasis Homo sapiens Hypersensitivity Hypromellose Institutional Animal Care and Use Committees Liquid Chromatography Liver Males Membrane Transport Proteins Metabolism Plasma Rats, Laboratory Rats, Wistar Rattus norvegicus Reproduction Rivers Serum Tandem Mass Spectrometry Tissues Tube Feeding Tween 80 Venipuncture

Genetic and Epigenetic Factors in PAAD

Genetic alterations, including gene mutations and copy number alterations, are the potential factors impacting expression. We evaluated the genetic alterations of CDCAs with Oncoprinter from cBioportal and the impacts of CDCAs on PAAD patient survival23 (link), 24 (link). DNA methylation is another risk factor that affects the expression of CDCAs. The influence of DNA methylation on CDCA expression was assessed by DNMIVE25 (link), and the impact of a single-methylation CpG site on the OS of PAAD patients was analyzed by MethSurv26 (link).

Xing C., Wang Z., Zhu Y., Zhang C., Liu M., Hu X., Chen W, & Du Y. (2021). Integrate analysis of the promote function of Cell division cycle-associated protein family to pancreatic adenocarcinoma. International Journal of Medical Sciences, 18(3), 672-684.

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Publication 2021

Chenodeoxycholic Acid Copy Number Polymorphism DNA Methylation Methylation Mutation Patients

Quantification of Bile Acids by UPLC/MS/MS

Serum BA extraction and quantification were described previously (15 ). Liver BA concentrations were quantified by a recent method using ultra performance liquid chromatography- tandem mass spectrometry (UPLC/MS/MS) (14 (link)). BA stock solutions were diluted with 50% methanol and spiked with internal standards (²H₄-GCDCA and ²H₄-CDCA) to construct standard curves between 5 and 20,000 ng/ml. All standard curves were constructed using a 1/concentration² weighted quadratic regression, and the correlation coefficient (r²) for all BAs was above 0.99. The limit of detection (signal/noise ratio=3) for the various BAs was in the range of 5-10 ng/ml, which equals 0.01-0.02 nmol/ml. For a preliminary analysis of hydroxylated BA, we obtained taurine-conjugated and unconjugated 3α,6α,7α,12α-tetrahydroxyl BA from Dr. Mary Vore (University of Kentucky, Lexington, KY). We optimized and obtained the multiple reaction monitoring (MRM) conditions for these two standards. Then we used the same MRM conditions to obtain chromatographs of tetrahydroxy BAs in BDL samples.

Zhang Y., Hong J.Y., Rockwell C.E., Copple B.L., Jaeschke H, & Klaassen C.D. (2011). EFFECT OF BILE DUCT LIGATION ON BILE ACID COMPOSITION IN MOUSE SERUM AND LIVER. Liver International, 32(1), 58-69.

Publication 2011

Chenodeoxycholic Acid Chromatography Liquid Chromatography Liver Methanol Serum Tandem Mass Spectrometry Taurine

Synthesis of Substituted Anilinyl-CDCA Conjugates

A series of substituted anilinyl conjugates glu-CDCA were synthesized using two synthetic approaches. In the first approach (used for synthesis of all targets except 2) α-benzyl glutamic acid was first coupled to CDCA via either N-hydroxysuccinimide (OSU) ester or benzotriazole (OBT) ester. Various substituted aniline probes were then coupled to glutamic acid by stirring either at RT or 60°C using O-Benztriazol-1-yloxytris-1,1,3,3 tetra methyl uranium hexaflourophosphate (HBTU) as the activating agent and triethylamine (TEA) as the base. The resulting neutral compounds were then subjected to hydrogenation in parr shaker for 1-2 h in ethanol (EtOH) and 10% palladium to remove the α-benzyl group, yielding the mono and dianionic targets. To synthesize 2 (Scheme 2), a second approach was needed.
All neutral compounds intermediates were purified by column chromatography using a gradient of hexane and ethyl acetate. All final target compounds were obtained as solids after deprotection. Identity and purity were confirmed by TLC, MS, NMR, and elemental analysis. All final target compounds possessed ≥95% purity.

Rais R., Acharya C., Tririya G., MacKerell AD J.r, & Polli J.E. (2010). Molecular Switch Controlling the Binding of Anionic Bile Acid Conjugates to Human Apical Sodium-dependent Bile Acid Transporter. Journal of medicinal chemistry, 53(12), 4749-4760.

Publication 2010

Anabolism aniline benzotriazole Chenodeoxycholic Acid Chromatography Esters Ethanol ethyl acetate Glutamic Acid Hexanes Hydrogenation Palladium Tetragonopterus triethylamine Uranium

Most recents protocols related to «Chenodeoxycholic Acid»

FXR Transactivation Assay Protocol

Direct FXR activity was evaluated using the LanthaScreen™ TR-FRET Farnesoid X Receptor Coactivator Assay kit (Cat# PV4833, ThermoFisher Scientific). Briefly, prepare a 12-point 100× dilution series of GDCA (Cat#IG2290, Solarbio), CDCA (Cat#IC0300, Solarbio), GW4064 (Cat# HY-50108, MCE) and GUDCA (Cat#IG0840, Solarbio) in a 96-well plate by serial dilution, respectively. Dilute each 100× serial dilution to 2× using Complete Coregulator buffer G. Then, the 2× serial dilutions were mixed with FXR-LBD-glutathione S-transferase fusion protein, fluorecein-SRC2-2 coactivator peptide and Lantha-screen Tb anti-GST antibody (Cat# PV4833, ThermoFisher Scientific, 1:1500) in the 384-well assay plate. Mix the 384-well plate and the TR-FRET signal was evaluated in a Multi-Mode Microplate Reader (Varioskan Flash, Thermo Fisher). Calculate the TR-FRET ratio by dividing the emission signal at 520 nm by the emission signal at 495 nm. Generate a binding curve by plotting the emission ratio vs. [ligand].

Tang B., Tang L., Li S., Liu S., He J., Li P., Wang S., Yang M., Zhang L., Lei Y., Tu D., Tang X., Hu H., Ouyang Q., Chen X, & Yang S. (2023). Gut microbiota alters host bile acid metabolism to contribute to intrahepatic cholestasis of pregnancy. Nature Communications, 14, 1305.

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Publication 2023

Antibodies, Anti-Idiotypic Biological Assay Buffers Chenodeoxycholic Acid Fluorescence Resonance Energy Transfer Glutathione S-Transferase GW 4064 Ligands Peptides Proteins Technique, Dilution

Comprehensive Bile Acid Profiling in Mice

Bile acids were extracted from liver, whole gallbladder bile, whole small intestine with content, and dried feces in 90% ethanol. Briefly, solid tissues and feces were homogenized in 90% ethanol and incubated at 50°C overnight. After centrifugation, the clear supernatant was used for total bile acid measurement with a bile acid assay kit. To collect fecal samples, an individual mouse was placed in a jar briefly and fresh feces were collected. Bile acid pool was calculated as the total bile acids in liver, gallbladder, and small intestine. For LC-MS analysis of bile acid composition, ethanol extracts were dried and then resuspended in injection buffer containing 0.1% formic acid in 1:1 water: mixture of acetonitrile and methanol (1:1) and subsequently analyzed on a Thermo Fisher Scientific UltiMate 3000 UHPLC with a Waters Cortecs C18 column (Waters Acquity UPLC HSS T3 1.8 um, 2.1x150 mm, part No. 186003540) and a TSQ Quantis triple quadrupole mass spectrometer. The running condition is as follow: Solvent A: 0.1% formic acid; Solvent B: 0.1% formic acid in 1:1 methanol: acetonitrile. Flow rate: 0.3 ml/min. Gradient: 52%–90% B in 18 min, 90% to 52%B in 0.1 min, hold for 4 min. Run time: 22 min. TSQ Quantis triple quadrupole mass spectrometer Ion Mode: Ion Source Type: H-ESI; Spray Voltage: Static; Negative Ion (V): 2500; Sheath Gas (Arb): 50; Aux Gas (Arb): 10; Sweep Gas (Arb): 1; Ion Transfer Tube Temp (°C): 325; Vaporizer Temp (°C): 350; Polarity: Negative; Cycle Time (sec): 0.8. Other LC-MS parameters (Retention time, ion monitoring) are listed in supplemental Table S1. Standard curves for bile acids and internal standard glyco-CDCA-d4 (G-CDCA-d4) were generated with purified compounds and relative area under the curve was calculated. To measure T-CDCA-d4 metabolism in fecal slurry mixtures, fresh fecal sample was resuspended in a reaction buffer consisting of 10% PBS (pH=7.4), and 90% 3 mM sodium acetate (pH = 5.2) to a final suspension of 4 mg fecal sample/ml. T-CDCA-d4 was added to a final concentration of 20 μg/ml and the mixture was incubated at 37°C for 6 h. An equal amount of methanol was added and the mixture was incubated on ice for 1 h to precipitate protein. After centrifugation, an aliquot of the supernatant was vacuum dried and resuspended in injection buffer. LC-MS measurement of bile acids was performed as described above.

Hasan M.N., Chen J., Matye D., Wang H., Luo W., Gu L., Clayton Y.D., Du Y, & Li T. (2023). Combining ASBT inhibitor and FGF15 treatments enhances therapeutic efficacy against cholangiopathy in female but not male Cyp2c70 KO mice. Journal of Lipid Research, 64(3), 100340.

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Publication 2023

acetonitrile Bile Bile Acids Biological Assay Buffers Centrifugation Chenodeoxycholic Acid Ethanol Feces formic acid Gallbladder Intestines, Small Liver Metabolism Methanol Mice, House Proteins Retention (Psychology) Sodium Acetate Solvents Tissues Vacuum Vaporizers

Bile Acid Metabolism and Liver Function Assay

Aspartate aminotransferase and alanine aminotransferase assay kits were purchased from Pointe Scientific (Canton. MI). GSK2330672 was purchased from MedChemExpress LLC (Monmouth Junction, NJ). Bile acid assay kit was purchased from Diazyme Laboratories (Poway, CA). AAV-FGF15 (under the control of an albumin promoter) was purchased from GeneCopoeia, Inc. (Rockville, MD). AAV-Null was purchased from Vector Biolabs Inc. (Malvern, PA). F4/80 antibody (Cat #. 70,076) was purchased from Cell Signaling Technology (Danvers, MA). Cytokeratin-19 antibody (ab52625) was purchased from Abcam (Waltham, MA). ZO-1 antibody (PA5-28858) was purchased from Thermo Fisher Scientific (Grand Island, NY).CDCA-d4 MaxSpec® Standard (CDCA-d4, No. 31366), tauro-conjugated CDCA-d4 MaxSpec® Standard (T-CDCA-d4, No. 31362), UDCA-d4 MaxSpec® Standard (UDCA-d4, No. 31368), and Tauro-conjugated UDCA-d4 MaxSpec® Standard (T-UDCA-d4, No. 31564) were purchased from Caymen Chemical Company (Ann Arbor, MI). FITC-dextran (MW:3000–5000) was purchased from Sigma Aldrich (St. Louis, MO).

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Publication 2023

Albumins Aspartate Transaminase Bile Acids Biological Assay Chenodeoxycholic Acid Cloning Vectors D-Alanine Transaminase fluorescein isothiocyanate dextran GSK2330672 Immunoglobulins Keratin-19 Ursodiol

Macrophage Activation by Hepatocyte Debris

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Publication 2023

Amino Acids antagonists Caimans Cells Chenodeoxycholic Acid Escherichia coli Glutamine Hepatocyte Lithocholic Acid Macrophage Macrophage Colony-Stimulating Factor Meglumine muricholic acid Mus Penicillins pregna-4,17-diene-3,16-dione, (17Z)-isomer Pyruvate Sodium Streptomycin TAK-242

Dual-Luciferase Reporter Assay for FXR

A dual-luciferase reporter assay was performed as described in our previous study (Hu et al., 2017 (link); Luo et al., 2016 (link)). Briefly, after being transfected with pBind FXR LBD and pGL5 luc and treated with CDCA and/or GUDCA, HEK-293T cells were lysed with 50 μL 1× passive lysis buffer. Then LAR II and Stop/Glo reagent were added respectively according to the manufacturer’s instructions. Luciferase fluorescence values were read using a multimode reader (Thermo, United States), and relative activity was normalized to Renilla luciferase fluorescence.

Zeng D., Zhang L, & Luo Q. (2023). Celastrol-regulated gut microbiota and bile acid metabolism alleviate hepatocellular carcinoma proliferation by regulating the interaction between FXR and RXRα in vivo and in vitro. Frontiers in Pharmacology, 14, 1124240.

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Publication 2023

Biological Assay Buffers Chenodeoxycholic Acid Fluorescence HEK293 Cells Luciferases Luciferases, Renilla

Top products related to «Chenodeoxycholic Acid»

Chenodeoxycholic acid by Merck Group

Sourced in United States, Germany, Switzerland, France, United Kingdom, Canada, Belgium

Chenodeoxycholic acid is a naturally occurring bile acid. It is a key component in the biosynthesis of bile salts and is involved in the regulation of cholesterol levels in the body.

Cholic acid by Merck Group

Sourced in United States, Germany, United Kingdom, Sao Tome and Principe, Switzerland, Canada, Japan, Macao, New Zealand, China

Cholic acid is a natural bile acid found in the human body. It is used as a basic laboratory compound for various research and analytical purposes.

Deoxycholic acid by Merck Group

Sourced in United States, Germany, United Kingdom, Switzerland, Belgium, China, Canada, France

Deoxycholic acid is a bile acid that is commonly used in laboratory settings. It is a white, crystalline powder with a molecular formula of C₂₄H₄₀O₄. Deoxycholic acid functions as a surfactant and is often utilized in various biochemical and cell biology applications.

Ursodeoxycholic acid by Merck Group

Sourced in United States, United Kingdom, Germany, Switzerland

Ursodeoxycholic acid is a chemical compound that is used as a pharmaceutical ingredient in various medical products. It is a naturally occurring bile acid that can be synthesized for use in laboratory and medical applications. The core function of ursodeoxycholic acid is to act as a bile acid and assist in the regulation of bile production and metabolism.

Lithocholic acid by Merck Group

Sourced in United States, Germany, United Kingdom, Switzerland

Lithocholic acid is a naturally occurring bile acid that is used in laboratory research and testing. It is a white, crystalline solid that is soluble in organic solvents. Lithocholic acid serves as a starting material or intermediate in the synthesis of other chemical compounds.

Taurocholic acid by Merck Group

Sourced in United States, United Kingdom, Switzerland, Germany, Sao Tome and Principe

Taurocholic acid is a bile acid that functions as a surfactant, facilitating the digestion and absorption of fats in the small intestine. It is a key component in the bile produced by the liver and plays a role in the emulsification and solubilization of lipids.

Taurochenodeoxycholic acid by Merck Group

Sourced in United States, Germany, United Kingdom, Switzerland

Taurochenodeoxycholic acid is a laboratory reagent used in biochemical research. It is a bile acid derivative that serves as a fundamental component in various analytical and experimental procedures. The core function of taurochenodeoxycholic acid is to facilitate specific chemical reactions and analyses in a controlled laboratory environment, though its precise applications may vary depending on the research context.

Glycocholic acid by Merck Group

Sourced in United States, Switzerland, United Kingdom, Germany

Glycocholic acid is a bile acid found in the human body. It is a crystalline compound that is used as a laboratory reagent in various biochemical and analytical applications.

Taurodeoxycholic acid by Merck Group

Sourced in United States, United Kingdom, Switzerland, Canada, Ireland

Taurodeoxycholic acid is a bile acid compound that is commonly used as a laboratory reagent. It serves as a solubilizing agent and is employed in various biochemical and cell culture applications.

Chenodeoxycholic acid cdca by Merck Group

Sourced in United States, Germany

Chenodeoxycholic acid (CDCA) is a laboratory chemical used in research and development. It is a naturally occurring bile acid found in the human body. CDCA is a primary bile acid that plays a role in the digestion and absorption of fats and fat-soluble vitamins. This chemical is commonly used in research applications, but its specific functions and intended uses should not be interpreted or extrapolated in this factual description.

What are the key functions of Chenodeoxycholic Acid in the body?

What are some of the therapeutic applications of Chenodeoxycholic Acid?

Are there different variations or types of Chenodeoxycholic Acid?

How can PubCompare.ai assist with Chenodeoxycholic Acid research?

PubCompare.ai's AI-driven platform can help researchers locate the best protocols from literature, preprints, and patents, using intelligenct comparisons to identify the most reliable and effective methods for Chenodeoxycholic Acid research. The platform allows you to screen protocol literature more efficiently, leveraging AI to pinpoint critical insights that can guide you towards the optimal use and comparison of Chenodeoxycholic Acid for your specific research goals. This can enhance reproducibility and accuracy in your Chenodeoxycholic Acid studies.

More about "Chenodeoxycholic Acid"

Chenodeoxycholic acid (CDCA) is a primary bile acid produced in the liver and plays a crucial role in the digestion and absorption of fats, cholesterol, and fat-soluble vitamins.
It is also known as chenodiol and can be used to treat certain liver and gallbladder disorders, such as gallstones and primary biliary cirrhosis.
CDCA is closely related to other bile acids like cholic acid, deoxycholic acid, ursodeoxycholic acid, and lithocholic acid, which are all involved in the bile acid metabolism and have various therapeutic applications.
Taurocholic acid, taurochenodeoxycholic acid, glycocholic acid, and taurodeoxycholic acid are also important bile acids that can conjugate with CDCA and affect its biological functions.
Research on the effective use of CDCA in therapeutic applications, such as treating liver and gallbladder conditions, is an active area of study.
PubCompare.ai's AI-driven platform can help researchers locate the best protocols from literature, preprints, and patents, using intelligent comparisons to identify the most reliable and effective methods for CDCA research.
Experience the power of data-driven insights and enhance the reproducibility and accuracy of your Chenodeoxycholic acid studiy.